Early detection of evolving critical illness myopathy with muscle velocity recovery cycles.

OBJECTIVE: To investigate the sensitivity of muscle velocity recovery cycles (MVRCs) for detecting altered membrane properties in critically ill patients, and to compare this to conventional nerve conduction studies (NCS) and quantitative electromyography (qEMG). METHODS: Twenty-four patients with intensive care unit acquired weakness (ICUAW) and 34 healthy subjects were prospectively recruited. In addition to NCS (median, ulnar, peroneal, tibial and sural nerves) and qEMG (biceps brachii, vastus medialis and anterior tibial muscles), MVRCs with frequency ramp were recorded from anterior tibial muscle. RESULTS: MVRC and frequency ramp parameters showed abnormal muscle fiber membrane properties with up to 100% sensitivity and specificity. qEMG showed myopathy in 15 patients (63%) while polyneuropathy was seen in 3 (13%). Decreased compound muscle action potential (CMAP) amplitude (up to 58%) and absent F-waves (up to 75%) were frequent, but long duration CMAPs were only seen in one patient with severe myopathy. CONCLUSIONS: Altered muscle fiber membrane properties can be detected in patients with ICUAW not yet fulfilling diagnostic criteria for critical illness myopathy (CIM). MVRCs may therefore serve as a tool for early detection of evolving CIM. SIGNIFICANCE: CIM is often under-recognized by intensivists, and large-scale longitudinal studies are needed to determine its incidence and pathogenesis.

Subdural intracranial pressure, cerebral perfusion pressure, and degree of cerebral swelling in supra- and infratentorial space-occupying lesions in children.

UNLABELLED: To our knowledge comparative studies of intracranial pressure (ICP) and degree of cerebral swelling during craniotomy for supratentorial or infratentorial space occupying lesion in children are not available. In this prospective study subdural ICP, cerebral perfusion pressure (CPP), dural tension, and the degree of cerebral swelling were analysed in supine and prone positioned children subjected to craniotomy for space occupying lesions. MATERIAL AND METHOD: 48 children with space occupying tumours were subjected to either isoflurane/nitrous oxide 50%/fentanyl (n = 22) or propofol/fentanyl/air/oxygen (n = 26). 25 children were operated supratentorially in supine position, while 23 patients were operated infratentorially in the prone position. Subdural ICP, mean arterial blood pressure (MABP), and CPP were measured just before opening of the dura. Dural tension was estimated before opening of dura, and the degree of cerebral swelling was estimated after opening of dura. RESULTS: The age and weight of children anaesthetised with isoflurane in the prone position were significantly lower than the propofol anaesthetised groups. No significant inter-group differences as regards tumour size, midline shift, rectal temperature, MABP or PaCO2 were found. ICP in prone positioned children averaged 16.9 mm Hg against 9.0 mm Hg in supine positioned children (p < 0.001). In prone positioned children the dura was significantly tenser, and the degree of brain swelling after opening of dura was significantly more pronounced. No significant difference as regard ICP was disclosed when isoflurane/nitrous oxide/fentanyl and propofol/ fentanyl anaesthetized children were compared, but MABP and CPP were significantly lower in isoflurane anaesthetised children. CONCLUSION: In children with cerebral tumours ICP is higher, and the degree of cerebral swelling more pronounced in the prone-compared with supine positioned children. Choice of anaesthesia did not influence ICP, but CPP was significantly lower during isoflurane anaesthesia.

The effects of indomethacin on intracranial pressure and cerebral haemodynamics in patients undergoing craniotomy: a randomised prospective study.

We compared the effects of indomethacin (bolus of 0.2 mg.kg-1 followed by an infusion of 0.2 mg.kg-1.h-1) and placebo on intracranial pressure and cerebral haemodynamics in 30 patients undergoing craniotomy for supratentorial brain tumours under propofol and fentanyl anaesthesia. Indomethacin was given before induction of anaesthesia and the infusion was terminated after opening of the dura. Subdural intracranial pressure was measured through the first burr hole and before opening the dura. Cerebral blood flow velocity, cerebral perfusion pressure, jugular bulb oxygen saturation, arterio-venous oxygen difference and carbon dioxide reactivity were measured; dural tension and the degree of brain swelling were estimated. Before induction of anaesthesia, indomethacin administration was associated with a significant decrease in cerebral blood flow velocity compared with placebo. After induction of anaesthesia, cerebral blood flow velocity and mean arterial blood pressure decreased significantly in both groups. Indomethacin was not associated with a decrease in intracranial pressure. There were no differences in cerebral perfusion pressure, dural tension or degree of brain swelling between the two groups. Carbon dioxide reactivity measured after induction of anaesthesia was significantly lower in the indomethacin group (p < 0.05). After removal of the bone flap, no significant difference in carbon dioxide reactivity was observed. We suggest that these findings are explained by propofol-induced cerebral vasoconstriction.

The effects of 10 degrees reverse trendelenburg position on ICP and CPP in prone positioned patients subjected to craniotomy for occipital or cerebellar tumours.

BACKGROUND: Control of ICP-hypertension is of utmost importance during craniotomy. The effects of reverse Trendelenburg position (RTP) upon ICP and CPP have recently been studied in supine positioned patients. METHOD: In this study we investigated changes in intracranial pressure (ICP), mean arterial blood pressure (MABP), CPP and jugular bulb pressure (JBP) before and one minute after 10( degrees ) RTP in 26 prone positioned patients with either occipital (n=12) or cerebellar tumours (n=14). ICP was measured by a subdural approach after removal of the bone flap. Tension of the dura was estimated by the surgeons by digital palpation before and after change in position. FINDINGS: In patients with occipital tumours ICP decreased from 21.0 to 15.6 mm Hg (p<0.05). MABP decreased from 87.9 to 83.3 mm Hg (p<0.05), JBP decreased from 14.3 to 7.7 mm Hg (P<0.05), while CPP was unchanged. In patients with cerebellar tumours ICP decreased from 18.3 to 14.2 mm Hg (p<0.05). MABP decreased from 93,8 to 90.5 mm Hg (p<0.05), JBP decreased from 12.1 to 5.0 mm Hg (P<0.05), while CPP was unchanged. There were no significant differences between the two groups with regard to changes in ICP, MABP, CPP and JBP. The change in ICP was accompanied by a significant decrease in dural tension (p<0.05). INTERPRETATION: In prone positioned patients 10 degrees RTP significantly reduces ICP, JPB and MABP within one minute, while CPP is unchanged.

No influence of the endothelin receptor antagonist bosentan on basal and indomethacin-induced reduction of cerebral blood flow in pigs.

BACKGROUND: The mechanism behind indomethacin-induced cerebral vasoconstriction is incompletely understood. We tested the hypothesis that the mixed endothelin-1 receptor antagonist bosentan would modify or prevent indomethacin-induced reduction of CBF in the anaesthetized pig. Furthermore, we investigated the effect of bosentan on resting CBF and CMRO2. METHODS: Twelve pigs were randomized in two groups of six, and received either bosentan and indomethacin (group 1), or placebo and indomethacin (group 2). Anaesthesia was induced with ketamine and midazolam and maintained with fentanyl, nitrous oxide and pancuronium. Baseline measurements of CBF and CMRO2 were performed before intravenous bolus injection of bosentan (10 mg/kg) or placebo (0.9% NaCl). The second CBF and CMRO2 measurement was performed 30 min after administration of bosentan/placebo. A 40-min infusion of indomethacin (0.05 mg/kg/min) was administered and the third CBF and CMRO2 measurement was performed 80 min after administration of bosentan/placebo. Independently, pharmacokinetic data of bosentan were generated in four pigs. RESULTS: In group 1, baseline CBF was 55 +/- 7 ml/100 cm3/min. Administration of bosentan i.v. did not change CBF significantly. Indomethacin decreased CBF to 41 +/- 5 ml/100 cm3/min (P < 0.002). In group 2, baseline CBF was 54 +/- 10 ml/100 cm3/min. Placebo did not change CBF while indomethacin decreased CBF significantly to 41 +/- 5 ml/100 cm3/min (P < 0.002). No significant changes in CMRO2 were observed. In group 2, a significant increase in MABP was observed after administration of indomethacin. No change in MABP was observed in the bosentan-treated animals. Total plasma concentrations of bosentan at the time of the first and the second PET measurement were 3.9 and 1.4 microg/ml, respectively. The corresponding values for the pharmacologically active metabolite Ro 48-5033 were 1.2 and 0.4 microg/ml. CONCLUSION: These findings indicate that endothelin receptor stimulation is not involved in indomethacin-induced cerebral vasoconstriction or maintenance of cerebrovascular tone in the anaesthetized pig. However, our results suggest that the increase in MABP is mediated through endothelin receptors.