Management of Acute Wounds-Expert Panel Consensus Statement.

Significance: The Wound Healing Foundation recognized the need for consensus-based unbiased recommendations for the treatment of wounds. As a first step, a consensus on the treatment of chronic wounds was developed and published in 2022. The current publication on acute wounds represents the second step in this process. Acute wounds may result from any number of conditions, including burns, military and combat operations, and trauma to specific areas of the body. The management of acute wounds requires timely and evidence-driven intervention to achieve optimal clinical outcomes. This consensus statement provides the clinician with the necessary foundational approaches to the causes, diagnosis, and therapeutic management of acute wounds. Presented in a structured format, this is a useful guide for clinicians and learners in all patient care settings. Recent Advances: Recent advances in the management of acute wounds have centered on stabilization and treatment in the military and combat environment. Specifically, advancements in hemostasis, resuscitation, and the mitigation of infection risk through timely initiation of antibiotics and avoidance of high-pressure irrigation in contaminated soft tissue injury. Critical Issues: Critical issues include infection control, pain management, and the unique considerations for the management of acute wounds in pediatric patients. Future Directions: Future directions include new approaches to preventing the progression and conversion of burns through the use of specific gel formulations. Additionally, the use of three-dimensional bioprinting and photo-modulation for reconstruction is a promising area for continued discovery.

A Quality Improvement Initiative to Increase the Number of Pediatric Resident Laceration Repairs.

BACKGROUND: Pediatric residents must demonstrate competence in several clinical procedures prior to graduation, including simple laceration repair. However, residents may lack opportunities to perform laceration repairs during training, affecting their ability and confidence to perform this procedure. OBJECTIVE: We implemented a quality improvement initiative to increase the number of laceration repairs logged by pediatric residents from a baseline mean of 6.75 per month to more than 30 repairs logged monthly. METHODS: We followed the Institute for Healthcare Improvement's Model for Improvement with rapid plan-do-study-act cycles. From July 2016 to February 2018, we increased the number of procedure shifts and added an education module on performing laceration repairs for residents in a pediatric emergency department at a large tertiary hospital. We used statistical process control charting to document improvement. Our outcome measure was the number of laceration repairs documented in resident procedure logs. We followed the percentage of lacerations repairs completed by residents as a process measure and length of stay as a balancing measure. RESULTS: Following the interventions, logged laceration repairs initially increased from 6.75 to 22.75 per month for the residency program. After the number of procedure shifts decreased, logged repairs decreased to 13.40 per month and the percentage of lacerations repaired by residents also decreased. We noted an increased length of stay for patients whose lacerations were repaired by residents. CONCLUSIONS: While our objective was not met, our quality improvement initiative resulted in more logged laceration repairs. The most effective intervention was dedicated procedure shifts.

Strengthening and neuromuscular reeducation of the gluteus maximus in a triathlete with exercise-associated cramping of the hamstrings.

STUDY DESIGN: Case report. OBJECTIVE: To highlight the effects of an intervention program consisting of strengthening and neuromuscular reeducation of the gluteus maximus in an elite triathlete with exercise-associated muscle cramping (EAMC). BACKGROUND: Researchers have described 2 theories concerning the etiology of EAMC: (1) muscle fatigue and (2) electrolyte deficit. As such, interventions for EAMC typically consist of stretching/strengthening of the involved muscle and/or supplements to restore electrolyte imbalances. CASE DESCRIPTION: The patient was a 42-year-old male triathlete with a primary complaint of recurrent cramping of his right hamstring muscle, which prevented him from completing races at his desired pace. Strength testing revealed gluteus maximus muscle weakness bilaterally. Electromyographic (EMG) analysis (surface electrodes, 1560 Hz) revealed that the right hamstrings were being activated excessively during terminal swing and the first half of the stance phase (48.1% maximum voluntary isometric contraction [MVIC]). OUTCOMES: Following the intervention, the patient was able to complete 3 triathlons without hamstring cramping. Strength testing revealed that the right hip extension strength improved from 35.6 to 54.7 kg, and activation of the hamstrings during terminal swing and the first half of the stance phase decreased to 36.4% of MVIC. DISCUSSION: A program of gluteus maximus strengthening and neuromuscular training eliminated EAMC of the hamstrings in this patient. Given that the hamstrings and gluteus maximus work as agonists to decelerate the thigh during terminal swing phase and control hip flexion during loading response of running, we postulate that strengthening of the gluteus maximus decreased the relative effort required by the hamstrings, thus reducing EAMC. The results of the EMG evaluation that was performed as part of this case report provides support for this hypothesis. LEVEL OF EVIDENCE: Therapy, level 4.

Physical therapist management of acute and chronic low back pain using the World Health Organization's International Classification of Functioning, Disability and Health.

BACKGROUND AND PURPOSE: The World Health Organization's Classification of Functioning, Disability and Health (WHO-ICF) model was developed to describe, classify, and measure function in health care practice and research. Recently, this model has been promoted as a successor to the Nagi model by some authors in the physical therapy literature. However, conceptual work in demonstrating use of the WHO-ICF model in physical therapist management of individual patients remains sparse. The purpose of this case report series is to demonstrate the application of the WHO-ICF model in clinical reasoning and physical therapist management of acute and chronic low back pain. CASE DESCRIPTION: Two patients, 1 with acute low back pain and 1 with chronic low back pain, were treated pragmatically using the WHO-ICF model and other applicable models of clinical reasoning. INTERVENTION: Manual therapy, exercise, and education interventions were directed toward relevant body structure and function impairments, activity limitations, and contextual factors based on their hypothesized contribution to functioning and disability. OUTCOME: Both patients demonstrated clinically significant improvements in measures of pain, disability, and psychosocial factors after 3 weeks and 10 weeks of intervention, respectively. DISCUSSION: The WHO-ICF model appears to provide an effective framework for physical therapists to better understand each person's experience with his or her disablement and assists in prioritizing treatment selection. The explicit acknowledgment of personal and environmental factors aids in addressing potential barriers. The WHO-ICF model integrates well with other models of practice such as Sackett's principles of evidence-based practice, the rehabilitation cycle, and Edwards and colleagues' clinical reasoning model. Future research should examine outcomes associated with the use of the WHO-ICF model using adequately designed clinical trials.

Surviving sepsis: bcl-2 overexpression modulates splenocyte transcriptional responses in vivo.

We hypothesized that spleen microarray gene expression profiles analyzed with contemporary pathway analysis software would provide molecular pathways of interest and target genes that might help explain the effect of bcl-2 on improving survival during sepsis. Two mouse models of sepsis, cecal ligation and puncture and tracheal instillation of Pseudomonas aeruginosa, were tested in both wild-type mice and mice that overexpress bcl-2. Whole spleens were obtained 6 h after septic injury. DNA microarray transcriptional profiles were obtained using the Affymetrix 430A GeneChip, containing 22,690 elements. Ingenuity Pathway Analysis software was used to construct hypothetical transcriptional networks that changed in response to sepsis and expression of the bcl-2 transgene. A conservative approach was used wherein only changes induced by both abdominal and pulmonary sepsis were studied. At 6 h, sepsis induced alterations in the abundance of hundreds of spleen genes, including a number of proinflammatory mediators (e.g., interleukin-6). These sepsis-induced alterations were blocked by expression of the bcl-2 transgene. Network analysis implicated a number of bcl-2-related apoptosis genes, including bcl2L11 (bim), bcl-2L2 (bcl-w), bmf, and mcl-1. Sepsis in bcl-2 transgenic animals resulted in alteration of RNA abundance for only a single gene, ceacam1. These findings are consistent with sepsis-induced alterations in the balance of pro- and anti-apoptotic transcriptional networks. In addition, our data suggest that the ability of bcl-2 overexpression to improve survival in sepsis in this model is related in part to prevention of sepsis-induced alterations in spleen transcriptional responses.

TAT-BH4 and TAT-Bcl-xL peptides protect against sepsis-induced lymphocyte apoptosis in vivo.

Apoptosis is a key pathogenic mechanism in sepsis that induces extensive death of lymphocytes and dendritic cells, thereby contributing to the immunosuppression that characterizes the septic disorder. Numerous animal studies indicate that prevention of apoptosis in sepsis improves survival and may represent a potential therapy for this highly lethal disorder. Recently, novel cell-penetrating peptide constructs such as HIV-1 TAT basic domain and related peptides have been developed to deliver bioactive cargoes and peptides into cells. In the present study, we investigated the effects of sepsis-induced apoptosis in Bcl-x(L) transgenic mice and in wild-type mice treated with an antiapoptotic TAT-Bcl-x(L) fusion protein and TAT-BH4 peptide. Lymphocytes from Bcl-x(L) transgenic mice were resistant to sepsis-induced apoptosis, and these mice had a approximately 3-fold improvement in survival. TAT-Bcl-x(L) and TAT-BH4 prevented Escherichia coli-induced human lymphocyte apoptosis ex vivo and markedly decreased lymphocyte apoptosis in an in vivo mouse model of sepsis. In conclusion, TAT-conjugated antiapoptotic Bcl-2-like peptides may offer a novel therapy to prevent apoptosis in sepsis and improve survival.

Accelerated lymphocyte death in sepsis occurs by both the death receptor and mitochondrial pathways.

Patients with sepsis are immune compromised, as evidenced by their failure to clear their primary infection and their propensity to develop secondary infections with pathogens that are often not particularly virulent in normal healthy individuals. A potential mechanism for immunosuppression in sepsis is lymphocyte apoptosis, which may occur by either a death receptor or a mitochondrial-mediated pathway. A prospective study of blood samples from 71 patients with sepsis, 55 nonseptic patients, and 6 healthy volunteers was undertaken to quantitate lymphocyte apoptosis and determine cell death pathways and mechanisms of apoptosis. Apoptosis was evaluated by flow cytometry and Western blotting. Lymphocyte apoptosis was increased in CD4 and CD8 T cells, B cells (CD20), and NK cells (CD56) in septic vs nonseptic patients. Samples taken sequentially from 10 patients with sepsis showed that the degree of CD3 T cell apoptosis correlated with the activity of his/her sepsis. In septic patients, apoptotic lymphocytes were positive for active caspases 8 and 9, consistent with death occurring by both mitochondrial-mediated and receptor-mediated pathways. In support of the concept that both death pathways were operative, lymphocyte apoptosis occurred in cells with markedly decreased Bcl-2 (an inhibitor of mitochondrial-mediated apoptosis) as well as cells with normal concentrations of Bcl-2. In conclusion, apoptosis occurs in a broad range of lymphocyte subsets in patients with sepsis and correlates with the activity of the disease. Lymphocyte loss occurs by both death receptor and mitochondrial-mediated apoptosis, suggesting that there may be multiple triggers for lymphocyte apoptosis.

Akt decreases lymphocyte apoptosis and improves survival in sepsis.

Sepsis induces extensive death of lymphocytes that may contribute to the immunosuppression and mortality of the disorder. The serine/threonine kinase Akt is a key regulator of cell proliferation and death. The purpose of this study was to determine whether overexpression of Akt would prevent lymphocyte apoptosis and improve survival in sepsis. In addition, given the important role of Akt in cell signaling, T cell Th1 and Th2 cytokine production was determined. Mice that overexpress a constitutively active Akt in lymphocytes were made septic, and survival was recorded. Lymphocyte apoptosis and cytokine production were determined at 24 h after surgery. Mice with overexpression of Akt had a marked improvement in survival compared with wild-type littermates, i.e., 94 and 47% survival, respectively, p < 0.01. In wild-type littermates, sepsis caused a marked decrease in IFN-gamma production, while increasing IL-4 production >2-fold. In contrast, T cells from Akt transgenic mice had an elevated production of IFN-gamma at baseline that was maintained during sepsis, while IL-4 had little change. Akt overexpression also decreased sepsis-induced lymphocyte apoptosis via a non-Bcl-2 mechanism. In conclusion, Akt overexpression in lymphocytes prevents sepsis-induced apoptosis, causes a Th1 cytokine propensity, and improves survival. Findings from this study strengthen the concept that a major defect in sepsis is impairment of the adaptive immune system, and suggest that strategies to prevent lymphocyte apoptosis represent a potential important new therapy.

Supplementation with micronutrients in addition to iron and folic acid does not further improve the hematologic status of pregnant women in rural Nepal.

Iron deficiency is one of the main causes of anemia during pregnancy, although other micronutrient deficiencies may play a role. We examined the effects of daily antenatal and postnatal supplementation with four combinations of micronutrients on maternal hematologic indicators in a double-masked randomized controlled community trial. Communities, called sectors, were randomly assigned to supplementation with folic acid (400 microg), folic acid plus iron (60 mg), folic acid plus iron and zinc (30 mg) and folic acid plus iron, zinc and 11 other micronutrients, each at the approximate recommended daily allowance for pregnancy all given with vitamin A as retinol acetate (1000 microg retinol equivalent), or vitamin A alone as the control group. Hemoglobin (Hb) and indicators of iron status were assessed at baseline and at 32 wk of gestation. At 6-wk postpartum, Hb assessment was repeated using a finger stick. Severely anemic women (Hb < 70 g/L) were treated according to WHO recommendations. Folic acid alone had no effect on maternal anemia or iron status. Hb concentrations were 14 g/L, [95% confidence limits (CL), 8.3-19.2], 10.0 g/L (CL, 5.2-14.8) and 9.4 g/L (CL, 4.7-14.1) higher in the groups receiving folic acid plus iron, folic acid plus iron and zinc and folic acid plus iron, zinc and multiple micronutrients, respectively, relative to the control. Anemia in the third trimester was reduced by 54% with folic acid plus iron, by 48% with folic acid plus iron and zinc and by 36% with folic acid plus iron, zinc and multiple micronutrients supplementation, relative to the control (P < 0.05). Thus, the combinations of folic acid plus iron and zinc and folic acid plus iron, zinc and multiple micronutrients provided no additional benefit in improving maternal hematologic status during pregnancy compared with folic acid plus iron. The level of compliance and baseline Hb concentrations modified the effect of iron.

Depletion of dendritic cells, but not macrophages, in patients with sepsis.

Dendritic cells (DCs) are a group of APCs that have an extraordinary capacity to interact with T and B cells and modulate their responses to invading pathogens. Although a number of defects in the immune system have been identified in sepsis, few studies have examined the effect of sepsis on DCs, which is the purpose of this study. In addition, this study investigated the effect of sepsis on macrophages, which are reported to undergo apoptosis, and MHC II expression, which has been noted to be decreased in sepsis. Spleens from 26 septic patients and 20 trauma patients were evaluated by immunohistochemical staining. Although sepsis did not decrease the number of macrophages, sepsis did cause a dramatic reduction in the percentage area of spleen occupied by FDCs, i.e., 2.9 +/- 0.4 vs 0.7 +/- 0.2% in trauma and septic patients, respectively. The number of MHC II-expressing cells, including interdigitating DCs, was decreased in septic, compared with trauma, patients. However, sepsis did not appear to induce a loss of MHC II expression in those B cells, macrophages, or DCs that were still present. The dramatic loss of DCs in sepsis may significantly impair B and T cell function and contribute to the immune suppression that is a hallmark of the disorder.