Biochemical alterations in the trapezius muscle of patients with chronic whiplash associated disorders (WAD) – A microdialysis study

The mechanisms behind the development of chronic trapezius myalgia in patients with whiplash associated disorders (WAD) appear to involve both peripheral and central components, but the specific contribution of alterations in muscle is not clear. Female patients with WAD and involvement of trapezius (N=22) and female controls (N=20; CON) were studied during an experiment compromised of rest (baseline), 20min repetitive low‐force exercise and 120min recovery. Their interstitial concentrations of serotonin (5‐HT), glutamate, lactate, pyruvate, potassium, interleukin‐6 (IL‐6), and blood flow were determined in the trapezius muscle using a microdialysis technique. Pressure pain thresholds (PPT) over trapezius and tibialis anterior muscles were also assessed. In WAD, we found signs of generalized hypersensitivity according to PPT. The WAD group had significantly higher interstitial [IL‐6] and [5‐HT] in the trapezius than the CON. [Pyruvate] was overall significantly lower in WAD, and with lactate it showed another time‐pattern throughout the test. In the multivariate regression analysis of pain intensity [5‐HT] was the strongest regressor and positively correlated with pain intensity in WAD. In addition, blood flow, [pyruvate], and [potassium] influenced the pain intensity in a complex time dependent way. These findings may indicate that peripheral nociceptive processes are activated in WAD with generalized hypersensitivity for pressure and they are not identical with those reported in chronic work‐related trapezius myalgia, which could indicate different pain mechanisms.     

Barbiturates in severe head injuries?

Possible mechanisms for the therapeutic effects of barbituric acid derivatives in severe head injuries have been discussed for half a century. In the following, a survey of the literature, and a discussion of three controlled clinical studies available until now is presented. A proven effect in terms of a beneficial long-term outcome for all injured patients has not been established.On the other hand there might be a subgroup of patients with an intact CO₂ reactivity of the brain vessels who may profit from barbiturates administered after head trauma.Dedicated to Marianne and Gerhard Winkler     

Insulin sensitivity is related to fat oxidation and protein kinase C activity in children with acute burn injury.

Impaired fatty acid oxidation occurs with type 2 diabetes and is associated with accumulations of intracellular lipids, which may increase diacylglycerol (DAG), stimulate protein kinase C activity, and inactivate insulin signaling. Glucose and fat metabolism are altered in burn patients, but have never been related to intracellular lipids or insulin signaling. Thirty children sustaining >40% total body surface area burns were studied acutely with glucose and palmitate tracer infusions and a hyper-insulinemic euglycemic clamp. Muscle triglyceride, DAG, fatty acyl CoA, and insulin signaling were measured. Liver and muscle triglyceride levels were measured with magnetic resonance spectroscopy. Muscle samples from healthy children were controls for DAG concentrations. Insulin sensitivity was reduced and correlated with whole body palmitate beta-oxidation (P = .004). Muscle insulin signaling was not stimulated by hyper-insulinemia. Tissue triglyceride concentrations and activated protein kinase C-beta were elevated, whereas the concentration of DAG was similar to the controls. Free fatty acid profiles of muscle triglyceride did not match DAG. Insulin resistance following burn injury is accompanied by decreased insulin signaling and increased protein kinase C-beta activation. The best metabolic predictor of insulin resistance in burned patients was palmitate oxidation.     

Implementation of a standardised treatment protocol for post resuscitation care after out-of-hospital cardiac arrest

BACKGROUND: Mortality among patients admitted to hospital after out-of-hospital cardiac arrest (OHCA) is high. Based on recent scientific evidence with a main goal of improving survival, we introduced and implemented a standardised post resuscitation protocol focusing on vital organ function including therapeutic hypothermia, percutaneous coronary intervention (PCI), control of haemodynamics, blood glucose, ventilation and seizures. METHODS: All patients with OHCA of cardiac aetiology admitted to the ICU from September 2003 to May 2005 (intervention period) were included in a prospective, observational study and compared to controls from February 1996 to February 1998. RESULTS: In the control period 15/58 (26%) survived to hospital discharge with a favourable neurological outcome versus 34 of 61 (56%) in the intervention period (OR 3.61, CI 1.66-7.84, p=0.001). All survivors with a favourable neurological outcome in both groups were still alive 1 year after discharge. Two patients from the control period were revascularised with thrombolytics versus 30 (49%) receiving PCI treatment in the intervention period (47 patients (77%) underwent cardiac angiography). Therapeutic hypothermia was not used in the control period, but 40 of 52 (77%) comatose patients received this treatment in the intervention period. CONCLUSIONS: Discharge rate from hospital, neurological outcome and 1-year survival improved after standardisation of post resuscitation care. Based on a multivariate logistic analysis, hospital treatment in the intervention period was the most important independent predictor of survival.