The metabolic syndrome is a clinical condition that is a powerful predictor for cardiovascular morbidity and mortality. Hypertension, abdominal obesity, high blood glucose levels, and abnormal blood lipid levels characterize metabolic syndrome. Therapeutic treatment of the metabolic syndrome confers a significant risk reduction for both type 2 diabetes and premature cardiovascular events. In the hospital setting, the management of hyperglycemia, one of the clinical components of the metabolic syndrome, has been secondary in importance to the condition that prompted admission. Hyperglycemia in the hospitalized patient has been associated with increased lengths of stay, higher rates of hospital-acquired infections, and increased mortality. Early recognition and treatment of hyperglycemia and the associated metabolic components that comprise the metabolic syndrome may reduce morbidity and mortality in the hospital setting. More aggressive interventions will aid in reducing costs while simultaneously improving patient care and safety.

The endocrine system maintains a delicate balance of physiologic processes including growth and sexual maturation, energy production and utilization, fluid and electrolyte balance, and circulatory function. Although endocrine regulation of growth and sexual maturation is a significant issue in general pediatrics, disorders of energy production and utilization, fluid and electrolyte balance, and circulatory function are the endocrine causes of critical illness in children. Care of the child with critical endocrine disease requires an understanding of endocrine pathophysiology, keen history taking and assessment skills, and knowledge of the pharmacology of synthetic hormone treatment. This article will provide an overview of common endocrine problems encountered in critically ill children with attention to endocrine problems that are unique to pediatrics and that may pose diagnostic and treatment dilemmas for healthcare providers without experience or education in pediatric critical care.

The prevalence of diabetes mellitus makes the occurrence of hyperglycemic emergencies a key component in clinical practice. The expert nurse is well positioned to manage both diabetic ketoacidosis and hyperosmolar hyperglycemic states. Patient care management includes a high index of suspicion for awareness for the possibility of diabetic ketoacidosis or hyperosmolar hyperglycemic states in patients based on a multifactorial etiology, evidence-based treatment of the emergent episode, and tertiary prevention to prevent recurrent episodes.

Hyperglycemia and insulin resistance are common among critically ill patients and occur in patients with or without a history of diabetes mellitus. All patients undergoing critical illness are at risk for stress-induced hyperglycemia. Some patients may be at greater risk for hyperglycemia than others when considering underlying disease states and iatrogenic factors. Many recent studies demonstrate that tight glucose control can decrease morbidity and mortality associated with critical illness. This article reviews the pathophysiology behind stress-induced hyperglycemia, the evidence to support tight glycemic control, and the importance of an intensive insulin therapy protocol to standardize treatment among critical care patients.

Severe stress, associated with critical illness, activates the hypothalamic- pituitary-adrenal (HPA) axis and stimulates the release of cortisol from the adrenal cortex. Cortisol is essential for general adaptation to stress and plays a crucial role in cardiovascular, metabolic, and immunologic homeostasis. During critical illness, prolonged activation of the HPA axis can result in hypercortisolemia and hypocortisolemia; both can be detrimental to recovery from critical illness. Recognition of adrenal dysfunction in critically ill patients is difficult because a reliable history is not available and laboratory results are difficult to interpret. The review in this article will illustrate how adrenal dysfunction presents in critically ill patients and how appropriate diagnosis and management can be achieved in the critical care setting.

One of the most debilitating neurological complications of human immunodeficiency virus (HIV), affecting nearly one in three patients, is painful peripheral neuropathy. Although HIV infection can cause distal sensory polyneuropathy (DSP), the advent of highly active antiretroviral therapy (HAART) to treat HIV infection has resulted in a significant number of patients developing a clinically indistinguishable form of toxic neuropathy. The predominant symptom, regardless of etiology, is excruciating unremitting pain, resistant to pharmacological treatments, that leads to a reduction in the ability to conduct activities of daily living and, eventually, inability to ambulate. Since withdrawal from nucleoside therapy is not typically recommended, a more thorough understanding of the etiology and pathophysiology underlying nucleoside-induced peripheral neuropathy, through basic and clinical research endeavors, will aid in the development of new therapeutic treatments aimed at alleviating or ameliorating pain. This article provides the latest information regarding the pathophysiology and clinical implications of HIV peripheral neuropathy.

More than one million Americans have been diagnosed with human immunodeficiency virus (HIV). Advances in prevention and treatment of HIV have led to an increased life expectancy for patients with HIV infection. Due to their increased life span, HIV+ patients are now presenting to hospitals with an increased number of diverse late-stage complications, such as cardiomyopathy and other cardiovascular conditions. These complications are as a direct or indirect result of HIV disease, HIV treatment modalities, comorbid conditions, dietary and lifestyle factors, and unknown etiologies. Cardiac complications, particularly HIV-related dilated cardiomyopathy, are potentially life-threatening diagnoses, with symptoms that may be minimized with appropriate cardiac-specific assessments and treatments, patient teaching, and collaboration among nurses caring for the HIV-positive client with cardiac disease.

The introduction of highly active antiretroviral therapy (HAART) has transformed human immunodeficiency virus (HIV) infection from a rapidly progressive catastrophic illness to a chronic condition. Individuals with HIV are living longer and developing conditions usually associated with aging, as well as complications from pre-existing or subsequently acquired conditions. In addition, toxicities associated with HAART may precipitate or exacerbate comorbid conditions. As opportunistic infections account for fewer admission and lower mortality rates, new patterns of illness are emerging. Complex interactions among multiple, sometimes overlapping conditions require focused yet comprehensive attention in care and management. Nurses will encounter HIV-infected patients in an increasing range of care settings, and an understanding of the range and interaction of potential comorbidities and their treatments with HIV and its treatment will be required to provide safe and effective care.

The Institute of Medicine report published in 1999 described a healthcare system in which 44,000 to 98,000 patients die each year from preventable medical errors. The healthcare industry has been charged with identifying and ameliorating risks to patients. The advanced practice nurse is in the optimal position to influence the patient care environment and contribute to a culture of patient safety. This article will review the role of the advanced practice nurse in the care of the neuroscience patient in identifying risks unique to this at-risk population. There will be a discussion of risk factors that contribute to errors, with advanced practice nurse-driven, evidence-based solutions. A case presentation of the role of the advanced practice nurse in reducing the incidence of deep vein thrombosis in the craniotomy patients with malignant tumors will be discussed.

There is a critical mismatch between available organs for transplant and acutely or critically ill patients with end-stage organ disease. Patients who may benefit from organ transplantation far outnumber available organs. The causes for this imbalance are multiple. One cause is family refusal to donate. A second cause is nonrecognition or delay in determination of brain death. A third cause is donor loss due to profound cardiopulmonary and metabolic instability consequent to brain-stem herniation and brain death. Family refusal may be addressed by education, public awareness, as well as close attention to social, cultural and ethical issues, and optimal communication with donor families. Brain death may be consequent to traumatic brain injury, ischemic versus hemorrhagic stroke, as well as massive cerebral anoxia/ischemic following cardiac arrest. Nonrecognition or delay in brain death determination may be addressed by clinician education and frequent clinical assessment to detect early stages of brain-stem herniation refractory to aggressive measures for control of intracranial pressure. Donor loss due to profound cardiopulmonary and metabolic instability may be addressed by aggressive, mechanism-based treatment for clinical instability based on affected body system, as well as measures to support metabolic activity at the cellular and tissue level in the brain-dead organ donor. This article explores cerebral physiology related to impending brain death and catastrophic intracranial pressure elevations. In addition, physiologic consequences of brain death are correlated with affected body systems and mechanism-based therapies to support organ function pending transplantation. Ethical/legal issues are explored as related to patient autonomy and optimal family outcomes. Effective family communication, astute clinical assessment, and optimal clinical management of the organ donor are illustrated using a case study approach, highlighting the role of the advanced practice nurse in donor management.

The goal of palliative care is to provide the alleviation or reduction of suffering and the support for the best possible quality of life for patients regardless of the stage of the disease. Palliative care can be provided in any patient care setting, including intensive care units. Death in intensive care units is a common occurrence, with literature suggesting that approximately 20% of deaths in the United States occur after a stay in the intensive care unit. Other studies suggest that approximately half of all chronically ill patients who die in a hospital receive care in the intensive care unit within 3 days of their deaths. Critical care nurses who work in neurological intensive care units are at the forefront of integrating palliative and critical care.

Patients with severe traumatic brain injury resulting in increased intracranial pressure refractory to first-tier interventions challenge the critical care team. After exhausting these initial interventions, critical care practitioners may utilize barbiturate-induced coma in an attempt to reduce the intracranial pressure. Titrating appropriate levels of barbiturate is imperative. Underdosing the drug may fail to control the intracranial pressure, whereas overdosing may lead to untoward effects such as hypotension and cardiac compromise. Monitoring for a therapeutic level of barbiturate coma includes targeting drug levels and using continuous electroencephalogram monitoring, considered the gold standard. New technology, the Bispectral Index monitor, utilizes electroencephalogram principles to monitor the level of sedation and hypnosis in the critical care environment. This technology is now being considered for targeting appropriate levels of barbiturate coma.

Aneurysmal subarachnoid hemorrhage is an increasing problem in the United States, affecting approximately 30,000 people every year. Despite advances in the neurosurgical field, approximately 50% of patients die within the first month after hemorrhage. Traditionally, craniotomy with aneurysmal clipping has been employed to manage these patients, but endovascular embolization is moving to the forefront of treatment, particularly for high grade (IV to V) aneurysms. Patient selection is often based on age, aneurysm size, location, characteristics and presentation, and patient hemodynamics. Postprocedure management relies on skilled observers to determine those potential complications that may occur, including vasospasm, rupture, bleeding, or vessel occlusion. Advanced practice nurses have an obligation to be aware not only of the procedure and its management, but also of the potential complications and ongoing care of the patients and families as well.

Use of technology in the management of the severely brain-injured patient has increased over the past decade and can be confusing and overwhelming to the critical care nurse clinicians who are new to the field of neurology. This article will describe normal physiology and cerebral dynamics and potential abnormal physiology encountered after brain injury. The technology reviewed will include intracranial pressure monitoring, cerebral blood flow monitoring and autoregulation, cerebral oxygen consumption and tissue oxygen monitoring, metabolism, sedation, and temperature monitoring. Integration of appropriate technology into patient management will be discussed using a case study to explore the utility of information at the bedside. Recognizing the difficult task of trying to control secondary injury in our patients is the first step to better outcomes. Implementing the use of technology to mitigate the situation must be done with careful consideration and a team approach to achieve the greatest benefit for the patient.

The brain is extraordinarily susceptible to changes in temperature. Hyperthermia has been shown to exacerbate the biochemical cascade of secondary brain injury. Inversely, hypothermia limits the damaging effects of secondary brain injury. There has been a great deal of investigation regarding the detrimental effects of hyperthermia and the neuroprotection of hypothermia in animal studies. Within the last decade, clinical trials have begun to establish how the brain reacts to both temperature extremes. In the future, studies of hypothermia will continue in the quest of the optimal timing and degree of hypothermia. Hyperthermia will be examined in depth for its detrimental effects on an injured brain. Interventions for the prevention and treatment of hyperthermia will be explored. Nurses will implement cooling strategies to induce hypothermia, applying interventions to prevent complications, and they will also diagnose hyperthermia, deciding when and if to intervene pharmacologically and therapeutically. These advanced nursing actions will be guided by knowledge and understanding of available evidence. This article presents the pathophysiology of secondary brain injury and how it is affected by both hypothermia and hyperthermia. A review of the research leading up to clinical trials is explored, as well as a discussion of the future of temperature modulation for the brain injury patient. This information will help healthcare providers understand the effect that both hypothermia and hyperthermia have on the acutely injured brain.