Improving Linkage for Patients With Injection-Drug-Use-Related Endocarditis and Osteomyelitis to Medications for Opioid Use Disorder Through a Telephone Intervention.

ABSTRACT: The opioid overdose crisis has continued to worsen, with a concomitant increase in serious injection-related infections, such as endocarditis and osteomyelitis. Usual care of these infections involves long-term intravenous antibiotics, typically administered via a peripherally inserted central venous catheter (PICC) at home. In patients with a history of opioid use disorder who inject drugs, a PICC has long been viewed as a high-risk intervention that may contribute to illicit substance use due to ease of venous access; thus, providers are often uncomfortable discharging these patients home to complete their antibiotics. As a result, many patients remain hospitalized or are discharge to skilled nursing facilities (SNFs) in order to complete their antibiotics. Challenges to this model include difficulty finding SNFs that will accept these patients, inability for these SNFs to continue their medication for opioid use disorder (MOUD), and inability to coordinate care with outpatient MOUD providers at SNF discharge. This quality improvement project sought to increase linkage to outpatient MOUD on SNF discharge via a telephone intervention. A total of 11 patients qualified for this intervention. Although patients were still in an SNF, 4/7 (57.1%) of patients were successfully contacted. Once they were discharged from the SNF, only 3/10 (30.0%) of patients were successfully reached. Of those 30.0% who were contacted, all of them had attended their outpatient MOUD appointment. We suggest that future linkage interventions in this population may benefit from utilizing existing care team members to facilitate linkage, to maximize the rapport built during an inpatient stay.

The Transition Trajectory for the Patient with a Traumatic Brain Injury.

The trajectory status of patients with mild, moderate, and severe traumatic brain injury from emergency room evaluation, through acute care (intensive care if severe) and discharge is discussed. Additional considerations for elderly population and common complications associated with severe traumatic brain injury are also covered.

Effect of neuromonitor-guided titrated care on brain tissue hypoxia after opioid overdose cardiac arrest.

INTRODUCTION: Brain tissue hypoxia may contribute to preventable secondary brain injury after cardiac arrest. We developed a porcine model of opioid overdose cardiac arrest and post-arrest care including invasive, multimodal neurological monitoring of regional brain physiology. We hypothesized brain tissue hypoxia is common with usual post-arrest care and can be prevented by modifying mean arterial pressure (MAP) and arterial oxygen concentration (PaO2). METHODS: We induced opioid overdose and cardiac arrest in sixteen swine, attempted resuscitation after 9 min of apnea, and randomized resuscitated animals to three alternating 6-h blocks of standard or titrated care. We invasively monitored physiological parameters including brain tissue oxygen (PbtO2). During standard care blocks, we maintained MAP > 65 mmHg and oxygen saturation 94-98%. During titrated care, we targeted PbtO2 > 20 mmHg. RESULTS: Overall, 10 animals (63%) achieved ROSC after a median of 12.4 min (range 10.8-21.5 min). PbtO2 was higher during titrated care than standard care blocks (unadjusted ß = 0.60, 95% confidence interval (CI) 0.42-0.78, P < 0.001). In an adjusted model controlling for MAP, vasopressors, sedation, and block sequence, PbtO2 remained higher during titrated care (adjusted ß = 0.75, 95%CI 0.43-1.06, P < 0.001). At three predetermined thresholds, brain tissue hypoxia was significantly less common during titrated care blocks (44 vs 2% of the block duration spent below 20 mmHg, P < 0.001; 21 vs 0% below 15 mmHg, P < 0.001; and, 7 vs 0% below 10 mmHg, P = .01). CONCLUSIONS: In this model of opioid overdose cardiac arrest, brain tissue hypoxia is common and treatable. Further work will elucidate best strategies and impact of titrated care on functional outcomes.

Traumatic shock: the fifth shock.

Although, historically, shock associated with traumatic injury has been evaluated through knowledge of the 4 recognized shock patterns--cardiogenic, obstructive, distributive, and hypovolemic--many trauma practitioners view traumatic shock as a unique fifth shock pattern. Although secondary to a systemic inflammatory response syndrome triggered by endogenous danger signals, traumatic shock represents a unique pathological condition that begins with multiple, usually blunt, trauma and may conclude with multiple organ dysfunction syndrome and death. While varying mechanisms of injury may lead to different presentations of shock and cardiovascular decompensation, a unifying theme of traumatic shock is an overwhelming inflammatory response driven by proinflammatory cytokines, and the downstream results of this cytokine storm including, but not limited to, acute respiratory distress syndrome, coagulopathy, sepsis, and multiple organ dysfunction syndrome. Treatment is primarily supportive; however, research into novel therapeutics for traumatic shock is ongoing and promises some direction for future care.