Does body mass index impact on muscle wasting and recovery following critical illness? A pilot feasibility observational study.

BACKGROUND: Critical illness is associated with muscle loss, weakness and poor recovery. The impact that illness and the ensuing metabolic response has on obese patients is not known. Objectives were to test if obese patients lose less muscle depth compared to non-obese patients; if a reduction in muscle depth was associated with reduced strength and recovery; and to assess the feasibility of these methods with a range of body mass index's (BMI). METHODS: A prospective observational pilot study of muscle depth in critically ill patients categorised by BMI was performed. Muscle depth changes were assessed by ultrasound on study days 1, 3, 5, 7, 12 and 14. Strength was measured via handgrip dynamometry and Medical Research Council (MRC) sum score on waking and at discharge from the intensive care unit. Level of dependency was measured with the Barthel index. RESULTS: 44 critically ill patients; 17 had normal BMI, 10 were overweight and 17 were obese. The three groups did not differ in baseline characteristics, except obese patients had significantly greater initial muscle depth. Muscle depth loss was similar between the BMI groups at each of the time points. Handgrip and MRC sum score were only possible in a small number of patients because of reduced alertness and weakness. Majority were deemed fully dependent based on the Barthel index. CONCLUSIONS: Obese patients lost muscle depth in a comparable manner to non-obese patients, suggesting that BMI may not prevent muscle depth loss. It was not possible to determine the effect on strength because the clinical condition of patients precluded reliable measurements.

Beyond the randomized clinical trial: citrate for continuous renal replacement therapy in clinical practice.

BACKGROUND: Premature circuit clotting is a major problem during continuous renal replacement therapy (CRRT). Six randomized controlled trials confirmed that regional anticoagulation with citrate is superior to heparin. Our objective was to compare circuit patency with citrate, heparin and epoprostenol in routine clinical practice. METHODS: We retrospectively analysed data on circuit patency of all circuits used in a single centre between September 2008 and August 2009. We differentiated between premature filter clotting, elective discontinuation and waste. RESULTS: 309 patients were treated with CRRT (n = 2,059 circuits). The mean age was 65.7; 63.8% were male. The methods to maintain circuit patency were unfractionated heparin (42.3%), epoprostenol (23.0%), citrate (14.7%), combinations of different anticoagulants (14.6%) and no anticoagulation (4.7%). Premature clotting was the most common reason for circuit discontinuation among circuits anticoagulated with heparin, epoprostenol or combinations of different anticoagulants (59-62%). Among circuits anticoagulated with citrate the main reason for discontinuation was elective (61%). Hazard regression analysis confirmed significantly better circuit survival with citrate. Changing from heparin to citrate decreased the risk of premature circuit clotting by 75.8%. CONCLUSION: In routine clinical practice, regional anticoagulation with citrate is associated with significantly better circuit patency than heparin or epoprostenol.

HTLV-I infection in the Free State region of South Africa: a sero-epidemiologic study.

Human T-lymphotropic virus type I (HTLV-1) is associated with tropical spastic paraparesis (TSP) and adult T-cell leukemia/lymphoma. HTLV-I infection is endemic in certain parts of the Natal/KwaZulu region of South Africa. No studies on the seroprevalence of HTLV-I infection in the Free State (FS) have been published. This study was designed to determine the prevalence of HTLV-I antibodies among different patient groups in the FS. Sera from 863 patients were analyzed. There were: 178 asymptomatic rural Blacks, 200 asymptomatic urban Blacks, 50 asymptomatic Whites, 60 patients with spastic myelopathy, 70 patients with other neurologic disorders, 12 patients with T-cell haematologic malignancies and 293 human immunodeficiency virus (HIV) seropositive patients. Sera were tested for the presence of HTLV-I/II antibodies using an enzyme linked immunosorbent assay (ELISA). Positive results were confirmed using a modified Western blot assay. None of the asymptomatic Whites were HTLV-I antibody positive (95 pc confidence interval (CI): 0 to 7 pc), while 2 pc (95 CI: 0.5 to 5 pc) of asymptomatic urban Blacks and 1.1 pc (95 pc CI: 0.14 to 4 pc) of asymptomatic rural Blacks had HTLV-I antibodies. Of the group of patients with spastic myelopathy 33.3 pc (95 pc CI: 21.7 to 46.7 pc had HTLV-I antibodies, while none of the patients with T-cell haematologic malignancies (95 pc CI: 0 to 26.5 pc) or other neurologic disorders (95 pc CI: 0 to 5 pc) had HTLV-I antibodies. Of the HIV seropositive patients 6.1 (95 pc CI: 4 to 9.5) were co-infected with HTLV-I. HTLV-I infection is present in the Free State. It is strongly associated with spastic myelopathy in this region. HIV seropositive patients have a high rate of HTLV-I co-infection.