By H. Lukjan. Olin College of Engineering. 2019.

Both the distal and second poles demonstrated this mid-diastolic potential aygestin 5 mg mastercard, which was slightly earlier in the distal tip buy cheap aygestin 5 mg. The sinus complexes that were recorded in the same electrograms demonstrated a late potential purchase aygestin paypal. Substrate Mapping In the presence of unstable monomorphic and/or polymorphic ventricular tachycardias, detailed activation mapping and entrainment mapping are not possible. Multisite data acquisition systems as described above may provide useful information in such cases as to the earliest site of activation. However, these methodologies do not necessarily allow one to do a discrete ablative procedure. As such, ablation in these arrhythmias must be aimed at producing larger lesions to disrupt the potential circuit. These are indirect methods based on identification of the arrhythmogenic substrate in patients with structural heart P. As such, abnormal electrograms were used for guiding surgical procedures in which these abnormal electrograms were encircled or removed in order to cure ventricular tachycardia. Substrate ablation was able to prevent induction and clinical recurrence of tachycardias, many of which were relatively stable. We have also used the electroanatomic mapping approach to identify the substrate in coronary disease and have shown that the site of successful ablation in the central, common pathway is located in infarcted tissue with late activation, low voltage, and often associated with late potentials (Fig. A: Ventricular pacing is being carried out at a presumed site in the central common pathway. The patient has been free of ventricular tachycardia for over 10 years, off medications. The concept of using voltage mapping to understand the morphology of ventricular scar and to plan ablation strategies is powerful. However, recent investigation suggests that there are significant limitations to this strategy which may explain, in part, the limited success rate of this technique. Although the voltage gradient in transmural infarction is very steep, repeated measures at the border of the infarct often are disparate, presumably related to the inherent inaccuracy of mapping with large tip catheters and differences in orientation; these errors would be expected to be magnified noninfarct related scar, in which the gradient is not always as steep. At times, isolated late potentials (a certain signal of slow conduction) can be sufficiently high enough in amplitude to not “qualify” as scar in electroanatomic mapping. These limitations may be further magnified when unipolar voltage mapping techniques (see below) are employed. During ventricular tachycardia, mid-diastolic potential was observed (small arrow). Ablation at this site terminated tachycardia by blocking between this diastolic site and a systolic electrogram. This suggested that block occurred between the central common pathway and the exit site of the tachycardia circuit. In addition, although substrate ablation was based initially on surgery, the analogy fails; nonmapping-guided subendocardial resection (i. The concern about the limitations of programmed stimulation (both preablation in identifying all possible morphologies, as well as afterward for test of success) has led to more extensive, surrogate strategies. Most strategies have been evaluated with relatively short-term follow-up in single center observational studies. In general, however, the trend is toward more extensive ablation, albeit limited to the area of scar. This is certainly less elegant than entrainment mapping, and in a way the quantity of lesions is an expression of our frustration with localization techniques, the vagaries of permanent lesion formation in abnormal tissue and concerns about progression of the substrate with time. Approximation of the circuit exit sites was performed with pace mapping at the edge of the voltage map abnormalities. From that fulcrum point, linear lesions are constructed through the exit site to an anatomic barrier or the interior of the scar. On the top left is an activation map that showed latest activation in the midinferior wall. In the upper right is a late potential map in which the latest activation is also shown in purple. Note that the whole inferior wall, which includes the late activation and late potential map site, is low voltage representing scar tissue. A linear lesion was made from the border zone through the site of best pace map to the dense scar. During sinus rhythm, the mapping catheter records a relatively high-voltage, bland electrogram. Electroanatomical maps are shown at the top of each panel, and analog recordings from the mapping catheter at three septal sites at the bottom of each. Both the analog recordings and the voltage map are significantly different with the change in rhythm. The concept of purely anatomic ablation is typically viewed as scar exclusion, usually by circumferential ablation at the border zone in many laboratories; in our laboratory we isolate the area with voltage ≤0. This would be exceptionally difficult (particularly given our documented trouble with durable ablation in the normal myocardium surrounding pulmonary veins! A conceptual variation of this idea is interrogating the “topography” of the scar using advanced imaging techniques, in an effort to determine areas that would be likely circuit sites. Channel-based strategies conceptually interrogate the scar to find distinctive characteristics (voltage, conduction slowing) that may identify putative circuit locations. Another recent take on a similar idea focuses on pace map sites that produce more than a single morphology, supporting the idea that each exit morphology is from a distinct channel (Fig. Ablation of these channels, usually performed with linear ablation near the edge of the scar, can result in inexcitability (inability to capture with high output pacing) within the entire excluded area (Fig. Note the dramatic isolated late potentials recorded on both bipoles of the ablation catheter. Isopotential mapping represents a color map of progression of activation throughout the ventricle as referenced by the location of steep qS unipolar electrograms. At each point in time, activation is shown in white, with recovery (or lower-voltage activation events) in the progression of colors from red to purple.

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The agents most commonly associated with the change from fibrillation to flutter are 1C agents and amiodarone purchase aygestin. The 1A agents have also been associated with this buy aygestin 5 mg visa, but their frequency of use has markedly diminished in the past decade order generic aygestin. An example of a patient with flutter-induced atrial fibrillation and completion of the flutter line that terminated the atrial fibrillation is shown in Figure 13-113. A larger series of patients needs to be evaluated to see how often flutter lesions can prevent atrial fibrillation and if we can better select those patients in whom this procedure might work. The major limiting features of this approach are failure of patient compliance, drug side effects, progressive disease process (e. As suggested above, failure to document pure isthmus-dependent flutter, as practiced in many laboratories, is another feature precluding a successful outcome. The top panel shows 1 of 30 paroxysms of atrial fibrillation experienced daily by this young physician. Following the administration of flecainide (second panel) atrial flutter resulted. This was shown to be isthmus- dependent with classical atrial activation sequences (and entrainment characteristics) (bottom panel). Linear ablation to the isthmus terminated this flutter at the site of the ablation (bottom panel). Bidirectional block was confirmed and the patient has been free of arrhythmias while maintaining flecainide for 4 years. Hybrid pharmacologic and ablative therapy—a novel and effective approach for the management of atrial fibrillation. We have also demonstrated this to be the case using intraoperative mapping techniques as described in Chapter 9. To date, the only technique that has been reproducibly shown to actually cure this type of atrial fibrillation is surgical ablation using the Maze procedure described by Cox et al. James Cox11 12 71 74, , , provided the first cure of persistent atrial fibrillation. The success rate for the Maze has ranged from 75% to 90%, for completely eliminating atrial fibrillation, but with perhaps as high as 25% incidence of pacemaker implantation because of sinus node or A-V node dysfunction. On the right an incision is carried out from the superior to the inferior vena cave and from the suture line of the right appendectomy to the anterolateral tricuspid annulus. Another lesion is made from the intercaval lesion perpendicularly and posterolaterally to the tricuspid annulus. A lesion is also made from the superior aspect of the coronary sinus and Eustachian ridge across the septum involving the fossa ovalis to intersect with the encircling pulmonary vein incision in the left atrium. The complexity of this surgery and the recent electrophysiologic data suggesting a lower incidence of multiple wavelet reentry has resulted in abandonment of the procedure except in a very few centers. The operation has been modified to be employed in combination with mitral valve surgery. A variety of other incisions have been employed in both the right and left atria, but they are more limited than the original Maze procedure. Reduction atrioplasty has also been incorporated into the procedure in order to eliminate excess tissue. The delayed left atrial activation and left atrial incisions make it difficult for me to believe that normal atrial transport is present. Moreover, even if the atria were to contract reasonably, the delayed and irregular atrial activation would unlikely lead to synchronous atrial contraction and appropriate filling of the left ventricle. A study282 compared patients undergoing the Maze procedure with mitral valve repair with patients with preoperative atrial fibrillation who did not have a Maze procedure accompanying mitral valve repair. Although survival was no different at 2 years, there was a marked reduction in atrial fibrillation in the Maze-treated group who also had better outcome in terms of the combined end point of stroke or anticoagulation-related bleeding. This suggests that a variant of the Maze procedure could be safely employed as a concomitant procedure in patients undergoing mitral valve repair or other cardiac surgery in whom atrial fibrillation has been a problem. Whether the Maze procedure alone as an isolated procedure for treating atrial fibrillation has long-term better outcomes and quality of life than either some of the newer catheter-based procedures to “cure” atrial fibrillation (e. At this point in time, permanent atrial fibrillation as an isolated clinical entity should be an unusual indication for Maze procedures. In the top panel, atrial flutter is present, which begins to change subtly as noted by a change in the relationship of the proximal coronary sinus electrogram with the other right atrial electrograms. Persistent atrial fibrillation subsequently developed as seen in the bottom panel. Radiofrequency ablation (after 45 minutes of atrial fibrillation) across the isthmus, when completed, terminates atrial fibrillation. The patient has had no episodes of flutter or fibrillation in 6 months off medicine. A: A narrow band of atrial tissue from the region of the sinus node to the A-V junction is isolated from the remainder of the atria. B: This maintains normal A-V synchrony while fibrillation or other atrial rhythms occur elsewhere. Perhaps the most impressive of these experiences has been logged by the Washington University group. Endocardial ablation is absolutely necessary for endoscopic transdiaphragmatic ablation using the nContact device. However, there were two periprocedural deaths in this experience, one from atrioesophageal fistula, although the risk of this has subsequently been markedly reduced with improved surgical techniques. Catheter-based procedures involving linear lesions in the right and left atria have also been employed to treat persistent, or even permanent, atrial fibrillation. Isolation of the superior vena cava and coronary sinus has been advocated in addition to pulmonary vein isolation in order to minimize the potential for development/maintenance of multiple wavelet reentry, as discussed above. As noted earlier, many investigators are targeting fractionated electrograms and “ganglia” as well. I occasionally will give lesions at the site of Bachmann bundle and/or the os of the coronary sinus in order to impair interatrial conduction. Total isolation of the coronary sinus from the left atrium has been suggested as part of an “individualized approach” to atrial fibrillation.

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Fortunately 5 mg aygestin for sale, cases of the occipital region emergency in our practice have been rare but they can occur generic aygestin 5 mg without a prescription, almost always including attacks of anxiety purchase generic aygestin on line. The anesthetist, in addition to dealing with unex- pected complications, can facilitate infiltration by performing an adequate sedation, which also allows reduction in the doses of local anesthetics. Prepare an anesthetic mixture (2 % lidocaine with a 1:100,000 dilution of adrenaline), which is injected in small and regular shots over the entire surface to be treated: since extensive undermining will be required, it is better to infil- trate both the median area and laterally, up to the retroauricu- vv lar sulcus, and frontally, up to the frontal recesses. Postoperatively, prescribe an appropriate antibiotic and corticosteroid therapy to reduce edema. With regard to pain, which is one of the main dissuasive factors of this method, we have developed a specific analge- sic therapy, such that this type of surgery can be considered just as any other procedure commonly performed in plastic surgery. With the patient in a semi-sitting position on the operation 7 cm away from “V” bed, with the marks already drawn and after the anesthesiol- F i g. Frontally, follows an ideal line joining the front edge of the incision to the anterior margin of the auricle • Toward the back, proceeds only along the median line, to avoid damaging the two occipital peduncles The undermining is performed along a practically avascu- lar plane, and in fact we usually perform homeostasis with an electroscalpel only along the incision line. V We can increase this size by means of a forced intraopera- tive extension with a multiple hook. To perform this maneuver, we hook the device to the galea of the two sides, and exercise a forced and repeated traction on at least three points per side. These actions, on the one hand, increase by about 25 % the removable part of bald area, and on the other increase the degree of postoperative pain, an unpleasant experience for the patient. Therefore it is better to limit these • On the transversal line actions only to selected cases (Fig. To remove more bald scalp extender, grasp it with a needle holder at one of the two metal 2. To avoid the unaesthetic median scar in the occipital bars, and, with a rotating movement, remove the hooks from region the galea, first on one side, then the other. To naturally direct hair growth downward to mask the We widely undermine the subgaleal plain, remove the scars that are no longer vertical, but horizontal (Fig. The ideal would be to perform the operation on flap; a portion of this tissue might be useful to suture the final a shaved head, but in general patients do not like this gap with less tension. Therefore, to avoid the possibility that surgi- sacrifice, and must also include the galea to avoid compro- cal maneuvers erase the preoperative drawings, we mark mising the vitality of the flaps. The width of the gap in the frontal region may 3 cm vary, at the Vertex it has to be 1 cm, in the occipital region it has to be 3 cm. In general, the scalp is very well supplied with blood vessels and tolerates precarious situations well. Diastasis of the scars, particularly of the median scar that starts from the vertex, and of the third flap on its caudal side, is possible. With regard to the diastasis of the median scar, the most frequent cause concerns the incomplete removal of the entire surface between the two series of hooks, an area that is compressed during the action of the extender and which, if not removed, extends itself. To overcome this inconvenience, in addition to the correct surgical technique we find it useful to place some robust nylon stitches to fix the galea to the periosteum. We put these stitches away from the breach so as to position a second series of smaller-sized stitches nearer to the edges. The skin can eventually be sutured with a colored non-absorbable thread, even 5-0, so that the scalp remains stable. To reduce tension on the third flap, in addition to the classical maneuver of fixing the occipital scalp to deeper levels we have introduced a modi- Fig. To match the size of the Skin Extenders 575 two sides of the breach, we decided to shorten the occipital 3. Dekker, New York, pp 785–793 then neglected, as it did not give rise to any aesthetic incon- 4. Slot occipital correction with three venience; on the contrary, in the event of autografting, it transposition flaps. In: Robbins R (ed) Textbook of dermatologic offered an additional harvesting area (Fig. Slot occipital correction with three Difficulty suturing the breach between the third flap and transposition flaps. In: Rusciani L, Robins P (eds) Textbook of der- the cephalic side of the occipital scalp may arise because of matologic surgery, vol 2. To solve this problem, we prepared a fourth Extension prolongée dans le traitment des calvities étendues. Kugler ity, we improved the scars and eliminated the graft: in these Publications, Amsterdam, New York, pp 125–137 cases, the major difficulty was to have the patient accept this 8. Other complications include: protrusion of the extender Imprimerie Lamy, Marseille, France, pp 55–77 11. J Dermatol Surg Oncol 10:967–969 and fistula along the scar from a tuft of hair trapped in the suture. London, England, 6–9 June 2002 The Suture of Nordstrom Manfredi Greco , Tiziana Vitagliano , and Rolf E. Nordstrom The extensive loss of tissue, especially if located in certain The introduction in surgical practice of tissue expanders parts of the body, often provokes serious problems for their has thus increased the possibility of scalp reduction or, reconstruction. The use of skin expanders where the skin is indeed, any approach to replacing extensive losses of tissue. Tissue the use of quantities of similar skin sufficient enough to expanders require several sessions of filling to achieve the reconstruct the defect. In addition, they require surgical inter- This method, known as tissue expansion, was introduced vention for their removal and confer a temporary deformity in surgical practice at the end of the 1950s when an article on almost never accepted by the patient, and the small donor the post-traumatic reconstruction of an ear using a device sites can hardly ever be expanded. The high cost of these filled with air passed through an external tube was published devices should not be underestimated. Tissue expanders widely used, determines a stretching force that reaches subsequently became popular, leading to the creation of 675 g, whereas as shown by many studies the ideal force to devices that exploit the elastic properties of the skin through be applied to a wound subjected to tension should range stretching by a tank filled progressively with saline. Depending on the shape they can be divided into rect- although it harbors certain limitations such as the need for angular, round, or crescent, and depending on the clinical repeated interventions to complete the areas of alopecia and expansion they can be spread in the same way over the entire the excessive tension that acts on the sides of the wound. These surface of the device or in a different way to achieve stronger factors can often lead to “stretch-back” and reappearance of expansion at a certain point in preference to another. Campanella”, Polo Oncologico di Eccellenza “Germaneto”, Catanzaro , Italy the later stages of scar contracture.

Women who have severe incontinence should cheap aygestin 5 mg with amex, in addition 5 mg aygestin mastercard, be assessed by a colorectal surgeon for a secondary sphincter repair or sacral nerve modulation buy generic aygestin 5mg. Women who have had a successful secondary sphincter repair for fecal incontinence should be delivered by cesarean section [84]. Some women with fecal incontinence may choose to complete their family prior to embarking on anal sphincter surgery. It would appear that these women may be allowed a vaginal delivery as the damage to the sphincter has already occurred and risk of further damage is minimal and probably insignificant in terms of outcome of surgery. The risk of worsening or de novo neuropathy has not been quantified and, in practice, does not appear to be clinically significant. If vaginal delivery is contemplated then these tests should be performed during the current pregnancy unless performed previously and found to be normal. Therefore, asymptomatic women who have no evidence of compromised anal sphincter function (ideally, confirmed by anal ultrasound and manometry) should be counselled accordingly and encouraged to have a vaginal delivery [82]. Therefore, unless it is the explicit wish of the woman, it should be reserved for those who are symptomatic or women who had undergone a successful secondary anal sphincter repair for fecal incontinence. Pathophysiology of urinary incontinence, fecal incontinence and pelvic organ prolapse. Third degree obstetric anal sphincter tears: Risk factors and outcome of primary repair. Incidence of third-degree perineal tears in labour and outcome after primary repair. Nordenstam J, Mellgren A, Altman D, Lopez A, Johansson C, Anzen B, Zhong-ze Li, Zetterstrom J. Immediate or delayed repair of obstetric anal sphincter tears—A randomised controlled trial. Increasing incidence of anal sphincter tears among primiparas in Sweden: A population-based register study. Fecal and urinary incontinence after vaginal delivery with anal sphincter disruption in an obstetrics unit in the United States. Anal incontinence in women with third or fourth degree perineal tears and subsequent vaginal deliveries. Detecting anal sphincter injury: Acceptability and feasibility of endoanal ultrasound immediately postpartum. Differences in outcomes after third- versus fourth-degree perineal laceration repair: A prospective study. Anal endosonographic findings in the follow-up of primarily sutured sphincteric ruptures. Anatomic and functional results of surgical repair after total perineal rupture at delivery. Anal sphincter damage after vaginal delivery: Functional outcome and risk factors for fecal incontinence. Third-degree obstetric perineal tear: Long-term clinical and functional results after primary repair. Anal sphincter tears at vaginal delivery: Risk factors and clinical outcome of primary repair. Effect of new guideline on outcome following third degree perineal tears: Results of a three-year audit. Anal incontinence after obstetric sphincter tears: Incidence in a Norwegian county. Primary repair of obstetric anal sphincter laceration: A randomized trial of two surgical techniques. A prospective cohort study of women after primary repair of obstetric anal sphincter laceration. Long-term ailments due to anal sphincter rupture caused by delivery—A hidden problem. Anal sphincter function and integrity after primary repair of third- degree tear: Uncontrolled prospective analysis. Risks of anal incontinence from subsequent vaginal delivery after a complete obstetric anal sphincter tear. Symptoms and anal sphincter morphology following primary repair of third degree tears. A randomized clinical trial comparing primary overlap with approximation repair of third degree obstetric tears. Early evaluation of bowel symptoms after primary repair of obstetric perineal rupture. Endosonography in the evaluation of anal function after primary repair of a third-degree obstetric tear. Objective methods cannot predict anal incontinence after primary repair of extensive anal tears. Anal incontinence after anal sphincter disruption: A 30-year retrospective cohort study. Management of obstetric anal sphincter injury: A systematic review and national practice survey. Anterior anal sphincter repair for fecal incontinence: Good long term results are possible. Long term results of overlapping anterior anal-sphincter repair for obstetric trauma. How to repair an anal sphincter injury after vaginal delivery: Results of a randomised controlled trial. The overlap technique versus end-to-end approximation technique for primary repair of obstetric anal sphincter rupture: A randomized controlled study. Overlapping compared with end-to-end repair of third- and fourth-degree obstetric anal sphincter tears: A randomized controlled trial. Overlapping compared with end-to-end repair of third-and fourth-degree obstetric anal sphincter tears: A randomized controlled trial. Overlapping compared with end-to-end repair of complete third-degree or fourth-degree obstetric tears: Three-year follow-up of a randomized controlled trial.

The former is readily demonstrated in the human infant or in patients with neuropathic bladder when the bladder wall tension exceeds the micturition threshold due to increased urine volume discount aygestin online amex. Voiding is initiated upon cessation of sympathetic and somatic input to the detrusor and sphincter buy discount aygestin, which causes sphincters to relax and the bladder neck to assume the shape of a funnel buy genuine aygestin, and the concomitant increased parasympathetic activity causes the detrusor contraction to generate pressure for overcoming resistance generated by the collapsed urethra. At this point, increased afferent firing from tension receptors in the bladder reverses the pattern of efferent outflow, producing firing in the sacral parasympathetic pathways and inhibition of sympathetic and somatic pathways. Reversal in efferent outflow in both sympathetic and somatic innervations to the urethra and sphincter causes a reflex relaxation followed in a few seconds by parasympathetic nerve– mediated detrusor contraction (Figure 23. As a result, the pressure inside bladder rises and the urethral pressure falls, which is a prerequisite for the urine expulsion. Elimination of urine is also facilitated by noncholinergic/nonadrenergic nitric oxide release onto the internal urethral sphincter, resulting in a relaxation of the urethral outlet [69,70] and by removal of excitatory inputs to the urethra. Secondary reflexes elicited by flow of urine through the urethra also facilitate bladder emptying [61,66,71]. These reflexes require the integrative action of neuronal populations at various levels of the neuraxis (Figure 23. Complete bladder emptying is facilitated by urethra to bladder reflex occurring while urine is flowing through urethra as demonstrated in anesthetized cat experiments by Barrington [72,73] (Figure 23. The other component was activated by a visceral afferent pathway in the pelvic nerve to facilitate voiding at the spinal micturition center [72]. Studies [71] in the anesthetized rat have further confirmed the seminal findings of Barrington [74]. At the initiation of micturition, intense vesical afferent activity activates the brainstem micturition center, which inhibits the spinal guarding reflexes (sympathetic and pudendal outflow to the urethra). Measurements of reflex bladder contractions under isovolumetric conditions during continuous urethral perfusion (0. Desensitization of the urethral afferent with intraurethral capsaicin also dramatically altered the micturition reflex. The existence of this pudendal nerve–mediated reflex has been confirmed as low-frequency electrical stimulation of afferent axons in the human pudendal nerve and the deep perineal nerve, a caudal branch of the pudendal nerve in cats that can initiate reflex bladder contractions and voiding [75,76]. The existence of urethra to bladder reflex may explain why stress incontinence and urge incontinence are comorbidities in women. Women with mixed incontinence may have detrusor overactivity activated by leakage of urine into the urethra due to stress incontinence, which support the theory of stress incontinence inducing urge incontinence [77]. Interestingly, surgical cure of the stress incontinence of women with mixed incontinence has resolved the urge incontinence in up to half of the patients. Inputs from supraspinal, spinal, and peripheral nervous system are necessary to maintain “switch-like” patterns of filling and voiding activity (Figures 23. The principal reflex components of these switching circuits are listed in Figures 23. Parasympathetic preganglionic axons that originate in the sacral spinal cord pass in the pelvic nerve to ganglion cells in the pelvic plexus and to distal ganglia in the organs. The pudendal and pelvic nerves also receive postganglionic axons from the caudal sympathetic chain ganglia. It is also possible that individual reflexes might be linked together in a serial manner to create complex feedback mechanisms. Thus, a bladder to sphincter to bladder reflex pathway could in theory contribute to the suppression of bladder activity during urine storage. Alterations in these primitive reflex mechanisms may contribute to neurogenic bladder dysfunction. Afferent Pathways 343 An intact afferent system is crucial to physiological voiding and bladder filling. During the filling phase, mechanoreceptors in bladder wall initiate visceral afferent (Aδ-fibers) activity that is carried by afferent axons in the pelvic nerve that synapse on spinal interneurons in lumbosacral spinal cord [62,80,81]. The pelvic nerve afferents consist of myelinated (A) and unmyelinated (C) axons to monitor the volume of the bladder and the amplitude of the bladder contraction (Figure 23. Visceral afferent fibers of the pelvic [82] and pudendal [83] nerves enter the cord and travel rostrocaudally within Lissauer’s tract. During neuropathic conditions and possibly inflammatory conditions, there is recruitment of C fibers from a new functional afferent pathway that can cause urge incontinence and possibly bladder pain. The suppression of detrusor overactivity in patients by sacral root stimulation may reflect in part the activation of the afferent limb of these visceral-bladder and somatic-bladder inhibitory reflexes [85–89]. Spinal and Supraspinal Pathways Involved in the Micturition Reflex In the spinal cord, afferent pathways terminate on second-order interneurons that relay information to the brain or to other regions of the spinal cord including the preganglionic sympathetic fibers from the intermediolateral cell column of the lower thoracic (T10) to upper lumbar (L2) spinal cord that form the thoracic and lumbar splanchnic nerves. Because polysynaptic pathways but not monosynaptic pathways mediate bladder, urethral, and sphincter reflex, interneuronal mechanisms play an essential role in the regulation of lower urinary tract function. Electrophysiological [90,91] and neuroanatomic [79,92–94] techniques have identified lower urinary tract interneurons in the same regions of the cord that receive afferent input from the bladder. Pharmacological experiments revealed that glutamic acid is the excitatory transmitter in these pathways [84]. Stimulation of afferent fibers from various regions (anus, colon–rectum, vagina, uterine cervix, penis, perineum, pudendal nerve) can inhibit the firing of sacral interneurons evoked by bladder distention [90]. This inhibition may be a result of presynaptic inhibition at primary afferent terminals or be due to direct postsynaptic inhibition of the second-order neurons. Direct postsynaptic inhibition of bladder preganglionic neurons can also be elicited by stimulation of somatic afferent axons in the pudendal nerve or visceral afferents from the distal bowel [95,96]. Peripheral Nervous System The lower urinary tract is innervated by three sets of the peripheral nerves involving the parasympathetic, sympathetic, and somatic nervous systems (Figure 23. Pelvic parasympathetic nerves arise at the sacral level of the spinal cord, excite the bladder, and relax the urethra. Lumbar sympathetic nerves inhibit the bladder body and excite the bladder base and urethra. Parasympathetic Pathways The preganglionic parasympathetic fibers arise from the ventral roots in the lateral part of the sacral intermediate gray matter in a region termed the sacral parasympathetic nucleus (S2–S4) and spinal cord to form the pelvic splanchnic nerves [63,82,84,98,99]. Upon coursing through and exiting the hypogastric and pelvic plexus, the fibers join the pelvic and pudendal nerves to synapse on terminal ganglia [1] and innervate the detrusor smooth muscle and urethra. The parasympathetic postganglionic neurons in humans are located not only in the detrusor wall layer but also in the pelvic plexus. This dual location can allow the possibility of afferent and efferent neuron interconnection at the level of the intramural ganglia in cauda equina or pelvic plexus injury [66,84]. Such injury leaves patients neurologically decentralized but may not be completely denervated.

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The division in anterior (skin and orbicularis oculi mus- neurosis buy aygestin on line amex, orbital septum and suborbicularis fascia on the deep cle) and posterior (tarsus and conjunctiva) lamella appears too surface of the orbicularis oculi muscle aygestin 5mg mastercard. On the upper eyelid it is possible levator palpebrae muscle as well as the trochlea that is to identify at least two fat bags (medial and central) order aygestin 5mg fast delivery, but an located in the medial portion of the orbit superoposteriorly to accessory lateral bag is identifiable in more than 20 % of the dissecting area should be avoided. The medial adipose bag is pale yel- low or white and it is located medial to the levator aponeurosis and at the root of the nose (Figs. Histologically, it Central fat pad Fusion line of and pre presents a larger quantity of connective tissue, vascularization the fascia and aponeurotica and sensitive innervation from the supratrochlear nerve. The orbital septum central and lateral bags have a bright yellow colour and are Medial fat pad Lacrimal located above the levator aponeurosis. A topical anaesthesia of the eye globe is per- tarsal plate) formed before the placement of the corneal protector, fol- lowed by local anaesthesia with epinephrine both on the skin and the conjunctiva. The area is then exposed with the appropriate retractor so as to incise the conjunctiva medially, 3–4 mm above the tar- Medial, central and lateral fat pads of the lower eyelid Fig. Orbital septum Lateral extension of pre aponeurotica Orbital Nasal fat pad Central fat pad fat fat (orbital fat) Lacrimal gland Levator Muscle of Muller aponeurosis Conjunctiva Tarsal plate Orbicularis oculi muscle Fig. References The quantity of fat to be removed depends on what protrudes from the incision and what is visible when gently pushing 1. Le Louarn C (2009) Muscular aging and its involvement in facial junctival margins. Can J Plast The better knowledge of the oculo-palpebral anatomy along Surg 17(3):102–103 with the need to minimize the undesired effects of tradi- 5. Bourguet J (1924) Les hernies graisseuses de l’orbite: notre traite- blepharoplasty for the lower and upper eyelid, allowing to ment chirurgical. Bull Acad Nat Med 92:1270–1272 reduce the risk of lid retraction with subsequent scleral show 7. Ophthalmology Usually the expert surgeon, that is able to perform both 96(7):1027–1032 the transcutaneous and transconjunctival blepharoplasty, 9. Plast Reconstr Surg 96(5):1053–1060 decisive factor in the choice for the most appropriate 10. Complications and their avoidance: a retrospective approach is usually for cases without skin excess. Arch Otolaryngol Head Neck contrary, but only in lower blepharoplasty, some authors Surg 119(9):993–999 11. In case a skin excess is also present, this Otolaryngol Head Neck Surg 120:172–177 is removed by sculpting a skin flap or by using the pinch 12. Dermatol Surg 21(5):407–410 sider the skin excess as relative, since a certain quantity of 14. Review skin is necessary to cover the remaining area after the fat Press Edit, New York bag removal. These Ophthalmol 127(5):614–616 procedures are able to effectively reduce the periocular 18. Plast Reconstr Surg 125(1):384–392 an easily performed surgical procedure that does not leave 20. Aesthet visible scars and respects the functional integrity of the Surg J 25(3):292–300 anatomical structures and the active support of the eyelid. Aesthetic Plast Surg 15:223 nal scars and for elder people preventing the development 23. Persichetti P, Di Lella F, Delfino S, Scuderi N (2004) Adipose com- of scleral show and ectropion, which are possible compli- partments of the upper eyelid: anatomy applied to blepharoplasty. Plast Reconstr Surg 113(1):373–378; discussion 379–380 Lateral Canthal Surgery in Blepharoplasty Glenn W. Jelks The development of lateral canthal surgical procedures par- had the disadvantage of distorting the lid margins and allels the understanding and treatment of lower eyelid mal- decreasing the functional fields of vision. They are surgical techniques employed at the mities associated with the tarsorrhaphies. Modifications of these atonic, or paralytic lower eyelid malpositions; (2) lateral can- procedures were described by Smith and Kazanjian and thal dystopia (lateral canthus lower than the medial canthus); Converse with a tarsoconjunctival wedge excised medially. Edgerton and Wolfort [2] described a de-epithelialized The concomitant use of autogenous auricular cartilage or dermal pennant of lateral canthal tissue that was passed palatal mucosa lower eyelid vertical spacer grafts, bone through a drill hole in the lateral orbital wall to correct lower anchors for suspension of the midface, myocutaneous flaps, eyelid malposition (Fig. Montandon [7 ] modified this skin grafts, and mucosal grafts allows reliable reconstruction procedure to include a lateral tarsorrhaphy (Fig. Lateral the lateral aspects of the upper and lower eyelids as they canthal suspensions have also been described via facelift interrelate with the lateral retinaculum. Direct lateral canthal incision access to the lateral orbital rim by Whitaker [14]. Indirect lateral canthal procedures support cial and cosmetic surgical interventions. These ancil- and Farkas described lateral canthal fixation via the conjunc- lary procedures are very effective in reconstruction of com- tival approach [16]. Jelks [3 , 11 , 13 , 22], Hinderer [20], and Flowers [18] Von Walther designed the simple lateral tarsorrhaphy pro- described variations in bone or periosteal fixation of the lat- cedure to correct the upper and lower eyelids laterally. Many surgeons developed their own methods of creating the lateral canthal angle by various suture techniques. Note there is no decrease in orbital bone fenestration and shortening of palpebral aperture with lat- horizontal palpebral aperture. Removal of epithelial elements from the lateral lower eyelid under laterally based periosteal flap (Baylis and Hamako 1980) (From creates a strip of tarsus corresponding to the amount of horizontal lid Jelks and Smith [13 ], pp 1720–1721) Lateral Canthal Surgery in Blepharoplasty 785 Anderson and Gordy [9], Jordan and Anderson [12], Lisman et al. Tenzel [6 ] described a lateral canthoplasty which passed through the upper lateral canthal retinacular structures to better approximate the lower lid to the globe (Fig. Bachelor and Jobe, Holt, Holt and van Kirk, and Leone described the use of periosteal flaps and temporalis fascia and palmaris longus tendons for lateral canthal reconstructions [13]. Lateral canthal procedures are designed to provide effec- tive lower eyelid tightening and lateral canthal elevation Fig. Zone V includes the contiguous periorbital structures of nasal, glabellar, brow, forehead, temple, malar, and naso- surrounding structures are divided into zones (Fig.

During relatively slow rates purchase aygestin 5 mg visa, 50 to 60 order genuine aygestin on line, the P waves become flat in these leads and the earliest onset of atrial activation is often recorded at the midlateral atrial sites purchase on line aygestin. To assess atrial conduction more accurately, we have used endocardial mapping of the atria in our laboratory for several years. A general assessment of intra-atrial conduction can be made using catheter recordings obtained from the high- and low-right atrium at the junctions with the venae cavae, midlateral right atrium, A-V junction (in the His bundle electrogram), proximal, mid- and distal coronary sinus, and/or left atrium. Detailed mapping of the left atrium requires a transseptal approach or use of a patent foramen ovale. Although the retrograde approach can be used, it is far more difficult to reproducibly map the entire left atrium. When mapping is performed, conduction times should be determined using the point at which the largest rapid deflection crosses the baseline or the peak of the largest deflection (both should be nearly the same in normal tissue). These measurements correlate to the intrinsicoid deflection of the local unipolar electrogram, which in turn has been shown to correlate with local conduction (phase 0) using simultaneously recorded microelectrodes. The peak and its crossing of the baseline are then easy to measure and are more accurate. This differs from the technique of measuring the onset of the His bundle deflection, in which the onset of depolarization of the entire His bundle rather than local activation is desired. Although close (1- to 2-mm) bipolar electrodes record local activity most discriminately, we have obtained comparable data using catheters with a standard (0. How to best measure activation times of a multicomponent atrial electrogram has not been established. In my opinion, all rapid deflections can be considered relatively local activations (i. Unipolar signals can help determine the component which is closest to any recording electrode (see Chapter 1). Such electrograms may be caused by a specific anatomic substrate producing nonuniform anisotropy leading to asynchronous activation in the region from which the electrogram is recorded (see Chapter 11). Our data have shown that normal atrial activation can begin in either the high or the midlateral right atrium, spread from there to the low atrium and A-V junction, and then spread to the left atrium. As noted previously, in our experience, earlier activation of the high-right atrium is more likely to occur at faster rates (i. Two possibilities exist, which are (a) the right atrium has a multitude of pacemaker complexes, the dominance of which is determined by autonomic tone, or (b) these different activation patterns may reflect different routes of exit from a single sinus node. Three routes of intra-atrial conduction are possible: (a) superiorly through Bachmann bundle, (b) through the midatrial septum at the fossa ovalis, and (c) at the region of the central fibrous trigone at the apex of the triangle of Koch. It can be demonstrated by distal (superior and lateral) coronary sinus activation preceding midcoronary sinus activation but following proximal (os) coronary sinus activation (Fig. The Carto system allows for accurate display of right and left atrial activation, since one can record several hundred sites in both atria. Left-to-right atrial activation during distal coronary sinus pacing rarely appears to use Bachmann bundle but primarily crosses at the fossa and low septum. Information about the antegrade and retrograde atrial activation sequences is critical to the accurate diagnosis of supraventricular arrhythmias (Chapter 8). Early observations using His bundle, coronary sinus, and high- right atrial recordings using quadripolar catheters suggested that retrograde atrial activation in response to ventricular premature beats or His bundle rhythms normally begins at the A-V junction, with apparent simultaneous radial spread to the right and left atria. Recently more detailed atrial mapping during ventricular pacing has demonstrated a complex pattern (see Chapter 8). Basically, at long-paced cycle lengths or coupling intervals atrial activation along a close-spaced (2-mm) decapolar catheter recording a His deflection at the tip is earliest. Secondary breakthrough sites in the coronary sinus catheter and/or posterior triangle of Koch occur in ∼50% of patients (Fig. The early left atrial breakthrough probably reflects activation over the left atrial extension of the A-V node. At shorter coupling intervals, particularly during pacing-induced Wenckebach cycles, retrograde activation changes and earliest activation is typically found at the posterior triangle of Koch, the os of the coronary sinus, or within the coronary sinus itself (Fig. Activation times are determined by the first rapid deflection as it crosses the baseline (arrows). Intraventricular Conduction Intracardiac analysis of intraventricular conduction has not been a routine procedure in most electrophysiologic laboratories. We, however, believe both right and left ventricular mapping are useful in analyzing intraventricular conduction defects, dispersion of ventricular activation and recovery of excitability, and localizing the site of origin of ventricular tachycardias. Differences in this timing relate to catheter placement more toward right ventricular apex or more toward the free wall at the base of insertion of the papillary muscle or after the takeoff of the moderator band. In addition, most investigators record from the proximal poles of a quadripolar catheter. This suggests left atrial activation occurs over both Bachmann bundle and the low atrial septum. We have actively pursued detailed evaluation of endocardial activation of the left ventricle during sinus rhythm in our laboratory. We performed characterization of electrograms, both qualitatively and quantitatively, and particularly, activation patterns in 15 patients with no evidence of cardiac disease. In all cases, we performed left ventricular mapping using a Josephson quadripolar catheter (0. We inserted the catheter percutaneously into the femoral artery and advanced it to the left ventricle under fluoroscopic guidance. We inserted one to two quadripolar catheters percutaneously in the right femoral vein and advanced to the right ventricular apex and P. We used the left ventricular mapping schema representing 12 segmental areas of the left ventricle (Fig. We recorded 10 to 22 electrograms in each patient with the catheter sites verified by multiplane fluoroscopy. We ensured stability by recording from each site for a minimum of 5 to 30 seconds. We made all electrogram measurements using 1-cm interelectrode distance, using the distal electrode paired with the third electrode of the catheter.

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