Timothy T. Houle

Predicting total knee replacement pain: a prospective, observational study.

To describe the natural history of pain after total knee arthroplasty and to identify factors predicting excessive postoperative pain, we used a prospective, observational study assessing clinical and radiographic variables preoperatively and at 1, 3, 6, and 12 months after knee replacement. Data sources included the visual analog pain scale and other measures of patient health, psychologic state, and component reliability. Regression analyses were conducted to identify specific factors predictive of postoperative pain, controlling for inequality of variables, and confirmed using regression diagnostics. For 116 patients (149 knees; mean age, 66 years; 55.2% women), significant pain was reported by 72.3%, 44.4%, 22.6%, 18.4%, and 13.1%, respectively. No intergroup differences existed for anesthesia, weight, age, or gender. Patients with greater preoperative pain had more postoperative pain, used more home therapy, and postoperative manipulations. Preoperative depression and anxiety were associated with heightened pain at 1 year. Pain after knee replacement resolves quickly, declining to approximately 1/2 by 3 months. However, one in eight patients report moderate to severe pain 1 year after surgery despite an absence of clinical or radiographic abnormalities. Development of office-based preoperative screening tools and interventions for these patients may reduce postoperative costs and improve patient-perceived outcomes.

Statistical evaluation of a biomarker.

A biomarker may provide a diagnosis, assess disease severity or risk, or guide other clinical interventions such as the use of drugs. Although considerable progress has been made in standardizing the methodology and reporting of randomized trials, less has been accomplished concerning the assessment of biomarkers. Biomarker studies are often presented with poor biostatistics and methodologic flaws that precludes them from providing a reliable and reproducible scientific message. A host of issues are discussed that can improve the statistical evaluation and reporting of biomarker studies. Investigators should be aware of these issues when designing their studies, editors and reviewers when analyzing a manuscript, and readers when interpreting results.

severity of acute pain after childbirth, but not type of delivery, predicts persistent pain and postpartum depression

Abstract Cesarean delivery rates continue to increase, and surgery is associated with chronic pain, often co‐existing with depression. Also, acute pain in the days after surgery is a strong predictor of chronic pain. Here we tested if mode of delivery or acute pain played a role in persistent pain and depression after childbirth. In this multicenter, prospective, longitudinal cohort study, 1288 women hospitalized for cesarean or vaginal delivery were enrolled. Data were obtained from patient interviews and medical record review within 36 h postpartum, then via telephone interviews 8 weeks later to assess persistent pain and postpartum depressive symptoms. The impact of delivery mode on acute postpartum pain, persistent pain and depressive symptoms and their interrelationships was assessed using regression analysis with propensity adjustment. The prevalence of severe acute pain within 36 h postpartum was 10.9%, while persistent pain and depression at 8 weeks postpartum were 9.8% and 11.2%, respectively. Severity of acute postpartum pain, but not mode of delivery, was independently related to the risk of persistent postpartum pain and depression. Women with severe acute postpartum pain had a 2.5‐fold increased risk of persistent pain and a 3.0‐fold increased risk of postpartum depression compared to those with mild postpartum pain. In summary, cesarean delivery does not increase the risk of persistent pain and postpartum depression. In contrast, the severity of the acute pain response to childbirth predicts persistent morbidity, suggesting the need to more carefully address pain treatment in the days following childbirth.

Multifactorial Preoperative Predictors for Postcesarean Section Pain and Analgesic Requirement

Background: The study aimed to determine predictive factors for postcesarean pain and analgesia using an assessment of pain threshold and suprathreshold thermal stimuli as well as degree of somatization and anxiety. Methods: Thirty-four healthy parturients scheduled for cesarean delivery under subarachnoid anesthesia were enrolled. Preoperative thermal pain threshold, intensity, and unpleasantness to heat stimuli applied to arm and lower back, State Trait Anxiety Inventory, and patient expectation for postoperative pain and need for analgesia were assessed. After surgery, overall, resting, and movement pain and analgesic consumption were recorded. Prediction of pain and analgesic use outcomes was made by principal component factor analysis, followed by stepwise linear regression. Results: Resting pain was predicted by two factors, thermal pain and unpleasantness and patient expectation (r2 = 0.26, P < 0.01), evoked pain by thermal pain threshold in the back (r2 = 0.20, P < 0.009), composite pain by thermal pain and unpleasantness and preoperative blood pressure (r2 = 0.28, P < 0.008), intraoperative analgesic need by preexisting pain (r2 = 0.22, P < 0.006), recovery room analgesia by thermal pain threshold and State Trait Anxiety Inventory (r2 = 0.27, P < 0.01), and total analgesic need by State Trait Anxiety Inventory (r2 = 0.22, P < 0.01). These models predicted the upper twentieth percentile of composite pain scores and analgesic requirement with sensitivity of 0.71 to 0.80 and specificity of 0.76 to 0.80. Conclusions: The authors’ results suggest a meaningful combination of preoperative patient responses from physical and psychological tests yields a valid multifactorial predictive model for postoperative pain and analgesic requirement with significant improvements over individual predictive variables.

Psychological Risk Factors in Headache

Headache is a chronic disease that occurs with varying frequency and results in varying levels of disability. To date, the majority of research and clinical focus has been on the role of biological factors in headache and headache‐related disability. However, reliance on a purely biomedical model of headache does not account for all aspects of headache and associated disability. Using a biopsychosocial framework, the current manuscript expands the view of what factors influence headache by considering the role psychological (i.e., cognitive and affective) factors have in the development, course, and consequences of headache. The manuscript initially reviews evidence showing that neural circuits responsible for cognitive–affective phenomena are highly interconnected with the circuitry responsible for headache pain. The manuscript then reviews the influence cognitions (locus of control and self‐efficacy) and negative affect (depression, anxiety, and anger) have on the development of headache attacks, perception of headache pain, adherence to prescribed treatment, headache treatment outcome, and headache‐related disability. The manuscript concludes with a discussion of the clinical implications of considering psychological factors when treating headache.

Guidelines for Trials of Behavioral Treatments for Recurrent Headache, First Edition: American Headache Society Behavioral Clinical Trials Workgroup

Guidelines for design of clinical trials evaluating behavioral headache treatments were developed to facilitate production of quality research evaluating behavioral therapies for management of primary headache disorders. These guidelines were produced by a Workgroup of headache researchers under auspices of the American Headache Society. The guidelines are complementary to and modeled after guidelines for pharmacological trials published by the International Headache Society, but they address methodologic considerations unique to behavioral and other nonpharmacological treatments. Explicit guidelines for evaluating behavioral headache therapies are needed as the optimal methodology for behavioral (and other nonpharmacologic) trials necessarily differs from the preferred methodology for drug trials. In addition, trials comparing and integrating drug and behavioral therapies present methodological challenges not addressed by guidelines for pharmacologic research. These guidelines address patient selection, trial design for behavioral treatments and for comparisons across multiple treatment modalities (eg, behavioral vs pharmacologic), evaluation of results, and research ethics. Although developed specifically for behavioral therapies, the guidelines may apply to the design of clinical trials evaluating many forms of nonpharmacologic therapies for headache.

Nosocomial Pneumonia Risk and Stress Ulcer Prophylaxis: A Comparison of Pantoprazole vs Ranitidine in Cardiothoracic Surgery Patients

BACKGROUND Stress ulcer prophylaxis (SUP) using ranitidine, a histamine H2 receptor antagonist, has been associated with an increased risk of ventilator-associated pneumonia. The proton pump inhibitor (PPI) pantoprazole is also commonly used for SUP. PPI use has been linked to an increased risk of community-acquired pneumonia. The objective of this study was to determine whether SUP with pantoprazole increases pneumonia risk compared with ranitidine in critically ill patients. METHODS The cardiothoracic surgery database at our institution was used to identify retrospectively all patients who had received SUP with pantoprazole or ranitidine, without crossover between agents. From January 1, 2004, to March 31, 2007, 887 patients were identified, with 53 patients excluded (pantoprazole, 30 patients; ranitidine, 23 patients). Our analysis compared the incidence of nosocomial pneumonia in 377 patients who received pantoprazole with 457 patients who received ranitidine. RESULTS Nosocomial pneumonia developed in 35 of the 377 patients (9.3%) who received pantoprazole, compared with 7 of the 457 patients (1.5%) who received ranitidine (odds ratio [OR], 6.6; 95% confidence interval [CI], 2.9 to 14.9). Twenty-three covariates were used to estimate the probability of receiving pantoprazole as measured by propensity score (C-index, 0.77). Using this score, pantoprazole and ranitidine patients were stratified according to their probability of receiving pantoprazole. After propensity adjusted, multivariable logistic regression, pantoprazole treatment was found to be an independent risk factor for nosocomial pneumonia (OR, 2.7; 95% CI, 1.1 to 6.7; p = 0.034). CONCLUSION The use of pantoprazole for SUP was associated with a higher risk of nosocomial pneumonia compared with ranitidine. This relationship warrants further study in a randomized controlled trial.

Local Anesthetic-Induced Cardiac Toxicity: A Survey of Contemporary Practice Strategies Among Academic Anesthesiology Departments

Though new local anesthetics (LA), effective test-dosing, and new regional anesthetic techniques may have improved the safety of regional anesthesia, the optimal management plan for LA-induced cardiac toxicity remains uncertain. Accordingly, we evaluated current approaches to LA cardiotoxicity among academic anesthesiology departments in the United States. A 19-question survey regarding regional anesthesia practices and approaches to LA cardiac toxicity was sent to the 135 academic anesthesiology departments listed by the Society of Academic Anesthesiology Chairs-Association of Anesthesiology Program Directors. Ninety-one anonymously completed questionnaires were returned, at a response rate of 67%. The respondents were categorized into groups according to the number of peripheral nerve blocks (PNBs) performed each month: >70 PNBs (38%), 51–70 PNBs (13%), 31–50 PNBs (20%), 11–30 PNBs (23%), and <10 PNBs (6%). Anesthesia practices administering >70 PNBs were 1.7-times more likely to use ropivacaine (NS), 3.9-times more likely to consider lipid emulsion infusions for resuscitation (P = 0.008), and equally as likely to have an established plan for use of invasive mechanical cardiopulmonary support in the event of LA cardiotoxicity (NS) than low-PNB volume centers. We conclude that there are differences in the management and preparedness for treatment of LA toxicity among institutions, but the safety implications of these differences are undetermined.

Resolution of pain after childbirth.

Background:Chronic pain after surgery occurs in 10–40% of individuals, including 5–20% of women after cesarean delivery in previous reports. Pain and depression 2 months after childbirth are independently associated with more severe acute post-delivery pain. Here we examine other predictors of pain at 2 months and determine the incidence of pain at 6 and 12 months after childbirth. Methods:Following Institutional Review Board approval, 1228 women were interviewed within 36 h of delivery. Of these, 937 (76%) were successfully contacted by telephone at 2 months, and, if they had pain, at 6 and 12 months after delivery. The primary outcome measure was presence of pain which began at the time of delivery. We also generated a model of severity of acute post-delivery pain and 2 month pain and depression. Results:Pain which began at the time of delivery was remarkably rare 6 and 12 months later (1.8% and 0.3% [upper 95% confidence limit, 1.2%], respectively). Past history of pain and degree of tissue damage at delivery accounted for 7.0% and 16.7%, respectively, of one aspect in the variability in acute post-delivery pain. Neither of these factors was associated with incidence of pain 2 months later. Conclusions:Using a definition of new onset pain from delivery, we show a remarkably low incidence of pain 1 yr after childbirth, including those with surgical delivery. Additionally, degree of tissue trauma and history of chronic pain, risk factors for pain 2 months after other surgery, were unimportant to pain 2 months after cesarean or vaginal delivery.

Stress and sleep duration predict headache severity in chronic headache sufferers

Summary Recent stress history and sleep quantity affect headache intensity for sufferers who experience daily or near‐daily headaches. ABSTRACT The objective of this study was to evaluate the time‐series relationships between stress, sleep duration, and headache pain among patients with chronic headaches. Sleep and stress have long been recognized as potential triggers of episodic headache (<15 headache days/month), though prospective evidence is inconsistent and absent in patients diagnosed with chronic headaches (⩾15 days/month). We reanalyzed data from a 28‐day observational study of chronic migraine (n = 33) and chronic tension‐type headache (n = 22) sufferers. Patients completed the Daily Stress Inventory and recorded headache and sleep variables using a daily sleep/headache diary. Stress ratings, duration of previous nights’ sleep, and headache severity were modeled using a series of linear mixed models with random effects to account for individual differences in observed associations. Models were displayed using contour plots. Two consecutive days of either high stress or low sleep were strongly predictive of headache, whereas 2 days of low stress or adequate sleep were protective. When patterns of stress or sleep were divergent across days, headache risk was increased only when the earlier day was characterized by high stress or poor sleep. As predicted, headache activity in the combined model was highest when high stress and low sleep occurred concurrently during the prior 2 days, denoting an additive effect. Future research is needed to expand on current findings among chronic headache patients and to develop individualized models that account for multiple simultaneous influences of headache trigger factors.