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.
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 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 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.
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.
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.
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.
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.
In this article, a preliminary conceptual framework is presented for exploring nursing interventions and research aimed at improving care of the unconscious brain-injured patient during the early subacute phase of brain injury. The cue-response framework presented is derived from multidisciplinary sources and has specific clinical relevance to critical care nurses caring for unconscious brain-injured patients. A key aspect of this framework is the attention focused on the timing of nursing interventions in response to how nurses interpret the physical, physiological, and secondary cues they observe when caring for comatose patients. A case exemplar is used to present one example of how this framework may be used in the clinical setting.