By: Edward T. F. Wei PhD
Without the appropriate bottle system impotent rage man avanafil 50 mg low price, infants are at risk for inefcient 498a impotence purchase avanafil 100mg online, calorie-wasting attempts to erectile dysfunction red 7 purchase avanafil mastercard suck impotence over 70 buy discount avanafil 50mg on-line, resulting in inadequate nutritional intake erectile dysfunction meme buy avanafil from india. Growth parameters must be monitored very closely in the frst few weeks to months of life. Infants with clefts involving the palate should be evaluated by nurses or feeding therapists with specialized training in feeding infants with clefts. This constellation of fndings was frst reported by the French stomatologist, Pierre Robin. If the baby appears to have this condition and is having difculty breathing due to obstruction by the tongue, the baby should be placed in the prone position. It is recommended to involve an experienced otolaryngologist if any of these interventions are needed. Consideration of supplemental nasogastric tube feedings or gastrostomy tube feedings may be necessary for some infants. These issues can be difcult to resolve, and generally require the coordinated eforts of pediatrics/primary care, otolaryngology, nursing, infant feeding therapy and respiratory therapy. Monitoring and managing these important early issues should be with a cleft lip/palate team and in a hospital where there is access to pediatric anesthesia. Infants with cleft palate are at high risk for recurrent and chronic middle-ear efusions or infections. Conductive hearing loss may result from middle-ear fuid, and 90-95% of infants with cleft palate will require ear tube placement, usually at the time of the palate repair. Genes and environmental factors are both thought to contribute to facial development, and families often have questions about why their child was born with a cleft and whether this will happen in a subsequent pregnancy. A visit with a clinical geneticist and genetic counselor should be ofered after the child is born, during adolescence, or whenever a family member has questions about etiology and recurrence risks. The possibility of a genetic syndrome should be considered if a patient has atypical facial features, developmental delays, or other anomalies. If the patient is followed by a cleft lip/palate team that is without a dysmorphologist or a geneticist, consider referral to an outside specialist. Dental issues are of paramount importance in the management of patients with cleft lip/palate. Thus once the teeth have erupted, preventive counseling should take place regarding baby bottle caries, proper tooth brushing, etc. Alveolar bone grafting is usually needed when clefts extend through the upper gum (alveolus). This procedure is generally performed between the ages of 7-10 years, depending upon dental development. The alveolar bone graft provides the foundation for the erupting teeth and support for the nasal base. Orthodontic evaluations and interventions are necessary before and after bone graft surgery. Some patients will also need jaw surgery because the defciency is too great for orthodontic compensation alone. Orthodontists, oral and maxillofacial surgeons, and craniofacial surgeons afliated with the cleft lip/palate teams generally evaluate and treat these issues. Several studies have shown that children with orofacial clefts have an increased risk for developmental delays and poor academic outcomes when compared to unafected peers. The potential reasons for these diferences are numerous but may include hearing loss during infancy associated with the cleft palate, difculty with speech production because of the anatomic diferences, school absences for clinic visits or surgeries, syndromic forms of clefting that are associated with other anomalies or developmental delays, or psychosocial issues associated with facial or speech diferences. All children, including those with orofacial clefts, require ongoing well-child care and access to medical care when they are sick. Adolescence is a difcult time for most people, but can be especially difcult for those who look or sound diferent from their peers. Psychosocial and Developmental Issues in Cleft Care Psychosocial issues are a critical part of the assessment and management of the child with cleft lip/palate, and must be addressed from the onset of care. The birth of a child is always a time of great family adjustment, and it is especially stressful when the child is born with a birth defect such as cleft lip/palate. Parents often experience feelings of sadness, guilt, anger and fear for their child’s future social acceptance. Some parents feel the extent of their emotional turmoil is unwarranted with such a reparable birth defect, and experience guilt that a facial deformity is so disturbing to them. In addition, the feeding difculties these infants experience can be threatening to new parents, who may doubt their own ability to feed and nurture an infant with such diferences. In part, through good psychosocial support and proper instructions, most families are able to work through their own emotional turmoil and efectively master the skills needed to feed and nurture these babies. Other issues of concern for new parents relate to accessing professional and community services, securing adequate fnancial resources and coping with the stress of sending a child to surgery. As the child grows, the family will have other concerns, often relating to teasing, peer acceptance, speech difculties, learning and behavior problems. For many families, securing appropriate community and fnancial resources remain important issues. Children should have their evolving decision-making role acknowledged, and should be personally addressed during appointments. During adolescence there are new challenges, as the maturing teen strives for independence and copes with being diferent in a highly appearance-conscious culture. Adolescents and pre-teens should be given the opportunity to confdentially share feelings and concerns with a qualifed professional. Psychosocial assessment and support may also become necessary when a high level of patient compliance and family commitment are required for certain interventions. When considering elective procedures such as lip scar revision or rhinoplasty to correct a facial diference, the maturing child’s preferences should be respected. By age 9 or 10, typically developing children should be included in decision making for these elective surgeries. Other important circumstances that are often addressed by a psychosocial professional include child abuse/neglect, substance abuse, domestic violence and other family dysfunction. It is not uncommon to see a child in a dysfunctional family become overly focused on “fxing my face” as a way for them to fx the dysfunction in the family. There is research to suggest that unless such emotional issues are addressed prior to surgery, such interventions alone are less likely to change self-image and improve quality of life. A detailed and specifc psychosocial assessment is appropriate for all families presenting to a cleft lip/palate team, regardless of socioeconomic status and perceived stability. In assessing children and families, their unique cultural and social characteristics must be taken into account, with a clear understanding of any implications for providing health care. Cultural diferences as well as other unexplored parental worries and concerns often contribute to behavior perceived and labeled by health care providers as “noncompliant. Learning Disorders and Behavioral Problems Children with cleft lip/palate are at increased risk for learning disorders. Fluctuating hearing loss associated with middle ear disease may impair speech and language development. Some children with clefts may have learning difculties associated with a syndromic diagnosis. However, children with isolated clefts (especially cleft palate), also appear to be at increased risk for learning problems. Children with cleft lip/palate may be at increased risk for behavioral disorders as well. Again, these disorders may be associated with a syndromic diagnosis, but can occur in children with isolated clefts as well. Symptoms may include social withdrawal, depression, conduct problems or school performance issues. Furthermore, social and educational circumstances, peer dynamics, problems in the child-parent relationship, and intrinsic characteristics of the child (including temperament and underlying cognitive problems) can combine to create a complex clinical picture. For all these reasons, children with cleft lip/palate should be monitored regularly for psychosocial, learning and behavioral problems. When such problems arise, relevant areas should be assessed, and the interaction of these variables recognized. Specialties suited to screen for these disorders include psychology, social work, nursing, developmental pediatrics, primary care, and speechlanguage pathology. However, all team members and primary care providers should be alerted to the potential for difculties in these areas, so when problems arise, appropriate referrals can be made. Cleft lip with or without cleft palate occurs in approximately 1:700 births worldwide, and 1:940 births in the United States. Although the majority of patients with cleft lip and palate are otherwise healthy, approximately 25% have associated birth defects/chromosomal abnormality, or a genetic 20–23 syndrome. Although there are more than 400 syndromes reported in association with cleft lip or cleft palate, the three syndromes that follow should receive special consideration. A complete medical history should be obtained on every child with a cleft, including a detailed prenatal history, teratogenic exposures, and a three-generation family history. This family history should include occurrences of clefting (and lower lip pits), hypodontia, other birth defects, developmental disabilities or known genetic syndromes. A complete physical examination by clinical geneticist or dysmorphologist should be pursued to identify dysmorphic features and/or associated birth defects or medical concerns. Additional studies, including opthalmologic consultation, echocardiography, other radiographic studies, and genetic testing should be directed by the examination and family history to facilitate genetic diagnoses. While the majority of children with cleft lip and/or palate will not have a genetic syndrome, these conditions may have prognostic implications that must be taken into account to help guide medical decisions and counseling. It should be noted that some physical features that suggest a genetic syndrome may not develop until later in infancy, so continued vigilance is needed. Children who were thought to have nonsyndromic clefting that are later identifed to have developmental delay should also be referred for genetic evaluation. Parents typically have many questions about the etiology of clefts to be addressed by the cleft lip/palate team. There is considerable cultural and social variability in family attitudes towards birth defects and their causation. These issues should be explored and, when appropriate, correct information supplied recognizing that western medical information will not necessarily supplant other cultural and ethnic beliefs. Since genetic factors play a role in clefting conditions even in children with nonsyndromic clefting, information on causation and empirical recurrence risks should be provided to all families with clefts based upon the family history. The risk is highest for bilateral cleft lip/palate (5-6%), compared to 2-3 % for cleft lip without cleft palate. This risk increases if there are additional family members with clefts, up to approximately 8-10% for nonsyndromic clefting. The recurrence risk for clefting associated with genetic syndromes varies with the mode of inheritance of the condition, and can range from 1-50%. Condition-specifc recurrence risks and prenatal testing options should be provided to families of a child with syndromic clefting condition. A discussion regarding the potential preventative role of preconception/ prenatal folate supplementation and avoidance of environmental risk factors (tobacco smoke, alcohol, and isotretinion) should be considered.
Althoughhavingprecise definitionsforhigh- erectile dysfunction johnson city tn buy discount avanafil 200 mg online,intermediate- creatine causes erectile dysfunction cheap avanafil 200mg, availability and expertise of outpatient diagnostic clinics erectile dysfunction doctor malaysia avanafil 200 mg on-line, and low-risk patient groups after an episode of syncope would and the lack of data demonstrating that hospital-based evaluabe useful for managing these patients impotence blog order 100 mg avanafil amex, evidence from current tion improves outcomes erectile dysfunction adderall avanafil 50 mg discount. In patients with a presumptive cause clinical studies renders this proposal challenging because of a of refiex-mediated syncope and no other dangerous medical large number of confounders. Risk markers from history, physconditions identified, hospital-based evaluation is unlikely to 35 ical examination, laboratory investigations, study endpoints, provide benefit. In patients with perceived higher risk, the adverse event rates, and time intervals between these events healthcare provider may recommend a hospital-based evaluaare variable from study to study. Risk markers are summarized in service use in the evaluation of syncope (Figures 1 and 64,67–70,72–75,82–98 105,111–113 Table 5. The types of events, event rates, 2), although there are currently insufficient data and study durations from investigations that estimated risk to advocate the use of specific decision support algorithms 64,65,76,81,87,89,92,97,99 scores are summarized in Table 6. Disposition After Initial Evaluation: Recommendations health service use and increased diagnostic rates. The evaluating provider must decide whether further workup However, the logistical and financial feasibility of specialized can continue in an outpatient setting or whether hospitalsyncope units in North American settings is unknown. The purpose of hospital-based acceptance of syncope units requires further evidence of evaluation is to expedite the treatment of identified serious improvement in clinical outcomes. Individual risk factors conditions or to continue the diagnostic evaluation in the (Table 5)andriskscores(Table 6) are correlated with shortand 105,106 long-term clinical outcomes, but they are not primary determiabsence of a presumptive cause of syncope. The disposition decision is complicated by varying renants for admission to hospital. Presence of 1 serious medical sources available for immediate testing, a lack of consensus condition, summarized in Table 7, is the key determinant for 90,98 on acceptable short-term risk of serious outcomes, varying further in-hospital management of patients after syncope. Finally, a large spectrum of noncardiac serious conditions may be associated with syncope and require management of the underlying problem. Both trials also allowed unstructured physician judgment to identify intermediate-risk patients. Primary providers can consider expedited referral to specialists with expertise in syncope, as indicated by availability of resources and provider’s assessment of short-term risk of serious outcomes, as an alternative to extended hospital-based evaluation. A broad-based use of additional testing the selection of a given diagnostic test, after the initial history, is costly and often ineffective. See Figure 3 for the algorithm for and a clear understanding of diagnostic and prognostic value additional evaluation and diagnosis for syncope. This section reviews circulating biomarkers, which the availability of simple and accurate biomarkers might are being evaluated as markers either of hypotension or understreamline risk stratification and diagnosis of the cause of lying disease processes. Data to support specific blood testing are largely descriptive data from case series and registries. Complete blood count and electrolyte panel are frequently obtained during syncope evaluation. The diagnostic yield is low when these are used routinely; however, when these blood tests are conducted in patients with a suspected related diagnosis. Thus, specific testing should stem from the assessment by history and physical examination when the nature of the syncope presentation or associated comorbidities suggests a diagnostic or more likely prognostic role for laboratory testing. See Online Data Although data to support biomarker testing are in general relatively weak, there are sufficient data to suggest that Supplements natriuretic peptide is elevated in patients whose subsequent cause for syncope is determined to be cardiac. The ability of troponin and natriuretic peptide 129 measurement to infiuence clinical decision making or patient outcome is unknown. There is little biological plausibility linking the remaining elements of broad-panel laboratory testing to the presentation or mechanism of syncope. Cardiovascular Testing: Recommendations the abnormalities found during cardiovascular testing may Cardiovascular causes of syncope are common. As such, cardiovascular testing can be a critical element in the evaluation and management of selected cardiovascular testing. Transthoracic echocardiography can be useful when healthcare providers are concerned about the presence of valvular disease. Although an echocardiogram may not be able to establish the immediate cause of syncope, it provides information for a potential disease substrate related to prognosis. These modalities offer superior spatial resolution in delineating cardiovascular anatomy. They provide information on the structural disease substrate relevant to the overall diagnosis and subsequent evaluation and follow-up in selected patients presenting with syncope. Unexpected findings on echocardiograms to explain syncope are uncommon; a “screening” echocardiogram is of low utility. Subjecting a patient to a treadmill exercise test to reproduce the symptoms or evaluate the hemodynamic response to exertion. However, bradyarrhythmia may ultimately be responsible for exertional syncope as well, and may only be elicited during stress testing. Cardiac Monitoring: Recommendations the choice of monitoring system and duration should be Although cardiac monitoring is often used in the evaluation appropriate to the likelihood that a spontaneous event will of palpitations or intermittent arrhythmias, the following recbe detected and the patient may be incapacitated and unable ommendations and discussion are focused primarily on the to voluntarily trigger the recording system. N/A the technology of cardiac rhythm monitoring is dynamic and advancing at rapid speed. Their selection and usefulness are highly dependent on patient characteristics with regard to the frequency of syncope and the likelihood of an arrhythmic cause of syncope. The effectiveness of any external cardiac Supplements monitoring device for syncope evaluation is related to the duration of monitoring, continuous versus intermittent 11 and 12. The patient activation, before or after an event, allows for symptom rhythm correlation; however, some external loop recorders are of limited use inpatientswhoare temporarilyincapacitatedaroundthetimeof syncope. Theadvantageofanexternal looprecorderoverHoltermonitoringstemsfromalonger 149,153 monitoring period, which confers a higher yield than Holter monitoring and may offer a diagnosis after a negativeHolterevaluation. One prospective, multicenter study of 392 patients (28% with syncope) reported a 4-week diagnostic yield of 24. The advances of new patch-based devices offer another and often less cumbersome means of identifying an arrhythmic cause for syncope. Some practices offer mobile continuous outpatient telemetry devices, which provide real-time arrhythmia monitoring and analysis. Importantly, there was a similar result in the subgroup of patients presenting with syncope or presyncope, with a significantly higher diagnostic yield in the mobile continuous outpatient telemetry group (89% versus 69%; p50. Table 8 Cardiac Rhythm Monitors Types of Monitor Device Description Patient Selection 151–153 Holter monitor A portable, battery-operated device Symptoms frequent enough to be detected Continuous recording for 24–72 h; up to 2 wk with newer within a short period (24–72 h) of monitoring* models Symptom rhythm correlation can be achieved through a patient event diary and patient-activated annotations Patient-activated, A recording device that transmits patient-activated data (live Frequent, spontaneous symptoms likely to recur transtelephonic or stored) via an analog phone line to a central remote within 2–6wk monitor (event monitoring station. However, the diagnostic yield of inpatient telemetry is low in the absence of high suspicion about an arrhythmic cause. In 1 prospective study of 2,240 patients admitted to a telemetry unit, patients admitted for syncope (10%) had low rates of unexpected intensive care transfer, and most were unrelated to arrhythmic conditions. A large, prospective evaluation of 2,106 patients admitted with syncope demonstrated high telemetry use (95%) but a diagnostic yield of only 5%. Electrophysiological Study: Recommendations or with low suspicion of an arrhythmic etiology. A positive response is defined as inducible presyncope or syncope associated with hypotension, with or without bradycardia (less commonly asystole). The hemodynamic response to the tilt maneuver determines 214 whether there is a cardioinhibitory, vasodepressor, or mixed response. There is general consensus that a tilt-table angle of 70 degrees for 30 to 40 minutes would provide optimal yield. This observation during tilt-table testing cannot necessarily define a causal etiology or be entirely conclusive of a refiex mechanism for syncope in the clinical setting. Correlation of tilt-table–induced findings to patients’ clinical presentation is critically important to prevent consequences of false-positive results from tilt-table testing. Prolonged convulsions and marked postictal confusion are uncommon in patients with syncope associated with convulsive movements,226 and fatigue is frequent after refiex syncope 226 and may be confused with a postictal state. Tilt-table testing has been shown to be of value in this clinical setting when a detailed history cannot clearly determine whether the convulsive movements were secondary to syncope, given the need for objective evidence to help distinguish this entity from true epileptic seizures. In a prospective study of 15 patients with recurrent unexplained seizure-like episodes who were unresponsive to antiepileptic therapy,223 67% had convulsive movements associated with hypotension and bradycardia during tilt-table testing. In another study of 74 patients with a questionable diagnosis of epilepsy (because of drug-refractory seizures or clinically suspected not to be true epilepsy), a cardiac diagnosis was established in 42% of patients, with. Neurological Testing: Recommendations persistent and often progressive generalized weakness, fatigue, visual blurring, cognitive slowing, leg buckling, and 3. These symptoms central or peripheral autonomic nervous system damage or may be provoked or exacerbated by exertion, prolonged dysfunction. Its causes should be sought so as to provide effistanding, meals, or increased ambient temperature. Such care may be provided by a neurologist, cardiologist, internist, or other physician who has sufficient training to treat these complicated patients. Central autonomic degenerative disorders include multiple system atrophy,241 Parkinson’s disease,242 and Lewy Body dementia. The evidence suggests that routine neurological Recommendations testing is of very limited value in the context of syncope evalMany patients undergo extensive neurological investigation uation and management; the diagnostic yield is low, with 36,77,78,251–260 after an uncomplicated syncope event, despite the absence very high cost per diagnosis. Neurological imaging may be indicated if significant head injury as a result of syncope is suspected. Management of Cardiovascular Conditions vant to and within the context of the specific stated cardiac the writing committee reviewed the evidence to support reccondition. Arrhythmic Conditions: Recommendations isting guideline recommendations in the present guideline, Cardiac arrhythmia is a common cause of syncope, and the except for the specific cardiac conditions in Sections 4. Management of paroxysmal and occult on initial evaluation—poses addipatients with syncope and heart disease would include treattional challenges and may warrant a more extensive evaluaing the immediate cause of syncope and further assessing tion (Section 3. The evidencecontinuestosupport,withoutchangefromthepreviousrecommendation,thenotionthatpermanentpacemakerimplantation is reasonable for syncope in patients with chronic bifascicular block when other causes have been excluded. The use of adenosine triphosphate in the evaluation of syncope in older patients continues to evolve. The writing committee has reached a consensus not to make a new recommendation on its use for syncope evaluation because of the limited data at this time. Comprehensive guidelines exist turepublished since publicationofthesedisease-specificguidefor diagnosis and management of many of these diseases, lines was performed to ensure that prior recommendations including sections on syncope. If new published data were of syncope is discussed in patients with underlying structural available, they were incorporated into the present document. Treatment of syncope is based on the specific cause of syncope, whereas treatment for the underlying cardiomyopathy impacts the long-term prognosis. A review of evidence supports previously published recommendations for patients with syncope in the presence of underlying cardiomyopathy. The mechanism is often hemodynamic, as opposed to arrhythmic, because of inability to augment and sustain cardiac output. In patients with valvular heart disease causing syncope, treatment is recommended by the latest guidelines. Inheritable Arrhythmic Conditions: of death in the patients with inheritable rhythm disorders, 25,26,220 Recommendations its impact on syncope recurrence is unknown. The prevalence of inherited arrhythmic conditions is low, rendering the clinical significance of an abnormal test a 4. Most of with type 1 morphology 2mmin 1 lead among the the publications included other cardiac events, such as carright precordial leads V1 and V2, occurring either spontadiac arrest and death, either at enrollment or as an neously or after intravenous administration of Class I antioutcome.
Blissett J erectile dysfunction at 17 buy genuine avanafil on line, Harris G erectile dysfunction treatment scams avanafil 100 mg fast delivery, Kirk J (2000) Growth hormone therapy and feeding problems in growth disorders erectile dysfunction rap beat buy avanafil 100 mg low cost. Blissett J erectile dysfunction doctors fort worth order cheapest avanafil, Harris G (2002) A behavioural intervention in a child with feeding problems impotence grounds for divorce in tn buy avanafil without prescription. Brodsky L (1997) Dysphagia with respiratory/pulmonary presentation: assessment and management. Brown R, Ogden J (2004) Children’s eating attitudes and behaviour: a study of the modelling and control theories of parental infiuence. Budden S, Meek F, Henighan C (1990) Communication and oral motor function in Rett syndrome. Caouette-Laberge L, Plamondon C, Larocque Y (1996) Subperiosteal release of the fioor of the mouth in Pierre Robin sequence: experience with 12 cases. Carruth B, Skinner J (2002) Feeding behaviors and other motor development in healthy children (2–24 months). Chatoor I, Conley C, Dickson L (1988) Food refusal after an incident of choking: a posttraumatic eating disorder. Dahl M, Sundelin C (1986) Early feeding problems in an affiuent society: categories and clinical signs. Mental Retardation and Developmental Disabilities Research Reviews 6(2): 125–30. DiScipio W, Kaslon K, Ruben R (1978) Traumatically acquired conditioned dysphagia in children. Field D, Garland M, Williams K (2003) Correlates of specific childhood feeding problems. Fischer-Brandies H (1989) Vertical development of the jaw in cases of trisomy 21: Interactions of form and function. Hagberg B (1985) Rett’s syndrome: Prevalence and impact on progressive severe mental retardation in girls. Haig D, Wharton R (2003) Prader-Willi syndrome and the evolution of human childhood. Kawahara H, Dent J, Davidson G (1997) Mechanisms responsible for gastroesophageal refiux in children. Kohda E, Hisazumi H, Hiramatsu K (1994) Swallowing dysfunction and aspiration in neonates and infants. Kovesi T, Rubin S (2004) Long-term complications of congenital esophageal atresia and/or tracheoesophageal fistula. Kramer S, Monahan-Eicher P (1993) the evaluation of pediatric feeding abnormalities. Lachman R, Funamura J, Szalay G (1981) Gastrointestinal abnormalities in the Cornelia de Lange syndrome. Li H-Y, Lo L-J, Chen K-S, Wong K-S, Chang K-P (2002) Robin sequence: review of treatment modalities for airway obstruction in 110 cases. MacDonald A, Holden C, Harris G (1991) Nutritional strategies in cystic fibrosis: Current issues. Acute clinical characteristics of paediatric dysphagia following traumatic brain injury. The Normal Acquisition of Oral Feeding Skills: Implications for Assessment and Treatment. Noerr B (2003) Current controversies in the understanding of necrotizing enterocolitis. Odman C, Kiliaridis S (1996) Masticatory muscle activity in myotonic dystrophy patients. Orenstein S, Shalaby T, Putnam P (1992) Thickened feedings as a cause of increased coughing when used as therapy for gastroesophageal refiux in infants. Papargyriou G, Kjellberg H, Kiliaridis S (2000) Changes in masticatory mandibular movements in growing individuals: a six-years follow-up. In Caruso A, Strand E (eds) Clinical Management of Motor Speech Disorders in Children. Reilly S, Carr L (2001) Foreign body ingestion in children with severe developmental disabilities: a case study. Reilly S, Skuse D (1992) Characteristics and management of feeding problems of young children with cerebral palsy. Reilly S, Skuse D, Poblete X (1996) Prevalence of feeding problems and oral motor dysfunction in children with cerebral palsy: a community survey. Robin P (1923) La chute de la base de la langue consideree comme une nouvelle cause de gene dans la respiration naso-pharyngienne. Rogers B (2004) Feeding method and health outcomes of children with Cerebral Palsy. Romero R, Chaiworapongsa T, Espinoza J (2003) Micronutrients and intrauterine infection, preterm birth and the fetal infiammatory response syndrome. Varan B, Tokel K, Yilmaz G (1999) Malnutrition and growth failure in cyanotic and acyanotic congenital heart disease with and without pulmonary hypertension. Antroduodenal motility in neurologically handicapped children with feeding intolerance. Before treatment and management can commence, however, there is a need for a thorough assessment of swallowing function. As detailed in Chapter 2, the infant swallow and the adult swallow are quite different and warrant individual discussions in their own right. Once cannot assume that assessment techniques that are suitable for adults will also be suitable for babies, infants and children. This chapter will discuss both (a) clinical assessments and (b) instrumental assessment techniques that are suitable for use with babies, infants and children. The ultimate goal of the clinical oral assessment is to define the pathophysiology and the extent of the feeding difficulties. In this problem-solving process, the evaluation of the oral cavity and its functions by observation plays a major role, and should occur prior to instrumental assessment. The feeding specialist must have a thorough understanding of normal function of the many interacting systems involved in feeding. In the clinical oral feeding evaluation, oral anatomy, motor skills, refiex activity, responsivity and swallowing are examined. With this information, referrals can be made for further diagnostic testing and multidisciplinary management where a specific treatment plan can be developed. The clinical oral examination should therefore always be the initial assessment scheduled in a team evaluation. Oral structures are examined for malformations and for abnormalities of muscle tone and muscle mass. The lips, cheeks, jaw, tongue, hard and soft palate are examined at rest and during spontaneous movement. Palatal and labial clefts, micrognathia, deviant dental occlusion, ankyloglossia and trismus are some of the most frequently seen anomalies. Assessment of oral motor function Oral motor skills have been described extensively in anatomy text books, developmental and rehabilitation literature (Morris, 1982). A brief discussion of the most clinically relevant oral refiexes in terms of infant sucking will be presented because the oral motor assessment in young infants occurs mainly by evaluation of the oral refiexes. These oral refiexes are defined as programmed responses to a specific sensory input, generally a tactile stimulus, and they become modified or integrated into functional activity with increased maturity. The expression of oral refiexes at any age can be quite varied, depending on a number of factors such as state of arousal or hunger. Eliciting specific oral refiexes during the clinical feeding evaluation provides information on the baby’s neurological maturity or integrity as well as on the quality of its response to tactile input (Wolf and Glass, 1992). The interplay of the refiexes with the child’s functional feeding skills is, however, more important than the presence or absence of specific refiexes (Ingram, 1962). Oral refiexes fall into two categories: temporary and permanent refiexes (see Table 14. Permanent refiexes such as the transverse tongue refiex, gag, cough and swallow develop quite early in utero but remain present during an individual’s lifetime. The cough and gag refiex are also called protective refiexes as they are designed to protect the airway during feeding and to expel aspirated foreign material. The second mechanism to protect the airway is bronchial receptor stimulation by excessive secretions with the purpose of clearing the lower airways of foreign material or mucus. It is important to observe the cough because the protective laryngeal cough is a prerequisite for safe feeding and excessive coughing suggests lack of suck-swallow-breath coordination. Although the presence of a cough is imperative for safe feeding, it does not guarantee that the subject is a safe feeder. Many children with swallow dysfunction cough sometimes, but do not when they aspirate during deglutition. As coughing is the mechanism that protects the airway, the presence and effectiveness of the cough, and not the gag, needs to be considered in regards to safe oral infant feeding (Wolf and Glass, 1992). The gag refiex is present at 18 weeks’ gestational age (Inniruberto and Tajani, 1981; Tucker, 1985). The purpose of the gag refiex is to protect the baby from ingesting large items that can block the airway. It is elicited by touch pressure to receptors located on the tongue or pharyngeal wall causing a reverse peristaltic movement in the pharynx. The spot triggering the gag refiex moves with increasing age: in the newborn gagging is elicited in the mid-tongue area; when the baby matures, the gag gradually moves back to the pharyngeal wall or posterior portion of the tongue (Wolf and Glass, 1992). The status of the gag refiex does not predict the swallow ability as they are innervated independently but does provide information on the responsivity of the pharyngeal receptors (Dodds, 1989; Leder, 1996). The swallowi ng response has been obser ved i n the foetus at 12 to 14 weeks (I n ni r uber to and Tajani, 1981) and is present throughout life. The transverse tongue refiex is triggered by unilateral stimulation of the anterior 1/3 lateral border of the tongue. Lateral tongue movement occurs towards the side of stimulation and should be elicited bilaterally. The temporary oral refiexes, which include rooting, sucking, palmomental refiex, Sandmyer refiex, and the phasic bite, assist in the acquisition of food, but disappear or are integrated by muscle function respectively at 3–6 months, 3–4 months, 1–2 years, 6–8 months and 9–12 months of age. The presence of this response is quite variable and is based on factors such as state. An absent refiex may refiect poor tactile sensitivity or neural integration (Wolf and Glass, 1992). Sucking is refiexive in the newborn with a gradual transition to full volitional control of sucking by 3 to 4 months of age. The elicitation of the refiex varies depending on the type of stimulus (nutritive or non-nutritive) and can be inhibited by factors such as state or satiation (Wolf and Glass, 1992). The palmomental (Babkin) refiex can be elicited by giving bilateral pressure to the palms resulting in mandible depression and sucking movements of the tongue.
They also allow more mobility erectile dysfunction medicine reviews generic avanafil 50 mg overnight delivery, the possibility of discharge to erectile dysfunction treatment youtube order avanafil 100mg on line the ward once off ventilatory support (thereby freeing up the bed for the next patient) erectile dysfunction gene therapy treatment quality avanafil 50 mg, and the recommencement of oral food and fiuids under the guidance of the speech pathologist erectile dysfunction treatment for diabetes 100 mg avanafil free shipping. The causes of upper airway obstruction are most often acute – burns erectile dysfunction at 17 50mg avanafil with mastercard, foreign bodies, corrosive gas/liquid exposure, infections or trauma. Occasionally such obstructions are slower in onset, especially if neoplastic in origin. Access to the airway for aspiration of secretions is most often needed in the post-intensive care setting when patients recovering from pneumonia or infective exacerbation of chronic obstructive lung disease are still producing copious amounts of secretions. The cough is very often weakened in this situation because of the inability of intensivists to provide enough nutrition in the acute illness setting to overcome the body’s tendency to break down muscles (including the diaphragm, accessory muscles and the intercostal muscles). It is debatable that even the delivery of enough calories would make a difference as the body produces certain chemical messengers (hormones and cytokines) that drive this process of muscle breakdown and prevent utilization of energy, whether delivered directly intravenously or indirectly enterally. This said, the most common reason for insertion of a tracheostomy is for the facilitation of weaning long-term ventilated patients from the ventilator. In Australia, we tend to use the cutoff of 2 weeks to define long-term ventilation – this does not mean that one necessarily waits 2 weeks, but if you think ventilation is very likely to be longer than two weeks, a tracheostomy is considered at the first clinically safe and technically feasible occasion. This is a historical practice that is currently being subjected to randomized trials of early versus late tracheostomies to try to work out the ideal time to insert one for patients with prolonged intubation. Indications for insertion of tracheostomies are as follows: • To bypass upper airway obstruction. For example: – burns; – foreign bodies; – corrosive gas/liquid exposure; – infections; – trauma. It is important to note that a tracheostomy tube does not guarantee protection from aspiration. It has been reported that aspiration may occur in up to 15% of patients managed with a tracheostomy (Irwin, 1999). Nevertheless, one must never assume that just because a tracheostomy is in place, even with the cuff balloon infiated, the patient is safe from aspiration and its consequences. A good general rule is always assume the cuff is not working and carry out all the mechanical procedures to minimize the risk of refiux and aspiration. The cuff allows infiation and occlusion of the airway to material from above – this, as mentioned previously, does not guarantee protection from aspiration and it has been noted that even the use of suctioning ports above the cuff does not reduce that risk. Smaller tracheostomies – the so-called ‘mini-trach’ – are often used in those patients with a weakened cough and/or excessive secretions to facilitate ‘tracheal toilet’. If the patient is not constantly on the ventilator, he or she can have a tube with holes (fenestrated) placed in or have a speaking valve put on the tracheostomy (with the cuff defiated) – these devices allow the passage of air from the lungs and up the trachea over the vocal cords. The speech pathologist’s role in the assessment and management of swallowing and communication for individuals with tracheostomy tubes is detailed in Chapter 9. Endotracheal tubes are associated with a change in the refiexes needed for swallowing due to changes in neurological sensitivity, muscular dysfunction and subacute injury even if the tube has only been in less than one day. These changes usually resolve rapidly and rarely need any formal intervention (DeLarminat et al. Should formal swallowing therapy be required, these would follow the principles outlined in Chapters 11 and 12. The most serious complications are bleeding, misplacement of the tube and obstruction. Bleeding can occur at an early stage – this is most often likely to be local and is more of an irritation than a serious concern. If it occurs at a late stage this is often serious, with 50% being due to erosion into the innominate artery (supplying the right arm and side of the head/brain) with catastrophic consequences. Misplacement may occur after dislodgement with faulty replacement, or as an initial insertion problem, and leads to a failure to ventilate. Obstruction is most often due to dried out and viscous secretions but can also be due to bleeding. There are a multitude of other complications – stoma infections, nerve injury (particularly the recurrent laryngeal nerve), pneumothorax, lung collapse, tracheo-oesophageal fistula and laryngomalacia. From the speech pathology point of view, the major complications of tracheostomy are dysphagia and aspiration. The cuffs are now designed to be more compliant even with high volumes of air in them resulting in less over-distension and less pressure on the airway – also most intensive care unit protocols call for either a leak test or a check of the cuff pressure to prevent excessive pressures being present in the cuff. Despite this, the cuff is often described in retrospect by patients as feeling like an orange stuck in the throat on attempting to swallow. A good general rule is to let the cuff down as soon as the patient is off the ventilator, especially when the patient is in the sitting position. Tracheostomies lead to delayed swallow triggering and pharyngeal pooling of contrast material on videofiuoroscopy (DeVita and Spierer-Rundback, 1990). There is poorer anterior movement of the pharynx in swallowing and laryngeal elevation is decreased as well. This is mostly due to fixation of the trachea to the skin by the tracheostomy although compression of the oesophagus by the cuff also plays a role. As mentioned before, endotracheal tubes can desensitize the nerves of the oropharynx and, likewise, tracheostomies and prolonged fasting/nil by mouth can desensitize the nerves involved with the sensation and coordination of swallowing. This leads to a loss of protective refiexes such as the cough or gag refiex and the refiex closure of laryngeal opening, which contributes to lack of coordination of the swallowing process. Basically, as soon as there is no further indication for the tracheostomy and the patient is considered safe, the tracheostomy should be removed. This decision should be arrived at after close coordination between the clinician caring for the patient and the speech pathologist reviewing the patient. It does not mean that one has to wait until the swallow is normal before removing the tracheostomy. The process of consultation and review does not stop there – depending on the underlying pathological process, the patient may never recover a normal swallowing process and most patients after decannulation will require ongoing speech pathology review. Therefore, those at risk of aspiration should be assessed by a qualified professional (a speech pathologist) before being allowed to have oral intake. Risk factors are readily identifiable – anything that interferes with muscle coordination or strength particularly cerebrovascular accidents or anything that depresses the level of consciousness. The care of a patient who has suffered aspiration or a patient who is coming off a tracheostomy requires close liaison between the clinician and the speech pathologist. Kidd D, Lawson J, Nesbitt R (1993) Aspiration in acute stroke: a clinical study with videofiuoroscopy. Drooling or saliva loss may occur where one or more of the phases of swallowing is impaired. Many of us only discover its importance when our mouth becomes dry while presenting at an important speaking engagement. Apart from moistening our tongues and lips while speaking, saliva has several major functions, which include the lubrication of the bolus for ease of swallowing, the maintenance of oral hygiene, and the regulation of acidity in the oesophagus. Where a person has no oral motor deficits there may still be problems with saliva production, which can result in changes in saliva viscosity. This may affect swallowing, and result in increased dental caries and periodontitis. Poor saliva control can occur in people with developmental, acquired or progressive disabilities. Hypersalivation is rare and not usually a cause of drooling (Tahmassebi and Curzon, 2003). Where a person has oral motor difficulties the problems with saliva may result in saliva overfiow (also called drooling or dribbling) and cause embarrassment and social isolation. Drooling is usually considered normal until a child is over 2 years of age (Morris and Dunn Klein, 2000). However some children with no obvious neurodevelopmental disabilities may drool until six or seven years (Johnson et al. Tahmassabi and Curzon (2003) suggested that, in children with cerebral palsy and an intellectual disability, drooling becomes less apparent after the development of permanent dentition. There are no separate prevalence rates available for those with an intellectual disability or other neurological conditions. People with acquired neurological conditions frequently encounter saliva control problems. Drooling in these conditions is related to impairment of oral control rather than an increase in saliva production. Secretion control problems are seen in adults where dysphagia occurs after multiple strokes involving both cerebral hemispheres or following a brain stem stroke. The problem is usually worse in the acute phase but may continue to be an issue depending on the site and extent of infarction (Smithhard, 1997). People with developmental disabilities, in particular cerebral palsy, often retain immature swallowing patterns. In this case, instead of the tongue collecting the saliva and then elevating itself to press against the hard palate to push the saliva into the pharynx, the tongue protrudes and retracts in much the same way an infant’s tongue moves. This tongue thrust pattern becomes more apparent as the person matures because the space in the oral cavity increases, resulting in protrusion of the tongue during the oral phase of swallowing and drooling. In Parkinson’s disease the characteristic paucity of movement affects the usually automatic, spontaneous swallowing of saliva. Drooling is most prominent when the anti-Parkinsonian medication is not effective. As Parkinson’s disease progresses the individual’s response to the medication diminishes and longer and more frequent ‘off’ periods are experienced. The tongue is particularly affected in motor neurone disease (Robbins, 1987) and consequently saliva cannot be collected and propelled into the pharynx. Because pharyngeal impairment frequently co-occurs with oral impairment, aspiration of saliva may be a problem. Understanding the mechanism of saliva fiow and production is essential if one is to understand the management of the range of difficulties with saliva. Diagrammatic representation of afferent and efferent pathways that are involved in refiex salivary secretion under the coordinating control of the salivary centres. The parotid glands are most active during chewing when the mechanical stimulation of the masseter and pterygoid muscles results in secretion of saliva via Stensen’s ducts into the mouth in the region of the second molars. The submandibular glands secrete via Wharton’s ducts, which are located on either side of the frenulum. Secretions from the sublingual glands fiow through the ducts of Rivius, situated on the fioor of the mouth (see Figure 6. The structure of the salivary glands is typical of all exocrine glands, being composed of small structures called acini, into which the epithelial cells secrete saliva, and ducts that transport the saliva. The parotid glands only produce serous secretions whereas the submandibular and sublingual glands produce both serous and mucoid secretions. Parasympathetic input increases the amount of saliva associated with eating and drinking. Sympathetic input reduces the quantity of secretion when not eating or drinking and during physical activity (see Figure 6. The average person produces and swallows approximately 600 ml of saliva a day (Watanabe and Dawes, 1988). This movement of the saliva is important to protect the teeth from developing caries.
Note also that high temperatures may be caused by conditions other than poor chest status erectile dysfunction over 70 order avanafil 100mg with visa. There are some medications that are known to erectile dysfunction va disability rating buy avanafil 100mg visa have adverse effects on swallowing function erectile dysfunction icd generic avanafil 50mg without a prescription. Medications that cause dryness of the oral erectile dysfunction drugs for diabetes buy cheap avanafil 200 mg on line, nasal or pharyngeal mucosae can make it difficult to erectile dysfunction cures discount avanafil 50mg on-line initiate a swallow (see Chapter 9). Other medications may produce side effects simulating extrapyramidal symptoms (see Chapter 9). The speech pathologist should also review the method by which medications are being administered (tablet, capsule, liquid, etc. Individuals with severe dysphagia may be unable to take medication in a tablet or capsule format and may require the pharmacist to see if there is an alternative method of administration. Also note that some capsules or tablets have special enteric coatings to ensure that they do not disperse before they reach the stomach. Placing these medications in a spoonful of thickened fiuids may assist the patient in swallowing the medication but reduces the effect of the medication if it disperses throughout the pharynx and oesophagus rather than in the stomach. If in doubt, always consult medical team members such as the pharmacist, doctor and nursing staff. Previous speech pathology intervention As part of any thorough background review, evidence of previous speech pathology intervention should also be sought. Knowledge of previous clinical reports or imaging studies such as videofiuoroscopy affords the clinician a baseline of swallowing function. Client-specific information It is important to remember that no two individuals are the same. We each have unique biographical, cultural and religious backgrounds, educational and vocational backgrounds and behaviours. This information should direct how we interact with and provide information to our patients. For example, in providing explanations for a swallowing assessment and how it is carried out one should be aware of the patient’s educational and vocational background. The explanation afforded a person with tertiary qualifications should be quite different from the explanation offered to an individual with little schooling. Cultural differences may be highlighted when it comes to discussions of the patient’s goals. For example, for individuals of Asian, European or Middle Eastern cultures, the Western texture modified diets offered may be unappealing to the point that they might cause a reluctance to eat, which then slows down recovery. This is another example of why it is important that each dysphagic individual be seen as unique, and treated as such. In addition to the above information, some general information should be gathered from the individual with dysphagia or their next of kin or carer. Questions for the individual with dysphagia and/or their next of kin are: • When did the swallowing problem beginfi Once the background information has been obtained, the individual should be observed. These are: • Is the patient alert and able to participate in an oromotor assessment and a swallowing evaluationfi The relationship between swallowing and respiration has been outlined in detail in Chapter 4, which includes normal respiratory rates that can be used as a reference. As noted in Chapter 4, if the resting respiratory rate is abnormal, the individual is automatically at an increased risk of aspiration. It is normal for there to be a small increase (approximately 10%) in respiratory rate after swallowing, however this rapidly returns to normal in a non-dysphagic individual (Hirst et al. Comprehension ability should be noted, and the need for hearing aids should also be established. Voice quality should also be subjectively noted (particularly for the parameters of wetness, hoarseness, breathiness or harshness). For example, the need for eye glasses or any disturbances in visuoperceptual skills such as those that might be found after a stroke. These may include, but are not limited to, up-to-date immunization of the speech pathologist. Disposal of contaminated materials such as gloves or tongue depressors should be carried out responsibly in the manner dictated by the workplace. Inspection of the oral cavity and oropharynx the clinician should be aware of any abnormalities of structures at rest within the oral cavity. For example, blisters only on the left buccal surface in a patient with a right hemisphere stroke may be indicative of the patient biting the left buccal region during eating and point to poor intraoral sensory perception for the affected side. Extensive dryness of the mouth makes it difficult to initiate a swallow, as does the presence of thick mucus (Miller, 1992). It should be noted whether patients care for their own oral hygiene or are reliant on carers. In conjunction with this the state of the person’s dentition should also be examined. Halitosis can be caused by – but is not limited to – decaying food that has been pooled in the buccal sulcii, or even in a pharyngeal pouch. There is research to suggest that poor oral hygiene may be a risk factor for respiratory tract infections, particularly for elderly institutionalized individuals. The mechanism for this includes aspiration of oral pathogens carried on saliva or food/fiuid particles (Langmore et al. Saliva management the issue of saliva management has been thoroughly examined in Chapter 6. Poor awareness may be indicated by drooling or pooling of saliva within the oral cavity. It should also be noted whether the patient wipes the mouth with a hand or tissue in an attempt to control saliva management. A patient’s ability to swallow his or her own secretions should also observed, particularly whether this is a spontaneous action or requires prompting by a carer to swallow pooled material. A gurgling vocal quality after swallowing of secretions may indicate pooled material in the pharynx. The clinician should also note symmetry or asymmetry of movement or loss of sensation. These nerves and their function in swallowing has been discussed in detail in Chapter 1. If there is asymmetry and the soft palate is sagging, the uvula will deviate towards the normal side as there is insufficient muscle tension from the affected side to hold it in the mid-line. If no response is elicited from the soft palate the clinician may wish to touch the posterior pharyngeal wall to see if a response can be elicited. This gives an indication of (a) ability to follow a command, (b) ability to perform a voluntary cough, (c) the strength of the cough. Observe also any refiexive coughs as these may be different in strength to voluntary coughs. Ask the patient to poke the tongue out, point up towards the nose, down towards the chin, protrude to the left and the right, and then move in a circular motion as if licking the lips. For patients where an apraxia appears to be present the clinician may, for example, try giving a cue that ‘there is something on your top lip, can you lick it offfi Airway protection • Ask the patient to voluntarily hold their breath for the count of two. Note that the apnoeic period may still be triggered refiexively during a swallow even if the individual cannot voluntarily hold their breath. Cranial nerve V – trigeminal nerve this nerve has both motor and sensory components. It provides general sensation for the anterior two-thirds of the tongue, and is motor to the masticatory muscles, and the fioor of the mouth. It provides sensory information in the form of taste from the anterior two-thirds of the tongue via the chorda tympani. The facial nerve is motor to the following muscles: orbicularis oculi and oris, zygomatic, buccinator, platysma, stylohyoid, and stapedius. Apart from important neurological information gained from this assessment which will help to ascertain the cause of the swallowing problem, this assessment also provides information about the person’s ability to keep the bolus within the oral cavity. It is responsible for taste for the posterior one third of the tongue and sensation of the soft palate. It is motor to stylopharyngeus, the otic ganglion, and partial to the middle/inferior pharyngeal constrictor. The glossopharyngeal nerve is responsible for elevation of the pharynx and larynx and contributes to pharyngeal constriction. It is motor to the inferior, middle and superior pharyngeal constrictors, levator veli palatini, uvular, cricothyroid, thyroarytenoid, cricoarytenoids, transverse and oblique arytenoids, and oesophagus. It is responsible for palatal elevation and depression, laryngeal movement, pharyngeal constriction and cricopharyngeal movement. A sluggish or absent gag refiex provides information about level of sensation in that region. It is designed to expel vomit and refiuxed material from below and foreign bodies such as an overly large bolus or the tongue depressor anteriorly. As such it works in the completely opposite way to a normal swallow, which is designed to propel the bolus through the pharynx. There is much confusion surrounding the gag refiex, not the least of which comes from the medical fraternity (Smithard and Spriggs, 2003). Many referrals suggest that swallowing is occurring safely because of an intact gag refiex. This assumption is often made regardless of how uncoordinated the swallow may actually be. The presence or absence of the gag refiex may be indicative of sensation in that region but one cannot assume that a gag refiex will be triggered in the event of pooled material in the pharynx. Neurology shows us that sensation for the soft palate, which is where the gag refiex is elicited, is mediated via the glossopharyngeal nerve, whereas sensation for the pharynx and larynx, which are where pooled material may accumulate after the swallow, is mediated via the vagus nerve. While these two nerves work in harmony the fact that one is working is not predictive that the other is also working. It is also very important to note that there is a large degree of variability in the gag refiex in healthy non-dysphagic adults. Logemann (1995) reports that approximately 40% of non-dysphagic men and 10% of non-dysphagic women do not have a gag refiex (Smithard and Spriggs, 2003). If the phonation sounds ‘wet’ or ‘gurgling’ it may indicate that there are secretions or pooled material over the surface of the cords or in the laryngeal vestibule. The length of time an individual can phonate for may also give an indication of their ability to control their respiratory system. Warms and Richards (2000) investigated the correlation between wet vocal quality and prediction of pooled material in the larynx/trachea as indicative of aspiration or penetration.
Purchase cheap avanafil online. Face shape before and after quitting smoking á´´á´° â–ˆâ–¬â–ˆ â–ˆ â–€â–ˆâ–€.