Medicina
-
The dangers of opioid overdose have been recognized for as long as the use of opium itself. When used correctly for medical purposes, opioids are remarkably safe and effective agents. ⋯ In a number of countries the use of heroin and other opioids in nonmedical contexts in associated with on increasing rate of overdose and often of fatal opioid overdose. This review article discusses opioid-receptor pharmacology, which is necessary for understanding of the signs and symptoms of opioid ingestion and management principles, clinical and toxic effects mediated with the opioids, the diagnosis and management guidelines in opioid intoxication, a clinical prediction rule to identify patients who can be safely discharge from hospital, the problems of the significant morbidity and mortality associated with opioid overdose.
-
Amniotic fluid embolism is a rare obstetric emergency in which amniotic fluid, fetal cells, hair, or other debris enters the maternal circulation. Amniotic fluid embolism is an incompletely understood obstetric complication unique to pregnancy presenting with the acute onset of hypoxia, hypotension and severe coagulopathy. ⋯ It cannot be predicted nor prevented. The epidemiology of amniotic fluid embolism, frequency, pathophysiology, clinical presentation, histologic findings, diagnosis, differential diagnosis, possible treatment, mortality rate, neonatal survival are discussed in this review article.
-
Severe acute adrenocortical insufficiency or adrenal crisis are often elusive diagnoses that may result in severe morbidity and mortality when undiagnosed or ineffectively treated. Although more than 50 steroids are produced within the adrenal cortex, cortisol and aldosterone are far the most abundant and physiologically active. In primary adrenocortical insufficiency, glucocorticoid and mineral-corticoid properties are lost; however, in secondary adrenocortical insufficiency (i.e., secondary to disease or suppression of the hypothalamic-pituitary axis), mineralocorticoid function is preserved. ⋯ The initial diagnosis and decision to treat are presumptive and are based on history, physical examination, and, occasionally, laboratory findings. Delay in treatment while attempting to confirm this diagnosis can result in poor patient outcomes. This article review data about physiology, pathophysiology of the adrenal cortex, physiologic effects of glucocorticoids, aldosterone, causes of primary and secondary adrenal insufficiency, frequency, clinical picture, laboratory and imaging studies of adrenal crisis, laboratory evaluation of adrenal function and emergency therapy, replacement therapy, mortality/morbidity of this pathology.
-
Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called noninsulin-dependent diabetes mellitus) is not as rare as was once thought. ⋯ The review discusses diagnostic procedures, laboratory evaluation, differential diagnosis and treatment: replacement of fluid and electrolytes, low-dose insulin therapy and recommendations for use of bicarbonate. A discussion of complications management of diabetic ketoacidosis (hypoglycemia, hypokalemia, cerebral edema, hyperchloremic metabolic acidosis, pulmonary edema, adult respiratory distress syndrome), mortality rate and prevention are included in this review.
-
Focal cerebral contusions can be dynamic and expansive, leading to a delayed neurological deterioration. In head--injured patients, the rise in intracranial pressure (ICP), subsequent to uncontrollable swelling, is the only and the most frequent cause of death. Studies show that brain swelling, after traumatic brain injury (TBI), is caused by brain edema rather than cerebral blood volume (CBV). ⋯ Histologically the loss of CA3 pyramidal cells in the hippocampus was observed ipsilaterally in the cortical contusion and bilaterally in diffuse axonal injury. Aggressive, early hyperventilation after TBI augments neuronal death in CA3 hippocampus. Due to high mortality associated with such cerebral contusions, a standard practice has evolved into evacuating contusions in patients who had deterioration in the level of consciousness, lesions more than 30 sec and CT suggestion of raised ICP.