By W. Mirzo. Northland College. 2018.
Major goals of management often and clarity of speech so that activities include maintaining joint range of motion of daily living and communication to prevent contractures and other defor- may be affected but the individual is mities cheap sildigra 25 mg visa erectile dysfunction treatment australia, and increasing muscle control and still able to function discount 50 mg sildigra otc erectile dysfunction quad mix. Physical therapy may be insti- and/or communicate is extensively tuted to increase and enhance motor skill compromised. Occupational therapy may be utilized to help individuals learn how to Lastly, cerebral palsy may be classiﬁed manage activities of daily living as well as according to muscle tone at rest: other daily functions. Isotonic, in which muscle tone is of prescribed braces or splints may be used normal to help prevent or correct deformity. Hypertonic, in which there is in- Braces can help individuals improve func- creased muscle tone tional mobility as well as appearance. Hypotonic, in which there is de- type of brace depends on the type of dis- creased muscle tone ability experienced. Medical interventions may also be in- Management of Cerebral Palsy volved in the management of cerebral pal- sy. In some instances medications may be Management of cerebral palsy is direct- prescribed to promote muscle relaxation ed toward providing functional supports to when excessive muscle spasticity or exces- 58 CHAPTER 2 CONDITIONS OF THE NERVOUS SYSTEM: PART I sive muscle tone is present. Anticonvul- alter the individual’s functioning ability or sant medications may be prescribed if well-being. Contractures can limit both individuals also have a seizure disorder passive and active joint movement and associated with cerebral palsy. Orthopedic can interfere with self-care, walking, and surgery may be needed to correct joint sitting. Some individuals with cerebral pal- deformities or to lengthen muscles or ten- sy also experience bowel and bladder in- dons in order to decrease muscle spasm. Be- and bladder incontinence can be managed cause of insufﬁcient muscle activity, some through training programs that help indi- individuals may be more prone to osteo- viduals establish dietary control and a reg- porosis, which in turn can cause pain and ular evacuation schedule, as well as increase susceptibility to fractures. Poorly programs to increase awareness of the sen- aligned joints may predispose them to sory stimuli that indicate a need for evac- degenerative joint disease, resulting in uation. In some dental problems through training in oral instances, if individuals have poorly sup- hygiene and regular dental care. A specif- ported sitting posture, scoliosis (lateral ic program of weight bearing and muscle curvature of the spine) may occur, com- activity as well as a diet adequate in cal- promising breathing as well as the func- cium can help to prevent osteoporosis. If coughing and Training that helps individuals increase swallowing ability is insufﬁcient, aspira- posture control and the use of braces and tion of food or ﬂuids may place individ- splints can retard the development of uals at risk of respiratory infections or degenerative joint disease and scoliosis. Training to help individuals develop Although not necessarily a complica- improved breathing patterns, coughing, tion, fatigue secondary to manifestations and lung expansion can decrease the of cerebral palsy can also interfere with chances of aspiration and consequently individuals’ ability to function efﬁciently. Because they may experience difﬁculty with Adequate rest at night as well as estab- motor control and coordination, more lishment of rest periods throughout the energy may be expended to carry out even day can decrease fatigue. Involuntary viduals’ total energy output and adjusting movement or spasticity may also increase their tasks and schedules to ﬁt their needs the amount of energy expended. As a can help preserve energy and prevent result, individuals with cerebral palsy excessive fatigue. Complications of Cerebral Palsy Psychosocial Issues in Cerebral Palsy Because of the manifestations of cere- Although data regarding the psychoso- bral palsy, a variety of complications that cial adjustment of adults with cerebral pal- are secondary to the condition itself can sy are limited, cerebral palsy as a develop- Conditions Affecting the Brain 59 mental disability poses many of the same For adolescents with cerebral palsy, problems as other developmental disabil- opportunities to participate in social activ- ities. Misunderstanding of the condition ities, information related to sexuality, and by parents, teachers, or others with whom opportunities to participate in sexual individuals with cerebral palsy come in exploration and relationships may have contact can perpetuate a sick and depend- been limited. In addition, adolescents ency status rather than one of empower- with cerebral palsy may have a distorted ment. How individuals with cerebral palsy body image and a low self-concept, which were treated in childhood can inﬂuence can affect their social competence, dating, their self-perception and functioning in and sexual behavior. With any type of developmen- als with cerebral palsy, as adolescents as tal disability there is the risk of overpro- well as adults, experience normal desires, tectiveness by parents and others, which they may lack the skills necessary to ful- can impede the individual’s emotional ﬁll those needs. In addition to barriers of development by restricting access to expe- inadequate information, skill, or opportu- riences that are vital to the development nity for appropriate sexual expression, of adequate coping strategies. As a result, they may also experience physical barri- children may learn, at an early age, to use ers because of their disability that make maladaptive behavior to achieve goals. Individu- overly dependent on parents, have been als with communication problems as the given little responsibility for home chores, result of cerebral palsy may have grown up have not been confronted with the typi- in an environment in which family, cal consequences of behavior, or have not friends, and others became accustomed to learned acceptable means of expressing their adaptive communication methods. For often been the focus of a wide variety of instance, those unfamiliar with the indi- services and activities from an early age vidual or with cerebral palsy itself may may continue these expectations into misinterpret problems with hearing or adulthood, demonstrating a sense of ego- unintelligible speech as lack of cognitive centricity that may limit positive social ability. In other instances, because the interactions and lead to further social iso- individual may be difﬁcult to understand, lation. If these behaviors persist into adult- acquaintances may begin to avoid inter- hood, they may become more of an actions with the individual who then impediment to social integration than the becomes socially isolated. At the severity and type of cerebral palsy, times brain damage associated with cere- decreased mobility, problems with eating, bral palsy may also create behavior deﬁcits or problems with personal hygiene may that can interfere with the development further restrict the individual’s social and maintenance of social relationships. Consequently, follow-up through- out the individual’s life may be necessary.
Conflicts between managed care organizations and emer- gency departments in California discount sildigra 50 mg otc impotence def. The impact of health maintenance organization care authorization policy on an emergency department before California’s new man- aged care law purchase sildigra 120 mg without a prescription erectile dysfunction caused by supplements. Emergency department patient literacy and the readability of patient- directed materials. Does determining serum alcohol concentrations in emer- gency department patients influence physicians’ civil suit liability? Lofsky, MD SUMMARY This chapter reviews the leading causes for anesthesiology mal- practice claims and the indemnity payments that result from dif- ferent patient injuries. Risk-management strategies are provided both to help prevent patient injuries and to make anesthesia claims more defensible. Key Words: Anesthesiology; American Society of Anesthesiolo- gists (ASA) monitoring standards; frequency; severity; claims trends; informed consent. INTRODUCTION In the 20 years since the widespread adoption of new monitoring technologies in anesthesia, the specialty has gone from high to low risk in the rating systems of most malpractice carriers. It is often cited as a role model for specialties seeking to improve patient outcomes and decrease the likelihood of malpractice litigation. Anesthesiology cur- rently has one of the lowest incidences of claim frequency among all specialties, with anesthesiologists sued an average of once every 8 years. The nature of the claims themselves has also changed with a marked decline in the percentages of claims for catastrophic injures From: Medical Malpractice: A Physician’s Sourcebook Edited by: R. As a result, in inflation-adjusted dol- lars, anesthesia is one of the few specialties to see declining premiums. This decrease in catastrophic cases is largely attributable to the monitoring capabilities supplied by the pulse oximeter and end-tidal carbon dioxide (CO2) monitors. These came into widespread use in the 1990s and are now included in American Society of Anesthesiologists (ASA) monitoring standards. These monitors, when used correctly, have virtually eliminated unrecognized esophageal intubations in the operating room and serve as an early warning sign of inadequate ven- tilation, something that only 15 years ago, surgeons first recognized by noticing darker blood in the surgical site. The practice of anesthesiology itself has undergone radical changes in recent years. General anesthesia now includes options of both inha- lational (gas) anesthetics and total intravenous agents. Difficult intubations are aided by newer visualization techniques or eliminated by the use of the laryngeal mask airway (LMA). Many cases can now be performed with monitored anesthesia care (MAC; intravenous seda- tion) or regional neurological block techniques. These newer alterna- tives have improved patient safety by allowing anesthetics to be specifically tailored to the patient’s needs and physical limitations. Many anesthesiologists now work outside the operating room in intensive care units or as pain specialists in freestanding office prac- tices. By working in these areas, anesthesiologists have overlapped the traditional practices of family practitioners, physical medicine physi- cians, and neurologists, among others. Malpractice insurance compa- nies have had to struggle to assess and appropriately price these new risks and to decide whether these anesthesiologists rightly belong to separate specialties, such as pain or intensive medicine. The discussion of pain and other nontraditional anesthesiology practices is beyond the scope of this chapter, which is intended to focus on claims related to operating room, surgery center, office operating room, and obstetrical anesthesia. CLAIMS To study anesthesia claim trends, The Doctors Company (TDC), a national physician-owned medical malpractice insurance company, looked at a representative sample of 500 consecutive anesthesia claims. Malprac- tice indemnity, by definition, is a dollar payout on behalf of the phy- Chapter 10 / Anesthesiology 117 Fig. Corre- spondingly, 89% of these anesthesia claims closed without any pay- ment being made to the plaintiff, which is a better defense rate than observed for many other specialties. Dental damage is the single most common allegation in anesthesia claims, accounting for nearly one-fourth of the claims studied here. About half of these are a result of trauma during endotracheal intubation, with the other half involving patients biting down on hard objects such as plas- tic oral airways and LMA shafts—often in the recovery period. The most commonly injured teeth in these claims are the upper front inci- sors, with injuries to prosthetic dental work such as crowns and bridges as another common allegation. Claims involving a patient death in the perioperative period occur in 14% of the claims in this series. Many of these claims do not involve obvious anesthesia errors; however, frequently in malpractice cases involving a death, numerous physicians are named initially and later dropped after discovery proceeds. However, those cases that did pay indemnity had an average payout of $225,000 to the decedent’s family. Malpractice claims alleging neurological injuries are almost evenly divided between general anesthetics, in which improper positioning may be an issue, and epidural and spinal block cases, in which direct nerve trauma can occur. Brain damage claims comprise 5% of claims in this series and include cases of severe anoxic injury resulting from loss of the airway and respiratory insufficiency. This category includes some of the most expensive claims in this series.
Electrical activity spreads across the atria discount 25 mg sildigra with visa erectile dysfunction drugs market share, through the atri- lective opening and closing of plasma membrane channels oventricular (AV) node sildigra 120 mg visa erectile dysfunction treatment hypnosis, through the Purkinje system, and for sodium, potassium, and calcium ions. Norepinephrine increases pacemaker activity and the calcium channels and the closing of potassium channels. Acetylcholine decreases pacemaker activity and the speed channels and the closing of sodium and calcium of action potential conduction. Pacemaker potentials are achieved by the opening of chan- regions of the heart are recorded by an electrocardiogram nels for sodium and calcium ions and the closing of chan- (ECG). Electrical activity is normally initiated in the sinoatrial (SA) rhythm, pattern of depolarization, and mass of electrically node where pacemaker cells reach threshold first. After initia- potential; phase 3 is the repolarization to the resting mem- tion, the electrical activity spreads throughout the heart, brane potential; and phase 4 is the resting membrane po- reaching every cardiac cell rapidly with the correct timing. In resting ventricular muscle The electrical activity of cardiac cells depends on the ionic cells, the potential inside the membrane is stable at approx- gradients across their plasma membranes and changes in per- imately 90 mV relative to the outside of the cell (see meability to selected ions brought about by the opening and phase 4, Fig. This chapter describes how these an action potential occurs (see Chapter 3). First, there is a ionic gradients and changes in membrane permeability result rapid depolarization from 90 mV to 20 mV (phase 0). Next, rapid repolarization (phase 3) returns the membrane potential to its resting THE IONIC BASIS OF CARDIAC ELECTRICAL value (phase 4). In contrast to ventricular cells, cells of the sinoatrial ACTIVITY: THE CARDIAC MEMBRANE POTENTIAL (SA) node and atrioventricular (AV) node exhibit a pro- The cardiac membrane potential is divided into 5 phases, gressive depolarization during phase 4 called the pace- phases 0 to 4 (Fig. When the membrane po- 219 220 PART IV BLOOD AND CARDIOVASCULAR PHYSIOLOGY A Major Channels Involved in Purkinje and +20 1 2 TABLE 13. Outward (transient) V Contributes briefly to Cardiac action potentials (mV) recorded rectifying K phase 1 by transiently FIGURE 13. K at positive Numbers 0 to 4 refer to the phases of the action potential (see text). Outward (delayed) V Cause phase 3 of action rectifying K potential by permitting tential reaches threshold potential, there is a rapid depolar- channels outflux of K after a ization (phase 0) to approximately 20 mV. The mem- (iKr, iKs) delay when membrane brane subsequently repolarizes (phase 3) without going depolarizes. IKr channel through a plateau phase, and the pacemaker potential re- is also called HERG channel. Other myocardial cells combine various character- G protein-activated L G protein operated istics of the electrical activity of these two cell types. The Cardiac Membrane Potential Depends on Transmembrane Movements of Sodium, Potassium, and Calcium 2 The membrane potential of a cardiac cell depends on con- Ca -ATPase and partially by an antiporter that uses en- 2 centration differences in Na , K , and Ca across the cell ergy derived from the Na electrochemical gradient to re- 2 membrane and the opening and closing of channels that move Ca from the cell. If the energy supply of myocar- 2 dial cells is restricted by inadequate coronary blood flow, transport these cations. Some Na , K , and Ca channels (voltage-gated channels) are opened and closed by changes ATP synthesis (and, in turn, active transport) may be im- in membrane voltage, and others (ligand-gated channels) paired. This situation leads to a reduction in ionic concen- are opened by a neurotransmitter, hormone, metabolite, tration gradients that eventually disrupts the electrical ac- and/or drug. The relative permeability to these cations at a par- membrane potentials are created and maintained by active ticular time depends on which of the various cation chan- nels listed in Table 13. The transport of Na and K is accomplished by the plasma membrane Na /K -ATPase (see Chapter 2). An equilibrium potential is not shown Mixed cation channel V Carries Na (mostly) and for Ca2 because, unlike Na and K , it changes during the ac- (funny, I )f inward when tion potential. This is because cytosolic Ca2 concentration activated by hyperpolarization. During the plateau of the action potential, the equilibrium potential for Ca2 Contributes to is approximately 90 mV. K channel (delayed V Contributes to phase 3 of outward rectifier, iK) action potential. Depolarization occurs when the membrane potential moves away from the K equilibrium potential and toward the Na equilibrium po- tential. In ventricular cell membranes, this occurs passively at first, in response to the depolarization of adjacent mem- meable only to K (potassium equilibrium potential). Once the ventricular cell mem- contrast, when open Na channels predominate (as occurs brane is brought to threshold, voltage-gated Na channels at the peak of phase 0 of the action potential), the measured open, causing the initial rapid upswing of the action poten- potential is closer to the potential that would exist if the tial (phase 0). The opening of Na channels causes Na membrane were permeable only to Na (sodium equilib- permeability to increase. The opening of Ca chan- permeability to K , the membrane potential approaches nels causes the membrane potential to be closer to the cal- the Na equilibrium potential, and the inside of the cell be- cium equilibrium potential, which is also positive; this comes positively charged relative to the outside.
For instance sildigra 50 mg with mastercard how to treat erectile dysfunction australian doctor, impulse-evoked release of this transmitter is prevented by the drug discount 25mg sildigra free shipping impotence of organic origin icd 9, vesamicol, which blocks uptake of acetylcholine from the cytoplasm into the terminal vesicles (Searl, Prior and Marshall 1991). Although most evidence supports vesicular exocytosis of acetylcholine (see Ceccarelli and Hurlbut 1980), some researchers contest this view. According to this scheme, opening of the pore is triggered by an increase in the concentration of intracellular Ca2 and allows gated release of aliquots of cytoplasmic acetylcholine. The vesicles are thought to serve merely as a reserve pool of transmitter and for sequestration of intracellular Ca2 (Dunant 1994). TRANSMITTER STORAGE VESICLES Electron microscopy and biochemical techniques, such as sucrose density-gradient centrifugation (see Fig. They are delivered to the terminals by fast axoplasmic transport and are the only type of vesicle to be found in axons (see Calakos and Scheller 1996). LDCVs are also found in nerve terminals but, in this part of the neuron, it is small synaptic vesicles (SSV: 40±50 nm)which predominate even though the proportion of LDCVs and SSVs varies from organ to organ (see Fillenz 1990). SSVs contain the classical transmitters (acetylcholine, monoamines and amino acids)which are mostly loaded in the nerve terminals. Whether SSVs are derived from LDCVs has been a matter of considerable debate but differences in the protein markers in their membranes, notably synapsin (see below), makes this unlikely (see De Camilli and Jahn 1990). Also, electron microscopic evidence has shown that LDCVs, unlike SSVs, dock at the axolemma at sites remote from the active zone at the synapse. This suggests that they have different functions and regulatory processes which, since they contain peptides, agrees with the finding that their release requires higher frequencies of nerve stimulation than does that of the classical neurotransmitters. Whether this is because LDCVs and SSVs are confined to different regions of the nerve terminal, or have different affinities for, or a topo- graphical relationship with, Ca2 channels is unresolved (Sihra and Nichols 1993). Electron microscopy certainly shows that their membranes are recovered after fusion with the axolemma but precisely how this occurs is unresolved. One possibility is that they are retrieved intact from the active zone, immediately after release has taken place. Alternatively, they could become incorporated into, and mix with, the components of the axolemma but are reformed after sorting of the different membrane elements (see Kelly and Grote 1993). Recent studies of exocytosis from retinula cells of the Drosophila fly suggest that both these processes for membrane retrieval can be found within individual cells. These studies have shown that there is rapid recovery of vesicular membrane from the active zone. However, a second slower process exists which takes place at sites remote from the active zone and involves the formation of invaginations in the axolemma. This process is thought to precede endocytosis because the formation of these invaginations is followed by the appearance of tubular cisternae within the nerve terminal from which new vesicles bud-off (Koenig and Ikeda 1996). This finding raises the interesting question of whether these different processes lead to the formation of two different populations of synaptic vesicles with different release characteristics. RELEASE VERSUS STORAGE POOL Evidence from measurements of transmitter turnover has long suggested that not all transmitter is immediately available for release. The reserve pool would then comprise vesicles which are docked, more remotely, on the neuronal cytoskeleton. It is thought that vesicles move from one pool to the other as a result of the actions of protein kinases which effect cycles of phosphorylation/dephosphorylation of proteins, known as synapsins, which are embedded in the vesicle membranes. NEUROTRANSMITTER RELEASE 95 SYNAPSINS Synapsins comprise a family of phosphoproteins that are found only in association with SSVs. Although they account for only about 9% of the total vesicular membrane protein they probably cover a large proportion of their surface. So far, synapsins Ia, Ib, IIa, IIb and III, which are the products of different genes, have been identified. Recent evidence suggests that, while synapsins might have a role in synaptogenesis, they also regulate the supply of vesicles to the release pool (Hilfiker et al. Experiments in vitro have shown that dephosphorylated synapsin I causes growth and bundling of actin filaments which are a major component of neuronal microfilaments. Such findings form the basis of the hypothesis that synapsin I forms a ternary complex with transmitter storage vesicles and the neuronal cytoskeleton, thereby confining vesicles to a reserve pool (Fig. Phosphorylated synapsin dissociates from the vesicles and F-actin, reduces the number of vesicle anchoring sites, and so frees the vesicles to the release pool. Synapsin I is the substrate for several protein kinases but one of these, Ca2/calmodulin protein kinase II (CAM kinase II), is bound to vesicle membranes to some extent. It is thought that phosphorylation of synapsin I by CAM kinase II is triggered by the influx of Ca2. This process would enable synapsin to act as a regulator of the balance between the releasable and reserve pools of vesicles.
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