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Sorin J Brull

Publications and source records attributed to Sorin J Brull.

10 recordsLinked to original sources
PubMed2006

Brief review: Nondepolarizing neuromuscular blocking drugs and critical illness myopathy.

PURPOSE: Critically-ill patients who receive nondepolarizing neuromuscular blocking drugs (NMBDs) may be at risk of developing profound muscle weakness that may last for months after the NMBD is discontinued, especially when large cumulative doses of NMBDs and corticosteroids are co-administered to septic, mechanically ventilated patients. This review focuses on the etiology and clinical features of critical illness myopathy (CIM), summarizes specific risk factors for its development, and discusses strategies that might be used to attenuate or even prevent the development of this potentially devastating syndrome. CLINICAL FEATURES: The etiology of CIM is unknown. Whether it can develop in at-risk patients who undergo lengthy operations during which they receive NMBDs is also unknown. In some patients following exposure to NMBDs their motor systems are impaired secondary to loss of thick (myosin) filaments that render the muscle unexcitable to direct electrical stimulation, while the sensory system is spared. Management of patients who develop NMBD myopathy is supportive, consisting of nutritional support, physical therapy, and daily trials of decreased ventilatory support. CONCLUSION: Recent guidelines recommend that NMBDs be used in critically ill patients only when absolutely necessary, that the depth of muscle paralysis be monitored to avoid overdosing and metabolite accumulation, and that drug administration be curtailed periodically to allow interruption of sustained NMBD effect.

Anesthesia↗
PubMed2005

Spinal anesthesia.

PURPOSE OF REVIEW: The aim of this article is to review current practice of spinal anesthesia regarding technique and medication use; review recent applications of spinal anesthesia to subspecialty care in outpatient, cardiac, and obstetrical anesthesia; and update risk assessment associated with spinal anesthesia. RECENT FINDINGS: Epidural volume extension enhances the spread of local anesthetics using a combined spinal-epidural technique. Chloroprocaine has become the agent of choice at some institutions. The growth in both the number and complexity of ambulatory surgery procedures has redefined the role of spinal anesthesia for outpatients. The 27-gauge Whitacre spinal needle is associated with a lower incidence of post-dural puncture headaches. Retrospective reviews can predict the incidence of rare complications such as neurologic injury and cardiac arrest. SUMMARY: Innovations in technology, equipment, and needle design improved safety and decreased complication rates from spinal anesthesia. The increased popularity of ambulatory surgical procedures has resulted in more frequent use of spinal anesthesia. Intrathecal narcotic analgesia is used increasingly in fast-tracking cardiac surgical protocols. Modern anesthetic and analgesic techniques include resurgence of older agents (2-chloroprocaine) as well as new agents (levobupivacaine and ropivacaine) that are used in conjunction with adjuvant intrathecal medications (opioids, vasopressors, and alpha-2 adrenergic agonists). Surgical thromboprophylaxis and the increased use of anticoagulants in patients with cardiovascular disease have challenged anesthesiologists to update clinical guidelines to minimize the risk of hemorrhagic complications such as epidural hematoma. The risk/benefit ratio of spinal anesthesia should be individualized. The continued popularity of spinal anesthesia is due to the safety, effectiveness and efficiency of this technique.

Journal Article↗
PubMed2004

Recovery of neuromuscular function after a combination of mivacurium and rocuronium.

PURPOSE: The present study was undertaken to evaluate onset, and early and late recovery of neuromuscular block after a combination of mivacurium (M) and rocuronium (R). METHODS: In this controlled, randomized study, 45 consenting ASA I-II patients were assigned to one of three treatment groups: 2.ED95 R alone (2R); 2.ED95 R plus 1.ED95 M (2R1M). or 2.ED95 R plus 2.ED95 M (2R2M). Neuromuscular monitoring of the ulnar nerve consisted of surface electrode stimulation and force transduction of the adductor pollicis muscle. Stable baseline stimulation (1 Hz, square-wave, supramaximal current) was established prior to relaxant administration and continued until 95 percent twitch height depression (onset). Thereafter, train-of-four stimulation every 10 seconds was used to record recovery data until 95 percent recovery (T(95%)). Data were analyzed using grouped t-tests, ANOVA, and Newman-Keuls multiple comparison tests. Significance was defined at the p < 0.05 level. RESULTS: The addition of mivacurium to rocuronium did not accelerate onset of block. The combination prolonged the clinical duration (time to 5 percent recovery, T(5%)), but did not affect subsequent recovery parameters: T(5%) in the 2R1M and 2R2M groups were 100 percent and 118 percent longer than in the 2R group, respectively (p < 0.05) the T(5-25%) (early recovery) and T(25-75%) (linear recovery) indexes were similar in all three groups. CONCLUSIONS: The present study did not note an acceleration of block onset when mivacurium was added to rocuronium. The findings suggest that the addition of mivacurium (1-2.ED95) to rocuronium (2.ED95) prolongs the clinical duration of the longer-acting agent, rocuronium, but has no effect on the early or linear recovery indexes of rocuronium. Thus, although clinical duration is prolonged, recovery from the combination regimens proceeds as if no mivacurium had been added to rocuronium.

Adolescent↗
PubMed2003

Intradermal sufentanil does not improve lidocaine-induced local anesthesia.

PURPOSE: Peripheral opioid receptors may result in antinociceptive effects when occupied by opioids. This study examined intradermally injected sufentanil (S), a highly lipid soluble opioid, administered with and without lidocaine (L), in a thermal pain model. METHODS: Nine volunteers were instructed on the method of magnitude estimation of pain before undergoing baseline testing with seven seconds thermal stimuli between 44 and 52 degrees C, delivered by a contact thermal stimulator at five cutaneous forearm sites. Then, four sites randomly received injections of equal volumes (0.1 mL) of either normal saline (NS), lidocaine 0.5% (L), sufentanil 0.75 microg (S), lidocaine 0.5% plus sufentanil 0.75 microg (L+S), and one site was not injected and served as reference (REF). Testing was repeated at six, 30, 60, 90, 120, and 150 min following injection. The pain elicited by each stimulus was normalized to the subject's response to the 50 degrees C stimulus at the REF site. RESULTS: Baseline testing showed small (P = ns) differences in pain scores. At six minutes, the lidocaine sites (L, L+S) had pain scores that were mean 83% (range 78-88%) lower than the other sites (P < 0.05), but there was no difference between the L and L+S sites or between the S and NS or REF sites. At 30 and 60 min these pain scores were mean 38% (29-44%) and 20% (8-30%) less than at the REF, NS, and S sites (P = ns). At 90 min and later times, the pain scores had returned to baseline. CONCLUSIONS: These results suggest that intradermal sufentanil alone has no analgesic effect. Further, in combination with lidocaine, sufentanil does neither potentiate nor prolong the analgesic effect of lidocaine.

Adult↗
PubMed2002

Thermosensitivity of large primary sensory neurons.

Spontaneous activity originating in the injured nerve or the dorsal root ganglion (DRG) has been implicated in the development and maintenance of neuropathic pain. The inherent characteristics of spontaneous activity and the causal factors that modulate its firing pattern and frequency are not fully understood. We attempted to assess the thermosensitivity of spontaneous activity in dorsal root ganglion (DRG) neurons in normal rats and in rats with chronic compression of the DRG (CCD) in an in vitro nerve-DRG preparation. Extracellular, dorsal root recording from 66 spontaneously active CCD Abeta fibers indicate that: (1) decreasing bath temperature from 37 to 36-26 degrees C significantly decreased the firing rate (FR) in 85% (56/66) of fibers tested, of which 19 fibers (34%) responded to temperature change at physiological range (36-37 degrees C), whereas the remaining fibers responded at lower temperature levels (26-36 degrees C); (2) cooling of the DRG increased the FR in 12% (8/66) of fibers tested; (3) similarly, the firing rate of 21/26 spontaneously active Abeta fibers from normal rats was decreased following temperature decrease; (4) intracellular recordings from 38 normal neurons revealed that cooling the DRG significantly increased the action potential (AP) threshold, AP duration, AP amplitude and afterhyperpolarization (AHP) duration, but decreased AHP amplitude, maximal depolarizing and repolarizing rates. There was no significant change in the rheobase currents or the resting membrane potential. The present study indicates that large sensory neurons with myelinated axons are temperature dependent. It also suggests that maintenance of a stable temperature is critical for reliable characterization of spontaneous activity of sensory neurons.

Action Potentials↗
PubMed2002

A comparison of chronic pain behavior following local application of tumor necrosis factor alpha to the normal and mechanically compressed lumbar ganglia in the rat.

To study the role of inflammatory cytokines in the initiation and persistence of radiculopathy as seen in humans, tumor necrosis factor alpha (TNF-alpha) was administered either to normal, uninjured L5 dorsal root ganglia (DRG) of rats via a hole drilled through the transverse process, or to chronically compressed L5 DRG via a hollow stainless steel rod inserted into the intervertebral foramen. In other experiments, a mixture of soluble TNF receptors (sTNF-Rs: sTNF-RIplus minussTNF-RII) was locally delivered to the chronically or acutely compressed DRG to neutralize the activity of endogenous TNF-alpha. Behavioral tests of mechanical allodynia were performed before and after TNF-alpha administration. Infusion of the normal DRG with TNF-alpha at a rate of 1 microl/h for 7 days induced ipsilateral mechanical allodynia (i.e. decreased mechanical withdrawal threshold) that lasted about 2 weeks. Infusion of the compressed DRG did not alter compression-induced allodynia within the first operative week but substantially enhanced the ipsilateral allodynia after the first postoperative week. Neutralizing the activity of endogenous TNF-alpha of the compressed DRG with sTNF-Rs reduced allodynia for 3 days, but was subsequently without effect. Similar results were obtained when sTNF-Rs were chronically administrated at the acutely compressed ganglion. Results demonstrated that exogenous TNF-alpha causes pain and mechanical allodynia when deposited at the normal DRG, and further enhances the ongoing allodynia when administrated at the compressed DRG. Results also suggest that endogenous TNF-alpha contributes to the early development of mechanical allodynia in rats with chronic DRG compression.

Animals↗
PubMed2002

Acute topical application of tumor necrosis factor alpha evokes protein kinase A-dependent responses in rat sensory neurons.

Local perfusion of the dorsal root ganglion (DRG) with tumor necrosis factor alpha (TNF-alpha) in rats induces cutaneous hypersensitivity to mechanical stimuli. Thus we investigated the cellular mechanisms of TNF-alpha-induced mechanical hyperalgesia. The L(4) and L(5) DRGs with the sciatic nerves attached were excised from rats for in vitro dorsal root microfilament recording. After baseline recording for 15 min, TNF-alpha (0.001, 0.01, 0.1, or 1 ng/ml) was applied to the DRG for 15 min, followed by washout for at least 30 min. Alternatively, H-89 or Rp-cAMPS, two specific cAMP-dependent protein kinase (PKA) inhibitors, was added to the perfusion solution for 15 min prior to TNF-alpha application. TNF-alpha (1 ng/ml) induced neuronal discharges in 67% (14/21) of C fibers and 27% (4/15) of Abeta fibers when applied topically to the DRG. Acute TNF-alpha application not only evoked discharges in silent fibers, but also enhanced ongoing activity of spontaneously active fibers and increased neuronal sensitivity to electrical stimulation of the peripheral nerves. H-89 (10 microM) and Rp-cAMPS (100 microM) each completely blocked the TNF-alpha-evoked response in most C and Abeta fibers tested but did not affect fiber conductivity. Our results demonstrates that exogenous inflammatory cytokines such as TNF-alpha can elicit a PKA-dependent response in sensory neurons and thus strongly suggest that endogenous TNF-alpha may contribute to the development of certain pathological pain states.

Administration, Topical↗
PubMed2002

Increased sensitivity of sensory neurons to tumor necrosis factor alpha in rats with chronic compression of the lumbar ganglia.

Proinflammatory cytokines may sensitize primary sensory neurons and facilitate development of neuropathic pain processes after peripheral nerve injury. The goal of this study was to determine whether responses of dorsal root ganglion (DRG) neurons to exogenous tumor necrosis factor alpha (TNF-alpha) are altered in a chronically compressed DRG (CCD) injury model. Extracellular recordings from teased dorsal root microfilaments demonstrated that acute topical application of TNF-alpha to the DRG for 15 min evoked C- and Abeta-fiber responses in both normal and CCD rats. However, the response latency was significantly shorter, and the peak discharge rate was higher, in CCD fibers than in normal fibers. Intracellular recordings from small- and large-sized neurons showed that TNF-alpha induced greater depolarization and greater decrease in rheobase in CCD neurons than in normal neurons. The proportion of both small- and large-sized neurons that were responsive to TNF-alpha increased significantly after CCD injury. Furthermore, TNF-alpha altered the discharge patterns of large, spontaneously active neurons in addition to enhancing their discharge rates. However, the depolarization caused by TNF-alpha in such neurons was minor (<2 mV). Inflammatory cytokines such as TNF-alpha increased the sensitivity of sensory neurons in normal and CCD rats. The CCD injury itself, on the other hand, increased neuronal responses to inflammatory cytokines.

Animals↗