Specific independent predictors of CPRA in medical vs. surgical patients on opioid and sedative therapy.

<p>Specific independent predictors of CPRA in medical vs. surgical patients on opioid and sedative therapy.</p

Risk factors for cardiopulmonary and respiratory arrest in medical and surgical hospital patients on opioid analgesics and sedatives

<div><p>Background</p><p>Opioid induced respiratory depression is a known cause of preventable death in hospitals. Medications with sedative properties additionally potentiate opioid-induced respiratory and sedative effects, thereby elevating the risk for adverse events. The goal of this study was to determine what specific factors increase the risk of in-hospital cardiopulmonary and respiratory arrest (CPRA) in medical and surgical patients on opioid and sedative therapy.</p><p>Methods</p><p>The present study analyzed 14,504,809 medical inpatient and 6,771,882 surgical inpatient discharges reported into the Premier database from 2008 to 2012. Patients were divided in four categories: on opioids; on sedatives; on both opioids and sedatives; and on neither opioids nor sedatives.</p><p>Results</p><p>During hospital admission, 57% of all medical patients and 90% of all surgical patients were prescribed opioids, sedatives, or both. Surgical patients had a higher incidence of CPRA than medical patients (6.17 vs. 3.77 events per 1000 admissions; Relative Risk: 1.64 [95%CI: 1.62–1.66; <i>p</i><0.0001). Opioids and sedatives were found to be independent predictors of CPRA (adjusted OR of 2.24 [95%CI: 2.18–2.29] for opioids and adjusted OR 1.80 [95%CI: 1.75–1.85] for sedatives in medical patients, and adjusted OR of 1.12 [95%CI: 1.07–1.16] for opioids and adjusted OR of 1.58 [95%CI: 1.51–1.66] for sedatives in surgical patients), with the highest risk in groups who received both types of medications (adjusted OR of 3.83 [95% CI: 3.74–3.92] in medical patients, and adjusted OR of 2.34 [95% CI: 2.25–2.42] in surgical patients) compared with groups that received neither type of medication. The common risk factors of CPRA in medical and surgical patients receiving both opioids and sedatives were Hispanic origin, mild liver disease, obesity, and COPD. Additionally, medical and surgical groups had their own unique risk factors for CPRA when placed on opioid and sedative therapy.</p><p>Conclusions</p><p>Opioids and sedatives are independent and additive predictors of CPRA in both medical and surgical patients. Receiving both classes of medications further exacerbates the risk of CPRA for these patients. By identifying groups at risk among medical and surgical in-hospital patients, this study provides a step towards improving our understanding of how to use opioid and sedative medications safely, which may influence our treatment strategies and outcomes. More precise monitoring of selected high-risk patients may help prevent catastrophic cardiorespiratory complications from these medications. As a retrospective administrative database analysis, this study does not establish the causality or the temporality of the events but rather draws statistically significant associations between the clinical factors and outcomes.</p></div

Incidence of CPRA in medical vs. surgical patients on sedatives, opioids, both sedatives and opioids, or neither sedatives nor opioids.

<p>Incidence of CPRA in medical vs. surgical patients on sedatives, opioids, both sedatives and opioids, or neither sedatives nor opioids.</p

Using heart rate variability to stratify risk of obstetric patients undergoing spinal anesthesia.

In this study, we evaluated whether point correlation dimension (PD2), a measure of heart rate variability, can predict hypotension accompanying spinal anesthesia for cesarean delivery. After the administration of spinal anesthesia with bupivacaine, hypotension was defined as systolic blood pressur

Multivariable logistic regression analysis of the incidence of CPRA.

<p>Multivariable logistic regression analysis of the incidence of CPRA.</p

Cocaine is pharmacologically active in the nonhuman primate fetal brain

Cocaine use during pregnancy is deleterious to the newborn child, in part via its disruption of placental blood flow. However, the extent to which cocaine can affect the function of the fetal primate brain is still an unresolved question. Here we used PET and MRI and show that in third-trimester pregnant nonhuman primates, cocaine at doses typically used by drug abusers significantly increased brain glucose metabolism to the same extent in the mother as in the fetus (∼100%). Inasmuch as brain glucose metabolism is a sensitive marker of brain function, the current findings provide evidence that cocaine use by a pregnant mother will also affect the function of the fetal brain. We are also unique in showing that cocaine’s effects in brain glucose metabolism differed in pregnant (increased) and nonpregnant (decreased) animals, which suggests that the psychoactive effects of cocaine are influenced by the state of pregnancy. Our findings have clinical implications because they imply that the adverse effects of prenatal cocaine exposure to the newborn child include not only cocaine’s deleterious effects to the placental circulation, but also cocaine’s direct pharmacological effect to the developing fetal brain