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By Y. Nasib. Radford University.

L1 bifurcates into an upper part (iliohypogastric and ilioinguinal nerves) and a lower part female viagra 50 mg on line, which joins with a branch from L2 to form the genitofemoral nerve buy generic female viagra. L3 purchase genuine female viagra, with portions of L2 and L4, divides into anterior and posterior divisions; the anterior division forms the obturator (L2–L4) and accessory obturator (L3, L4, when present) nerves, whereas the posterior division forms the lateral (femoral) cutaneous nerve of the thigh (L2–L3) and the femoral nerve (L2–L4). Figure 36-13 Schematic diagrams of the lumbar (left; L1–L4) and sacral (right; L4–S4) plexuses. In anatomic relation to the psoas major muscle, the obturator (L2–L4) and accessory obturator nerves emerge from its medial border, the genitofemoral (L1, L2) pierces the muscle to lie on its anterior surface, and all others emerge from its lateral border. Terminal nerves of the lumbar plexus are discussed in the Lower Extremity section. Inguinal Nerves 2379 The iliohypogastric nerve penetrates the transverse abdominis muscle just above the iliac crest, supplies the muscle, and divides into anterior and lateral cutaneous branches: • The anterior branch pierces and supplies the internal oblique muscle just 2 cm medial to the anterior superior iliac spine. It then courses deep to the external oblique muscle and superior to the inguinal canal and pierces the external oblique aponeurosis about 2 to 3 cm above the superficial inguinal ring, terminating subcutaneously in the skin of the suprapubic region. The ilioinguinal nerve pierces and supplies the internal oblique muscle and then enters the inguinal canal, where it traverses outside the spermatic cord to emerge through the superficial (external) inguinal ring (the external oblique aponeurosis), providing cutaneous innervation to the skin of the scrotum (or labium majus) and adjacent thigh. Important landmarks that contain the plexus during its course include the psoas compartment, bordered posteriorly by the quadratus lumborum muscle and anteriorly by the posterior fascia of the psoas muscle, and, more distally, the substance of the psoas major muscle. The anatomy of the terminal nerves is examined later, as are the formation and branches of the sacral plexus. Sacral Plexus: Formation and Branches At the medial border of the psoas major muscle, the lumbosacral trunk is formed by the union of a branch of L4 and the anterior ramus of L5. After exiting through the anterior sacral foramina, the anterior primary rami of S1– S4 join the lumbosacral trunk to form the sacral plexus (Fig. The nerves of the plexus converge toward the greater sciatic foramen anterior to the piriformis muscle on the posterior pelvic wall. The main terminal nerves are the sciatic nerve (continuation of the plexus) and the pudendal nerves (“terminal branches”). The gluteal vessels (superior and inferior) generally follow the course of the sacral nerves in the anterior plane and can be used to help identify the sciatic nerve at its proximal course. Sciatic, Tibial, and Common Peroneal Nerves The sciatic nerve—the largest nerve of the body—is usually the conjunction of two trunks initially enveloped in a common sheath: A lateral trunk (L4–S2), which eventually emerges as the common peroneal nerve and a medial trunk (L4–S3), which later becomes the tibial nerve. These combined nerves exit through the sciatic notch and pass anteriorly to the piriformis muscle to then lie between the ischial tuberosity and the greater trochanter of the femur. At a variable distance within the posterior thigh (often high in the popliteal fossa), the sciatic nerve bifurcates into the tibial and common peroneal nerves. The common peroneal nerve descends along the medial border of the biceps femoris muscle and then on the lateral border of the gastrocnemius muscle. At the fossa, it gives off the lateral sural nerve, which forms the lateral sural cutaneous nerve by joining the medial sural nerve supplied by the tibial nerve. It winds around neck of the fibula and terminates as the deep and superficial peroneal nerves. In the posterior thigh, the tibial nerve is covered medially by the semitendinosus and semimembranosus muscles and 2381 laterally by the biceps femoris muscle. Beyond the knee joint, it is covered by both heads of the gastrocnemius muscle and then deep to the soleus muscle, before coming to an end on the tibialis posterior muscle and finally on the posterior surface of the tibial shaft medial to the medial malleolus. Within the fossa, it gives off muscular branches (gastrocnemius, soleus, popliteus, and plantaris muscles) as well as the medial sural nerve (to join its lateral counterpart from the common peroneal nerve). In the lower leg and foot, it gives off muscular, articular (ankle), and cutaneous branches and terminates as the medial and lateral plantar nerves. Terminal Nerves of the Lumbar Plexus Genitofemoral Nerve (L1, L2) This nerve leaves the lumbar plexus at the lower border of the L3 vertebra. It pierces and then lies anterior to the psoas major muscle before descending subperitoneally and behind the ureter, where it divides into two branches (genital and femoral) at a variable distance above the inguinal ligament. The genital branch crosses the external iliac artery and traverses the inguinal canal. It supplies the cremaster muscle and skin over the scrotum and adjacent thigh (males) or the skin over anterior part of labium majus and mons pubis (females). The femoral branch descends lateral to the external iliac artery, passes under the inguinal ligament, enters the femoral sheath lateral to the femoral artery, and pierces the anterior layer of the femoral sheath and fascia lata. It innervates the skin immediately below the crease of the groin anterior to the upper part of the femoral triangle. Lateral Cutaneous Nerve of Thigh (aka, Lateral Femoral Cutaneous Nerve) (L2, L3) This nerve passes obliquely from the lateral border of the psoas major muscle over the iliacus to enter the thigh below or through the inguinal ligament, variably medial to the anterior superior iliac spine (Fig. On the right side of the body, the nerve passes posterolateral to the cecum, and on the left it traverses behind the lower part of the descending colon. The nerve lies on top of the sartorius muscle before dividing into anterior (supplies skin over the anterolateral aspect of the thigh) and posterior (supplies skin on the lateral aspect of thigh from the greater trochanter to the mid-thigh) branches. Occasionally, this nerve is a branch of the femoral nerve rather than its own nerve. Femoral Nerve (L2–L4) 2382 The femoral nerve is the largest nerve of the lumbar plexus, supplying muscles and skin on the anterior aspect of the thigh. It descends through the psoas major muscle and emerges low at its lateral border, coursing inferiorly between the iliacus and psoas major muscles to enter the thigh under the inguinal ligament (Fig. At the inguinal ligament (line running between anterior superior iliac spine and the medial pubic tubercle) and just distal to it (in the femoral triangle), the nerve lies slightly deeper (0. At the femoral (inguinal) crease (a few centimeters caudad to the inguinal ligament), the nerve lies underneath the fascia iliaca (iliopectineal fascia), deep to the fascia lata. Beyond the femoral triangle, the nerve branches into anterior (quite proximally) and posterior divisions. The anterior division gives muscular branches to the pectineus and sartorius muscles and cutaneous branches (intermediate and medial cutaneous nerves of thigh) to the skin on the anterior aspect of the thigh. The posterior division sends muscular branches to the quadriceps femoris muscle and gives rise to the saphenous nerve, its largest cutaneous branch. The saphenous nerve follows the femoral artery, lying lateral to it within the adductor (Hunter’s, subsartorial) canal and then crossing it anteriorly to lie medial to the artery. Distal to the canal, the saphenous nerve leaves the artery to lie superficial at the medial aspect of the knee; the nerve then continues inferiorly (subcutaneously) with the long (great) saphenous vein along the medial aspect of the leg down to the tibial aspect of the ankle. The saphenous branch supplies the skin on the medial aspect of the leg below the knee and on the medial aspect of the foot; it provides articular branches to the hip, knee, and ankle joints. Needle insertion sites (•) for blocking the lateral femoral cutaneous, femoral, and obturator nerves are shown. Obturator Nerve (L2–L4) The obturator nerve emerges from the medial border of the psoas major muscle at the pelvic brim to pass behind the common iliac vessels and lateral to the internal iliac vessels. It then courses inferiorly and anteriorly along the lateral wall of the pelvic cavity on the obturator internus muscle toward the obturator canal, through which it enters the upper part of the medial aspect of the thigh above and anterior to the obturator vessels. The nerve divides into its anterior and posterior branches near the obturator foramen (Fig. It supplies the adductor longus, gracilis, adductor brevis (usually), and pectineus (often) muscles. Cutaneous branches supply the skin on the medial aspect of the thigh and perhaps to the medial knee. The nerve’s posterior branch pierces the obturator externus muscle anteriorly and supplies it, then passes behind the adductor brevis muscle (sometimes supplies it) to descend on the anterior aspect of the adductor magnus muscle (medial to the anterior branch), which it supplies.

Focused cardiac ultrasound: recommendations from the American Society of Echocardiography buy female viagra 50 mg mastercard. Routine pre-operative focused ultrasonography by anesthesiologists in patients undergoing urgent surgical procedures cheap 100 mg female viagra. Brief group training of medical students in focused cardiac ultrasound may improve diagnostic accuracy of physical examination 100mg female viagra mastercard. Development and evaluation of methodologies for teaching focused cardiac ultrasound skills to medical students. Impact assessment of perioperative point-of- care ultrasound training on anesthesiology residents. Focused transthoracic echocardiography training in a cohort of Canadian anesthesiology residents: a pilot study. Focus cardiac ultrasound: the European Association of Cardiovascular Imaging viewpoint. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians. The “5Es” of emergency physician- performed focused cardiac ultrasound: a protocol for rapid identification of effusion, ejection, equality, exit, and entrance. Transthoracic echocardiography for 1899 cardiopulmonary monitoring in intensive care. This moves the provider’s point of view past the tongue, avoiding the need for a direct line of sight to the glottis. Perspectives on Airway Management In the nearly three decades since the publication of the first edition of this text, the field of airway management has undergone a vigorous revolution. Although many of the tools available in 1988 remain in use, the array of devices, algorithms, and pharmaceuticals in the modern airway armamentarium can be daunting. Fortunately, careful planning and expertise in a limited, albeit complementary, set of tools typically suffices. The final decade of the last century saw a resolute swing toward the application of supraglottic ventilation. Along with offering the provider better tools, technology has also aided in the creation of large databases of airway-related records from which a wealth of information can be collected retrospectively. Techniques and practices in airway management have long been an 1902 important concern of anesthesia societies, as illustrated by the publication and revision of various difficult airway guidelines. A significant decrease in claims related to death/brain death at the induction of anesthesia is not matched with similar progress during emergence and in the postoperative period. Although the closed claims data is useful, it has significant4 limitations, including its retrospective nature and the lack of a denominator. This chapter will reflect the need to7 consider these five factors when approaching any patient who requires or may require airway control. This text will focus on routine and rescue airway management techniques that are the fundamentals upon which all airway management is based. Review of Airway Anatomy The term airway refers to the upper airway—consisting of the nasal and oral cavities, pharynx, larynx, trachea, and principal bronchi. Because the oroesophageal and nasotracheal passages cross each other, anatomic and functional complexities have evolved for protection of the sublaryngeal airway against aspiration of food passing through the pharynx. As are other bodily systems, the airway is not immune from the influence of genetic, nutritional, and hormonal factors. The anatomically complex airway undergoes significant changes in its size, shape, and relationship to the cervical spine from infancy into childhood. Note that the cricoid cartilage is <1 cm in height in its anterior aspect, but may be 2 cm in height posteriorly. The laryngeal skeleton consists of nine cartilages (three paired and three unpaired); together, these house the vocal folds, which extend in an anterior– posterior plane from the thyroid cartilage to the arytenoid cartilages. The shield-shaped thyroid cartilage acts as the anterior “protective housing” of the vocal mechanism (Fig. Movements of the laryngeal structures are controlled by two groups of muscles: the extrinsic muscles, which move the larynx as a whole; and the intrinsic muscles, which move the various cartilages in relation to one another. The larynx is innervated by the superior and recurrent laryngeal nerves, which are branches of the vagus nerve. Because the recurrent laryngeal nerves supply all of the intrinsic muscles of the larynx (with the exception of cricothyroid muscle), trauma to these nerves can result in vocal cord dysfunction. With unilateral recurrent laryngeal nerve injury, hoarseness is the primary symptom, though the protective role of the larynx in preventing aspiration may be compromised. Bilateral injury can 1904 result in complete airway obstruction due to fixed cord adduction and may be a surgical emergency. The membrane has a central portion known as the9 conus elasticus and two lateral thinner portions. Because of anatomic variability in the course of veins and arteries and the membrane’s proximity to the vocal folds (which may be 0. This2 should lead to routine examination of laryngeal structures, including the marking of surface anatomy, and the use of ultrasound identification, especially in at-risk patients (Fig. This cartilage is approximately 1 cm in height anteriorly, but almost 2 cm in height in its posterior aspect as it extends in a cephalad direction (Fig. The tracheal cartilages are 1905 interconnected by fibroelastic tissue, which allows for expansion of the trachea in both length and diameter with inspiration/expiration and flexion/extension of the thoracocervical spine. Inferiorly, the trachea is suspended from the cricoid cartilage by the cricotracheal ligament. The trachea measures approximately 15 cm in adults and is circumferentially supported by 17 to 18 C-shaped cartilages, with a membranous posterior aspect overlying the esophagus. The trachea ends at the carina (opposite the fifth thoracic vertebra), where it bifurcates into the principal bronchi. The right principal bronchus is larger in diameter than the left and deviates from the sagittal plane of the trachea at a less acute angle. Cartilaginous ring support continues through the first seven generations of the bronchi. History of Airway Management Prior to 1874, mechanisms of airway obstruction were poorly understood. Opening the mouth with a wooden screw and drawing the tongue forward with a forceps or a steel-gloved finger was the height of nonsurgical airway management. Not until 1880 was it recognized that most airway obstruction12 resulted from the tongue falling against the posterior pharyngeal wall. Over the next 50 years, several modifications of the basic13 oropharyngeal airway were described. In the 1930s, Ralph Waters introduced the now-familiar flattened tube oral airway.

This point deserves special emphasis buy female viagra 100mg online, particularly in view of the fact that monitored anesthesia care is often provided to the elderly or debilitated patient who has been deemed “unfit” for general anesthesia; these are the patients most likely to suffer adverse reactions to local anesthetic drugs proven female viagra 100mg. Even if the anesthesiologist does not perform the block personally buy line female viagra, he 2081 or she is in a unique position to fulfill an important “preventive” role by advising the surgeon about the most appropriate volume, concentration, and type of local anesthetic drug or technique to be used. Systemic local anesthetic toxicity occurs when plasma concentrations of drug are excessively high. Plasma concentrations will increase when the rate of entry of drug into the circulation exceeds the rate of drug clearance from the circulation. The clinically recognizable effects of local anesthetics on the central nervous system are concentration dependent. At low concentrations, sedation and numbness of the tongue and circumoral tissues and a metallic taste are prominent features. As concentrations increase, restlessness, vertigo, tinnitus, and difficulty focusing may occur. Higher concentrations result in slurred speech and skeletal muscle twitching, which often herald the onset of tonic–clonic seizures. The conduct of monitored anesthesia care may modify the individual’s response to the potentially toxic effects of local anesthetic administration and adversely affect the margin of safety of a regional or local technique. For example, a patient with compromised cardiovascular function may experience a further decline in cardiac output during sedation. The resultant reduction in hepatic blood flow will reduce the clearance of local anesthetics that are metabolized by the liver and have a high hepatic extraction ratio, thereby increasing the likelihood of achieving toxic plasma concentrations. A patient receiving sedation may experience respiratory depression and a subsequent increase in arterial carbon dioxide concentration. By increasing cerebral blood flow, hypercarbia will increase the amount of local anesthetic that is delivered to the brain, thereby increasing the potential for neurotoxicity. By reducing neuronal axoplasmic pH, hypercarbia increases the intracellular concentration of the charged, active form of local anesthetic, thus also increasing its toxicity. In addition, hypercarbia, acidosis, and hypoxia all markedly potentiate the cardiovascular toxicity of local anesthetics. Furthermore, the administration of sedative–hypnotic drugs may interfere with the patient’s ability to communicate the symptoms of impending neurotoxicity. However, the anticonvulsant properties of benzodiazepines and barbiturates may attenuate the seizures associated with neurotoxicity. In both of these circumstances, it is possible that the symptoms of cardiotoxicity will be the first evidence that an adverse reaction has occurred. Thus, appropriate treatment is delayed or inadvertent intravascular injection is continued because of the absence of any clinical evidence of neurotoxicity. Cardiovascular toxicity usually occurs at a higher plasma concentration than neurotoxicity, but when it does occur, it is usually much more difficult to manage than neurotoxicity. Although cardiotoxicity is usually preceded by neurotoxicity, it may on occasion be the initial presenting feature. Deep sedation is occasionally delivered by trained specialists, including emergency department physicians and intensivists. The specific reasons for nonanesthesiologist involvement differ from institution to institution and from case to case and include convenience, availability, and scheduling issues; perceived lack of anesthesiologist availability; perceived increased cost; and a perceived lack of benefit concerning patient satisfaction and safety when sedation and analgesia are provided by anesthesiologists. Despite our frequent noninvolvement in these cases, anesthesiologists are indirectly involved in the care of these patients by being required to participate in the development of institutional policies and procedures for sedation and analgesia, as mandated by the Joint Commission. The practice guidelines emphasize that sedation and analgesia represent a continuum of sedation wherein patients can easily pass into a level of sedation deeper than intended. This statement contains a chart representing the clinical progression along this continuum (Table 30- 9). The importance of continuous patient monitoring is discussed—in particular, the response of the patient to commands as a guide to the level of sedation. The appropriate monitoring of ventilation, oxygenation, and hemodynamics is also discussed, and recommendations are made for the contemporaneous recording of these parameters. The task force strongly suggests that an individual other than the person performing the therapeutic or diagnostic procedure be available to monitor the patient’s comfort and physiologic status. Specific educational objectives include the potentiation of sedative-induced respiratory depression by concomitantly administered opioids, adequate time intervals between doses of sedative/analgesics to avoid cumulative over-dosage, and familiarity with sedative/analgesic antagonists. At least one person with Basic Life Support training should be available during moderate sedation, with immediate availability (1 to 5 minutes) of personnel trained in Advanced Life Support. This individual should have the ability to recognize airway obstruction, establish an airway, and maintain oxygenation and ventilation. The practice guidelines recommend that appropriate patient- size emergency equipment be readily available, specifically including equipment for establishing an airway and delivering positive pressure ventilation with supplemental oxygen, emergency resuscitation drugs, and a working defibrillator. Adequate postprocedure recovery care with appropriate monitoring must be provided until discharge. Controversy exists regarding the level of training required for nonanesthesiologists to be credentialed to provide moderate and deep sedation. These “anesthesia” services must be provided by: A qualified anesthesiologist; a doctor of medicine or osteopathy, a dentist, oral surgeon, or podiatrist who is qualified to administer anesthesia under state law; an appropriately supervised Certified Registered Nurse Anesthetist or Anesthesia Assistant, all who are separate from the practitioner performing the procedure. Failure to follow these recommendations could put patients at increased risk of significant injury or death. These devices integrate patient monitoring variables with the programmed delivery of propofol. The manufacturer of this system required that it should only be used in facilities where an anesthesia professional is immediately available to assist or consult as needed. However, the device worked in conjunction with a single administered dose of fentanyl given 3 minutes prior to the start of a propofol infusion in an attempt to yield some analgesic effect. After a maintenance infusion rate escalation, further increases were limited by a 3-minute lockout period. There were several safety mechanisms in place to ensure both adequate depth of sedation, and prevention of oversedation. An automated responsiveness monitor actuated by the patient assessed his/her responsiveness by requiring interaction with a hand-held device when prompted by vibratory or auditory stimulation. Oxygen delivery was also automatically titrated as determined by oxygen saturation measurement. There were alarm systems to alert the provider to low respiratory rate, low oxygen saturation or apnea events. Monitored anesthesia care presents an opportunity for our patients to observe us at work. For the anesthesiologist, monitored anesthesia care presents an opportunity to provide a more prolonged and intimate level of care and reassurance to our patients that is in contrast to the more limited exposure that occurs during and after general anesthesia. Our airway management skills and our daily practice of applied pharmacology make us uniquely qualified to provide this service. Monitored anesthesia care presents us with an opportunity to display these skills and increase our recognition in areas outside the operating room. The availability of drugs with a more favorable pharmacologic profile allows us to tailor our techniques to provide the specific components of analgesia, sedation, anxiolysis, and amnesia with minimal morbidity and to facilitate a prompt recovery. As the population ages, increasing numbers of patients will become candidates for monitored anesthesia care.

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