Malegra FXT Plus

By M. Will. Saint Louis Christian College.

In the lateral view order 160mg malegra fxt plus mastercard, the nasal the narrowest segment of the nasal airway discount malegra fxt plus 160mg free shipping, with a cross-sec- dorsum starts at the deepest point of the frontonasal angle tional area of ~55 to 83mm2 buy line malegra fxt plus,3 and an acute angle of ~1 generic malegra fxt plus 160mg overnight delivery. Dorsal hump removal is an important com- dorsum and the nasal tip and contributes to the appearance of ponent of reduction rhinoplasty. The Nasal projection is defined as the distance that the nose proj- procedure of removing the osseous nasal vault consists of excis- ects from the face in a horizontal direction. The third line connects the Reduction of the bony dorsum often accompanies reduction two previous lines and traverses through the nasal tip in a hori- of the cartilaginous dorsum. An adequate subperiosteal pocket is first created over tion is to measure the distance from the alar crease to the nasal the midline nasal bones with a Joseph elevator prior to per- tip. The bony rasp is often used for Theoretically, 50 to 60% of the distance from the alar crease to smaller bony humps or for fine dorsal contouring. Dorsal removal it is important to ensure that no palpable small bony particles techniques are performed when the dorsal structures and/or or irregularities are retained, especially in the thin-skinned their relationships with the face are not ideal. Larger bony humps can be removed with a straight 105 Management of the Dorsum Fig. The osteotome is engaged at the infe- rior aspect of the midline nasal bone and the osteotomy carried superiorly toward the nasion with careful attention to the Fig. This method uses a ratio of the nasal tip projection to the performed immediately after reduction of the cartilaginous length of the face. After bony reduction, it is not unusual to find an open-roof Additionally, nasal dissection should maintain the integrity of deformity at the nasal bones. If not corrected, an open roof can the mucoperichondrium to avoid further damage to the nasal lead to a depressed, wide, and flattened nasal dorsum. These grafts Alternatively, Skoog described an en bloc dorsal reduction 9 6 can be used as supportive maneuvers in primary rhinoplasty technique. The excised dorsal fragment is sculpted and reposi- when aggressive resection of a nasal hump is needed and/or tioned in the dorsum as a free graft. A large propor- tion of post-rhinoplasty nasal obstruction is a consequence of Various functional and aesthetic complications can be attrib- nasal hump removal. Functional problems can be encoun- tors must be considered in the preoperative analysis of each tered with each of these deformities. Postsurgical dynamic and static airway obstruction can be attributed to these changes. However, in the hourglass deformity, there is a nor- mal nasal bone width and a smoother dorsal transition. Although various conditions can cause a saddle nose, prior surgery accounts for the majority of the cases. Daniel also outlines the use of the follow- ing techniques: onlay grafts, spreader grafts and columellar struts, autologous rib grafts, and composite reconstructions. In secondary rhinoplasty, they can be used to correct complications of exces- sive dorsal hump removal. The surgical techniques include autologous cartilaginous grafts and reconstructive sutures. The main goal of these surgical maneuvers is to rebuild the middle nasal vault infrastructure, improving aesthetic and functional problems. Spreader grafts can gery or many years later from skin and soft tissue contraction. The aesthetic spreader grafts are used when nasal dorsal asymmetries are consequences include an inappropriate relationship between present. The wider end of the graft is orientated cephalically to the nasal tip and dorsal projection. A classification system create a thicker width in this region and reproduce an adequate of saddle nose deformities and the various reconstructive nasal contour. The grafts will then be nasal vault is the placement of onlay cartilaginous grafts. Butterfly grafts, as described by Clark and Cook,15 are another type of onlay graft. These grafts are typi- cally placed on the nasal dorsum, on top of the existing middle external. Ideally,conchalcartilageisused,astheintrinsic for the grafts to be precisely sutured into position. Tempo- rally, the graft is attached to the dorsal septum with a 27-gauge needle. After the graft(s) are positioned, they are sutured to the nasal septum in a horizontal mattress fashion with a 5–0 long-acting monofilament absorbable suture. The spreader graft technique provides both aesthetic and functional improvement of the middle nasal vault. An anterior approach is used to raise a skin flap, obtaining a concave cartilage graft. The caudal portion of the graft is placed be harvested with cartilage only or the graft can contain bone. The general goal of these reconstructive techniques mize the natural tendency for rib cartilage to warp. Because of their high flexibil- ity and good long-term results, Daniel prefers grafts consisting 14. In comparison, cadaveric rib cartilage is 110 Management of the Nasal Dorsum can manifest shortly after surgery or may present many years 14. Frequently, rhinoplasty maneuvers designed to improve aes- To prevent postsurgical problems of the middle nasal vault, thetics can diminish nasal infrastructure and have untoward functional nasal anatomy must be understood and respected. This is especially true after reduction This enables the surgeon to diagnose preexisting conditions that rhinoplasty when components of the nasal infrastructure are may contribute to postoperative middle vault complications removed or weakened. Many prophylactic surgical techni- Surgical weakening of the nasal infrastructure produces vari- ques are used to prevent nasal vault complications after rhino- ous functional complications. Furthermore, weak- spreader grafts or onlay butterfly grafts) and suture techniques ening the nasal infrastructure can lead to aesthetic problems. These techniques allow reduction of the Aesthetic complications related to cartilaginous dorsal hump dorsal nasal projection while maintaining nasal width and struc- include inverted-V deformity, hourglass deformity, and saddle tural support. These aesthetic and functional complications and maintains or improves preoperative nasal function. This patient has a weak middle nasal third and is predisposed for internal nasal collapse. Facial Plast Surg Clin cedures may result in cosmetic and functional complications. Spreader graft: a method of reconstructing the roof of the middle Surg 2008; 24: 327–338 nasal vault following rhinoplasty. Bending of the upper lateral cartilages for 2009; 17: 91–113 nasal valve collapse. Plast Reconstr Surg 2008; 122: 1883–1891 113 Management of the Dorsum 15 anagem ent of Naso-septal L-strut Deform ities David W. Kim and Theresa Gurney reconstructing the nose as rhinectomy was a common form of 15. It wasn’t until the 19th century that surgical tech- Early in the training of every nasal surgeon, we are admonished niques to correct the septum were introduced and documented to have great respect for the nasal septum. Adams in 1875 recommended fractur- that “where the septum goes, so goes the nose” and the septum ing the septum, with subsequent splinting. The During this time, directed removal of deviated cartilage was value of this minimal width varies from surgeon to surgeon, no introduced. Ingals began with attempts to excise a small por- doubt born out of surgical training and perhaps modified by tion of anterior cartilage. A common value for this dimension is sive excisional approach as others utilized saws and chisels to 1. There is little involved excisions that sometimes extended to the vomer and in the literature revealing from where this value originates; perpendicular plate of the ethmoid and usually included the nonetheless, it remains a concept that likely every surgeon has overlying mucosa on one or both sides. One certainly can imagine the resultant cosmetic deformities This ingrained reverence for the L-strut, while helpful in pre- and functional complications of these often extensive, exci- venting saddle noses and ptotic tips, may contribute to a differ- sional approaches. The senior author recalls began to propose more conservative techniques in addressing performing a submucous resection of septal quadrangular carti- the septum while preserving its structure.

It is invariably associated with falciparum malaria order line malegra fxt plus, in those who had taken antimalarial drugs irregularly or in non-immune person purchase discount malegra fxt plus line, who had taken irregular antimalarial prophylaxis buy malegra fxt plus without a prescription. Clinical features: High fever with chill and rigor safe 160 mg malegra fxt plus, vomiting, diarrhoea, dark to black urine (haemoglobinuria), collapse and renal failure. Sometimes, fever may be irregu- lar, low grade continuous, occasionally undulant fever (pyrexia followed by apyrexial period). Remember the following points: • Human is the only reservoir in Indian subcontinent. Causes of death in Kala-azar: If no treatment is given, patient may die within 1 to 2 year due to: • Secondary infection. Detection of antigen: Done by latex agglutination test (Katex) for detecting leishmanial antigen in urine. This test is very simple, more specifc than antibody-based test, highly sensitive (96%) and also specifc (100%). Antigen is detected in urine within a week and disappears from urine within 3 weeks after successful treatment. So, this test is helpful for early diagnosis and also to see the response to therapy. Blood for total protein and A:G ratio (high total protein, low albumin and high globulin). Culture is done for identifcation of species and if the number of organisms is less, it may grow in culture media. A: As follows: 1st line therapy: Liposomal Amphotericin B, Miltefosine, Paromomycin or combination therapy. Also avoid in women of child bearing age not using contraceptives regularly, breast feeding women, children less than 2 yrs of age. If alternative 1st line agents are not available, then a 2nd line agent should be used. Drug of choice is Liposomal Amphotericin B (5 mg/kg body weight on alternate days for 3 doses). Treatment should be given as follows: If diagnosed at 1st trimester, then it should be treated at 2nd trimester. Presentation of a Case: • There are multiple, pale, pink, reddish, wart like nodules of variable size and shape involving nose, cheek and ear lobule. A: It is non-ulcerative, cutaneous lesion that occurs after successful treatment of visceral leishmania- sis. Initially starts as macules, then erythematous patches, followed by wart-like nodular lesions on the face, ear lobules and limbs. Following treatment, visceral infection disappears, but organisms may remain in skin. In India, it occurs in a small minority of patients, 6 months to 3 years or more after the initial infection, creating a persistent human reservoir. The patient usually presents with macules, papules, nodules (most common) and plaques on the face, mainly around the chin. Hypopigmented macules can occur over all parts of the body and are highly variable in extent and location. A: In early case, depigmented macules, erythematous, well-circumscribed lesions may be seen. Later, wart like nodules, or only multiple nodules of variable sizes and shapes are seen involving nose, cheek and ear lobule. A: As follows: First line treatment: Usually miltefosine should be given: • Adult: 50 mg twice daily for 12 weeks. A: Because: • The mass is in the right hypochondrium and in the epigastrium (left lobe). A: Yes, if it is pushed downward by any pathology in the right side of chest, such as emphysema, pleural effusion or pneumothorax. A: Investigations should be done according to the history and suspicion of cause: 1. A: 4 methods: • Percutaneous (by Vim–Silverman needle, Menghini needle or Tru-cut needle). If bilirubin is high, liver biopsy should not be done, as liver tissue does not take the stain. A: By percussion, upper border of liver dullness is in the sixth intercostal space or rib in right midcla- vicular line and the distance between this upper border and lower border is called liver span. It is character- ized by fever, pain in the right hypochondrium with radiation to right shoulder, tender hepatomegaly, hepatic rub and small right pleural effusion. Treatment: Tetracycline or doxycycline or erythromycin or azithromycin are used for Chlamydia infection. A: Because, the liver is hard, irregular, nodular, non-tender and there is hepatic bruit. Q:How to differentiate between primary carcinoma (hepatoma) and secondary carcinoma? Metabolic abnormalities are polycythaemia, hypercalcaemia, hypoglycaemia and porphyria cutanea tarda. A:Rarely, fbrolamellar hepatocellular carcinoma, common in young adults, affecting equally in male and female, in the absence of hepatitis B and cirrhosis. Other (rare) primary tumours are haemangioendothelial sarcoma, cholangiocarcinoma, hepatoblastoma, leiomyosarcoma, fbrosarcoma. Surgical resection, if pressure symptoms, also if pregnancy is desired (as size is increased in pregnancy). A: Because liver has dual blood supply causing relatively more blood fow (by portal vein and hepatic artery). A: It is a normal component of plasma protein, produced by the foetal liver older than 6 weeks and reaches maximum concentration at 12 to 16 weeks of foetal life. My diagnosis is tender hepatomegaly, which may be due to: • Acute viral hepatitis. Remember the following points: • Clinical features and pathological features are same by all viruses. But in cholestatic hepatitis or obstructive jaundice, alkaline phosphatase may be very high). A: As follows: • Acute fulminating hepatic failure (by B and sometimes E in pregnancy. It is seen in anxious patient who complains of malaise, anorexia, nausea, vomiting, right hypochondrial pain or discomfort in the absence of clinical or biochemical evidence of liver disease. In many cases, there is no active liver disease, normal or slightly raised transaminase and the patient is not highly infective, do not develop progressive liver disease although some patients develop reactive hepatitis. Decompensated cirrhosis can also be treated with oral antiviral agents, but liver transplantation may be required. Organism and animal hosts of different types of Leptospirosis: • Leptospira icterohaemorrhagiae of rat (rodent). The organism is excreted in the urine and may survive in the soil for several weeks. Entry into the human host is through cuts and abrasions on the skin, or through intact mucous membranes or contaminated water. Pathology: Replication occurs in the blood, tissue and multisystem involvement may occur. Initial or septicaemic phase—Persists for 4 to 7 days, characterized by high fever, headache, myalgia, abdominal pain, anorexia, nausea, vomiting, skin rash (macular, maculopapular or haemorrhagic), conjunctival ingestion (blood-shot eyes). Liver failure, myocarditis, cardiac failure, encepha- litis, aseptic meningitis, meningism, may occur. Haemolytic anaemia, thrombocytopenia, uveitis, haemolytic uremic syndrome may occur. Second or immune phase—There is development of antibody and leptospira disappears from blood. Features are usually mild, but meningism or aseptic meningitis and iridocyclitis may occur. Any case with high fever and combination of hepatitis, renal failure, bleeding manifestations and carditis is highly suggestive of Weil’s disease. Antibiotic should be started as early as possible in suspected case: • Doxycycline (100 mg 12 hourly for 1 week).

In selected circumstances buy malegra fxt plus from india, high-dose progestin therapy and repeat of the endometrial sampling in 2 to 3 months is possible for those who desire a pregnancy generic malegra fxt plus 160 mg on line. The chronic est rogen exposure wit hout progestin is the reason for development of endometrial cancer purchase 160 mg malegra fxt plus. She denies the use of steroid medica- t ion s purchase 160mg malegra fxt plus visa, we ig ht ch an g e s, or a fam ily h istory of h irsut ism. Exami- n at ion of the e xte rn al g e n it alia re ve als p ossib le clitorom e g aly. Pe lvic e xam in a- t ion sh ows a n orm al u te ru s an d ce rvix an d an 8-cm, rig ht ad n e xal m ass. She denies t he use of steroid medicat ions, weight changes, or a family history of hirsutism. Most likely diagnosis: An ovar ian t u mor, pr obable Ser t oli– Leyd ig cell t u mor. Know the typical history and physical examination and treatment for the vari- ous causes of hirsutism. Co n s i d e r a t i o n s This 42-year-old woman has the onset of excess male-pattern hair over the past 6 months, as well as features of virilism (clitoromegaly). T his woman has a large adnexal mass, and so t he diagnosis is st raight - for ward. Sh e h as irregular men ses becau se of the an drogen effect of in h ibit ing ovulation. The patient does not have the stigmata of Cushing disease, such as hypertension, buffalo hump, abdominal striae, and central obesity. A Sertoli– Leydig cell tumor of t he ovary is a solid st romal t ype of tumor, t he androgen cou nt er par t of gr anu losa-t h eca cell t umor (wh ich secret es est r ogen s). T h ese tumors are usually of low malignant potent ial and slow growing, but nevertheless may metastasize and often recur. It is most commonly associated with anovulation; however, other causes of increased androgen levels, such as adrenal and ovarian diseases, need to be ruled out. The most sensitive marker of excess androgen production is hirsutism, followed by acne, oily skin, increased libido, and virilizat ion. Virilization con sist s of clit or om eg- aly, deepening of the voice, balding, increased muscle mass, and male body habitus. Adrenal hyperplasia or androgen-secret ing t umors of the adrenal gland or ovary are causes of virilizat ion. Differences in hair gr owt h bet ween et h n ic gr oups are secon d ar y t o var iat ion s in h air follicle con - cent r at ion an d 5-alph a-r edu ct ase act ivit y. H air gr owt h can be divid ed int o t h r ee phases: anagen (growing phase), catagen (involution phase), and telogen (quies- cent phase). H airs found on the face, axilla, chest, breast, pubic area, and anterior thighs are termed “sex hair” because they respond to sex hormones. Androgens (especially testosterone) initi- ate t he growt h of pubic hair and increase the diameter and pigment at ion of pubic hair. Androgens may be produced by the ovary, adrenal gland, or by peripheral conver sion. The appearance and cosmetic changes associated with hirsutism depend on the number of follicles present, ratio of growth to resting phases, asynchrony of growth cycles, and t h ickness and degree of pigment at ion of individual h airs. The history should focus on the onset and duration of symptoms (faster growth is associated with tumors of the adrenal gland and ovary, whereas slow onset since menarche is more likely polycystic ovarian syndrome). The severit y of sympt oms sh ould also be char- act erized (eg, virilizat ion is rare and is usually associat ed wit h androgen-secret ing tumors). The physical examination should focus on the location of hair growth and it s severit y, t hyromegaly, body shape and habitus, the presence of breast dis- ch ar ge, skin ch an ges (acant h osis or abd om in al st r iae), adn exal or abd om in al m asses, and t he external genit alia. A markedly elevat ed t est ost erone level suggest s an androgen-secret ing ovarian t umor, such as a Sert oli– Leydig cell tumor. The differential diagnosis for hirsutism (Table 53–1) includes anovulation, late- onset adrenal hyperplasia, androgen-secreting tumors (adrenal or ovarian in ori- gin ), Cu sh in g d isease, med icat ion s, t h yr oid disease, an d h yp er pr olact in emia. Treatment options include weight loss, combined oral cont racept ion pills, spironolact one (a diuret ic that is an androgen antagonist), progesterone-containing medications, electrolysis, laser vaporizat ion, waxing, and shaving. The patient must be warned that there is a slow response t o t reat ment wit h medicat ions (an average of 6 mont hs). To help wit h more immediate result s, nonmedical t herapies (waxing and shaving) may be used initially until the new medication begins to work effectively. Isosexual (no virilization) precocious puberty with an adnexal mass usually is a granulosa cell tumor of the ovary. They present as a pelvic mass that causes pain due to its rapidly enlarging size, however, t hey do not cause isosexual precocious pubert y. A Sertoli–Leydig cell tumor is t he androgen count erpart t o t he granulose-t heca cell t u m or. W it h a Ser t oli– Leydig cell t u m or, t est ost er on e levels are mar k- edly elevat ed, and pat ient s t ypically present wit h hirsut ism, virilism, and an adnexal mass. Congenital adrenal hyperplasia is the most common cause of ambiguous genit alia in t he newborn; however, late onset can present in adult women wit h sympt oms of h irsut ism and anovulat ion. T h e m o s t co m m o n n e o n a t a l e n d o cr i n e ca u s e o f d e a t h ( s a lt w a s t i n g) i s con- genital adrenal hyperplasia ( 2 1 -hydroxylase deficiency). An elevat ed t est ost er- one level would be found with a Sertoli–Leydig cell tumor. A dexamet h ason e suppression t est is used in t he diagnosis of Cushing syndrome. A karyotype may be used in find- ing t he et iology beh ind a young girl’s present at ion of primary amenorrhea or pubertal delay. Sin ce the sympt oms were n ot of r apid on set, the et iology is not likely t o involve a tumor. Int raut erine inseminat ion is usually indicat ed for the rare cer vical fact or in fer t ilit y, an d n ot ovulatory dysfunction. Polycystic ovarian syndrome is the most common cause of hirsutism and irregular menses. Sympt om s d o n ot cor r elat e wit h an ovar ian t u mor (sin ce the patient has abnormal hair growth, hirsutism); also, laboratory values indicate normal adrenal function, thus ruling out adrenal tumor and Cushing syndrome. Sh e h a s a n o ld e r sist e r wh o e xp e rie n ce d m e n - arch e at the ag e of 12 ye ars. He r b re a st s ap p e ar to b e Tan n e r st ag e I, an d h e r p ub ic h air p at te rn is also con siste nt wit h Ta n n e r s t a g e I. Th e e x t e r n a l g e n i - t alia are n orm al for a p re p ub e sce nt fe m ale. Know that the absence of secondary sexual characteristics by the age of 14 years constitutes delayed puberty. Know that the most common cause of sexually infantile delayed puberty, gon ad al d ysgen esis, is u su ally associat ed wit h a ch r om osom al abn or m alit y. Know that the definition of precocious puberty is the onset of secondary sex- ual characteristics > 2 st andard deviat ions from the mean (age 7 years in Cau- casian women an d 6 year s in Afr ican -Am er ican women ). Know that the most common cause of precocious puberty in women is idio- pathic and treated with gonadotropin-releasing hormone agonist. Co n s i d e r a t i o n s This 16-year-old adolescent woman has never menstruated and, therefore, has pri- mary amenorrhea. Furthermore, she has not yet experienced breast development (which should occur by an age of 14 years) and thus has delayed puberty. The lack of breast development means a lack of estrogen, which may be caused by either a cent r al n er vou s syst em pr oblem ( low gon ad ot r opin levels) or an ovar ian pr oblem (elevated gonadotropins). T h e absen t p u bic an d axillar y h air are con sist en t wit h d elayed p u ber t y. T h e most likely diagnosis without further information would be gonadal dysgenesis, such as Turner syndrome. There are four stages of pubertal development: ( 1 ) the l a r ch e, ( 2 ) p u b a r ch e / adrenarche, (3) growt h spurt, and (4) menarche. The first sign of pubert y is t he appearance of breast budding (thelarche), which occurs at a mean age of 10. This is followed b y the ap p ear an ce of p u b ic an d axillar y h air ( p u b ar ch e/ adrenarche), usually at 11 years. The onset of menses (menarche) is the final event of puberty, occur- ring approximately 2. N ormal puberty takes place between the ages of 8 and 14 years, with an average duration of 4.

Corticosteroids • Short courses of oral steroids for acute exacerbations in patients with reversible airflow obstruction or allergic bronchopulmonary aspergillosis cheap malegra fxt plus 160mg without prescription. Lung transplantation Epidemiology 71700–2200 procedures performed for all conditions annually worldwide buy 160mg malegra fxt plus mastercard. Cause of respiratory failure Primary graft dysfunction • Develops in the first 72h post transplantation buy malegra fxt plus us. Survival • The overall median survival of lung transplantation is 5 years (data from the International Society for Heart and Lung Transplantation 2007) purchase malegra fxt plus 160mg on-line. Management of immunosuppression in severe illness • Patients with lung transplants may present with severe sepsis, or indeed other coincidental illnesses. Steroids should be continued and doses may need to be increased in severely unwell patients. Amyloid light chain amyloid Immunoglobulin light chain as precursor protein, associated with plasma cell dyscrasias, e. Amyloid A amyloid Amyloid A (acute phase protein) as precursor protein, associated with chronic inflammatory or infective disorders. Pulmonary manifestations • Tracheobronchial infiltration may cause hoarseness, stridor, endobronchial obstruction. Extra-pulmonary manifestations Heart • Cardiomyopathy, dysrhythmias, myocardial ischaemia. Gastrointestinal • Hepatomegaly +/– splenomegaly, bleeding, dysmotility, malabsorption. Neurological • Carpal tunnel syndrome, mixed sensory and motor peripheral neuropathy. Pulmonary manifestations • Dyspnoea, cough, chest pain, fever, malaise, and weight loss (asymptomatic in 20%). Extra-pulmonary manifestations Skin • Papular rash, oral and genital ulcers, gingival hypertrophy. Treatment • Smoking cessation—mandatory • Corticosteroids may be beneficial in nodular disease. Lymphangioleiomyomatosis Pathophysiology • Proliferation of atypical smooth muscle cells around and within the bronchovascular structures and lymphatics. Pulmonary manifestations • Progressive formation of diffuse thin-walled cysts measuring 0. Extra-pulmonary manifestations • Renal angiomyolipomas (benign tumours made up of adipose tissue, smooth muscle cells, and thickened blood vessels). A pattern then found a strong relationship between “crooked noses and facial emerges where these four findings are often but not exclusively growth retardation. These patients were subdivided into three groups: where subtle differences may only be seen after strict photo- those with deviated noses and asymmetric faces (57. There Their analysis utilized measurements between the lateral structures are derived from different processes during embryo- canthus and mouth corner as well as the distance between the logical development and can independently develop in a sym- rhinion to the most lateral cheek projecting point. Findings often cited, such as a higher eyebrow these frontal views measured the craniocaudal and mediolat- or chin deviation toward the side of hypoplasia, are again some- eral or transverse maxillary vectors but did not assess the ante- times but not always associated with midfacial hypoplasia and roposterior vector. Pre- and postoperative photographs showing deviation correction using foundation rhinoplasty techniques alone. Pre- and postoperative views of a combined foundation rhinoplasty and cosmetic rhinoplasty approach. Foundation rhino- plasty alone without nasal bone osteotomy provided airway correction. Persistent right midvault asym- metry due to partial onlay graft resorption is present. The patient did not desire additional corrective maneuvers and was pleased with the outcome. Vertical height differences (lateral canthus to mouth corner) having facial asymmetry. Lateral alar, medial canthus, and lateral canthus excursion There was an even higher degree of association between the was noted to be a significant predictor of the face as asymmet- lateral or transverse measurements (rhinion to lateral cheek ric. Commissure deviation and tragal height differences were point) than the vertical one. Overall, 76% reported a subjective improvement in the perception of facial of their patients with facial asymmetry had nasal deviation, and asymmetry in these patients as well. A previous study by Yao et al used base view analysis Another important finding within this study was the high of patients with nasal deviation and facial hypoplasia. A significant number of those pared with angulation of the alar attachment to the face on patients had also had orthodontic interventions during their base view. A 72% satisfaction between these two measurement points, indicating a high rate was noted within this group of respondents. This base-view soft tissue analysis indi- satisfaction included persistent deviation, asymmetric nostrils, rectly looks at the anteroposterior maxillary volume and asymmetric alar rims. Note the starting nasal point between the pupils and the tip position essentially at the philtrum (vertical lines). Postoperatively, an improved but persis- tent nasal axis deviation is present (horizontal lines). Note the increased deviation correc- tion and alignment of facial structures on the vertical plane compared with the patient in ▶Fig. This propa- separates the face into thirds and also considers the three- gates as a vomerine spur with bony septal deviation toward dimensional development of each segment emerges. The caudal septum may traverse the crest to area or vector can be deficient in isolation, but typically the ultimately lie on the side of tip deviation (ipsilateral) or entire maxilla is hypoplastic. With respect to the nose, it is the remain on the same side (contralateral) as the deeper medial maxillary projection that matters most. Sig- nificant difficulties arise with asymmetric development of the As a surgeon becomes more experienced with nasal corrective anterior nasal spine. The position of the anterior nasal spine procedures, certain patterns of deformity typically become should be determined preoperatively and verified intraopera- internalized into the individual physician’s thought process and tively. If the spine lies in a paramedian position, then deviation surgical treatment plan. Drawing upon past patient experiences correction must be done using a method that transposes the helps one to define corrective maneuvers that will work and posterior septal angle to the opposite side of the spine, rather those that will not. The surgeon should also be aware of The senior author has had significant experience correcting the increased potential for postoperative deprojection, unless deviated noses for both functional and cosmetic reasons. Within the context of this experience, a pattern for congenital The degree of deviation correction with paramedian crests, in nasal deviation associated with midfacial hypoplasia has devel- the senior author’s experience, is also harder to achieve and oped and, although not exclusive, represents a starting point for predict. Another significant variation is seen in patients with midline Congenitally deviated noses are typically linear, but traumati- nasal bones. Deviation correction does not mandate osteoto- cally deviated noses are typically curvilinear. A linear deviation, mies, as corrective maneuvers of the lower nasal two-thirds are which is almost exclusively seen with midfacial hypoplasia, is reliably predictable in this circumstance. Deviation is typically most pronounced at the rhinion due 17 Rhinoplasty Assessment Fig. Pre- and postoperative views of foundation rhinoplasty correction without nasal bone osteotomy or suture tip modification. The tip typically is only slightly off midline due to tractional pull from the caudal sep- The nasal bones are the most commonly fractured bones in tum, and base view analysis does not show significant angulation the face4 and thus are a leading cause of an asymmetric nose. The overall effect creates the Facial injuries may lead to surface depressions, irregularities, appearance of a curved nose, due to the relatively midline tip posi- and disruption of the traditional nasal support mechanism, tion. These patients also do not typically have maxillary crest and which may or may not cause nasal deviation and/or dysfunc- vomerine spurs associated with the deviation unless the trauma tion. Nasal collapse may occur from upper lateral cartilage occurred in childhood. Septal dislocations may create new- onset nasal airway asymmetry, which causes functional obstructive symptoms. Patients with severe facial injuries, typically as a result of high-speed automobile accidents or Lefort I fractures, can develop traumatic nasal tip deviation. Loss of lateral supporting elements of the maxilla exerts its effect upon the nasal tip through the sesamoid complex and intervening fibrofatty tis- sue. Volume addition to the lat- eral pyriform rim or subalar region can result in significant tip medialization in these patients. In contradistinction, patients with tripod fractures or isolated zygomatic arch fractures do not typically have changes to the position of the nasal tip.

Which of the following nerves provides the innervation to the scalp in this region? The temporal artery is deep to the temporalis muscle and sometimes is associated with inflammation (temporal arteritis) cheap 160 mg malegra fxt plus free shipping. Temporal arteritis or giant cell arteritis is associated with headache and multiple joint pain cheap malegra fxt plus 160 mg mastercard. He lost consciousness briefly but woke up after about 45 s and had no neurological deficits order malegra fxt plus mastercard. Four hours later buy malegra fxt plus with amex, while being observed, he complained of an increasing headache and had a seizure. On exami- nation, the patient’s right pupil appeared dilated and reacted sluggishly to light. Four hours later, he developed an increasing headache, a dilated and sluggish right pupil, and had a seizure, consistent with increased intracranial pressure. After waking up, he had no neurological deficits; however, after 4 h, there were signs of increased intracranial pressure. The most likely explanation is disruption of the middle meningeal artery, which underlies the temporal bone. This scenario of a loss of consciousness followed by a lucid interval and a second loss of consciousness is very typical for epidural hematoma. Emergent cerebral decompression and surgical control of the bleeding are paramount. The dura mater is a thick, strong membrane (pachyme- ninx) that is closely apposed to the deep surface of the cranium. Immediately deep to the dura is the arachnoid layer, a thin, nearly transparent membrane that adheres to the deep surface of the dura. The dura mater that covers the external surface of the brain consists of two layers, an external periosteal layer attached to the bone and an internal men- ingeal layer. The falx cerebri courses along the midline and separates the left and right cerebral hemispheres. Running at right angles, the tentorium cerebelli separates the two lobes of the cerebrum from the cerebellum. On the inferior surface of the tentorium is attached the small falx cerebelli, which also runs along the midline and partially separates the cerebellum into lobes. Another important dural infolding the diaphragma sellae, covers the pituitary fossa. Normally, the two dural layers are tightly apposed, but they may split to form the dural sinuses (Figure 44-1). The major dural sinuses are the superior sagittal sinus, which courses along the superior edge of the falx cerebri, and the transverse sinus, which courses along the posterior border of the tentorium cerebelli. The transverse sinus continues laterally as the sigmoid sinus and empties into the internal jugular vein. On the inferior surface of the falx cerebri, the inferior sagittal sinus continues as the straight sinus after joining the great vein of Galen, which drains the brain. The superior, straight, and transverse sinuses come together at the confluence of sinuses, a landmark on the internal surface of the occipital bone. Other important sinuses are the superior and inferior petrosal sinuses and the cavernous sinus. The vessels that supply the dura mater are branches of the middle meningeal artery. This artery arises in the infratemporal fossa from the first part of the maxil- lary artery and enters the cranial cavity through the foramen spinosum. The artery runs within the dura mater and separates into anterior and posterior divisions. An external landmark for the middle meningeal artery is the pterion, where the fron- tal, parietal, temporal, and sphenoid bones converge. The vessels that supply the brain arise from the circle of Willis (see Case 46 for more details). This anasto- motic formation originates from the internal carotid and vertebral arteries. The major branches tend to course along the surface of the brain and give off penetrating branches. The dura and meninges: 5 = superior sagittal sinus, 6 = inferior sagittal sinus, 18 = lateral lacuna, 19 = emissary vein (connects sinuses to scalp veins), 20 = arachnoid granulation (resorption of cerebrospinal fluid). Blood accu- mulates in potential spaces surrounding the brain, expanding their volume, and placing pressure on the brain. For example, rupture of the middle meningeal artery will lead to accumulation of blood in the epidural potential space, between the external periosteal layer of the dura and the calvaria. Blood from a cerebral artery due, for example, to a ruptured cerebral aneurysm, will accumulate in the subarachnoid space. Head trauma may result in rupture of veins as they enter a sinus, usually resulting in accumulation of blood in the subdural potential space between the dural and arachnoid layers. These veins may be cerebral veins that drain the brain or emissary veins that drain the scalp. After careful questioning, it was discovered that the infant was shaken before the change in mental status. The neurosurgeon suspects that the skull fracture and underlying hematoma occurred at the junction of the four major bones of the skull. Infants who are shaken are vulnerable to laceration of the emissary veins that are found below the dura. The pterion is a landmark of the skull where the four major bones of the skull (frontal, parietal, temporal, and sphenoidal) come together. On examination, she is noted to have edema and tenderness of the left submandibular region. Palpation of her mouth reveals a 4-mm, irregular, nonmobile, hard mass in the mucosa of her mouth. On examination, she has tenderness of the left submandibular salivary gland and a palpable, irregular, 4-mm mass along the floor of her mouth. Occlusion of the duct by a stone will cause secreted saliva to accumulate proximally to the stone, thus causing distention and pain. Pain after a meal is due to the accumulation of saliva proximal to the occluded duct, which stretches the duct or the capsule of the gland. The pathogenesis of sialolithiasis is unknown but appears to be due to lodging of a small particle in the duct, which serves as a nucleus for deposition of organic and inorganic material. The particle could be food, bacteria, or an inorganic constituent of tobacco smoke. Treatment would be excision of the stone under endoscopy and administration of antibiotics. Be able to describe the salivary glands and the course of their ducts to the oral cavity 2. The parotid gland lies superficial and posterior to the ramus of the mandible and inferior to the ear. The submandibular gland lies below the angle and the body of the mandible superficial to the mylohyoid muscle. The sublingual gland lies in the floor of the mouth between the mandible and the genioglossus muscle. All of the glands secrete saliva into the oral cavity through characteristic ducts. The parotid duct crosses over the masseter muscle and pierces through the buccinator muscle to open into the oral cavity, typically at the level of the second upper molar. The sub- mandibular duct forms from the deep lobe of the submandibular gland, deep to the mylohyoid muscle. The duct runs anteriorly on the surface of the hyoglossus muscle and opens into the oral cavity through the submandibular caruncles, just lateral to the lingual frenulum. The sublingual glands give rise to numerous small ducts that empty at the base of the tongue. The submandibular duct has a close relation to several important structures in the floor of the mouth. The submandibular gland folds around the free posterior border of the mylohyoid muscle, and the duct arises from the deep lobe of the gland. It courses anteriorly between the mylohyoid and hyoglossus muscles and then on Duct of parotid gland Parotid gland Buccinator muscle Sublingual Masseter muscle ducts Sublingual gland Sternocleidomastoid muscle Anterior belly of digastric muscle Mylohyoid muscle Submandibular duct Submandibular salivary gland figure 45-1.

If airway resistance or inspiratory flow rate increase buy malegra fxt plus visa, the curve is offset to the right-hand side order malegra fxt plus 160 mg on line, as demonstrated in Fig discount 160 mg malegra fxt plus fast delivery. V V mL mL 800 800 600 600 400 400 200 200 Paw Flow cmH2O L/min 0 0 –10 0 20 40 –100 –50 0 50 Fig purchase malegra fxt plus 160mg. If lung over-distension occurs during tidal ventilation, the slope of the inspiratory limb will reduce towards the end of the inspiratory phase (Fig. This is the equivalent of the upper inflection point on a static pressure–volume loop. Static loops Pressure–volume loop The classic static pressure–volume loop is obtained using the ‘super syringe’ method where the lung is progressively inflated in a stepwise manner with small increments of volume (50mL) and the associated change in airway pressure measured during conditions of no gas flow. Under these conditions, the effects of resistance are removed and the pressure–volume curve reflects the elastic properties of the lung. This allows the zone of maximum compliance to be identified, with lower and upper inflection points representing lung volumes where compliance is significantly reduced due to de-recruitment and over-inflation respectively (Fig. Many ventilators now offer the facility to perform a ‘quasi-static’ pressure–volume curve using the slow inflation technique. The low flow rate limits the pressure changes required to overcome the resistive forces such that the pressure–volume curve generated is a reasonable reflection of the true static pressure–volume curve. The procedure generally requires that the patient is deeply sedated and paralysed to ensure no spontaneous respiratory effort during the manoeuvre. Upper and lower inflection points may then be identified, although their clinical utility remains debated. In a significant number of patients these inflection points are not clearly identified. Accurate measurements require that the patient is sedated and making no spontaneous respiratory efforts. Many ventilators now display breath-by-breath dynamic measurements of compliance and resistance. These are derived from the continuous analysis of the pressure–, flow–, and volume–time curves. All measurements of compliance and resistance assume that patients are not making significant respiratory efforts (see box). Any values measured during periods when patients make effective respiratory efforts will not be accurate and should be interpreted with caution. Serial measurements of resistance are useful for assessing the response to bronchodilators. This produces conditions of no flow and the pressure within the lungs equilibrates with that in the ventilator. The patient must be relaxed and not make any respiratory effort during the measurement, which usually requires deep sedation and often a muscle relaxant. This requires the insertion of an oesophageal balloon to estimated pleural pressure and is not commonly undertaken. Other measurements Maximal inspiratory pressure This is the maximum negative inspiratory pressure that can be generated by a patient during occlusion of the airway and is used to assess respiratory muscle strength. However, the measurement does not have adequate specificity or sensitivity for routine use in clinical practice. However, low values may also be associated with failure to wean due to either inadequate respiratory drive or severe respiratory muscle weakness. Predictors of successful weaning Respiratory frequency <35/min Tidal volume >5mL/kg Rapid shallow breathing index (F/Vt) <80 Occlusion pressure (P0. Accurate measurements use a transducer that is placed at the ‘Y’ piece that combines in-line capnography with a pneumotachograph. A sudden and marked increased in physiological dead space in a ventilated patient may indicate a pulmonary embolus. Barotrauma In the early days of positive pressure mechanical ventilation large (10–15mL/kg) tidal volumes were recommended to prevent alveolar collapse. It was soon recognized that the use of large tidal volumes was associated with high airway pressures, which could cause the rupture of lung parenchyma. As this was initially thought to be primarily a pressure effect, the term ‘barotrauma’ was used to describe the associated lung injury. Histological studies have confirmed that over-inflation of normal lung units during mechanical ventilation produces stress fractures at the alveolar–capillary interface that can allow alveolar gas to escape into the pulmonary parenchyma and beyond. Cyclical de-recruitment/re-recruitment of alveolar units results in shear stress in the parenchyma between adja- cent units (atelectrauma). This inflammatory reaction may also spill cytokines into the systemic circulation and produce a systemic inflam- matory response syndrome. The production and release of inflammatory mediators in response to the mechanical stress of ventilation is termed ‘biotrauma’. This strategy was shown to decrease mortality and reduce the duration of mechanical ventilation, but the rates of pneumothorax and air leaks were unchanged. The transpulmonary pressure (the pressure difference between the alveoli and the pleural space) determines alveolar distension. Alveolar pressure equals proximal airway pressure when there is no gas flow, such as at the end of inspiration (end inspiratory pause pressure or plateau pressure) or during an inspiratory hold. While overall transpulmonary pressure in these circumstances may be acceptable, regional differences in lung mechanics mean that it is less certain that all distal lung units are protected to the same degree. This usually occurs deep within the lung and the air dissects along fascial planes to produce pulmonary interstitial emphysema. The air may track into the mediastinum to produce pneumo- mediastinum and pneumopericardium. In turn, mediastinal gas can move into the neck to produce subcutaneous emphysema or pass below the diaphragm to produce pneumoperitoneum. If the visceral pleura ruptures, air will collect in the pleural space and produce a pneumothorax. Tension pneumothoraces occur when pleural air, under pressure, displaces mediastinal structures (heart and great vessels), resulting in cardiovascular collapse. Diagnosis Clinical features Clinical features may be non-specific, subtle, or absent, and gas exchange may not change markedly. Radiographic features See b Pleural disease, p 481 Treatment Tension pneumothoraces should be decompressed as an emergency. Classical management involves needle decompression in the second inter- costal space, mid clavicular line, followed by formal drainage. This is usually a consequence of positive pressure ventilation rather than evidence of a tension pneumothorax. Most persistent air leaks in mechanically ventilated patients are due to parenchymal necrosis and an air leak distal to a seg- mental bronchus. This is the largest type of air leak but even so most are not of sufficient magnitude (i. There is no evidence that any of the meas- ures outlined below affect mortality or any other outcome. With severe lung disease, where relatively high pressures are required in order to keep the patient alive, a large air leak may have to be tolerated. Permissive hypercapnia, an increase in FiO2, and perhaps permissive hypoxia may have to be accepted. This may result in hyperventilation, respiratory alkalosis, the inappropriate escalation of sedatives, and the use of neuromuscular blocking agents. During conventional mechanical ventilation, gas flows preferentially through a fistula because it has low airway impedance. However, this increase in airway impedance becomes less important in patients with reduced compliance in the rest of the lung. This is because of the proximity of the lobar ostia to the carina on the right main bronchus. Right-sided tubes are available and may need to be used in disease of the proximal left main bronchus. Disadvantages include the additional skills required at placement, tube displacement, bronchial ischemia, stenosis, and rupture from the high pressure generated by the endobronchial cuff. It has been common practice to place thoracostomy tubes on suction on the assumption that this promotes early resolution of air leaks by eliminating residual space and encouraging pleural apposition. Intermittent inspiratory chest tube occlusion This synchronizes chest tube occlusion on inspiration, potentially reducing the leak and facilitating distribution of tidal volume to the rest of the lung.