SFAT-AM: Short Family Therapy in Ambulatory Medicine. Treatment Approach in 10-15 Minute Encounters

The question of the possibilities latent within an appointmentlasting on average only 10–15 minutes, under the pressuresof a heavy workload in a public clinic, has occupied the authorsfor three years. S FAT-AM: Short Family Therapy in AmbulatoryMedicine, has been developed with aim of offering solutionsto this question. The theoretical background is taken from familymedicine with a biopsychosocial (b.p.s.) systems approach. Theauthors formulated series of basic doctor-patient encounterswhich last on average 10–15 minutes. The basic encounteris a kind of didactic checklist model which presents to thedoctor possibilities latent within. Emphasis is placed on theart of treatment and the meeting itself as therapeutic. Duringthe meeting, patient's satisfaction, psychosocial informationand the doctor's inner voice help the participants adjust toeach other and move from stage to stage. The approach also relatesto the possibility of joint work together with colleagues orwith members of different teams in the clinic. The doctor makesuse of communication techniques and reaches a b.p.s. diagnosiswhich will be the basis for suggesting a treatment. The presentedmodel was tried by the authors and by trainees as part of aspecialization course in family medicine. The trainees receivedbetween 20 and 70 academic hours of instruction. From the doctors'report it can be seen that SFAT-AM can be used in a primaryclinic. Future research should give more specific answers toquestions about the model's desirability, cost-efficiency, andjob satisfaction. (Doctors will be referred to in the male genderthroughout the article).     

QRS Axis and the Benefit of Cardiac Resynchronization Therapy in Patients with Mildly Symptomatic Heart Failure Enrolled in MADIT‐CRT

Cardiac Resynchronization Therapy and QRS Axis . Background: Mildly symptomatic heart failure (HF) patients derive substantial clinical benefit from cardiac resynchronization therapy with defibrillator (CRT‐D) as shown in MADIT‐CRT. The presence of QRS axis deviation may influence response to CRT‐D. The objective of this study was to determine whether QRS axis deviation will be associated with differential benefit from CRT‐D. Methods : Baseline electrocardiograms of 1,820 patients from MADIT‐CRT were evaluated for left axis deviation (LAD: quantitative QRS axis ‐30 to ‐90) or right axis deviation (RAD: QRS axis 90–180) in left bundle branch block (LBBB), right bundle branch block (RBBB), and nonspecific interventricular conduction delay QRS morphologies. The primary endpoints were the first occurrence of a HF event or death and the separate occurrence of all‐cause mortality as in MADIT‐CRT. Results: Among LBBB patients, those with LAD had a higher risk of primary events at 2 years than non‐LAD patients (20% vs 16%; P = 0.024). The same was observed among RBBB patients (20% vs 10%; P = 0.05) but not in IVCD patients (22% vs 23%; P = NS). RAD did not convey any increased risk of the primary combined endpoint in any QRS morphology subgroup. When analyzing the benefit of CRT‐D in the non‐LBBB subgroups, there was no significant difference in hazard ratios for CRT‐D versus ICD for either LAD or RAD. However, LBBB patients without LAD showed a trend toward greater benefit from CRT therapy than LBBB patients with LAD (HR for no LAD: 0.37, 95% CI: 0.26–0.53 and with LAD: 0.54, 95% CI: 0.36–0.79; P value for interaction = 0.18). Conclusions: LAD in non‐LBBB patients (RBBB or IVCD) is not associated with an increased benefit from CRT. In LBBB patients, those without LAD seem to benefit more from CRT‐D than those with LAD. (J Cardiovasc Electrophysiol, Vol. 24, pp. 442‐448, April 2013)     

Acute Increase in Serum Tonicity Following Exchange Transfusion

ABSTRACT. We analysed the data of difference in serum sodium (DIFNA) and glucose (DIFGLU) concentrations and difference in serum tonicity (DIFTON) following exchange transfusion (ET) with CPD blood during 122 consecutive procedures performed in 82 newborn infants. Mean (± SE) gestational age (GA) was 30.8 ± 0.45 weeks, mean birthweight was 1568.6 ± 81.4 g, and mean age at time of ET (AGEH) was 60.6 ± 4.3 h. Following the ET, mean serum sodium concentration increased in 110 cases, by 5.4 ± 0.7 mmol/1, and the mean DIFTON rose by 14.6 ± 1.46 mOsm/kg H₂O. Mean DIFGLU rose in 111 cases by 3.8 ± 0.3 mmol/1. Significant correlations were found between DIFNA and AGEH (p<0.02), and between DIFTON and AGEH (p<0.02). ET performed < 48 h after birth produced higher DIFTON values than later transfusions (21.2 vs. 8.2 mOsm/kg H₂O, p<0.001) particularly in the VLBW infants (31.1 in < 28 weeks vs. 15.1 mOsm/kg H₂O in >28 weeks). VLBW neonates appear to be at greatest risk of developing extreme increments in serum tonicity following ET performed within the first 48 h of life.     

Hyperbaric oxygen in acute ischaemia due to allergic vasculitis

A case of a child with allergic vasculitis to penicillin is presented. The patient received successful treatment with hyperbaric oxygen (HBO) therapy. The pathophysiological mechanism of acute peripheral anoxia and the infleunce of HBO treatment on it is described.     

Post-Obstructive Urinary Concentrating Defect A Case Study in the Role of Prostaglandins

ABSTRACT. A child with post-obstructive urinary concentrating defect was studied for the possible pathophysiological role of prostaglandins and an eventual therapeutic approach. Increased urinary excretion of prostaglandins was corrected by indomethacin, with resultant increased nephrogenous cyclic AMP and partial improvement in the concentrating defect. The addition of a thiazide restored urinary concentration. These results add clinical support to the conception of the important role of prostaglandins in the mechanism of post-obstructive hyposthenuria. This therapeutic regimen is advocated for prolonged post-obstructive concentrating defect.     

EFFECT OF NEUROMUSCULAR ELECTRICAL STIMULATION ON THE RECOVERY OF PEOPLE WITH COVID-19 ADMITTED TO THE INTENSIVE CARE UNIT: A NARRATIVE REVIEW

The rehabilitation of patients with COVID-19 after prolonged treatment in the intensive care unit is often complex and challenging. Patients may develop a myriad of long-term multi-organ impairments, affecting the respiratory, cardiac, neurological, digestive and musculoskeletal systems. Skeletal muscle dysfunction of respiratory and limb muscles, commonly referred to as intensive care unit acquired weakness, occurs in approximately 40% of all patients admitted to intensive care. The impact on mobility and return to activities of daily living is severe. Furthermore, many patients experience ongoing symptoms of fatigue, weakness and shortness of breath, in what is being described as “long COVID”. Neuromuscular electrical stimulation is a technique in which small electrical impulses are applied to skeletal muscle to cause contractions when voluntary muscle contraction is difficult or impossible. Neuromuscular electrical stimulation can prevent muscle atrophy, improve muscle strength and function, maintain blood flow and reduce oedema. This review examines the evidence, current guidelines, and proposed benefits of using neuromuscular electrical stimulation with patients admitted to the intensive care unit. Practical recommendations for using electrical muscle stimulation in patients with COVID-19 are provided, and suggestions for further research are proposed.Evidence suggests NMES may play a role in the weaning of patients from ventilators and can be continued in the post-acute and longer-term phases of recovery. As such, NMES may be a suitable treatment modality to implement within rehabilitation pathways for COVID-19, with consideration of the practical and safety issues highlighted within this review. LAY ABSTRACTMany patients with COVID-19 are admitted to the intensive care unit with ongoing symptoms of fatigue, weakness and shortness of breath. Neuromuscular electrical stimulation is a technique in which small electrical impulses are applied to skeletal muscle to cause contractions when voluntary muscle contraction is difficult or impossible. It can prevent muscle atrophy, improve muscle strength and function, maintain blood flow and reduce oedema. This review examines the evidence, current guidelines, and proposed benefits of using neuromuscular electrical stimulation with patients admitted to the intensive care unit. Practical recommendations for using electrical muscle stimulation with COVID-19 patients are provided and suggestions for further research are proposed. Evidence suggests NMES may play a role in the weaning of patients from ventilators and can be continued in the post-acute and longer-term phases of recovery. As such, NMES may be a suitable treatment modality to implement within rehabilitation pathways for COVID-19, with consideration of the practical and safety issues highlighted within this review. Key words: critical care, rehabilitation, neuromuscular electrical stimulation, muscular atrophy, coronavirus infection, COVID-19

The COVID-19 pandemic has seen unprecedented numbers of people being treated in intensive care units (ICUs) worldwide. Many patients have received artificial ventilation, and some have been ventilated for many weeks. Those that survive are often left with long-term disabilities as a result of the effects of both the disease and of the treatments necessary to keep them alive. A myriad of multi-organ impairments is associated with COVID-19 including respiratory, cardiac, neurological, bowel and kidney dysfunction (1). The unexpectedly large number of COVID-19 patients requiring a prolonged stay in ICU additionally increases the risk of dysfunction of both respiratory and skeletal muscle, commonly referred to as ICU-acquired weakness (ICUAW). A conspicuous feature of COVID-19 is the persistence of symptoms, which may appear to resolve, but then recur. As a result, many survivors are left needing significant rehabilitation at a time when such services are under great stress. This has led to the blanket term “long COVID”, which describes ongoing symptoms, which may include fatigue, weakness and delayed recovery (2).Strikingly, in the first 7 months of 2020, there were more than 10,000 COVID-19 admissions to critical care in the UK National Health Service (NHS), which is 4 times greater than historic annual cases of viral pneumonia (3). Our experience of COVID-19 in the UK is that critically unwell patients generally require a longer course of respiratory support, exacerbating other risk factors for ICUAW (3). At present, ICUAW is seen in approximately 20–50% of patients with COVID-19 admitted to the ICU (4). General deconditioning, muscle atrophy, inflammation, and functional disability often necessitate transfer from the ICU to a long-term care facility. Exacerbations of chronic comorbidities and the cycle of prolonged bed rest, ongoing inflammation and malnutrition can lead to continued functional disability, immobility and continued ventilation support. Data from the UK Intensive Care National Audit and Research Centre (ICNARC) database indicates that older age, obesity, multiple deprivation, and the requirement for assistance in activities of daily living (ADL) are predictors for severe disease requiring admission to critical care (3). These risk factors are associated with a reduced level of background fitness, malnutrition and neuropathy. Infection with COVID-19 characteristically causes myalgia, lethargy and a loss of appetite, which are likely to exacerbate this pre-morbid condition. Further deconditioning may result from constrained normal daily activities. This may be due to the disease itself, causing shortness of breath on exertion or delirium (5), or may be the result of supportive interventions and infection control measures. It is also noteworthy that proximal myopathy is associated with the use of therapeutic dexamethasone, a drug that has been shown to reduce 28-day mortality in COVID-19 (6).Table IRisk factors for deconditioning and intensive care unit associated weakness (ICUAW) in patients with COVID-19 in comparison with those with viral pneumonia (3)

Novel ψ-S-CH2 peptide-bond replacement and its utilization in the synthesis of nonpeptidic surrogates of the Leu-Asp-Val sequence that exhibit specific inhibitory activities on CD4+ T cell binding to fibronectin

The Leu-Asp-Val-(LDV)-containing amino acid sequence, derived from the alternatively spliced first connecting segment region of fibronectin (FN), was shown to be recognized primarily by the α₄β₁-integrin receptor expressed on the surface of various cell types. This adhesion epitope may therefore inhibit integrin-mediated cell interactions with the extracellular matrix glycoprotein, including adhesion, migration, activation and differentiation. To probe the structural requirements for LDV recognition by integrins and examine the feasibility of inhibition of LDV-dependent cell-FN interactions, we have designed and constructed a novel ψ-S—CH₂ peptide bond surrogate that was employed in the formation of LDV surrogates. The synthesis of the ψ-S–CH₂ surrogates reported herein is based on Michael addition of 4-methylpentane thiol to an itaconic acid diester to form an S–CH₂ bond. We have found that the LDV surrogates comprises of 4-methylpentanoate-Asp-i-butyl amide and 8-methyl-3-(2-methylpropylaminocarbonyl)-5-thianonanoic acid interfered with CD4⁺ human T-cell adhesion to FN in vitro, with an ED₅₀ of 280 μg/mL. A control structural mimetic of the Leu-Glu-Val (LEV) peptide did not interfere with the T-cell-FN interaction. The specificity of the reaction was substantiated by the finding that the LDV mimetics did not interfere with T-cell adhesion to laminin, another major cell-adhesive glycoprotein of the extracellular matrix. That the nonpeptidic mimetics of LDV interfered markedly with T-cell-FN adhesive interactions indicate that the peptide bond and the amine and carboxyl end groups of the tripeptide makes only a minor contribution to the integrin binding affinity. Thus, consistent with our recent report on the production of Arg-Gly-Asp surrogates, we suggest that these constructs could provide novel insights into the fundamental mechanisms of integrin-ligand interactions, and serve as competitive antagonists of conceivable therapeutic value.