ABSTRACT
Quantitative pupillometry provides a noninvasive and objective assessment within the neurological examination. This review details the physiology of the pupillary light response, the clinical significance of changes in pupillary reactivity, and the variables that compose the Neurological Pupil index or NPi are discussed. This article reviews the most recent applications and advances in quantitative pupillometry for noninvasive intracranial pressure monitoring, postcardiac arrest prognostication, and subarachnoid hemorrhage. Also discussed are the limitations and confounders of quantitative pupillometry in the modern neurological intensive care unit.
Subject(s)
Neurologic Examination , Reflex, Pupillary , Heart Arrest/diagnosis , Humans , Intensive Care Units , Intracranial Pressure , Pupil , Subarachnoid Hemorrhage/diagnosisABSTRACT
As intracerebral hemorrahge becomes more frequent as a result of an aging population with greater comorbidities, rapid identification and reversal of precipitators becomes increasingly paramount. The aformentioned population will ever more likely be on some form of anticoagulant therapy. Understanding the mechanisms of these agents and means by which to reverse them early on is critical in managing the acute intracerebral hemorrhage.
Subject(s)
Anticoagulants/adverse effects , Blood Coagulation/drug effects , Cerebral Hemorrhage/therapy , Coagulants/therapeutic use , Factor Xa Inhibitors/adverse effects , Plasma , Warfarin/adverse effects , Antibodies, Monoclonal, Humanized/therapeutic use , Blood Coagulation Factors/therapeutic use , Cerebral Hemorrhage/blood , Cerebral Hemorrhage/chemically induced , Coagulants/adverse effects , Factor VIIa/therapeutic use , Factor Xa/therapeutic use , Humans , Recombinant Proteins/therapeutic use , Treatment Outcome , Vitamin K/antagonists & inhibitors , Vitamin K/therapeutic useABSTRACT
This report describes the successful management of a case of central neurogenic hyperventilation (CNH) refractory to high dose sedation by increasing the mechanical dead space. A 46-year-old male presented with a history of multiple neurological symptoms. Following an extensive evaluation, he was diagnosed with primary diffuse CNS lymphoma and started on high dose steroids. After initial symptomatic improvement, the patient developed increasing respiratory distress and tachypnea. He was intubated and transferred to the neurointensive care unit (neuro ICU). While in the ICU the patient remained ventilator dependent with significant tachypnea and respiratory alkalosis resistant to fentanyl and propofol. This prompted an attempt to normalize the PaCO2 via an increase of the mechanical dead space. This approach successfully increased PaCO2 and bridged the patient until ongoing therapy for the underlying disease resolved the pervasive breathing pattern typical of CNH. Further investigation is warranted to evaluate this strategy, which upon review of the literature appears underused.
ABSTRACT
Induced hypothermia has been used for neuroprotection in cardiac and neurovascular procedures. Experimental and translational studies provide evidence for its utility in the treatment of ischemic cerebrovascular disease. Over the past decade, these principles have been applied to the clinical management of acute stroke. Varying induction methods, time windows, clinical indications, and adjuvant therapies have been studied. In this article the authors review the mechanisms and techniques for achieving therapeutic hypothermia in the setting of acute stroke, and they outline pertinent side effects and complications. The manuscript summarizes and examines the relevant clinical trials to date. Despite a reasonable amount of existing data, this review suggests that additional trials are warranted to define the optimal time window, temperature regimen, and precise clinical indications for induction of therapeutic hypothermia in the setting of acute stroke.
