Management of an epidural abscess after continuous epidural catheter infusion.

OBJECTIVE: To increase awareness of the possibility of epidural infection after continuous epidural infusion. Outline the salient diagnostic features of epidural infection. Outline a strategy to manage epidural infection and minimize morbidity. SETTING: Academic multidisciplinary pain clinic. PATIENT: A patient with a left knee meniscal tear with a history of Chronic Regional Pain Syndrome Type I (CRPS I) of the left foot. INTERVENTIONS: Attempted control of CRPS I symptoms with a tunnelled epidural catheter infusion. RESULTS AND CONCLUSIONS: The patient developed an epidural abscess diagnosed on the 11th postoperative day. The catheter was removed and the patient was treated successfully with intravenous antibiotics.

Common nerve blocks in chronic pain management.

Anesthesiologists have become increasingly involved with the management of chronic pain patients in the operating room, on the surgical floor, and in the outpatient pain facility setting (often interdisciplinary). Based upon the authors' practice of regional anesthesia, the most specific contribution to chronic pain management arguably remains the practice of diagnostic, prognostic, and therapeutic injections of the neuraxis, peripheral nerves, and the autonomic nervous system.

Implantable spinal cord stimulator to treat the ischemic manifestations of thromboangiitis obliterans (Buerger's disease).

Thromboangiitis obliterans (Buerger's disease) is a segmental inflammatory vasculitis that involves the small-sized and medium-sized arteries, veins, and nerves. It is causally related to tobacco use. The diagnosis is usually made on the basis of the presence of distal arterial disease in individuals who smoke and in whom other disease entities have been excluded. The most effective treatment for Buerger's disease is smoking cessation. Without strict adherence to tobacco avoidance, disease progression is likely. Methods to control ischemic pain include medications, sympathectomy, or surgical revascularization. The effect of sympathectomy is unpredictable, and the chances of a successful revascularization procedure are rare because distal target vessels often are extensively diseased. Herein, we describe a patient whose condition did not respond to the usual conservative therapy but did respond dramatically to the implantation of a permanent spinal cord stimulator. Although these devices have been used for more than 20 years in various other peripheral arterial diseases, their use in Buerger's disease has been limited.

Hemodynamic responses to dobutamine during acute normovolemic hemodilution.

The effects of dobutamine (DOB) on myocardial performance, systemic hemodynamics, and oxygen delivery during acute normovolemic hemodilution in anesthetized rats were studied. Forty-two Sprague Dawley rats (body weight 375 to 425 g) were divided into six equal groups. Hemodynamic and cardiac indices were measured or calculated at baseline, 30 minutes after the initiation of hemodilution (HD), and 15 minutes after DOB or saline infusion. Myocardial performance in response to acute pressure or volume loads was studied in all groups of animals. HD to a hematocrit (Hct) value of 20% resulted in no change in heart rate (HR), increased CI, SVI, and LV dP/dt, and decreased MAP, SVRI, and oxygen delivery index (O2DI). HD increased peak SV and CI after preload stress while the left ventricular developed pressure (LVDP) was unchanged. Infusion of DOB as 7.5 or 15 micrograms/kg/min increased HR, CI, and LV dP/dt as well as LVDP. At the same time, DOB decreased MAP and SVR, whereas the SVI remained unchanged. In non-HD animals both doses of DOB increased LVDP, but only the larger dose increased CI, whereas peak SV decreased with the smaller dose. Arterial carbon dioxide tension (PaCO2) increased, whereas pH and arterial oxygen tension (PaO2) decreased; however, O2DI remained unchanged. Concomitant hemodilution and DOB infusion resulted in attenuation of HR response to DOB, exaggerated the drop in MAP and SVR, and increased LV dP/dt. Only the larger dose of DOB increased the CI, whereas neither dose could alter the SVI in HD animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Fentanyl stimulates atrial natriuretic peptide secretion.

The effects of fentanyl on ultrastructure, protein biosynthesis, and atrial natriuretic peptide (ANP) secretion were studied in neonatal rat cardiomyocytes (CM). Ventricles from 2-day-old American Wistar rats were digested with 1% collagenase in perfusion buffer. Eight hundred thousand to 1.0 million cells/ml were incubated in tissue culture media, to which fentanyl citrate (Sublimaze) was added in a dose of 10-50 ng/ml. Fentanyl increased the spontaneous CM beating rate, which became rather fibrillary in nature. Protein biosynthesis also increased in a time-related manner. Simultaneous incubation with naloxone (10(-6) M) did not alter the beating rate or protein synthesis. Ultrastructurally, several criteria of myocyte growth were observed: an increase in myofilaments and the appearance of newly formed organized sarcomeres, which were preceded by an increase in the ribosomes and cisternae of rough endoplasmic reticulum, and the appearance of large, adult-type mitochondria with increased matrix granules and long parallel cristae. The latter replaced the elongated thin fetal mitochondria. This was associated with a network of developing sarcoplasmic reticulum and T-tubular system as well as the formation of intercalated discs between the CM. Furthermore, exposure to fentanyl increased ANP immunoreactivity in the culture media while simultaneous incubation with naloxone blocked the effect of fentanyl on ANP secretion. On the other hand, naloxone alone did not alter ANP secretion. Therefore, it could be concluded that fentanyl stimulated protein biosynthesis and ANP secretion as evidenced both biochemically and ultrastructurally. Although the molecular mechanism of ANP secretion by fentanyl is still unclear, yet an opioid receptor mediation could be possible as ANP secretion was blocked by an opioid receptor antagonist (naloxone).

Acute morphological effects of cocaine on rat cardiomyocytes.

The cardiovascular actions of cocaine in vivo are varied and often antagonistic. Cocaine produces excitatory sympathomimetic effects by interfering with re-uptake of norepinephrine at adrenergic nerve terminals. However, the local anaesthetic properties of cocaine exert depressant effects on the myocardium. In an attempt to differentiate the direct effects of cocaine from the indirect sympathomimetic effects on the myocardium, primary cultures of neonatal rat cardiomyocytes were established under serum-free conditions and exposed to cocaine and/or norepinephrine. After 36-48 h in culture, spontaneously contracting cells were treated with cocaine (10-1,000 micrograms/ml) and contractile rate (beats/min) quantitated, after which the cells were processed for ultrastructural examination. The contractile rate was reduced at all dosages with nearly 80% reduction at the highest concentration studied. Recovery of beating rate was observed 24 h after removal of cocaine. Pronounced cytoplasmic vacuolation of the cells occurred at concentrations > or = 100 micrograms/ml. Ultrastructural examination revealed extensive myofibrillar disruption, membrane damage, and a near complete loss of organized sarcomeres. Nuclear morphology remained unaffected. Within 24 h after removal of cocaine from the medium, myocytes recovered their characteristic cytoplasmic architecture, indicative of sarcomere reassembly. The results observed in response to cocaine were distinctly different from the response to norepinephrine. In these myocytes, the contractile rate was enhanced twofold and morphological damage was not observed. These findings suggest that cocaine can directly alter myocardial morphology independent of its sympathomimetic effects.

The localization of cholecystokinin immunoreactivity in the rat ovary and uterine tube.

The presence of cholecystokinin (CCK) immunoreactive nerve fibres in the rat ovary and uterine tubes was detected using the peroxidase antiperoxidase (PAP) technique. The antibody used was anti CCK 4562 which reacts with CCK-4, CCK-8, CCK-12 and CCK-33 (Larsson and Rehfeld, 1977). CCK-immunoreactive nerve fibres were found between the interstitial cells of the ovary, along blood vessels, and close to smooth muscle fibres in the ovary and tubal wall. A possible role of CCK-nerves in modulation of the sensitivity of the ovarian components to other humoral and nervous stimuli is discussed. The possible control of CCK over smooth muscle fibres in the ovary and the uterine tube and its role in ovulation is a matter of further studies.

Portal-like microcirculation in rat sympathetic ganglia.

The fine structure of intraganglionic blood vessels of rat superior cervical sympathetic ganglia is studied with the light microscope and with both conventional and ultrastructural histochemical methods. Two sets of small capillaries together with larger sinusoidal ones are identified. One set of capillaries is associated with the clustered (type II) small catecholamine-containing (CC) cells and exhibits features suggestive of fluid transport function (multiple wide fenestrae and active pinocytosis). The second set of capillaries is in direct relation to the sympathetic neurons (SN) and shows characteristics suggestive of absorptive function (microvilli and pinocytotic vesicles). The larger sinusoidal capillaries are observed in the vicinity of type II CC cells, extend parallel to the long axes of the perikarya of the neurons and occasionally form loops around them. The latter are assumed to be larger blood spaces connecting the two capillary sets and serve to slow the circulation around the neurons. A pattern of portal-like intraganglionic microcirculation through which type II CC cells participate in modulating the SN is postulated. Type II CC cells secrete a catecholamine modulator which, driven by concentration gradient, gains access to the circulation through the fenestrated capillaries. The sinusoidal capillaries serve to perfuse the SN with a slow stream of blood rich in the catecholamine modulator. The latter can be filtered through the microvilli and pinocytotic vesicles of the second set of capillaries to induce slow inhibitory postsynaptic potential on the SN.

Propranolol-induced changes in the catecholamine-containing cells and vesicles of SHR sympathetic ganglia.

The ultrastructural effects of long-term propranolol administration on the catecholamine-containing (CC) cells of cervical sympathetic ganglia were studied in spontaneously hypertensive rats. After 2 months of propranolol administration, there were hydrops of mitochondria, together with swelling and vesiculation of Golgi complex and rough endoplasmic reticulum. Such swollen organelles seemed to coalesce with each other, resulting in transformation of major parts of the cytoplasm into large membrane bound saccules. In that group of animals, the number of CC vesicles showed a significant decrease (P less than 0.025) compared to the control. Moreover, such vesicles looked more electron dense, with decreased electron-lucent haloes compared to the control. Blood pressure recording via rat tail cuff showed a significant drop (P less than 0.0001) of the mean systolic blood pressure in the treated animals. One month after stopping propranolol administration, resorption of the cytoplasmic saccules occurred, but the cytoplasm looked lighter and lost its granular appearance. The mitochondria regained their normal shape, though they appeared fewer in number. The CC vesicles were significantly reduced in number (P less than 0.001) and were less electron dense compared to the control. The possible implications of these findings on the mechanism of action of propranolol as an antihypertensive agent are discussed.

New synapses associated with the granule-containing cells of rat sympathetic ganglia.

The synapses of the rat superior cervical sympathetic ganglion were studied with both conventional and ultrastructural histochemical methods. Besides the cholinergic synapses polarized from preganglionic fibers to sympathetic ganglion neurons, two morphologically and functionally different types of synapses were observed in relation to the small granule-containing (catecholamine-containing) cells of the rat superior cervical ganglion. The first type is an efferent adrenergic synapse polarized from granule-containing cells to the dendrites of the sympathetic ganglion neurons. This type of synapse might mediate the inhibitory effects (slow inhibitory postsynaptic potentials) induced by catecholamines on the sympathetic neurons. The second type is a reciprocal type of synapse between the granule-containing cells and the cholinergic preganglionic fibers. Through such synapses, these cells could exert a modulating effect on the excitatory preganglionic fibers. Therefore, we propose that these cells, through their multiple synaptic connections, exhibit a local modulatory feedback system in the rat sympathetic ganglia and may serve as interneurons between the preganglionic and postganglionic sympathetic neurons.