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Since the first human electroencephalogram (EEG) was recorded in 1929 by Hans Berger, enormous advances have been made in EEG recording technology and data analysis [, ]. The recording period was extended and long-term EEG monitoring became technically feasible when computer applications were introduced in the 1970s and digital EEG recording systems established. However, the use of long-term EEG monitoring was mostly limited to epilepsy monitoring units and only subsequently found its way to the intensive care unit (ICU).

Stroke remains a major source of morbidity and mortality throughout the world representing the third leading cause of death in North America and the second leading cause of death in Asia []. Large hemispheric strokes account for a majority of these deaths and represent a significant proportion of stroke patients treated in an intensive care unit (ICU). Our understanding of the secondary processes that occur after the initial stroke has changed our approach to the management of this population. We will review and discuss the new management strategies that have been developed to decrease the morbidity and mortality of patients with large hemispheric infarctions.

Acute brain injury is a frequent cause of disability and death worldwide. Common forms of acute brain injury include perinatal birth asphyxia, traumatic brain injury (TBI), stroke, and out-of-hospital cardiac arrest. These conditions affect patients with a wide age range from the young to the elderly. Interruption of cerebral oxygen and nutrient delivery by cardio-respiratory insufficiency or by a vascular lesion may precipitate cerebral ischemia. The initial pathology may not induce immediate cell death, but can precipitate a complex biochemical cascade leading to delayed neuronal loss, the end result being death or disability (Fig. 1). This chapter reviews the current evidence on temperature reduction after neuronal injury.

Non-traumatic subarachnoid hemorrhage (SAH) has distinct risk factors, demographics, and treatment from other forms of stroke. Spontaneous SAH, mostly aneurysmal, accounts for about 2–5% of all strokes, afflicting 37,500 cases of stroke per year in the United States []. A cerebral aneurysm is an outpouching of the brain arteries that eventually ruptures. The incidence of non-traumatic aneurysmal SAH has remained stable over the past 30 years []. Although the incidence of non-traumatic SAH varies from region to region, the aggregate worldwide incidence is about 10.5 per 100,000 person years [, ]. Women have a 1.6 times (95% confidence interval [CI] 1.5–2.3) higher risk than men [] and people of African descent a 2.1 times (95% CI 1.3–3.6) higher risk than whites []. The major risk factors for non-traumatic SAH include cigarette smoking, hypertension, cocaine use, and habitual heavy alcohol intake []. Other factors, such as a family history of first-degree relatives with the disease and heritable connective-tissue disorders, also play a role [].

Management strategies for subarachnoid hemorrhage (SAH) include early aneurysm obliteration, pharmacologic prevention of vasospasm, therapeutic (but not prophylactic) hyperdynamic therapy, targeted critical care, and rehabilitation. Despite recent advances, major gaps in our knowledge remain, and many potentially salvageable patients have devastating outcomes. Neuroprotective, prognostic, and pharmacologic developments are especially promising. This chapter highlights areas of intensive study in SAH management, with hopes that the efforts of dedicated clinician-scientists will come to fruition in the near future. I mean to highlight promising areas of active study with preliminary data or research funding, not today’s state-of-the-art. There are no express or implied guarantees about actual progress.

Nitric oxide (NO) is a cell membrane-permeable free radical gas and is the smallest known biologically active molecule. NO can be produced by nearly all tissues of the body. NO is synthesized from the semi-essential amino acid, L-arginine, by the enzyme, nitric oxide synthase (NOS). Three isoforms of NOS exist: Endothelial (eNOS), neuronal (nNOS), and inducible (iNOS). Agents that selectively inhibit the individual isoforms of NOS, as well as transgenic mice that are deficient in each of the isoforms of NOS, have played important roles in understanding the normal functions of NO and the changes in NO metabolism that occur with neurological disorders like traumatic brain injury (TBI) [].

The modulation of arterial pressure is an important stage in the care of a patient with a cerebral lesion. International guidelines recommend a level of cerebral perfusion pressure (CPP = mean arterial pressure [MAP] – intracranial pressure [ICP]) that is superior to 60 mmHg. On the other hand, a level that exceeds 70 mmHg in the absence of cerebral ischemia must be avoided given the risk of acute respiratory distress syndrome (ARDS) []. Moreover, a single episode of hypotension defined as systolic arterial pressure <90 mmHg in a patient with severe head trauma is associated with an increase in mortality and morbidity [].

Until a few years ago, the occurrence of delirium or ‘intensive care unit (ICU) psychosis’ was regarded as a routine feature of life in the ICU. Delirium occurred with such a high frequency that it was often considered to be a routine consequence of prolonged stay — a combined effect of the patient’s underlying illness and perhaps the administration of large amounts of sedatives.

The natural history of serious burns is characterized by burn shock, which can be fatal within the first few hours to days, particularly in those with untreated large burns. Burn wound sepsis is the major cause of mortality among those who survive the burn shock. Survival and outcome after major burn injury have improved over the last 20 years due to improved understanding of the pathophysiologic nature of burn injury, better resuscitation, and advances in control of post-burn sepsis including early, aggressive surgical treatment [].

Burns account for around 700,000 emergency department visits every year resulting in around 50,000 admissions to hospital in the United States []. Around 50% of these admissions have burns of less than 10% total body surface area (TBSA) and, as such, have near normal metabolic rates. For the remainder, the rise in metabolic rate is linked to burn size and for those with severe thermal injuries (>40% TBSA) the change in patient metabolism is, if left unchecked, set to last for more than 12 months. The change contributes, at least in part, to long term deleterious effects on the individual. It has been previously shown that the ensuing period of hypermetabolism and catabolism following a severe burn leads to impaired immune function, decreased wound healing, erosion of lean body mass, and hinders rehabilitative efforts delaying reintegration into normal society. However, the magnitude and longevity of these changes has yet to be fully elucidated. Strategies for attenuating these maladaptive responses may be divided into pharmacological and non-pharmacological. Non-pharmacological approaches include prompt, early excision and closure of wounds, pertinacious surveillance for and treatment of sepsis, early commencement of high protein high carbohydrate enteral feeding, elevation of the immediate environmental temperature to 31.5°C (± 0.7°C), and early institution of an aerobic resistive exercise program. Several pharmacotherapeutic options are also available to further reduce metabolic rate and as such attenuate the erosion of lean body mass; these include anabolic agents such as recombinant human growth hormone, insulin, and oxandrolone and also beta blockade using propranolol.