Ketamine was discovered in the 1960s and released for public use in 1970. Originally developed as a safer alternative to phencyclidine, ketamine is primarily used in clinical settings for analgesia and sedation. In recent years, other uses have been developed, including pain management and treatment of asthma and depression. Clinical use of ketamine causes dissociation and emergence delirium. These effects have led to recreational abuse. Although death from direct pharmacologic effects appears rare, the disinhibition and altered sensory perceptions caused by ketamine puts users at risk of environmental harm. Ketamine has also been implicated in nonconsensual sexual intercourse. Data continue to build that chronic ketamine use may lead to morbidity. Impairment of memory and persistent dissociative, depressive, and delusional thinking has also been reported with long-term use. Lower urinary tract symptoms, including cystitis have been described. Gastric and hepatic pathology have also been noted, including abnormal liver function tests, choledochal cysts and dilations of the common bile duct. S-ketamine, an enantiomer in racemic ketamine, has been shown to be hepatotoxic in vitro. Abstinence from ketamine may reduce the adverse effects of chronic use and is considered the mainstay of treatment. Specialized urine drug testing may be required to detect use, as not all point of care urine drug screens include ketamine.

Objective: Dopamine administration results in variable effects on blood pressure in hypotensive preterm infants. The clinical benefits of dopamine administration in increasing cerebral blood flow (CBF) and reducing adverse neurological outcomes in hypotensive preterm neonates are unclear. The objective of this study was to examine the efficacy of dopamine for treatment of hypotension and investigate the changes in cerebral hemodynamics and central nervous system injury in hypotensive preterm infants following dopamine administration.Study Design: Standard meta-analytic techniques, including random and fixed effects models, were used to calculate combined effect size correlations and significance levels.Result: Random effects meta-analysis found that dopamine increases mean arterial blood pressure (12 studies; N ¼ 163; r ¼ 0.88, 95% confidence interval (CI) ¼ 0.76 to 0.94) and systolic blood pressure (8 studies; N ¼ 142; r ¼ 0.81, 95% CI ¼ 0.42 to 0.94). For the increase in blood pressure, dopamine administration was associated with a significantly greater overall efficacy than dobutamine (seven studies; N ¼ 251; r ¼ 0.26; 95% CI ¼ 0.20 to 0.32), colloid (two studies; N ¼ 67; r ¼ 0.60; 95% CI ¼ 0.41 to 0.74) and hydrocortisone (one study; N ¼ 28; r ¼ 0.40; 95% CI ¼ 0.034 to 0.67). CBF increased following dopamine administration (five studies; N ¼ 75; r ¼ 0.36; 95% CI ¼ À0.059 to 0.67) and the increase in CBF was greater in hypotensive than normotensive preterm infants (eight studies; N ¼ 153; r ¼ 0.16; 95% CI ¼ À0.0080 to 0.32). There were no statistically significant differences in adverse neurological outcome between dopamine and dobutamine (three studies; N ¼ 118; r ¼ À0.13; 95% CI ¼ À0.31 to 0.059), epinephrine (two studies; N ¼ 46; r ¼ 0.06; 95% CI ¼ À0.23 to 0.34), colloid (two studies; N ¼ 80; r ¼ 0.0070; 95% CI ¼ À0.218 to 0.23) or hydrocortisone administration (one study; N ¼ 40; r ¼ À0.10; 95% CI ¼ À0.40 to 0.22).Conclusion: Dopamine administration increases mean and systolic blood pressure in hypotensive preterm infants, and is more effective than dobutamine, colloid or hydrocortisone alone. Dopamine administration is associated with increased CBF, with greater increases in CBF in hypotensive than in normotensive preterm infants. Dopamine is not associated with a greater incidence of adverse effects than other therapies used to treat hypotension.

Delirium is a neuropsychiatric disorder characterized by acute disturbances in attention, consciousness, cognitive processing, perception, and the sleep-wake cycle. The few studies investigating treatment of delirium in critically ill children and adolescents have used differing diagnostic criteria, and have not employed control groups or procedures to blind observations. The objective of this study was to examine the efficacy of olanzapine for the treatment of delirium in the pediatric intensive care unit (ICU) using methodological procedures to reduce bias and allow greater generalization. Psychiatric records of 59 patients admitted to the pediatric ICU or cardiothoracic ICU over a 4 yr period with the diagnosis of delirium were examined. The delirium rating scale was used to assess delirium severity at the time of initial psychiatric evaluation and five days later. Raters were blinded to medication administration. Patients who were diagnosed with delirium, but did not receive olanzapine, or any other antipsychotic medication, served as the control group. Greater improvement of delirium symptoms was found for the olanzapine group (n?=?31) than the control group (n?=?28) (F (1,40)?=?4.86, r?=?0.33, 95% confidence interval?=?0.020?0.58). This finding remained statistically significant after controlling for initial delirium severity (F (1, 20)?=?28.62, r?=?0.77, 95% confidence interval?= 0.50?0.90). This study demonstrates patients with delirium administered olanzapine had greater reduction of delirium symptom severity than controls. It supplements the existing literature by using a study design that reduces expectancy effects and allows examination of the natural history of delirium symptoms without medication administration.