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Resection of a portion of the caudal lower lateral cartilages are then secured with through-and- septum can allow for the infratip lobule to rotate superiorly order januvia 100mg visa, through sutures order 100 mg januvia amex. Kridel et al16 performed a retrospective leading to increased tip rotation; however cheap januvia 100 mg amex, one must be careful review of all patients undergoing the tongue-in-groove tech- to not overresect the caudal septum, leading to iatrogenic com- nique over a 10-year period and found 278 of 287 patients plications. The author concluded that the tongue-in-groove techni- Dynamic collapse of the external nasal valve manifests upon que is best utilized in the patient with a ptotic nasal tip but inspiration with inward collapse of the ala, leading to obstruc- adequate projection. Malposition of the lateral crura of the lower lateral carti- nique should be utilized in patients with an underprojected lage represents one common cause of dynamic collapse of the ptotic nasal tip and the lateral crural overlay in patients with external nasal valve. If necessary, the tongue-in- “malpositioned lateral crura,” which he later stated were groove technique can be combined with caudal extension actually normal anatomic variants. In normal subjects, the lat- grafts to correct abnormalities of the caudal septum. Byrd et eral crura of the lower lateral cartilages diverge from the alar al18 described the use of caudal septal extension grafts used margin at an angle of 30 to 45 degrees. In some individuals, in combination with the tongue-in-groove technique as a the angle of divergence of the lateral crura from the alar mar- reliable means to set the nasal tip position and achieve long- gin exceeds 45 degrees, leading to lack of structural support of lasting results. For example, Daniel21 pre- modified back-to-back auricular cartilage graft used as a cau- viously stated that in a review of 50 patients, the lower lateral dalseptalextensiongraftcombinedwiththetongue-in- crura being located greater than 7mm from the midalar mar- groove method to extend the medial crura, providing tip gin was predictive of cephalic malpositioning and its functional support, projection, and rotation. Constantian22 reported that 27 of 61 patients circumstances, the tongue-in-groove technique with or with- (47%) presenting for rhinoplasty exhibited lateral crural 269 Tip Rhinoplasty malpositioning. A few patients complained of increased full- rospective review of 200 patients undergoing rhinoplasty and ness of their lateral nasal wall secondary to the graft; however, reported that 68% of primary rhinoplasty patients and 87% the noted fullness decreased over time secondary to scarring of secondary rhinoplasty patients exhibited lateral crural and decreased edema. Sheen20 described mobilization significant improvement in their breathing, with six patients and repositioning of the lateral crura, which he later abandoned noting minor aesthetic fullness in the lateral nasal wall. Gunter and Friedman24 described the the support and strength of the lateral nasal wall; however, alar use of lateral crural strut grafts with or without lateral crural rim grafts are placed in a nonanatomic position and are largely repositioning to address cephalic positioning of the lateral crus limited to the treatment of external nasal valve collapse. Oktem et al25 described repositioning of procedure can be performed via an external or endonasal rhi- the lateral crus with a cartilage Z-plasty technique in which the noplasty approach. A precise pocket along the alar margin is lateral crus on each side is transected and the anterior segment fashioned and an alar rim graft (usually 2 to 3mm wide and 1 attached to the domes is sutured to the caudal aspect of the to 2cm long) is placed within the pocket. No suture is necessary posterior segment, thus repositioning the majority of the lateral if an appropriate pocket is fashioned; however, a suture can be crus and providing more support to the external nasal valve. Similar to normally positioned lateral crura secondary to weakness of the ala rim grafting, Rohrich et al28 performed a retrospective cartilage, which can be congenital, iatrogenic, or secondary to review of 123 patients undergoing alar rim grafting (termed trauma or infection. Multiple surgical techniques have been “alar contour graft”) during a 6-year period and noted that 91% described to bolster support of the lateral crus, thus preventing of patients experienced correction of their alar notching or inspiratory collapse of the external nasal valve. Boahene and Hilger29 retrospec- monly used techniques utilized to bolster the support of the tively reviewed 150 rhinoplasty cases over a 1-year period and external nasal valve and the lateral crus of the lower lateral car- identified 31 cases (21%) in which alar rim grafting was used. In all cases in which alar rim grafting was utilized for internal nasal valve collapse. Alar batten grafts are commonly external nasal valve collapse, there was increased alar support fashioned from septal or conchal cartilage and are placed in an and decreased external nasal valve collapse noted postopera- appropriately sized pocket at the site of maximal collapse of the tively without any complications in the series. Gunter and Friedman24 described the use of lateral 63 patients undergoing placement of alar batten grafts for crural strut grafts placed underneath the lateral crus after dis- either internal or external nasal valve collapse or both. The section of the vestibular skin in patients with weakness or authors noted that 98% of patients noted improvement in their cephalic malpositioning of the lateral crus. A cartilage graft harvested from the ear or septum is placed in an appropriately sized pocket spanning the pyriform aperture and overlapping at least the medial aspect of the lateral crura of the lower lateral cartilages. Cartilage grafts are sutured to the underside of the lower lateral crura of the lower lateral cartilages after elevating the vestibular skin. A graded approach to repairing the technique and advocate the use of this technique for alar con- stenotic nasal vestibule. Lateral crural steal and lateral crural overlay: an objec- The nasal tip is a complex area that has significant implications tive evaluation. Arch Otolaryngol Head Neck Surg 1999; 125: 1365–1370 for functional and aesthetic outcomes following rhinoplasty. Tongue-in-groove technique and septorhinoplasty: A 10-Year Abnormalities of the nasal tip can lead to static or dynamic col- Experience. The tongue-in-groove technique in septorhi- lapse of the external nasal valve, leading to nasal obstruction noplasty. Arch Facial Plast Surg 1999; 1: 246–256, dis- and aesthetic abnormalities, in turn leading to the appearance cussion 257–258 of a boxy, bulbous, ptotic, and/or pinched tip. Septal extension grafts: a method the nasal tip; however, no single technique can be utilized to ofcontrolling tip projection shape. Modified back-to-back autogenous conchal cartilage familiar with multiple techniques to address both functional graft for caudal septal reconstruction: the medial crural extension graft. Arch and aesthetic abnormalities of the nasal tip to achieve optimal Facial Plast Surg 2011; 13: 20–25 outcomes. The two essential elements for planning tip surgery in primary References and secondary rhinoplasty: observation based on review of 100 consecutive patients. Plast Reconstr Surg 1997; 99: 943–952, discus- 1986; 112: 726–728 sion 953–955  Pitanguy I. Cartilage Z plasty on lateral crus for treat- 2001; 107: 264–266 ment of alar cartilage malposition. Applications of the M-arch model in nasal tip refine- of alar rim deformities in rhinoplasty. Alar rim grafting in rhinoplasty: indications, techni- the cantilevered spring model. Arch Facial Plast Surg 2009; 11: 285–289 271 Tip Rhinoplasty 35 Nuances in Tip odification: Specific Applications of Cartilage Splitting in Rhinoplasty Anil R. Shah and Minas Constantinides Division of lower lateral cartilages in rhinoplasty has long been inexperienced rhinoplasty surgeon but is often necessary to maligned for producing unnatural results and unpredictable achieve an acceptable rhinoplasty outcome. The original manifestation of this technique resulted help in analyzing recognition of these specific nasal deformities from the Goldman tip rhinoplasty, stereotyped by the nar- in which cartilage-splitting techniques may improve the ulti- rowed, pinched noses of previous decades. In addition, technical details will be given in recently, use of several modifications of this technique in the order for the reader to produce the achieved results.
In the event of severe bleeding cheap januvia 100 mg with mastercard, infusion of abciximab and heparin should be discontinued buy discount januvia 100mg on line. The drug—neither an antibody nor a peptide—was modeled after a platelet inhibitor isolated from the venom of the saw-scaled viper januvia 100 mg, a snake indigenous to Africa. Thrombolytic (Fibrinolytic) Drugs As their name implies, thrombolytic drugs are given to remove thrombi that have already formed. This contrasts with the anticoagulants, which are given to prevent thrombus formation. In the United States three thrombolytic drugs are available: alteplase, reteplase, and tenecteplase. Principal differences among the drugs concern specific uses, duration of action, and ease of dosing. All thrombolytics pose a risk for serious bleeding and hence should be administered only by clinicians skilled in their use. Because of their mechanism, thrombolytic drugs are also known as fibrinolytics (and informally as clot busters). The alteplase-plasminogen complex then catalyzes the conversion of other plasminogen molecules into plasmin, an enzyme that digests the fibrin meshwork of clots. In addition to digesting fibrin, plasmin degrades fibrinogen and other clotting factors. In all three settings, timely intervention is essential: the sooner alteplase is administered, the better the outcome. Results for alteplase were as follows: among patients treated within 2 hours of symptom onset, the death rate was only 5. Clearly, outcomes are best when thrombolytic therapy is started quickly, preferably within 2 to 4 hours of symptom onset, and even earlier if possible. In addition to its use for acute thrombotic disease, alteplase can be used to restore patency in a clogged central venous catheter. The drug has a very short half-life (5 minutes), owing to rapid hepatic inactivation. Within 5 minutes of stopping an infusion, 50% of the drug is cleared from the blood. Bleeding occurs for two reasons: (1) plasmin can destroy preexisting clots and can thereby promote recurrence of bleeding at sites of recently healed injury; and (2) by degrading clotting factors, plasmin can disrupt coagulation and can thereby interfere with new clot formation in response to vascular injury. Likely sites of bleeding include recent wounds, sites of needle puncture, and sites at which an invasive procedure has been performed. Accordingly, high-dose therapy with these drugs must be avoided until thrombolytic effects of alteplase have abated. Patients who require blood replacement can be given whole blood or blood products (packed red blood cells, fresh-frozen plasma). Absolute and relative contraindications to thrombolytic therapy are shown in Table 89. Preparations Alteplase is available under two trade names: Activase and Cathflo Activase. Alteplase is usually given by an “accelerated” or “front-loaded” schedule, in which the infusion time is only 90 minutes, compared with 3 hours as routinely done in the past. Dosage is based on patient weight but should not exceed 100 mg because doses in excess of 100 mg are associated with an increased risk for intracranial bleeding. However, because of this small structural change, the pharmacokinetics of tenecteplase are much different. As a result, thrombolysis develops faster, and emergency personnel are spared the trouble of monitoring a prolonged infusion. Because tenecteplase is so easy to administer, it has the potential to allow dosing before the patient reaches a hospital. Thirty days after treatment, outcomes were equivalent with respect to mortality (6. Of significance, the incidence of major hemorrhage (other than intracranial) was lower with tenecteplase (4. Tenecteplase dosage is based on body weight as follows: • Less than 60 kg: dose 30 mg • 60 to 69. Reteplase has a short half-life (13–16 minutes), owing to rapid clearance by the liver and kidneys. The risk for bleeding is increased by concurrent use of heparin, aspirin, and other drugs that impair hemostasis. In addition to its antidysrhythmic applications, lidocaine is employed as a local anesthetic (see Chapter 21). Effects on the Heart and Electrocardiogram Lidocaine has three significant effects on the heart: (1) like other class I drugs, lidocaine blocks cardiac sodium channels and thereby slows conduction in the atria, ventricles, and His-Purkinje system; (2) the drug reduces automaticity in the ventricles and His-Purkinje system by a mechanism that is poorly understood; and (3) lidocaine accelerates repolarization (shortens the action potential duration and event-related potential). In contrast to quinidine and procainamide, lidocaine is devoid of anticholinergic properties. If the drug were administered orally, most of each dose would be inactivated on its first pass through the liver. Because lidocaine is rapidly degraded, plasma drug levels can be easily controlled: if levels climb too high, the infusion can be slowed and the liver will quickly remove excess drug from the circulation. Antidysrhythmic Use Antidysrhythmic use of lidocaine is limited to short-term therapy of ventricular dysrhythmias (Table 89. Consequently, whenever lidocaine is used, equipment for resuscitation must be available. The usual loading dose is 50 to 100 mg (1 mg/kg) administered at a rate of 25 to 50 mg/min. An infusion rate of 1 to 4 mg/min is used for maintenance; the rate is adjusted on the basis of cardiac response. To avoid toxicity, dosage should be reduced in patients with impaired hepatic function or impaired hepatic blood flow (e. Procainamide Procainamide blocks cardiac sodium channels, thereby decreasing conduction velocity in the atria, ventricles, and His-Purkinje system. In contrast to quinidine, procainamide is only weakly anticholinergic and hence is not likely to increase ventricular rate. Procainamide is effective against a broad spectrum of atrial and ventricular dysrhythmias. However, because prolonged therapy is often associated with serious adverse effects, procainamide is less desirable than quinidine for long- term use. In contrast to quinidine, procainamide can be used to terminate ventricular tachycardia and ventricular fibrillation.
It is important to appreciate that drug therapy of dysrhythmias is highly empiric (i order januvia 100 mg visa. In practice order januvia 100mg, this means that cheap januvia 100 mg on-line, even after a dysrhythmia has been identified, we cannot predict with certainty just which drugs will be effective. Frequently, trials with several drugs are required before control of rhythm is achieved. If the atria drive the ventricles at an excessive rate, diastolic filling will be incomplete and cardiac output will decline. Of course, if treatment did abolish the dysrhythmia, this outcome would not be unwelcome. Atrial Fibrillation Atrial fibrillation is the most common sustained dysrhythmia, affecting about 2. The disorder is caused by multiple atrial ectopic foci firing randomly; each focus stimulates a small area of atrial muscle. In addition to compromising cardiac performance, atrial fibrillation carries a high risk for stroke because, in patients with atrial fibrillation, some blood can become trapped in the atria (rather than flowing straight through to the ventricles), thereby permitting formation of a clot. When normal sinus rhythm is restored, the clot may become dislodged and then may travel to the brain to cause stroke. Treatment of atrial fibrillation has two goals: improvement of ventricular pumping and prevention of stroke. Pumping can be improved by either (1) restoring normal sinus rhythm or (2) slowing ventricular rate. For those undergoing treatment to restore normal sinus rhythm, warfarin should be taken for 3 weeks before the procedure and for 4 weeks after. For those taking an antidysrhythmic drug long term to control ventricular rate, warfarin must be taken long term too. Alternatives to warfarin include three new oral anticoagulants—apixiban [Eliquis], dabigatran [Pradaxa], and rivaroxaban [Xarelto]—and antiplatelet drugs (either aspirin alone or aspirin plus clopidogrel). Atrial Flutter Atrial flutter is caused by an ectopic atrial focus discharging at a rate of 250 to 350 times a minute. Like atrial fibrillation, atrial flutter poses a risk for stroke, which can be reduced by treatment with anticoagulants. With these drugs, ventricular rate will be slowed even if the dysrhythmia persists. When the dysrhythmia has been controlled, beta blockers and/or calcium channel blockers can be taken orally to prevent recurrence. Ventricular Dysrhythmias In contrast to atrial dysrhythmias, which are generally benign, ventricular dysrhythmias can cause significant disruption of cardiac pumping. Because the ventricles cannot pump effectively at these rates, immediate intervention is required. Ventricular Fibrillation Ventricular fibrillation is a life-threatening emergency that requires immediate treatment. This dysrhythmia results from the asynchronous discharge of multiple ventricular ectopic foci. Because many different foci are firing, and because each focus initiates contraction in its immediate vicinity, localized twitching takes place all over the ventricles, making coordinated ventricular contraction impossible. Electrical countershock (defibrillation) is applied to eliminate fibrillation and restore cardiac function. Digoxin-Induced Ventricular Dysrhythmias Digoxin toxicity can mimic practically all types of dysrhythmias. With proper treatment, digoxin-induced dysrhythmias can almost always be controlled. If antidysrhythmic drugs are required, lidocaine and phenytoin are the agents of choice. Torsades de Pointes Torsades de pointes is an atypical, rapid, undulating ventricular tachydysrhythmia that can evolve into potentially fatal ventricular fibrillation. Principles of Antidysrhythmic Drug Therapy Balancing Risks and Benefits Therapy with antidysrhythmic drugs is based on a simple but important concept: treat only if there is a clear benefit—and then only if the benefit outweighs the risks. As a rule, this means that intervention is needed only when the dysrhythmia interferes with ventricular pumping. Treatment offers two potential benefits: reduction of symptoms and reduction of mortality. Symptoms that can be reduced include palpitations, angina, dyspnea, and faintness. For most antidysrhythmic drugs, there is little or no evidence of reduced mortality. Because of their prodysrhythmic actions, antidysrhythmic drugs can exacerbate existing dysrhythmias and generate new ones. Because of their prodysrhythmic actions, antidysrhythmic drugs can increase mortality. Properties of the Dysrhythmia to Be Considered Sustained Versus Nonsustained Dysrhythmias As a rule, nonsustained dysrhythmias require intervention only when they are symptomatic; in the absence of symptoms, treatment is usually unnecessary. In contrast, sustained dysrhythmias can be dangerous, so the benefits of treatment generally outweigh the risks. Asymptomatic Versus Symptomatic Dysrhythmias No study has demonstrated a benefit to treating dysrhythmias that are asymptomatic or minimally symptomatic. In contrast, therapy may be beneficial for dysrhythmias that produce symptoms (palpitations, angina, dyspnea, faintness). Supraventricular Versus Ventricular Dysrhythmias Supraventricular dysrhythmias are generally benign. The primary harm comes from driving the ventricles too rapidly to allow adequate filling. The goal of treatment is to either (1) terminate the dysrhythmia or (2) prevent excessive atrial beats from reaching the ventricles (using a beta blocker, calcium channel blocker, or digoxin). In contrast to supraventricular dysrhythmias, ventricular dysrhythmias frequently interfere with pumping. Accordingly, the goal of treatment is to terminate the dysrhythmia and prevent its recurrence.
The parents also report that she has appeared weak and listless over the last several months purchase januvia 100 mg line, and has not been eating well buy januvia 100mg with amex. Review of systems reveals a normal order januvia 100mg fast delivery, varied diet and a history of multiple epi- sodes of diarrhea per day for the past 2 years. Clinical examination shows a Tanner stage 2 male at fifth percentile for height with multiple perianal skin tags. Infants drinking goat’s milk must have nutritional supplementation with vitamin B12, folate, and iron. The results reported are not typical for iron deficiency, and neither an iron panel nor iron supplementation is warranted. At this point, your workup should include checking folate and B12 levels; supple- mentation of these compounds is not yet justified. Myelodysplasia or leukemia is in the differential, but is probably less likely with a normal white blood cell count and differential (no atypical cells); referral to pediatric hematology may ultimately be required, but some preliminary data can be gathered first. A smooth, red, and tender tongue may be observed in juvenile pernicious anemia, a rare autosomal recessive condition in which the child is not able to secrete intrinsic factor and cannot absorb vitamin B12. Supplies of vitamin B12 passed to the fetus from the mother typically are sufficient for at least the first 1 to 2 years of life. A deficiency in transcobalamin results in megaloblastic ane- mia in infancy because transcobalamin is required for B12 transport and utiliza- tion; therefore, vitamin B12 provided by the mother cannot be used effectively. Petechiae may occur with vitamin C or K deficiency, muscle fasciculation with vitamin D and calcium disturbance, and hair loss with zinc deficiency. Although iron deficiency is the most common cause of microcytic anemia in patients with Crohn disease, macrocytic anemia is also possible with this disorder. Chronic inflammation involving the terminal ileum can result in fibrosis, limiting absorption of vitamin B12. In addition, stricture formation, necessitating surgical resection of the terminal ileum, is also a risk factor for the development of anemia. The family reports that they had moved to Baltimore from the Midwest 3 months ago. The child was the product of a normal pregnancy and delivery, and he had experienced no medical problems until the move. The parents report that he has developed emotional lability, abdominal pain, “achy bones,” and intermit- tent vomiting and constipation. They initially attributed his behavior to the move and to the chaos in their house, which is being extensively renovated. He may have been exposed to lead-containing dust in the renovation environment, or he may have displayed pica (the eating of nonfood substances such as paint chips, dirt, or clay). During the evaluation and treatment, other children in the home must be screened for elevated lead levels given their shared exposure risk. In the northeastern United States, older homes undergoing renovation are a common source of exposure. A complete investi- gation includes a travel history and an accounting of lead exposures through hob- bies (such as stained glass), home renovation, welding, radiator repair, furniture refinishing, pottery glazing, and similar activities. Previous sources (gasoline, foods, beverage cans) have been eliminated; lead-containing paint in older homes is now the major source. Less com- mon sources include foodstuffs from countries where regulations are not strict, traditional ethnic remedies, glazed pottery, ingestion of leaded items (jewelry, fishing equipment), exposure through burning of lead-containing batteries, or through hob- bies involving lead smelting. The signs and symptoms of lead exposure vary from none (especially at lower lead levels) to those listed in this case. Anorexia, hyperirritability, altered sleep pattern, and decreased play are commonly seen. Abdominal com- plaints (occasional vomiting, intermittent pain, and constipation) are sometimes noted. Persistent vomiting, ataxia, altered consciousness, coma, and seizures are signs of encephalopathy. Permanent, long-term consequences include learning and cognitive deficits and aggressive behavior; with less lead in the environment and decreasing average lead levels, these more subtle findings are now more common than acute lead encephalopathy. Other findings (free erythrocyte protoporphyrin, basophilic stippling, glycosuria, hypophosphatemia, long bone “lead lines,” and gastrointestinal tract radiopaque flecks) in symptomatic patients are less specific. Admission to the hospital, stabilization, and chelation are appropriate for symptomatic patients. Therapy for asymptomatic patients could involve simple investigation of the child’s environment, outpatient chelation, or immediate hospitalization (Table 25–1). Newer research has cast doubt on the utility of chelation therapy in asymptom- atic children with lead levels less than 45 μg/dL. Lead levels do decrease acutely with chelation therapy, but affected children do not show improvement in long-term cognitive testing. The most recent literature suggests that no “safe” lead level exists; even lead levels less than 10 μg/dL have been shown to have a deleterious impact on neuro- cognitive development. This evidence places further importance upon the primary prevention of lead exposure in children. As part of the visit, you obtain a blood lead level and a hemoglobin level in accordance with your state’s Medicaid screening guide- lines. The following week, the state laboratory calls your clinic to report that the child’s blood lead level is 14 μg/dL. Appropriate management of this level should include which of the following actions? All lead sources in the home have since been removed (verified by dust wipe samples), and the parents do not work in occupations prone to lead exposure. After a course of outpatient chelation therapy, the 3-year-old’s lead level dropped to 5 μg/dL. Your examination reveals a microcephalic infant with low birth weight who does not respond to sound. In your discussions with the family, you discover this is the parents’ first child.