The influence of flushing epidural catheters before use on detection of intravenous placement: an in vitro and in vivo study.

Undetected intravenous placement of epidural catheters is rare but potentially fatal and no perfect identification method exists. Epidural catheters may be flushed before insertion to identify faulty epidural catheters, or to prime the system with local anaesthetic. We hypothesised that flushing epidural catheters before insertion may delay the detection of intravenous placement. We investigated our theory using both in vitro and in vivo models. The in vitro component examined flowrates in flushed and unflushed epidural catheters, using conditions designed to mimic epidural venous pressure. The in vivo component examined the flow within flushed and unflushed epidural catheters inserted into the forearm veins of 20 anaesthetised patients, using a randomised crossover design. The end-point utilised for both components was the time taken for frank blood to reach the 20 cm mark on the epidural catheter. Blood flow to the 20 cm mark on the epidural catheter was significantly faster in the unflushed catheters than the flushed catheters, both in vitro and in vivo (in vitro, unflushed median = 18.6 s (range: 18.0 to 20.5 s), flushed 37.6 s (32.6 to 91.2 s), P = 0.0009; in vivo, unflushed 9.2 seconds (range 5.0 to 35.3 s), flushed 19.2 s (10.6 to 47.4 s), P = 0.003 in vivo). Flushed catheters also demonstrated a greater variability in the range of flowrates. Flushing epidural catheters before insertion may delay the detection of intravenous placement.

Detection of intravascular epidural catheter placement: a review.

Intravascular placement of an epidural catheter is recognised as a potentially fatal complication of epidural anaesthesia and analgesia. Up to 10% of epidural catheters may be inserted into an epidural vessel, the majority of which will be recognised; however, a proportion (1% of all epidural catheters inserted) may not be identified as lying intravascularly. Opinions differ on the optimal method for identifying intravascular catheters and no perfect method exists. Some debate the need for a test of correct location, as a lack of specificity may mean that a proportion of correctly located catheters are withdrawn and resited. This review outlines the incidence and risk factors associated with intravascular placement and aims to evaluate the detection methods that have been described, in an attempt to answer the question: "What is the optimal way of detecting intravascular placement of an epidural catheter?"

Physical and chemical effects of red cells in the shear-induced aggregation of human platelets.

Both chemical and physical effects of red cells have been implicated in the spontaneous aggregation of platelets in sheared whole blood (WB). To determine whether the chemical effect is due to ADP leaking from the red cells, a previously described technique for measuring the concentration and size of single platelets and aggregates was used to study the shear-induced aggregation of platelets in WB flowing through 1.19-mm-diameter polyethylene tubing in the presence and absence of the ADP scavenger enzyme system phosphocreatine-creatine phosphokinase (CP-CPK). Significant spontaneous aggregation was observed at mean tube shear rates, (G) = 41.9 and 335 s-1 (42% and 13% decrease in single platelets after a mean transit time (t) = 43 s, compared to 89 and 95% decrease with 0.2 microM ADP). The addition of CP-CPK, either at the time of, or 30 min before each run, completely abolished aggregation. In the presence of 0.2 microM ADP, CP-CPK caused a reversal of aggregation at (t) = 17 s after 30% of single cells had aggregated. To determine whether red cells exert a physical effect by increasing the time of interaction of two colliding platelets (thereby increasing the proportion of collisions resulting in the formation of aggregates), an optically transparent suspension of 40% reconstituted red cell ghosts in serum containing 2.5-micron-diameter latex spheres (3 x 10(5)/microliters) flowing through 100-microns-diameter tubes was used as a model of platelets in blood, and the results were compared with those obtained in a control suspension of latex spheres in serum alone. Two-body collisions between microspheres in the interior of the flowing ghost cell or serum suspensions at shear rates from 5 to 90 s-1 were recorded on cine film. The films were subsequently analyzed, and the measured doublet lifetime, tau meas, was compared with that predicted by theory in the absence of interactions with other particles, tau theor. The mean (tau meas/tau theor) for doublets in ghost cell suspensions was 1.614 +/- 1.795 (SD; n = 320), compared to a value of 1.001 +/- 0.312 (n = 90) for doublets in serum. Whereas 11% of doublets in ghost cell suspensions had lifetimes from 2.5 to 5 times greater than predicted, in serum, no doublets had lifetimes greater than 1.91 times that predicted. There was no statistically significant correlation between tau meas/tau theor and shear rate, but the values of tau meas/tau theor for low-angle collisions in ghost cell suspensions were significantly greater than for high-angle collisions.

Extracellular-free Ca++ accounts for the sex difference in the aggregation of human platelets in citrated platelet-rich plasma.

It has been shown in Poiseuille flow, that the ADP-induced aggregation of human platelets in citrated plasma from female donors is significantly greater than from male donors over a range of mean tube shear rate, G, from 41.9 s-1 to 1920 s-1 and mean transit time, t, from 0.2 to 86 s. The present work verifies the sex difference at G = 335 s-1 and t = 43 s and deals with the effect of free Ca2+ on it. An inverse correlation between the extent of single platelet aggregation and donor hematocrit, and between hematocrit and the plasma ionized calcium concentration, [Ca2+], as well as a positive correlation between the extent of single platelet aggregation and [Ca2+] was found. This indicated that the sex difference is due to hematocrit-dependent differences in the [Ca2+] that result when a fixed volume of the chelating agent citrate is used to anticoagulate blood. When the initial citrate concentration was adjusted to compensate for the variable volume dilution of citrate in plasma among donors and the [Ca2+] of males raised above that of females, the sex difference was reversed. Again, aggregation correlated with [Ca2+]. At the physiological [Ca2+] in both heparinized PRP and hirudinized PRP, the rate of aggregation and aggregate size were much greater than in citrated plasma but no sex difference was detected.

The effect of red blood cells on the ADP-induced aggregation of human platelets in flow through tubes.

The effect of red blood cells, rbc, and shear rate on the ADP-induced aggregation of platelets in whole blood, WB, flowing through polyethylene tubing was studied using a previously described technique (1). Effluent WB was collected into 0.5% glutaraldehyde and the red blood cells removed by centrifugation through Percoll. At 23 degrees C the rate of single platelet aggregation was upt to 9 x greater in WB than previously found in platelet-rich plasma (2) at mean tube shear rates G = 41.9, 335, and 1,920 s-1, and at both 0.2 and 1.0 microM ADP. At 0.2 microM ADP, the rate of aggregation was greatest at G = 41.9 s-1 over the first 1.7 s mean transit time through the flow tube, t, but decreased steadily with time. At G greater than or equal to 335 s-1 the rate of aggregation increased between t = 1.7 and 8.6 s; however, aggregate size decreased with increasing shear rate. At 1.0 microM ADP, the initial rate of single platelet aggregation was still highest at G = 41.9 s-1 where large aggregates up to several millimeters in diameter containing rbc formed by t = 43 s. At this ADP concentration, aggregate size was still limited at G greater than or equal to 335 s-1 but the rate of single platelet aggregation was markedly greater than at 0.2 microM ADP. By t = 43 s, no single platelets remained and rbc were not incorporated into aggregates. Although aggregate size increased slowly, large aggregates eventually formed. White blood cells were not significantly incorporated into aggregates at any shear rate or ADP concentration. Since the present technique did not induce platelet thromboxane A2 formation or cause cell lysis, these experiments provide evidence for a purely mechanical effect of rbc in augmenting platelet aggregation in WB.

Adenosine diphosphate-induced aggregation of human platelets in flow through tubes. I. Measurement of concentration and size of single platelets and aggregates.

A double infusion flow system and particle sizing technique were developed to study the effect of time and shear rate on adenosine diphosphate-induced platelet aggregation in Poiseuille flow. Citrated platelet-rich plasma, PRP, and 2 microM ADP were simultaneously infused into a 40-microliters cylindrical mixing chamber at a fixed flow ratio, PRP/ADP = 9:1. After rapid mixing by a rotating magnetic stirbar, the platelet suspension flowed through 1.19 or 0.76 mm i.d. polyethylene tubing for mean transit times, t, from 0.1 to 86 s, over a range of mean tube shear rate, G, from 41.9 to 1,000 s-1. Known volumes of suspension were collected into 0.5% buffered glutaraldehyde, and all particles in the volume range 1-10(5) microns 3 were counted and sized using a model ZM particle counter (Coulter Electronics Inc., Hialeah, FL) and a logarithmic amplifier. The decrease in the single platelet concentration served as an overall index of aggregation. The decrease in the total particle concentration was used to calculate the collision capture efficiency during the early stages of aggregation, and aggregate growth was followed by changes in the volume fraction of particles of successively increasing size. Preliminary results demonstrate that both collision efficiency and particle volume fraction reveal important aspects of the aggregation process not indicated by changes in the single platelet concentration alone.

Adenosine diphosphate-induced aggregation of human platelets in flow through tubes. II. Effect of shear rate, donor sex, and ADP concentration.

The effect of shear rate on the adenosine diphosphate-induced aggregation of human platelets in Poiseuille flow was studied using the method described in part I (Bell, D.N., S. Spain, and H.L. Goldsmith. 1989. Biophys. J. 56:817-828). The rate and extent of aggregation in citrated platelet-rich plasma were measured over a range of mean transit time from 0.2 to 8.6 s and mean tube shear rate, G, from 41.9 to 1,920 s-1. At 0.2 microM ADP, changes in the single platelet concentration with time suggest that more than one type of platelet-platelet bond mediates platelet aggregation at physiological shear rates. At low G, a high initial rate of aggregation reflects the formation of a weak bond of high affinity, the strength of which diminishes with time. Here, the fraction of collisions yielding stable doublets, the collision efficiency, reached a maximum of 26%. The collision efficiency decreased with increasing G and was accompanied by a progressive delay in the onset of aggregation. However, the gradual expression of a more shear rate-resistant bond at high shear rates and long mean transit times produced a subsequent increase in collision efficiency and a corresponding increase in the rate of aggregation. Although the collision efficiencies here were less than 1%, the high collision frequencies were able to sustain a high rate of aggregation. At 0.2 microM ADP, aggregate size generally decreased with increasing G. At 1.0 microM ADP, aggregate size was still limited at high shear rates even though the rate of single platelet aggregation was much higher than at 0.2 microM ADP. Platelet aggregation was greater for female than for male donors, an effect related to differences in the hematocrit of donors before preparing platelet-rich plasma.

Otitis externa. A common, often self-inflicted condition.

Otitis externa can be caused by trauma to the ear canal, skin disorders, and viral and bacterial infections. Often the disease is self-inflicted; insertion of an object into the canal in an attempt to clean the ear interferes with the ear's own cleansing mechanism and causes inflammation and infection. Swimmers, persons who wear a hearing aid, and persons who have had an ear disorder are especially prone to infection and may need to take special precautions. Appropriate treatment, including instillation of drops, cleansing of the canal, and drug therapy, usually prevents recurrence. Surgical intervention may be necessary to enlarge a tiny canal or remove exostoses and osteomas. A rare form of otitis externa is "malignant" external otitis, which usually affects diabetic patients and has a high mortality.

Platelet aggregation in poiseuille flow: II. Effect of shear rate.

Using a double infusion technique described in the previous paper, the effect of shear rate, G, on platelet aggregation was studied in citrated platelet-rich plasma in Poiseuille flow over a range of mean linear flow rates, u3 from 50 to 1500 microns-1 corresponding to G from 2 to 54 sec-1. At 1 micron ADP, aggregates were formed at all u3 and, except at the lowest flow rate, both the degree of aggregation (net fraction of cells in aggregates, A') and size of the aggregates increased with distance down the tube. The degree of aggregation was both time and shear rate-dependent. Over the first 10 sec, A' appeared to be independent of the mean transit time indicating that the collision capture efficiency decreased with increasing G. Thereafter, A' increased with increasing shear rate leading to the formation of an appreciable number of aggregates greater than 10 cells at G greater than 24 sec-1. Small aggregates initially formed near the tube wall and, as they grew in size, migrated toward the axis as their rotation was physically impeded by the wall. In addition, the values of A' in cPRP from five female donors were significantly greater than those from five male donors.

Platelet aggregation in poiseuille flow: I. A double infusion technique.

This paper describes the design of a double infusion microtube and its use to directly observe the aggregation of platelets undergoing Poiseuille flow immediately after the introduction of 1 microM ADP. Citrated human platelet-rich plasma flowed between two reservoirs through a 100-microns-diameter flow tube at the entrance of which ADP was simultaneously infused through the tip of a concentrically located micropipet . With the aid of microcinematography, the time course of platelet aggregation was followed by measuring the number distribution of single cells and aggregates across the median plane of the tube at various distances downstream of the micropipet . Preliminary studies covering a range of mean tube shear rates from 2 to 30 sec-1 showed that, for a given donor, the fraction of platelets in aggregates, both in control runs (infusion of Tyrodes ) and in experimental runs (infusion of ADP) was reproducible to within +/- 1%. Except at the lowest shear rate, the extent of aggregation increased with increasing distance down the tube.

Trigeminal neurotization of paralyzed facial musculature. Modification of the Lexer-Rosenthal surgical procedure.

We introduce a modification of the Lexer-Rosenthal surgical technique for reinnervation of the facial muscles by trigeminal neurolization in patients with facial paralysis. Four patients with such paralysis were seen in the Cranial Nerve Research Clinic, Oakland, Calif. Three of the four patients had their paralysis surgically treated, and recovery of facial motion was compared with that in one patient, in whom spontaneous trigeminal neurotization occurred. Those patients whose facial paralysis was surgically treated had fair to excellent results, and the technique is considered superior to alternative hypoglossal or spinal accessory anastomosis.

Herpes simplex virus in idiopathic facial paralysis (Bell palsy).

Sera from all 41 adult patients with idiopathic facil paralysis (Bell palsy) and 35 (85%) of 41 matched controls who had never had Bell palsy contained antibodies to herpes simplex virus (P smaller than.05). The frequency of antibodies to herpes zoster virus did not differ in patients and controls. A rise in antibody titer, indicating primary herpes simplex virus infection, was not found in these patients. That Bell palsy may be caused by reactivation of herpes simplex virus is suggested by (1) clinical, neurologic, laboratory, and immunologic similarities between idiopathic facial paralysis and known manifestations of reactivated herpes simplex virus infection, and (2) the known neurotropism of herpes simplex virus, including its presence in latent form in the trigeminal ganglia, and parallels with known facial paralysis due to varicella zoster virus, a closely related agent. The presence of antibodies to herpes simplex virus is the only common factor among the patients tested in this study.