Validation of an electronic tool for flagging surgical site infections based on clinical practice patterns for triaging surveillance: Operational successes and barriers.

BACKGROUND: Surveillance is an effective strategy for reducing surgical site infections (SSIs); however, current identification methods are resource-intensive. Therefore, we sought to validate an electronic SSI triaging tool for detection of probable infections and identify operational barriers and challenges. METHODS: A retrospective cohort study was conducted among all Veterans Affairs Surgical Quality Improvement Program (VASQIP)-reviewed surgeries at 2 Veterans Affairs medical centers from October 1, 2011-September 30, 2014. During the postoperative period, clinical and administrative variables associated with SSI (relevant microbiology order, antibiotic order, radiology order, and administrative codes) were extracted from the electronic medical record and used to score the probability (high, intermediate, and low) that an SSI occurred. VASQIP manual chart review was used as the gold standard of comparison. RESULTS: VASQIP manual review identified 118 SSIs out of 3,700 surgeries (3.2%). There were 2,041, 1,428, and 231 surgeries that met criteria for low, intermediate, and high probability for SSI. The tool's area under the curve was 0.86 (95% confidence interval, 0.82-0.89). The sensitivity among low-probability surgeries was 92.4%, and the specificity among high-probability surgeries was 95.1%. CONCLUSIONS: The electronic SSI tool has the potential to be used for triaging VASQIP surveillance toward the high-probability surgeries and to avoid manual review of surgeries with low probability of SSI.

Reduced hippocampal volume in association with p50 nonsuppression following traumatic brain injury.

Traumatic brain injury (TBI) may produce persistently impaired auditory gating. This cholinergic-dependent, hippocampally mediated preattentive cognitive function that facilitates filtering of auditory stimuli may be indexed by the P50 evoked waveform to paired auditory stimuli. Abnormal P50 suppression post TBI is believed to result from injury to the hippocampus and/or its afferent cholinergic projections. This hypothesis was tested by comparing hippocampal and total brain volumes on MRI between ten P50-nonsuppressing TBI patients and ten normal control subjects matched for age, gender, and education. TBI subjects had highly significant bilateral hippocampal volume reductions, even when covaried for reductions in total brain volume. Degree of volume loss was not correlated with initial TBI severity. Findings support the hypothesis that hippocampal injury underlies P50 nonsuppression post TBI and suggest that such structural abnormalities may be observed even in "mildly" injured persons.

Neuropsychiatric Aspects of Traumatic Brain Injury.

Traumatic brain injury (TBI) may produce a variety of neuropsychiatric problems, including impaired cognition, depression, mania, affective lability, irritability, anxiety, and psychosis. Despite the common occurrence of these symptoms following TBI, there are relatively few studies that provide clear guidance regarding management. Many symptoms (eg, irritability, affective lability, fatigue, sleep disturbance, and impaired cognition) are primarily consequences of brain injury rather than symptoms of a comorbid psychiatric disorder such as major depression. Although it is difficult to study the complicated treatments needed for such symptom complexes, we are able to recommend an approach to the evaluation and treatment of neuropsychiatric problems following traumatic brain injury. A thorough assessment of the patient is a prerequisite to the prescription of any treatment. This assessment should include a thorough developmental, psychiatric, and medication history; a detailed mental status examination; a complete neurologic examination; and quantification of neuropsychiatric symptoms using standardized and accepted inventories (eg, Neurobehavioral Rating Scale, Neuropsychiatric Inventory ). All symptoms must be evaluated in the context of the patient's premorbid history and current treatment because neuropsychiatric symptoms may be influenced by either factor or by both factors. Psychotherapy is an important component of the treatment of neuropsychiatric problems following TBI. Additionally, patients should be encouraged to become involved with local TBI support groups. When medications are prescribed, it is essential to use cautious dosing (low and slow) and empiric trials with continuous reassessment of symptoms using standardized scales and monitoring for drug-drug interactions. In general, medications with significant sedative, antidopaminergic, and anticholinergic properties should be avoided, and benzodiazepines should be used sparingly, if at all. Although patients with TBI may be particularly susceptible to adverse effects of psychopharmacologic medications, at times dosages similar to those used for the non-brain-injured psychiatric patient may be needed. When a single medication does not provide adequate relief of symptoms or cannot be tolerated at therapeutic doses, an alternative strategy is to augment the effect of one medication by using a second low-dose agent with a different mechanism of action.

Impaired auditory gating and P50 nonsuppression following traumatic brain injury.

Traumatic brain injury (TBI) can produce persistent attention and memory impairment that may in part be produced by impaired auditory sensory gating. The P50 evoked waveform response to paired auditory stimuli appears to be a useful measure of auditory gating. The first controlled measurement of the P50 ratio in TBI patients is described: when 20 patients with persistently symptomatic TBI were compared with 20 control subjects, the P50 ratio was significantly greater in the TBI group. The potential neurophysiologic and therapeutic implications of this finding in TBI patients who report symptoms consistent with impaired auditory gating are discussed.

The neuropsychiatry of pathologic affect: an approach to evaluation and treatment.

The ability to skillfully regulate the internal experience and outward expression of emotion is among the most complex and recently acquired functions of the human brain. When the capacity for emotional regulation is compromised by disease or injury the impact on individuals and their families may be considerable, both with regard to psychological well-being and social and occupational function. This article describes first a framework for the description, evaluation, and treatment of affective dysregulation. We review the literature regarding disorders of affective regulation, and in particular affective lability. Although disorders of affect as they occur in common neuropsychiatric disorders (eg, stroke, multiple sclerosis, traumatic brain injury, and so on) are the focus of this article, the review incorporates information from the study of patients with primary psychiatric disorders and hence the discussion herein may also be relevant to the understanding and treatment of affective lability in these conditions. An overview of the neurobiology that appears most relevant to understanding such problems is presented, along with several specific methods that appear to be useful in the evaluation of patients with affective lability. Finally, we review the literature regarding the treatment of disorders of affect and offer some practical suggestions for the treatment of patients with these problems.

Attention and memory dysfunction after traumatic brain injury: cholinergic mechanisms, sensory gating, and a hypothesis for further investigation.

Traumatic brain injury (TBI) is a common occurrence, with a rate of nearly 400,000 new injuries per year. Cognitive and emotional disturbances may become persistent and disabling for many injured persons, and frequently involve symptomatic impairment in attention and memory. Impairments in attention and memory have been well characterized in TBI, and are likely related to disruption of cholinergic functioning in the hippocampus. Additionally, disturbances in this neurotransmitter system may also account for disturbances in sensory gating and discriminative attention in this population. The electroencephalographic P50 waveform of the evoked response to paired auditory stimuli may provide a physiologic market of impaired sensory gating among TBI survivors. The first application of this recording assessment to the TBI population is reported. Preliminary findings in three cases are presented, and the interpretation of impaired sensory gating in this population is discussed. Given the impact of TBI on cholinergic systems, the effects of cholinergic augmentation on attention and memory impairment, and the availability of an electrophysiologic marker of cholinergic dysfunction responsive to cholinergic agents, a testable cholinergic hypothesis for investigation and treatment of these patients is proposed.