Coreg

Thunderbird School of Global Management. D. Campa, MD: "Purchase online Coreg - Effective online Coreg no RX".

However buy cheap coreg 12.5 mg on-line blood pressure levels up and down, large daily oral doses can be just as effective buy coreg 6.25 mg lowest price blood pressure what is too low, as can weekly intranasal doses coreg 6.25mg pulse pressure nursing. During prolonged therapy purchase 12.5 mg coreg free shipping blood pressure normal unit, treatment should be periodically assessed: plasma levels of vitamin B12 should be measured every 3 to 6 months, blood samples should be examined for the return of macrocytes, and blood counts should be performed. Potential Hazard of Folic Acid Treatment with folic acid can exacerbate the neurologic consequences of B12 deficiency. Recall that folic acid, by itself, can reverse the hematologic effects of B12 deficiency—but will not alleviate neurologic deficits. So, by correcting the most obvious manifestation of B12 deficiency (anemia), folic acid can mask the fact that deficiency of B12 still exists. As a result, use of folic acid can lead to undertreatment with B itself12 and can thereby permit neurologic damage to progress. Clearly, folic acid is not a substitute for vitamin B12, and vitamin B12 deficiency should never be treated with folic acid alone. Whenever folic acid is employed during treatment of vitamin B12 deficiency, extra care must be taken to ensure that B12 dosage is adequate. Folic Acid Deficiency In one respect, folic acid deficiency is identical to vitamin B12 deficiency: in both states, megaloblastic anemia is the most conspicuous pathology. However, in other important ways, folic acid deficiency and vitamin B12 deficiency are dissimilar (Table 45. Consequently, when a patient presents with megaloblastic anemia, it is essential to determine whether the cause is deficiency of folic acid, vitamin B12, or both. Under normal conditions, activation occurs through a pathway that employs vitamin B12 (see Fig. However, when large amounts of folate are ingested, some can be activated through an alternate pathway—one that does not employ vitamin B12. Fate in the Body Folic acid is absorbed in the early segment of the small intestine and then transported to the liver and other tissues, where it is either used or stored. That is, folate from the liver is excreted into the intestine, after which it is reabsorbed and then returned to the liver through the hepatic-portal circulation. In contrast to vitamin B12, folic acid is not conserved rigidly: every day, significant amounts are excreted. As a result, if intake of folic acid were to cease, signs of deficiency would develop rapidly (within weeks if body stores were already low). Good sources include peas, lentils, oranges, whole-wheat products, asparagus, beets, broccoli, and spinach. Folic Acid Deficiency: Causes, Consequences, and Diagnosis Causes Folic acid deficiency has two principal causes: (1) poor diet (especially in patients who abuse alcohol), and (2) malabsorption secondary to intestinal disease. Alcoholism Alcoholism, either acute or chronic, may be the most common cause of folate deficiency. Deficiency results for two reasons: (1) insufficient folic acid in the diet and (2) derangement of enterohepatic recirculation secondary to alcohol- induced injury to the liver. Fortunately, with improved diet and reduced alcohol consumption, alcohol-related folate deficiency will often reverse. Sprue Sprue is an intestinal malabsorption syndrome that decreases folic acid uptake. Because sprue does not block folate absorption entirely, deficiency can be corrected by giving large doses of folic acid orally. Consequences With the important exception that folic acid deficiency does not injure the nervous system, the effects of folate deficiency are identical to those of vitamin B12 deficiency. As with B12 deficiency, the most prominent consequence of folate deficiency is megaloblastic anemia. Because we already noted that many of the consequences of vitamin B12 deficiency result from depriving cells of active folic acid, the similarities between folate deficiency and vitamin B12 deficiency should be no surprise. The Developing Fetus Folic acid deficiency very early in pregnancy can cause neural tube defects (e. Accordingly, it is imperative that all women of reproductive age ensure adequate folate levels before pregnancy occurs. Preventive Services Task Force now recommends that all women who may become pregnant consume 400 to 800 mcg of supplemental folic acid each day—in addition to the folate they get from food. Other Consequences As discussed in Chapter 65, folic acid deficiency may increase the risk for colorectal cancer and atherosclerosis. One form is inactive as administered (but undergoes activation after being absorbed). Both forms have several generic names: the inactive form is referred to as folacin, folate, pteroylglutamic acid, or folic acid; the active form is referred to as leucovorin calcium, folinic acid, or citrovorum factor. Indications Folic acid has three uses: (1) treatment of megaloblastic anemia resulting from folic acid deficiency; (2) prophylaxis of folate deficiency, especially during pregnancy and lactation; and (3) initial treatment of severe megaloblastic anemia resulting from vitamin B12 deficiency. However, as noted in Chapter 65, even moderately large doses (1000 mcg/day), when taken long term, may increase the risk for some cancers, including colorectal cancer and cancer of the prostate. Dosage For treatment of folate-deficient megaloblastic anemia in adults, the usual oral dosage is 1000 to 2000 mcg/day. For prophylaxis during pregnancy and lactation, doses up to 1000 mcg/day may be used. Leucovorin Calcium (Folinic Acid) Leucovorin calcium is an active form of folic acid used primarily as an adjunct to cancer chemotherapy. Leucovorin is not used routinely to correct folic acid deficiency because folic acid is just as effective and cheaper. Guidelines for Treating Folic Acid Deficiency Choice of Treatment Modality The modality for treating folic acid deficiency should be matched with the cause. If the deficiency is due to poor diet, it should be corrected by dietary measures— not with supplements (except for women who may become pregnant). Ingestion of one serving of a fresh vegetable or one glass of fruit juice a day will often suffice. In contrast, when folate deficiency is the result of malabsorption, diet alone cannot correct the deficiency, so supplemental folate will be needed. Even in the presence of intestinal disease, oral folic acid can be effective, provided the dosage is high enough. Prophylactic Use of Folic Acid Folic acid should be taken prophylactically only when clearly appropriate. The principal candidates for prophylactic folate are women who might become pregnant and women who are pregnant or lactating. Because folic acid may mask vitamin B12 deficiency, indiscriminate use of folate should be avoided. Treatment of Severe Deficiency Folic acid deficiency can produce severe megaloblastic anemia. Folic acid should be given orally in a dosage of 1000 to 2000 mcg/day for 1 to 2 weeks.

Production of active drug is especially erratic in newborns order coreg 6.25mg fast delivery 2014 2014, infants coreg 12.5 mg with amex arrhythmia pronunciation, and young children order 25 mg coreg overnight delivery blood pressure questionnaire. Chloramphenicol is highly lipid soluble and widely distributed to body tissues and fluids buy coreg 12.5 mg with amex arrhythmia definition medical. As a result, chloramphenicol is of special value for treating meningitis and brain abscesses caused by susceptible bacteria. In patients with liver impairment, the half- life is prolonged and accumulation can occur. Because the kidneys serve only to excrete inactive metabolites, there is no need for dosage reduction in patients with renal impairment. In neonates, hepatic metabolism is not fully developed, and hence the half-life of chloramphenicol is prolonged. Because chloramphenicol has a low therapeutic index, and because serum levels of the drug can vary substantially among patients, monitoring drug levels is frequently indicated. Monitoring is especially important for neonates, infants, and young children because chloramphenicol levels in these patients can be especially variable. For most infections, effective therapy is achieved with peak serum drug levels of 10 to 20 mcg/mL and trough levels of 5 to 10 mcg/mL. The risk for dose-dependent bone marrow suppression is significantly increased when peak levels rise above 25 mcg/mL. However, use dropped sharply when its ability to cause fatal aplastic anemia became evident. Today, chloramphenicol is indicated only for life-threatening infections for which safer drugs are ineffective or contraindicated. Adverse Effects The most important adverse effects are gray syndrome and toxicities related to the blood. Gray Syndrome Gray syndrome, originally known as gray baby syndrome, is a potentially fatal toxicity observed most commonly in newborns. Initial symptoms are vomiting, abdominal distention, cyanosis, and gray discoloration of the skin. Newborns are especially vulnerable to gray syndrome because (1) hepatic function is insufficient to detoxify chloramphenicol and (2) renal function is insufficient to excrete active drug. Although gray syndrome is usually observed in neonates, it can occur in older children and adults if dosage is excessive. If drug use is discontinued immediately when early symptoms appear, the syndrome is usually reversible. The risk for gray syndrome in infants can be reduced by using low doses and by monitoring chloramphenicol levels in serum. Reversible Bone Marrow Suppression Chloramphenicol can produce dose-related suppression of the bone marrow, resulting in anemia, and sometimes leukopenia and thrombocytopenia. The cause of bone marrow suppression appears to be inhibition of protein synthesis in host mitochondria. To promote early detection of bone marrow suppression, complete blood counts should be performed before therapy and every 2 days thereafter. Chloramphenicol should be withdrawn if evidence of bone marrow suppression is detected. Suppression of bone marrow usually reverses within 1 to 3 weeks after drug withdrawal. The anemia associated with toxic bone marrow suppression is not related to aplastic anemia (discussed next). B l a c k B o x Wa r n i n g : C h l o r a m p h e n i c o l Rarely, chloramphenicol produces aplastic anemia, a condition characterized by pancytopenia and bone marrow aplasia. Aplastic Anemia Aplastic anemia develops in 1 of 35,000 patients and is not related to dosage. The mechanism underlying aplastic anemia has not been determined, but toxicity may result from a genetic predisposition. Other Adverse Effects Gastrointestinal effects (vomiting, diarrhea, glossitis) occur occasionally. Neurologic effects (peripheral neuropathy, optic neuritis, confusion, delirium) develop rarely, usually in association with prolonged treatment. Other rare toxicities include superinfection of the bowel, allergic reactions, and fever. Drug Interactions Chloramphenicol can inhibit hepatic drug-metabolizing enzymes, thereby prolonging the half-lives of other drugs. Agents that may be affected include phenytoin (an anticonvulsant), warfarin (an anticoagulant), and two oral hypoglycemics: tolbutamide and chlorpropamide. If any of these drugs are taken concurrently with chloramphenicol, their dosages should be reduced. Preparations, Dosage, and Administration Chloramphenicol sodium succinate is available as a powder for reconstitution to a 100-mg/mL solution. As a rule, the dosing objective is to produce peak chloramphenicol plasma levels that range between 10 and 20 mcg/mL. For infants more than 7 days old, the recommended dosage is 25 mg/kg every 12 hours. Tigecycline is active against a broad spectrum of bacteria, including many drug-resistant strains. Unfortunately, tigecycline is associated with an increased mortality (see later), and hence using another antibiotic drug should be considered. Mechanism of Action and Resistance Tigecycline is a bacteriostatic inhibitor of protein synthesis. Antimicrobial Spectrum Tigecycline is a broad-spectrum antibiotic with activity against gram-positive and gram-negative bacteria, including many strains that are drug resistant. Susceptible gram-negative organisms include Acinetobacter baumannii, Stenotrophomonas maltophilia, B. Of note, tigecycline is not active against Pseudomonas aeruginosa or Proteus species. To delay emergence of resistance, tigecycline should be used only when other drugs are considered likely to fail. Pharmacokinetics Tigecycline is administered intravenously and undergoes moderate binding to plasma proteins (about 80%). Adverse Effects Tigecycline is a tetracycline analog and hence may have adverse effects like those of the tetracyclines. Like the tetracyclines, tigecycline may pose a risk for pseudotumor cerebri (a benign elevation of intracranial pressure) and may increase sensitivity to ultraviolet light, thereby increasing the risk for sunburn. Acute pancreatitis, including fatal cases, has occurred during tigecycline treatment. B l a c k B o x Wa r n i n g : Ti g e c y c l i n e Among patients treated for severe infections, mortality is higher for those receiving tigecycline than for those receiving other antibiotics. Tigecycline does not affect the cytochrome P450 system and hence will not alter the kinetics of drugs metabolized by P450.

Infammatory thyroid disease (subacute Glands thyroiditis) can cause a transient form of hyperthyroidism Figure 32-1 purchase coreg 25 mg otc hypertension vision. The goals iodide uptake and the synthesis of thyroid hormones triiodothyronine (T3) of therapy are to eliminate excessive thyroid hormone pro- and tetraiodothyronine (T4 buy generic coreg 6.25mg on line prehypertension natural remedies, thyroxine) buy discount coreg 25 mg online pulse pressure femoral artery. The choice of treatment depends on the type and severity of hyperthyroidism and on the individual characteristics of the patient generic coreg 25mg with visa hypertension with stage v renal disease. Antithyroid agents are primarily used for the short-term treatment of hyperthyroidism, either to induce Hypothyroid patients may note lethargy, cold intolerance, remission of Graves disease or to control the symptoms of weight gain, and constipation. Myxedema coma is characterized often results in chronic hypothyroidism, which necessitates by hypothermia, hypoglycemia, weakness, stupor, and lifelong thyroid hormone replacement therapy. As the disease progresses, however, choice for thyroid hormone replacement in persons with the T4 level usually falls below normal. Thyroid hormones obtained The most common cause of hypothyroidism in adults from animal glands were used to treat thyroid disorders is autoimmune thyroiditis (Hashimoto disease). Pituitary ity and their potential to cause allergic reactions to animal or hypothalamic dysfunction can cause secondary proteins contained in these preparations. The synthetic thyroid hormone preparations include Several types of drugs can induce thyroid disorders. However, an analysis antiarrhythmic drug that can cause either hypothyroidism of controlled trials concluded that combined T4 and T3 was or hyperthyroidism through a variety of mechanisms that not superior to T4 alone with respect to fatigue, depression, alter multiple thyroid functions. Thyroperoxidase catalyzes the iodination of tyrosine residues of thyroglobulin and the coupling of iodotyrosines to form triiodothyronine (T3) and tet- raiodothyronine (T4, thyroxine). Thioamide drugs inhibit the synthesis of thyroid hormones by inhibiting iodination and coupling of tyrosine residues. Elevated iodide concentrations and lithium inhibit the release of thyroid hormones. Her symptoms and laboratory values are indicative has also had more trouble than usual with constipation and of mild hypothyroidism. On physical examina- centration is the primary test used to evaluate replacement tion, her temperature is 97. Suppressive therapy thereby reduces Pharmacokinetic Properties goiter size and thyroid gland volume. Relative potency 1 4 Oral bioavailability 80% (variable) 95% Adverse Effects Elimination half-life 7 days 1 day Thyroid hormone preparations rarely cause adverse reac- Daily doses 1 1-3 tions if dosage is appropriate and is carefully monitored during the initial treatment of hypothyroidism and perio- dically thereafter. Excessive doses produce symptoms of pharmacologic and pharmacokinetic properties of levothy- hyperthyroidism. Interactions Levothyroxine Aluminum hydroxide, calcium supplements, cholestyramine, Pharmacokinetics ferrous sulfate, and sucralfate are among the drugs that The oral bioavailability of levothyroxine is about 80%. These ferent brands and generic formulations of levothyroxine vary drugs should be administered 2 hours before or after levo- in hormone content and bioavailability, and formulations thyroxine is administered. For this roxine be taken at the same mealtime each day in order to reason, the dosage of levothyroxine usually does not need to achieve consistent blood levels. Because the half-life of levo- be adjusted in persons who are taking steroid hormones. Liothyronine Because about 35% of T4 is converted to T3 in peripheral As shown in Table 32-1, liothyronine (T3) is more potent tissues, levothyroxine administration produces physiologic than levothyroxine (T4) and has a higher oral bioavailabil- levels of both T4 and T3. It is seldom used in the treatment of hypothyroidism, however, because it has several disadvantages. Liothyronine Indications has a much shorter half-life than levothyroxine, and mul- Levothyroxine is the drug of choice for thyroid hormone tiple daily doses may be needed to obtain a smooth response replacement in patients with hypothyroidism, because it is during hormone replacement therapy. Liothyronine does chemically stable, is nonallergenic, and can be given orally not increase plasma T4 levels, so it is diffcult to monitor once a day. Liothyronine also causes pool of T4 that is converted to T3 at a steady and consistent more adverse cardiac effects and is more expensive than rate. The dose is then increased ism include thioamide drugs, β-adrenoceptor antagonists, at monthly intervals until a full replacement dose is achieved. A gradual increase in the dose prevents excessive stress on The thioamide drugs inhibit the synthesis of thyroid hor- the cardiovascular and other organ systems and thereby mones, whereas suffcient doses of iodide salts inhibit the causes fewer adverse reactions. The β-blockers are used to control higher doses per kilogram of body weight than do adults. Levothyroxine is also the drug of choice for suppressive Drug Properties therapy in patients with thyroid nodules, diffuse goiters, or Mechanisms. The thioamide drugs are well azole is not bound to plasma proteins, and it readily crosses absorbed from the gut after oral administration. The thioamide drugs are appears to be the drug of choice just before and during the extensively metabolized before undergoing renal excretion. The effects of thioamide drugs are delayed Thyroid hormones and the sympathetic nervous system act because it takes about 4 to 8 weeks of therapy before the synergistically on cardiovascular function. This explains why glandular hormone stores are depleted and circulating increased levels of thyroid hormones cause tachycardia, hormone levels start to return to the normal range. They act immediately the objective is long-term remission of Graves disease, and are particularly useful during severe acute thyrotoxicosis patients usually remain on the drug for 12 to 24 months. They are also used to control symptoms of About 45% of patients will eventually achieve a permanent hyperthyroidism in patients awaiting either surgery or a remission. Persons with persistent thyroid-stimulating antibodies Iodide Salts have a higher incidence of relapse than do persons without Iodide salts are contained in potassium iodide tablets and persistent antibodies. Pruritic maculopapular rash, arthralgia, and Lugol solution (elemental iodine and potassium iodide). Less frequently, a lupus erythematosus–like patients with acute thyrotoxicosis, to prepare patients for syndrome, hepatitis, or gastrointestinal distress is reported. Iodide salts can also be used to with a white blood cell count of less than 4000/µL. Potassium iodide preparations acterized by a granulocyte count of less than 250/µL. Severe are available without prescription for this purpose (Thyro- agranulocytosis usually develops during the frst 3 months Safe, ThyroShield). Patients and fatal liver failure, but a recent analysis of adverse drug with hyperthyroidism usually obtain symptomatic improve- reactions by the U. The isotope is rapidly • β-Adrenoceptor antagonists are used to control the absorbed from the gut and concentrated by the thyroid cardiovascular symptoms of hyperthyroidism in pati- gland. In the gland, it emits β-particles that destroy thyroid ents who are suffering from acute thyrotoxicosis, are tissue. Potassium iodide solutions are used β-blockers alone are not adequate to control these symp- to control symptoms of acute thyrotoxicosis, to reduce toms. A man is given a drug to reduce thyroid gland size and vascularity before surgical thyroidectomy. A woman with weight loss, nervousness, heat intolerance, pling of iodotyrosines to form T3 and T4. Which serious adverse effect has • The thyroid hormones, which activate cytoplasmic been associated with this medication? In the (A) gastrointestinal bleeding nucleus, they activate gene transcription and thereby (B) thromboembolism increase the metabolic rate and accelerate a wide (C) agranulocytosis range of cellular activities required for normal growth (D) hepatic failure and development and for the maintenance of normal (E) esophageal ulcer metabolism.

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 cheap 12.5mg coreg blood pressure quiz pdf, leading to obstruc- adequate projection cheap coreg 6.25 mg with amex high blood pressure medication and zyrtec. 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 order 6.25 mg coreg with amex blood pressure numbers chart. If necessary buy coreg 6.25mg with mastercard hypertension vs hypotension, 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 [5] 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. With proper execution of technique and appropriate selection of patients, lower lateral 35. Goldman originally described his technique in a 1957 land- Typically, in patients with excessively long lateral crura relative mark article. An overly long lateral crus refine and maintain natural nasal tip appearance without the may exist coincidentally or independently from the tension requirement of grafts or implants. Unfortunately, dividing the nose or overly long nasal septum and must be distinguished cartilage without reapproximation often led to tip asymmetries from a ptotic nasal tip. Since this first description, of the relationship between the lower lateral cartilages and newer insight into nasal tip dynamics has broadened the appli- septum. The ptotic nose will not have a downward snarl in cation and use of division of lower lateral cartilages as an appearance and the nasal tip support is often weak. On the Anderson originally described the nasal tripod theory to pro- other hand, in the patient with excess long lateral cruses, the vide a simple explanation of tip dynamics. Surgeons who neglect to address the long legs of the tripod, and the conjoined medial crura and caudal lateral cartilage with appropriate modification will invariably septal attachments correspond to the third leg. Kridel and Konior first described the tech- instance, techniques that augment or lengthen the medial cru- nique of lateral crural overlay.