Fit for Duty: Lessons Learned from Outpatient and Homebound Hematopoietic Cell Transplantation to Prepare Family Caregivers for Home-Based Care.

In the past decade, the demand for home-based care has been amplified by the Coronavirus disease 2019 pandemic. Home-based care has significant benefits for patients, their families, and healthcare systems, but it relies on the often-invisible workforce of family and friend caregivers who shoulder essential health care responsibilities, frequently with inadequate training and support. Hematopoietic cell transplantation (HCT), a potentially curative but intensive treatment for many patients with blood disorders, is being increasingly offered in home-based care settings and necessitates the involvement of family caregivers for significant patient care responsibilities. However, guidelines for supporting and preparing HCT caregivers to effectively care for their loved ones at home have not yet been established. Here, informed by the literature and our collective experience as clinicians and researchers who care for diverse patients with hematologic malignancies undergoing HCT, we provide considerations and recommendations to better support and prepare family caregivers in home-based HCT and, by extension, family caregivers supporting patients with other serious illnesses at home. We suggest tangible ways to screen family caregivers for distress and care delivery challenges, educate and train them to prepare for their caregiving role, and create an infrastructure of support for family caregivers within this emerging care delivery model.

A qualitative exploration of the feasibility and acceptability of Meaning-Centered Psychotherapy for Cancer Caregivers.

OBJECTIVE: Caregivers of patients with cancer are at significant risk for existential distress. Such distress negatively impacts caregivers' quality of life and capacity to serve in their role as healthcare proxies, and ultimately, contributes to poor bereavement outcomes. Our team developed Meaning-Centered Psychotherapy for Cancer Caregivers (MCP-C), the first targeted psychosocial intervention that directly addresses existential distress in caregivers. METHOD: Nine caregivers of patients with glioblastoma multiforme (GBM) enrolled in a pilot randomized controlled trial evaluating the feasibility, acceptability, and effects of MCP-C, and completed in-depth interviews about their experience in the therapy. One focus group with three MCP-C interventionists was also completed. RESULTS: Four key themes emerged from interviews: (1) MCP-C validated caregivers' experience of caregiving; (2) MCP-C helped participants reframe their "caregiving identity" as a facet of their larger self-identity, by placing caregiving in the context of their life's journey; (3) MCP-C enabled caregivers to find ways to assert their agency through caregiving; and (4) the structure and sequence of sessions made MCP-C accessible and feasible. Feedback from interventionists highlighted several potential manual changes and overall ways in which MCP-C can help facilitate caregivers' openness to discussing death and engaging in advanced care planning discussions with the patient. SIGNIFICANCE OF RESULTS: The overarching goal of MCP-C is to allow caregivers to concurrently experience meaning and suffering; the intervention does not seek to deny the reality of challenges endured by caregivers, but instead to foster a connection to meaning and purpose alongside their suffering. Through in-depth interviews with caregivers and a focus group with MCP interventionists, we have refined and improved our MCP-C manual so that it can most effectively assist caregivers in experiencing meaning and purpose, despite inevitable suffering.

Prognostic awareness and communication preferences among caregivers of patients with malignant glioma.

OBJECTIVE: Malignant glioma (MG) is a devastating neuro-oncologic disease with almost invariably poor prognosis, yet many families facing malignant glioma have poor prognostic awareness (PA), or the awareness of the patient's incurable disease and shortened life expectancy. Accurate PA is associated with favorable medical outcomes at end-of-life for patients and psychosocial outcomes for informal caregivers (ICs) through bereavement. To date, however, no study has specifically examined PA among MG ICs and the information they receive that shapes their awareness. METHODS: Thirty-two ICs of patients with malignant glioma completed a semi-structured assessment of their awareness of the incurability and life expectancy of their loved one's illness, and to understand their sources of prognostic information and preferences for communication of prognostic information. RESULTS: Twenty-two (69%) ICs had full PA-awareness of the incurability of malignant glioma and accurate estimates of their loved ones' life expectancy. Twenty-three (72%) felt that prognostic information was extremely or very important to possess, and 16 (50%) desired more prognostic information. The majority of ICs received prognostic information from physicians and the Internet. Qualitative analyses revealed that many ICs had difficulty navigating medical encounters in which they concurrently wanted to elicit prognostic information from physicians and protect patients from such information. CONCLUSIONS: Accurate and timely PA is necessary for ICs to serve as critical members of health care teams. Interventions are needed to foster ICs' skills in navigating prognostic communication with patients and health care providers and thereby improve their ability to advocate for their loved one's wishes.

Exploring the cancer caregiver's journey through web-based Meaning-Centered Psychotherapy.

OBJECTIVE: Psychosocial interventions are historically underutilized by cancer caregivers, but support programs delivered flexibly over the Internet address multiple barriers to care. We adapted Meaning-Centered Psychotherapy for cancer caregivers, an in-person psychotherapeutic intervention intended to augment caregivers' sense of meaning and purpose and ameliorate burden, for delivery in a self-administered web-based program, the Care for the Cancer Caregiver (CCC) Workshop. The present study evaluated the feasibility, acceptability, and preliminary effects of this program. METHODS: Eighty-four caregivers were randomized to the CCC Workshop or waitlist control arm. Quantitative assessments of meaning, burden, anxiety, depression, benefit finding, and spiritual well-being were conducted preintervention (T1), within 2-weeks postintervention (T2), and 2- to 3-month follow-up (T3). In-depth semistructured interviews were conducted with a subset of participants. RESULTS: Forty-two caregivers were randomized to the CCC Workshop. Attrition was moderate at T2 and T3, with caregiver burden and bereavement as key causes of drop-out. At T2 and T3, some observed mean change scores and effect sizes were consistent with hypothesized trends (eg, meaning in caregiving, benefit finding, and depressive symptomatology), though no pre-post significant differences emerged between groups. However, a longitudinal mixed-effects model found significant differential increases in benefit finding in favor of the CCC arm. CONCLUSIONS: The CCC Workshop was feasible and acceptable. Based on effect sizes reported here, a larger study will likely establish the efficacy of the CCC Workshop, which has the potential to address unmet needs of caregivers who underutilize in-person supportive care services.

A scoping review of caregiver burden during allogeneic HSCT: lessons learned and future directions.

The extant literature documents burden among caregivers of patients undergoing a hematopoietic stem cell transplantation (HSCT), but little is known about the burden of caregivers of patients receiving outpatient and homebound HSCTs. This scoping study sought to evaluate what is known about the burden of the increasing number of adult caregivers of patients receiving outpatient HSCTs and to create practice guidelines for how to best support this vulnerable group. Online databases were searched for studies that evaluated caregiver burden in adult caregivers of HSCT patients since 2010 (the publication date of the most recent systematic review on HSCT caregiver burden). Of the 1271 articles retrieved, 12 met the inclusion criteria, though none specifically examined outpatient or homebound caregivers. Overall, studies corroborated existing literature on the experience of significant burden among HSCT caregivers across the HSCT trajectory, and highlighted the emotional costs of outpatient transplants on caregivers and the need to identify caregivers at high risk for burden early in the transplant process. Future studies of outpatient caregivers should include a comprehensive assessment of burden and seek to identify points along the transplant trajectory at which caregivers are at particular risk for negative outcomes and when intervention is most appropriate.

Activation of mitogen-activated protein kinases in human heart during cardiopulmonary bypass.

Mitogen-activated protein kinases (MAPKs) have been shown to be activated in both in vitro and in vivo models of cardiac tissue in response to ischemia/reperfusion injury. We investigated whether MAPKs are activated in human heart during coronary artery bypass grafting (CABG) surgery. During elective CABG surgery of 8 patients, 3 right atrial appendage biopsies were obtained at baseline, at the end of cross-clamping, and after coronary reperfusion. The expression of the p38-MAPK, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinases (ERK1/2) MAPKs was not altered during CABG. The phosphorylation and activation of both ERK1/2 and p38-MAPK were increased approximately 2-fold by ischemia and even more (8- and 4-fold, respectively) by reperfusion. Although the ischemic period did not result in a significant activation of JNK, an approximately 6-fold increase in JNK activity could be observed after reperfusion. In conclusion, distinct activation patterns of ERK1/2, p38, and JNK MAPKs can be observed in human heart during CABG.

Atrial tachycardia as the presenting sign of a left atrial appendage aneurysm.

A patient presented with atrial tachycardia. The work-up, guided by the tachycardia morphology, led to the diagnosis of left atrial appendage aneurysm. Surgical removal of the atrial appendage resulted in cure of the tachycardia and associated symptoms.

Surgical management of tetralogy of Fallot in the first year of life.

BACKGROUND: The surgical approach to tetralogy of Fallot (TOF) continues to evolve and now many centers favor early repair for TOF. METHODS: Our experience includes 82 consecutive patients less than 1 year old with TOF (n = 74) and TOF with pulmonary atresia (n = 8) who were operated on between January 1992 and March 1998. Mean age at repair was 5.2 +/- 1.2 months and mean weight was 4.5 +/- 0.4 kg. Seven patients (anomalous left anterior descending artery [n = 1], pulmonary atresia with hypoplastic pulmonary arteries [n = 6]), underwent palliative procedures in the neonatal period followed by complete repair. Forty-nine patients (59%) were symptomatic (severe cyanosis or hypoxic spells), and 33 patients (41%) were asymptomatic. A combined transatrial-transpulmonary approach was employed in 28 patients (34%), and transannular patch or conduit for reconstruction of the right ventricular outflow tract (RVOT) was required in 54 patients (66%). The mean Nakata index was 160 +/- 25 mm2/m2. RESULTS: There were no hospital deaths. Mean post-repair peak right ventricular/systemic pressure ratio was 0.48 +/- 0.1. There were no late deaths or reoperations during a mean follow-up of 23 +/- 5 months. All patients are currently asymptomatic and in New York Heart Association class 1. Postoperative evaluation by two-dimensional and Doppler echocardiography or cardiac catheterization showed minimal pulmonary artery stenosis with a mean pressure gradient of 15 +/- 6 mm Hg across the RVOT. CONCLUSIONS: Our experience suggests that early repair of TOF can yield excellent results and initial palliation does not preclude early complete repair.

Barbarians at the gates? Combating some new threats to hospital security professionals.

This article shows how security directors can answer simplistic security formulas used by some consultants and contractors with meaningful measurements. It presents ideas and approaches for cost-cutting, and may help the security director, if called on, to cut costs in a way that will continue to provide the most security per dollar spent.

Coronary pathology predicts conduction disturbances after coronary artery bypass grafting.

Conduction disturbances after coronary artery bypass grafting may result from compromised septal blood flow. To examine this hypothesis we reviewed the preoperative coronary angiography of 55 consecutive patients undergoing coronary artery bypass grafting. Thirty-five patients had either no lesion or a discrete lesion in the left anterior descending coronary artery that did not include the septal perforator (type I anatomy). Twenty patients had a lesion of the left anterior descending coronary artery at the origin of the first septal branch, a lesion of the first septal artery, or a pair of lesions in the left anterior descending coronary artery that straddled the origin of the first septal artery; all lesions were proximal to the graft site (type II anatomy). None of the patients with type I anatomy had a major conduction disturbance after coronary artery bypass grafting. Eleven of the patients with type II anatomy had major conduction disturbances after coronary artery bypass grafting; right bundle-branch block in 1, right bundle-branch block and left anterior hemiblock in 2, left bundle-branch block in 5, and complete atrioventricular block that required pacemaker implantation in 3 (p less than 0.001). In the 20 patients with type II anatomy, the appearance of conduction disturbances correlated well with the absence of retrograde flow to the septal branches from the right coronary artery (p less than 0.01). Pathological lesions in the left anterior descending coronary artery that compromise flow in the first perforator and that do not provide an adequate circulation produce localized damage and conduction disturbances after coronary artery bypass grafting. This can be predicted from the preoperative angiographic anatomy.

Aspartate-induced neuronal necrosis in infant mice: protective effect of carbohydrate and insulin.

Infant mice given large doses of glutamate or aspartate develop hypothalamic neuronal necrosis. Studies by others demonstrated that simultaneous administration of carbohydrate or prior injection with insulin markedly decreased glutamate-induced neuronal damage. We investigated whether carbohydrate and insulin exert a similar protective effect against aspartate-induced neuronal necrosis. Eight-day-old mice administered aspartate at 750 and 1000 mg/kg body weight developed neuronal necrosis (45.9 +/- 7.2 and 80.8 +/- 17.3 necrotic neurons/section, respectively). When carbohydrate (1 g/kg body weight) was administered simultaneously no lesions were detected in mice administered 750 mg/kg body weight aspartate, while 30.1 +/- 14.2 necrotic neurons/section were noted at 1000 mg aspartate/kg body weight. Mice administered 1000 mg/kg body weight aspartate with prior injection of insulin had 28.4 +/- 12.6 necrotic neurons/section, while 4.2 +/- 1.4 necrotic neurons/section were noted in insulin treated mice given 750 mg aspartate/kg body weight. Carbohydrate and insulin treatments has only minimal effects on plasma aspartate concentrations.

Guide wire entrapment during PTCA: a potentially dangerous complication.

The tip of a "high-torque" floppy guide wire became entrapped in a coronary artery during elective PTCA in four patients. In two it was removed through the guiding catheter, in the third an operative intervention was needed in order to free the wire, and in the fourth the remnant was left in situ. Interventional cardiologists should be aware of this potential complication.

Utilization of intravenously administered glycogen by young pigs.

Previous studies evaluated solutions of small oligosaccharides as potential sources of carbohydrate-derived energy for patients fed intravenously. Although results with these solutions were disappointing, the data suggested that very large oligosaccharides were potential sources of intravenous carbohydrate. To test this hypothesis, four young pigs (3.6 +/- 0.2 kg; mean +/- SD) were infused with sterile solutions for a 6-d period. On days 1 and 6, a balanced isotonic electrolyte solution was infused. On days 2-5 a 9% solution of glycogen was infused at a rate providing 17.7 +/- 0.77 g/d. For each study day the remaining portion of the energy, protein, essential fatty acids and micronutrients was supplied enterally. No adverse reactions were noted during glycogen infusion, and the animals continued to grow. Glycogen utilization was 66.4 +/- 4.3%. Of the total carbohydrate excreted, 85.4% was composed of oligosaccharides of maltotetraose size or larger. Free glucose accounted for 3.5% of the total excreted, while maltose plus maltotriose accounted for 11.1%. Plasma concentrations of oligosaccharide-bound glucose increased during glycogen infusion, rising from a base-line value of 11.0 +/- 14 mg/dL to an overall mean value for the 4-d period of 100.3 +/- 31.6 mg/dL.

Correlation of glutamate plus aspartate dose, plasma amino acid concentration and neuronal necrosis in infant mice.

Eight-day-old mice were given by gavage glutamate and aspartate mixtures providing each amino acid at 125, 250 or 500 mg/kg body weight (250, 500 and 1000 mg total dicarboxylic amino acids/kg) and the degree and extent of neuronal necrosis were determined. Similar studies were carried out in mice given monosodium L-glutamate at 250 or 500 mg/kg body weight. Plasma aspartate and glutamate concentrations were determined at each dose level. No animal given either glutamate or the glutamate plus aspartate mixture at 250 mg/kg developed neuronal necrosis. However, neuronal necrosis developed in 30% of animals given glutamate at 500 mg/kg (12+/-2 necrotic neurons/section in the region of maximal damage) and in 17% of animals given 250 mg glutamate/kg plus 250 mg aspartate/kg (11-13 necrotic neurons/section in the region of maximal damage). The threshold mean peak plasma glutamate plus aspartate concentration associated with neuronal necrosis was 128+/-24 mumol/dl. Using these data, and previously published data for aspartate-induced neurotoxicity (Finkelstein et al. Toxicology 1983, 29, 109), the individual threshold plasma glutamate and aspartate concentrations associated with neuronal necrosis were calculated to be 110 mumol/dl for aspartate and 75 mumol/dl for glutamate.

Effect of carbohydrate ingestion on plasma aspartate concentrations in infant mice administered sodium L-aspartate.

Previous studies of infant pigs have demonstrated that simultaneous ingestion of carbohydrate (1 g/kg body weight) and glutamate (300 mg/kg body weight) resulted in markedly lower mean peak plasma glutamate concentration and a smaller area under the plasma glutamate concentration-time curve (AUC) than ingestion of the equivalent amount of glutamate alone. This study was carried out to investigate whether a similar carbohydrate-induced effect occurred with the other dicarboxylic amino acid, aspartate. Eight-day-old mice were administered sodium L-aspartate at 250, 500 and 1000 mg/kg body weight with and without 1.0 g/kg body weight of partially hydrolyzed cornstarch. Mean peak plasma aspartate concentration and plasma aspartate AUC values increased in proportion to the aspartate dose. The addition of carbohydrate to the aspartate solution had no significant effect on either mean peak plasma aspartate concentrations or AUC values at aspartate doses of 250 and 500 mg/kg body weight. A modest, but significant effect of carbohydrate was noted on the mean peak plasma aspartate levels in animals administered 1000 mg/kg body weight aspartate (P less than 0.05, Student's t-test). However, analysis of variance showed no significant carbohydrate effect and plasma AUC values were not significantly affected. These data indicate that carbohydrate affects the metabolism of aspartate and glutamate differently.

Correlation of aspartate dose, plasma dicarboxylic amino acid concentration, and neuronal necrosis in infant mice.

Eight-day-old mice were administered aspartate at 0, 1.88, 3.76, 4.89, 5.64 and 7.52 mmol/kg body wt and the degree and extent of neuronal necrosis determined. In addition, plasma aspartate and glutamate concentrations were determined at each aspartate dose. Animals administered aspartate at 0, 1.88 and 3.76 mmol/kg body wt did not develop neuronal necrosis. Hypothalamic neuronal necrosis (7.33 +/- 1.52 necrotic neurons/section of maximal damage) was found in 3 of 10 animals administered aspartate at 4.89 mmol/kg body wt. The extent of neuronal necrosis was proportional to dose once a neurotoxic dose of aspartate was reached. All 12 animals administered aspartate at 5.64 mmol/kg body wt developed lesions (49.5 +/- 7.2 necrotic neurons/section of maximal damage). Similarly, all 18 mice administered aspartate at 7.52 mmol/kg developed hypothalamic lesions (80.8 +/- 17.8 necrotic neurons/section of maximal damage). Infant mice administered the highest dose of aspartate not producing neuronal necrosis (3.76 mmol/kg) had a mean (+/- S.D.) peak plasma aspartate concentration of 87 +/- 23 mumol/dl and a mean peak plasma glutamate concentration of 64 +/- 22 mumol/dl. Thus, the toxic threshold for these amino acids must be greater than those values.

Utilization of intravenously administered beta-cellobiose and maltose by young pigs.

Intravenous solutions of glucose oligosaccharides are potential sources of carbohydrate-derived energy for patients requiring intravenous feeding. Relatively little is known about utilization of glucose oligosaccharides linked by beta-glucosidic bonds. We compared the utilization of maltose (alpha-D-glucosyl-1,4-D-glucose) and beta-cellobiose (beta-D-glucosyl-1,4-D-glucose) when administered intravenously (19 g per day) to young pigs for a 5-day period. Animals infused with maltose excreted 15% of the infused disaccharide over the 5-day infusion period. No evidence of maltose accumulation was noted in plasma, and kidney morphology was normal. Animals infused with beta-cellobiose excreted 95% of the infused disaccharide in the urine. The mean (+/- SD) plasma total glucose concentration increased significantly over base-line values of 114 +/- 39 mg/dl to a value of 180 +/- 28 mg/dl during cellobiose infusion, indicating accumulation of cellobiose in body water. Kidney morphology in cellobiose-infused animals was normal. Intravenously infused beta-cellobiose is poorly utilized by the pig when compared with the utilization of its alpha-1,4 linked isomer, maltose.

Constrictive pericarditis following coronary-artery bypass grafting in a patient with chronic asymptomatic pericardial disease.

Constrictive pericarditis is a rare complication of open-heart surgery. We describe a patient who was found at the time of coronary artery bypass surgery to have asymptomatic pericardial thickening and subsequently developed rapidly progressive constrictive pericarditis. At operation for pericardiectomy, the bypass graft to the posterior descending coronary artery was found to be strangled by fibrous tissue while the remaining two bypass grafts were patent. Following pericardiectomy, the patient made a good recovery.

Segmental localization of sensory cells that innervate the bladder.

The present study labels the neuronal cell bodies that give rise to afferent fibers that innervate the bladder of cat and rat. The method used was the retrograde transport of horseradish peroxidase (HRP) from its injection site in the bladder to cells in various dorsal root ganglia. In the rat, the labelled cells are located in the L1-L2 and L6-S1 dorsal root ganglia. In the cat, the labelled cells are located in the L2-L5 and S1-S4 dorsal root ganglia. This confirms older clinical findings, and for the first time directly demonstrates the afferent cell bodies for the bladder. The bladder afferents are small ganglion cells in both rat and cat, and because there is a correlation between the size of axon and the cell body from which it originates, we conclude that the great majority of bladder afferents are small myelinated or unmyelinated axons. In addition, by restricting the HRP to one side of the bladder, we are able to show that some afferent cell bodies send their distal processes across the midline. These results will be useful in considerations of the neural control of bladder function.