By W. Anog. Dickinson State University. 2019.
Eventration Unilateral hypoplasia of a hemidiaphragm (very (Figs C 46-1 and C 46-2) rarely both) with the thinned buy 5 mg olanzapine free shipping, weakened muscu- lature inadequate to restrain the abdominal viscera buy olanzapine 2.5mg with amex. Localized eventration primarily involves the anteromedial portion of the right hemidia- phragm purchase 2.5mg olanzapine overnight delivery, through which a portion of the right lobe of the liver bulges olanzapine 5 mg amex. In a posterior eventration, upward displacement of the kidney can produce a rounded mass. Eventrations may have paradoxical diaphragmatic motion (though more commonly seen in diaphragmatic paralysis). Phrenic nerve paralysis Unilateral or bilateral diaphragmatic elevation (Fig C 46-3) with characteristic paradoxical motion of the diaphragm (tends to ascend rather than descend with inspiration). Results from any process interfering with the normal function of the phrenic nerve (inadvertent surgical transection, primary bronchogenic carcinoma, or mediastinal metas- tases); intrinsic neurologic disease (poliomyelitis, Erb’s palsy, peripheral neuritis, hemiplegia); injury to the phrenic nerve, thoracic cage, cervical spine, or brachial plexus; pressure from a substernal thyroid or aneurysm; or lung or mediastinal infection (paralysis may be temporary). Also perinephric, hepatic, or splenic abscess; pancre- atitis; cholecystitis; and perforated ulcer. Intra-abdominal mass Unilateral or bilateral diaphragmatic elevation (Fig C 46-4) caused by enlargement of the liver or spleen; abdominal tumor or cyst of the liver, spleen, kidneys, adrenals, or pancreas; or distended stomach or splenic flexure (left hemidiaphragm). Primary bronchogenic carcinoma (arrow) involving the phrenic nerve causes paralysis of the right hemidiaphragm. Tumor or cyst of diaphragm Very rare lesion that simulates unilateral dia- phragmatic elevation. On (Fig C 46-6) frontal views, the peak of the pseudodiaphragmatic contour is lateral to that of a normal hemi- diaphragm (situated near the junction of the middle and lateral thirds rather than near the center). Altered pulmonary volume Unilateral or bilateral diaphragmatic elevation due to atelectasis (associated pulmonary opacity); postoperative lobectomy or pneumonectomy (rib defects, sutures, shift of the heart and mediastinum); hypoplastic lung (crowded ribs, mediastinal shift, absent or small pulmonary artery, sometimes the scimitar syndrome). Diaphragmatic hernia Mimics unilateral diaphragmatic elevation on (Figs C 46-7 and C 46-8) frontal views. Lateral views show the characteristic anterior location of Morgagni’s hernia or the posterior position of Bochdalek’s hernia. Injury diaphragm to the right side causes herniation of the soft-tissue (Figs C 46-9 and C 46-10) density of the liver into the right hemithorax. On the left, air-containing stomach and bowel herniate into the chest (may mimic diaphragmatic elevation if the bowel loops are filled with fluid). The peak of the pseudodiaphrag- due to splinting secondary to a right lower lung infiltrate. Herniation of a portion of the splenic flexure (arrow), with obstruction to Fig C 46-8 the retrograde flow of barium. Also (Fig C 47-1) pleural, vascular, and bronchial interfaces with occurs in patients with asbestosis and colla- normal parenchyma. The predominant pattern of ground-glass (rather than reticular) opacities is seen in nearly all patients, reflecting the presence of intra-alveolar macrophages and interstitial inflammation. Typical litis, chronic eosinophilic pneumonia, and collagen peribronchial thickening. In most patients, however, no cause is found and the condition is referred to as idiopathic or cryptogenic. Scan at the level of the right upper lobe bronchus in a woman with id- iopathic pulmonary fibrosis shows a reticular pattern and irregular in- terfaces predominantly in the sub- pleural lung regions. Scan at the carinal level shows patchy areas of air- space opacification (“ground-glass” density). Air-space consolidation in the subpleural regions associated with peribronchial thickening (arrows). Usually most evident in the lung periphery, where (Fig C 47-5) the septa appear as lines running perpendicular to the pleura. Sarcoidosis Irregular nodules or interstitial thickening along In late stages, fibrosis typically radiates from the (Fig C 47-6) the bronchovascular bundles. Scan through the septa (small arrows) and ill-defined centrilobular opac- right lower lung shows extensive abnormalities with ities (large arrows). Note also the thickening of the thickening of the interlobular septa (straight arrows), peribronchovascular interstitium, with peribronchial major fissure, and bronchovascular bundles (curved 88 87 cuffing. Nodu- lar thickening of the interlobular septa (curved arrow) and subpleural granulomas (white arrows) are also identified. Supine scan shows moderate thickening of interlobular septal (arrows) and peribronchial (arrow- heads) structures in the nondependent subpleural Fig C 47-8 parenchyma. Scan through the right middle lobe shows an irregu- pleural honeycombing (curved arrow). The interlobar fis- lar mass with aerated lung interposed between it and the adjacent sures are thickened, and there is serration of the pleural thickening. A focal band of soft tissue can be seen in con- lung-pleural interface at sites of interstitial fibrosis, tact with the pleura. The mass was stable on serial radiographs and changes indicative of visceral pleural fibrosis. Scattered calcifications are visible in the right anterior costal plaque (arrows). Extrinsic allergic alveolitis Fine nodular or reticulonodular pattern in the Hypersensitivity disease of the lungs caused by (Fig C 47-11) subacute stage. Bilateral areas of hazy increased inhalation of antigens contained in certain organic density (ground-glass opacification) with dusts. In the acute stage, there is diffuse air-space preservation of underlying vascular markings consolidation that resolves to an interstitial pattern may occur. Repeated exposure to the antigen may lead to acute and subacute changes superimposed on chronic fibrosis. Pulmonary Langerhans cell Small irregular nodules and cystic air spaces Histologically an infiltrative lung disease of histiocytosis that diffusely involve the upper two-thirds of the Langerhans cells. Scan at the level of the right hemidiaphragm shows patchy areas of hazy interstitial density (“ground-glass” density; arrows) that typically do not obscure the underlying vascular markings. Often associated with volume Late stage of radiation-induced lung injury, which (Fig C 47-14) loss, traction bronchiectasis, and pleural thick- develops gradually in patients with radiation ening that results in a sharp demarcation pneumonitis when complete resolution does not between normal and irradiated lung. It evolves within the previously irradiated field, 6–12 months after radiation therapy, and usually becomes stable within 2 years after treatment. Scan through the right upper lobe shows numerous thin-walled cystic air spaces of vari- ous sizes. Note the traction bronchiectasis due to fibrosis and the sharp demarca- tion between normal and irradiated lung. This (Figs C 48-1 and C 48-2) appearance suggests active and contagious disease, especially when associated with adjacent cavitary nodules within the lungs. The terminal tufts of the “tree-in-bud” pattern may represent lesions in the bronchioles and alveolar ducts, whereas the stalk may reflect a lesion affecting the last-order bronchus in the secondary pulmonary lobule.
To approach to restore lost volume purchase olanzapine 2.5 mg visa, smooth contours cheap 20 mg olanzapine mastercard, and enhance facial paraphrase Hungerford purchase olanzapine 5 mg line, “beauty may actually reside in the Phi (eye) features naturally2 (see Chapter 7) discount 10mg olanzapine with mastercard. Although truly the domain of autologous fat and pharmaceuti- Injection therapy restores youth by sofening aging lines, reestab- cally available “dermal” fllers, botulinum-based neuromodulators lishing fullness of features, and smoothing contours with gradual can also play a signifcant role in optimizing beauty by generating transitions. Individual ideal facial proportions can be dynamic expression, but the position of facial elements in the rest- obtained with the aid of a golden mean caliper—a tool for dynami- ing state through static muscle tension. Create Phi beauty, and youth accom- flling agents, the efect is quite ofen synergistic, optimizing both panies it—but pursuing youth does not necessarily create beauty the patient’s experience and outcome. An overly concave temple can detract from True facial beauty arouses the senses to an emotional level of pleasure facial attractiveness, and signify a stigma of advancing age. Perception excess convexity in a female temple can portend a masculine look of beauty is innate, as borne out by numerous studies confrming and distort the beautiful facial oval (or heart shape) preferred by most that newborn infants prefer attractive faces. Furthermore, in modern day ofering a more balanced and harmonious look to the upper face. Extensive research has further shown that regardless of our Deposition of botulinum toxin into the temporalis muscle within racial background, we seem to have similar subjective ideas about its fossa can reduce upper facial bulkiness and provide the initial what constitutes an attractive face. Leonardo Da Vinci, one of the world’s most superfcial temporalis muscle will lead to a hernia-type deformity of celebrated thinkers, insisted that there was a mathematical basis to its untreated deeper counterpart (similar to masseteric hypertrophy). Across the centuries, many other of the incobotulinum; 25 u of abobotulinum toxin) spaced 2 cm apart into world’s greatest intellectual minds, including Galileo, Michelangelo, the maximum convexity of the muscle usually sufce, followed by and Einstein were in awe of the fact that natural beauty appeared several minutes of pressure to minimize the risk of bruising from the dependent on this divine ratio. Furthermore, although maximal clench is dimin- bc), commonly regarded as one of the greatest of all classical Greek ished,17 no detrimental efect on chewing has been observed, as the sculptors. In simple algebraic terms, the golden section is the only masseter and pterygoid muscles remain the principle contributors to point dividing a line into two parts where the smaller segment in mastication. As such, the superior portion of the muscle is frmly adherent to the underlying bone and devoid of interposing fascia. Te periosteum and deep fascia of the forehead (galea aponeuro- (a) (b) tica) as they traverse the upper face under the frontalis muscle can- not continue under the temporalis muscle and as such lie over the muscle as the deep and superfcial temporal fascia respectively. This anatomical oddity, of a deep fascia lying on the surface of the mus- cle which bears its name, provides a resistant plane that is apprecia- bly felt when penetrating the region with a needle. Overlying this fascia in the posterior leaves of the superfcial temporal fascia are the superfcial temporal vessels (arteries and veins) and specifcally the frontal ramus of the superfcial temporal artery. Located in the depth of the muscle are the anterior and posterior deep temporal arteries (branches of the internal maxillary artery, second division), the middle temporal artery (connecting the deep and superfcial arterial system), and the prominent middle temporal vein approxi- mately 2 cm above the zygomatic arch. Deposition of botulinum toxin deep to the fascial layer is mandatory to access the bulky deep muscle as outlined above, and will require a 30-gauge needle of minimum ½ inch length. Prudent technique would require aspira- (c) tion before injection of toxin into the temporal muscle to mini- mize the possibility of intravascular washout limiting the clinical result. Post-injection pressure for several minutes, regardless of the appearance of blood through the puncture site, will diminish the possibility of delayed unsightly bruising. T e Beautiful Glabella and Botulinum Toxin Subtle diferences in glabellar appearance have a profound efect on beauty and youthfulness. Aging skin changes and actinic expo- sure lead to the appearance of lines, creases, and dyschromias com- pounded with tissue atrophy and volume loss. Bone remodeling leads to an increase in glabellar height and width, which can ofen be evi- denced by a paradoxical elevation of the medial brow in the elderly (Figure 8. This is to be distinguished from an elevated eyebrow resulting from increased frontalis activity as compensation for an upper eyelid partial levator dehiscence. Simply stated, com- cial gliding muscles, the frontalis (elevator) and the procerus (depres- plete loss of the tethering efect of medial corrugator pull, in combina- sor); and two deep brow depressor muscles, the paired corrugator tion with the unopposed oblique pull of the frontalis muscle, can lead and depressor supercilii. Trough their sof tissue attachments into to unnatural eyebrow splay post-treatment (Figure 8. Patients at the skin of the region, these antagonistic muscles both animate the risk for this medial canthal splay afer corrugator chemodenervation medial brow, and position it through resting tension depending on typically have mobile glabellar tissue that widens easily with digital the individual’s emotional state. Once these patients and depressors is somewhat stratifed as the frontalis blends superf- are identifed, the addition of a small amount of toxin into the upper cially with the deeper depressors. Varying the height and depth of toxin deposition according to the muscle action being targeted can alter the resting posi- tion of the medial brow. Phi harmony in the upper face dictates that the medial brows begin in a vertical line above the medial canthii at a 1. This technique is indicated when medial eyebrow position is too high and superior medial orbital hollowing is present to accom- modate the potentially redundant skin that may occur as a result of treatment. Te medial eyebrow Unlike other regions of the face where moderation is desirable to begins vertically above the medial canthus at a height equal to 0. It then extends laterally at an angle of 10–20 degrees to a maintain natural animation, it is ofen the goal of glabellar injec- peak located Phi (equal to the intercanthal distance) of the entire length of the tion therapy to obliterate depressor function that is responsible for eyebrow (1. Te corrugator supercilii runs from In summary, thorough observation and palpation of the glabellar a deep osseous origin to a lateral superfcial insertion into the dermis complex of muscles and overlying skin’s resistance to spread is neces- of the middle third of the eyebrow. Te dimensions of the corrugator sary in order to individualize the pattern of neurotoxin injections to supercilii muscle are more extensive than previously described and optimize beauty in the region. It arises from the frontal process of the maxilla approxi- within 1 mm from a line drawn vertically from the medial iris. Te triangular procerus is Needle injections of toxin in the region are best performed avoiding more superfcial and can be considered as a musculoaponeurotic these exact topographical landmarks to minimize bruising. Te frontalis is actually comprised of paired fat muscles originat- T e Beautiful Eyebrow and Botulinum Toxin ing from the occipitofrontal-musculoaponeurotic system of the scalp From its origin overlying the supraorbital ridge above the medial can- in an angulated direction from lateral to a more medial insertion into thus, the beautiful female eyebrow slopes upward and laterally at an the confuence of the glabellar complex and overlying dermis of the angle of 10–20 degrees. Te dermal insertion is beneath the eyebrow in its medial laterally at 0–10 degrees. Te frontalis glides easily over the frontal bone in its mimetic female brow is ideally located at the golden section of the brow length function due to the underlying galea, a thick fascia that is inter- (0. Individualizing the dose and location of upper muscle is limited to around 8 mm of vertical movement. Te authors contend that to raise a sagging forehead promontory has few signifcant vessels (periosteal branches brow is virtuous, but to contour it, divine. Although the more in-depth pre-injection assessment to determine those patients frontalis is considered to be a paired muscle with a midline aponeu- who may beneft from eyebrow positional changes. For instance, indi- rotic gap and lateral extent to the temporal fusion line, occasional viduals with a pre-existing high lateral arch to the eyebrow may obtain muscle fbers have been demonstrated both centrally as well as later- an accentuated and exaggerated arch if injections more efectively ally beyond the temporal crest margin. Te aesthetic injector should reduce the caudal displacement efects of the lateral sub-brow orbi- be wary of these variations in anatomy that are the culprit for post- cularis oculi muscle. This typically results in secondary lines above toxin residual central furrowing or lateral “Spocking” of the brow the lateral brow that disrupt the overall aesthetics. Te outlying tail of the eyebrow beyond cal palpebral aperture (“squintier” eyes in the elderly) (Figure 8. Like a skin-tightening procedures remain the workhorses of beautifcation cantilever, it must rely on the frontalis’ upward pull on the adjacent and rejuvenation in the middle face. In patients who demonstrate a sig- sofening of dynamic lines or unwanted tics and grimaces.
Te original cyst grows 2–3 cm per year; as the cyst enlarges order 10mg olanzapine otc, it starts to form internal daughter cysts ( order 10mg olanzapine free shipping. Humans are intermediate hosts who are infected with the parasite by Grading of the Liver Lesions by E generic olanzapine 5 mg on line. On the diferent radiological imaging modalities order olanzapine 20mg on line, diferent Afer the parasite is ingested, the eggs hatch, and the shapes of the hydatid cyst may be encountered. This is due to embryos penetrate the intestinal mucosa, enter the portal cir- the fact that the cysts undergo diferent stages of life and culation, and are carried to various organs. Te second wall is an outer acellular layer intact endocysts, and patients with grade 1 lesions (ectocyst), and the third is an inner cellular wall (endocyst). It mimics a solid pulmonary mass and may lead to a false diagnosis of pulmonary tumor. Absence of symptoms and presence of other cystic lesions within the liver are important clues. This is an important sign that grade is characterized by the appearance of diferent diﬀerentiates a grade 1 hydatid cyst from a simple intracystic textures. It is seen as collapse of the hydatid membrane (pericyst) over the residual endocysts. This grade is characterized by intrahepatic biliary dilatation with hydatid vesicle escape from the mother cyst into the biliary radicals, causing regional biliary obstruction (. Leakages involving the mesentery and the intraperitoneal structures of the hydatid fuid into the peritoneum cause severe irritation and peritonitis. Notice the right lobe cyst with dilated biliary radicals ruptured hydatid cyst with ﬂoating water lily sign (arrowheads ). Notice around it, with an intrabiliary daughter cyst (arrow ) the cystic wall mimicking a cavity (arrow ) 11. Notice the large hydatid cyst occupying a large portion of the right lobe of the liver (arrowhead), with compensatory. As the liver has the ability to regenerate, com- pensatory hypertrophy of the liver is usually seen when a large segment of the liver parenchyma is atrophied. Te cyst is small (1–10 mm in diameter) and forms multilocular alveolar cysts that resemble lung alveoli, hence D i ﬀ erential Diagnoses and Related Diseases the name alveolaris. This will later result in a of a major hepatic or portal vein or biliary tree branch results fbrous, tumor-like lesion composed of E. Stenosis of the porta hepatic with the hepatic veins within the lesion is a commonly found. Te disease is one of the most common public health problems in South America from Texas to Argentina. Te bite occurs around the face, ofen at night, and outer wall of the ventricle below the pericardium the parasite is found in the bug’s feces. Te parasite invades and enters Apical aneurysm with thrombus formation is a the host cells, particularly the muscles, the glia, and the reticulo- common finding. Multiplication occurs by binary fssion until the cells rupture, and the parasite enters the blood or invades more tissues. At the site of multiplication, severe infammatory reaction occurs with local lymphangitis, which is known as cha- goma. Soon afer that lymphatic spread to regional lymph nodes occurs, which is usually seen in the frst 2 weeks postinfection. Afer an incubation period of 2 weeks, patients ofen present with fever that can persist for months, malaise, loss of appetite (anorexia), vomiting, diarrhea, and muscle pain. Hyaline necrosis of isolated myocardial fbers(Magarinos – Torres’ lesion) is a characteristic feature of Chagas’ myocarditis. Te try- Subacute Chagas’ Disease panosomes may enter the conjunctiva in up to 50 % of patients, causing upper or lower eyelid edema, conjunctiva chemosis, T is stage is ofen seen in young adults, and the patient pres- and preauricular lymph nodes enlargement (Romana ’ s sign). Doppler tissue imaging to access systolic T is stage develops afer many years and is characterized by function in Chagas’ disease. Radiological diagnosis of Chagas’ disease contractility and hypertrophy of the circular smooth mus- (American trypanosomiasis). Signs on Plain Chest Radiograph 5 The dilated esophagus is seen as a mediastinal mass along the entire right side of the 11. Schistosoma are fatworms that do not have a 11 5 Raised left hemidiaphragm due to splenic flexure digestive tract and are commonly known as trematodes or dilatation may be found. Schistosomiasis is commonly known as “bilhar- ziasis,” afer Bilharz, the discoverer of the parasite in 1815. Later, the eggs 5 The esophagus is massively dilated (>7 cm), with are hatched into larvae, which maturate in freshwater snails. Food may be found snails and enter into humans by penetrating the exposed lodged within the esophagus. Te parasites lie in the lymphatic system for almost 21 days before they enter the hepatic portion of the portal venous system into the liver, where they further mature and mate. Depending on the type of the Schistosoma, the parasites migrate into the intestinal or the bladder venous system to lay their eggs. Te adult worms are strictly intravenous and do not evoke the immune system, while both the cercariae and the eggs stimulate the immune system, resulting in the formation of granulomas around the eggs and the systemic cercariae, which will cause tissue fbro- sis and calcifcation of the afected organ in advanced stages of the disease. T ere are four types of Schistosoma worldwide: 5 Schistosoma japonicum is found within eastern Asia, is located within the intestinal tract veins, and releases its. The liver shows an internal echogenic polygonal network 5 Schistosoma intercalatum is found only in equatorial Africa due to periportal ﬁbrosis and calciﬁcation, which causes and mainly afects the intestinal tract and the portal system. Weeks later, systemic manifestations like hematuria, There is internal periportal ﬁbrosis (low-density bands) fever, weight loss, diarrhea, and abdominal pain arise. As the ova penetrate the wall of the intestine or the urinary bladder, they may cause chronic bleeding (resulting in anemia), be trapped in the wall of the organ, or enter the blood and circu- late as emboli. Te dead worms initiate a severe infamma- tory reaction within the veins, causing thrombophlebitis, which can block the afected vein. T e clinical and radiological manifestations of schistoso- miasis can be classifed according to the parasite type. In the small bowel, the duo- schistosomiasis demonstrates the internal periportal denum and the jejunum are mainly afected. When the eggs die, fbrosis within the venules results in a polygonal network of peripor- Schistosomiasis by S. Tere is a high incidence of liver carcinoma with tous colitis, which causes loss of haustration and strictures later S. If the small intestine is afected, regional ileitis and protein-losing enteropathy may develop. In uncommon cases, when the calcifcation is so severe as to include all the layers of the colon wall, the ova start to accumu- late freely within the peritoneal cavity outside the wall. This causes infammation and fbrosis within the peritoneal cavity and the pericolic region, resulting in a pericolic mass that can- not be diferentiated from carcinoma on imaging. In the liver, the parasite deposits its eggs around the main portal vein at the liver hilum, later resulting in Symmers’ pipestem fbrosis. Symmers’ pipestem fbrosis is a condition that arises when egg granulomas aggregate around the portal vein, resulting in vascular fbrosis that causes obstruction of the small veins and presinusoidal cirrhosis.
It has a floor which means the exposed surface of the ulcer and it has a base on which the ulcer rests olanzapine 7.5 mg. In a spreading ulcer olanzapine 2.5 mg low cost, the edge is inflamed and oedematous whereas in a healing ulcer the edge buy olanzapine 2.5 mg low price, if traced from the red granulation tissue in the centre towards periphery order 7.5 mg olanzapine with visa, will show a blue zone (due to thin growing epithelium) and a white zone (due to fibrosis of the scar). Five common types of ulcer edge seen in surgical practice are;— (i) Undermined edge — is mostly seen in tuberculosis. The disease causing the ulcer spreads in and destroys the subcutaneous tissue faster than it destroys the skin. Every healing ulcer has a sloping edge, which is reddish purple in colour and consists of new healthy epithelium, (iv) Raised and pearly-white beaded edge — is a feature of rodent ulcer. This type of edge develops in invasive cellular disease and becomes necrotic at the centre, (v) Rolled out (Everted) edge — is a characteristic feature of squamous cell carcinoma or an ulcerated adenocarcinoma. This ulcer is caused by fast growing cellular disease, the growing portion at the edge of the ulcer heaps up and spills over the normal skin to produce an everted edge. Marked induration of the edge is a characteristic feature of a carcinoma be it a squamous cell carcinoma or adenocarcinoma. A certain degree of induration or thickness is expected in any chronic ulcer, whether it is atrophic ulcer, gummatous ulcer or a syphilitic ulcer. When floor is covered with red granulation tissue, the ulcer seems to be healthy and healing. Wash-leather slough (like wet chamois leather) on the floor of an ulcer is pathognomonic of gummatous ulcer. A trophic ulcer penetrates down even to the bone, which forms the floor in this case. If an attempt is made to pick up the ulcer between the thumb and the index finger, the base will be felt. Slight induration of the base is expected in any chronic ulcer but marked induration (hardness) of the base is an important feature of squamous cell carcinoma and Hunterian chancre. Ulcers associated with mal-nutrition, anaemia, avitaminosis and rheumatoid arthritis are also included in this group. But these ulcers occur more commonly where the skin is closely applied to bony prominences e. Occasionally, particularly in older people, a single ulcer confined to the lower leg is due to chronic staphylococcal infection. These ulcers heal quickly and do not become chronic unless supervened by infection or ischaemia, which may turn this ulcer to chronicity. These occur in those parts of the limbs which are subjected to repeated pressure and trauma. Prolonged pressure on one part of the foot causes ischaemic damage to the tissues and if the circulation is inadequate then the tissues cannot repair themselves and ischaemic ulcer develops. These ulcers are mostly due to peripheral arterial disease and poor peripheral circulation. Atherosclerosis of the peripheral arteries is the commonest cause of this condition. It is due to episodes of trauma and infection that destroy the skin which fails to heal because of poor arterial supply. These ulcers tend to occur on the anterior and lateral aspects of the leg, on the toes, dorsum of the foot or the heel (the parts exposed to trauma). These ulcers tend to be punched out and destroy the whole skin and the deep fascia (unlike the venous ulcer) and may expose the tendons in the floor of the ulcer. The basic cause of venous ulcer is abnormal venous hypertension in the lower-third of the leg, ankle and dorsum of the foot. The neurological conditions which predispose to formation of such ulcer include diabetes, alcoholic peripheral neuritis, tabes dorsalis, spina bifida, leprosy, peripheral nerve injury, paraplegia and syringomyelia. These ulcers are commonly seen on the heel and ball of the foot when the patient is ambulatory; on the buttock and on the back of the heel when the patient is non-ambulatory. Trophic ulcers are included in this group which are caused by various factors such as impairment of nutrition of the tissues, inadequate blood supply and neurological deficit. These ulcers have punched out edge with slough in the floor thus resembling a gummatous ulcer. These ulcers develop as the result of repeated trauma to insensitive part of the body. Syphilitic ulcers are classified under the heading of specific group of ulcers and are not included here. Every effort should be made to detect the cause behind the ulcer and to treat accordingly. Pain is an important symptom and this is often accompanied by acute lymphadenitis. Gradually pustules develop and burst in two or three days forming ulcers whose edges are undermined and raised. Copious serosanguineous discharge with considerable pain is the most important feature. Such lesion results from excessive vasoconstriction of the skin arterioles of the affected area. When any part of the body is exposed to wet cold below freezing point, ischaemic changes occur in the skin and subcutaneous tissues. Such ischaemic changes are due to arteriolar spasm followed by stasis of blood in the capillaries. This alongwith exposure of the tissues below freezing point will lead to freezing of tissues and denaturation of intracellular protein with destruction of enzyme systems. These ulcers occur in patients over 50 years of age who are usually hypertensive or atherosclerotic. A local patch of skin on the back or outer side of the calf suddenly necroses and sloughs away leaving a punched-out ulcer FiS-H-3— Martorell’s ulcer. Pathology is sudden obliteration of the end arterioles of the skin of this region which is already having a sparse arterial supply from atherosclerosis. Since this is an ischaemic lesion, it has a long painful course and may take months to heal. These patients have thick ankles with abnormal amount of subcutaneous fat, combined with an abnormally poor arterial supply to the ankle skin. The blood supply of the lower-third of the leg and the ankle are derived from a number of fine perforating arteries arising from the posterior tibial and peroneal arteries. In erythrocyanoid cases these arteries may be abnormally small or even absent causing low grade ischaemia of the whole ankle region. The patient finds that the ankle skin is abnormally sensitive to temperature changes. In hot weather chronic reactive hyperaemia becomes evident with the ankle becomes hot, oedematous, swollen and painful. Palpation of the leg will reveal small, superficial and painful nodules which breakdown to form ulcers. Anything liable to cause an ulcer (incompetent perforating vein, trauma or infection) produces its effect much more quickly and in a more severe degree in the relatively ischaemic fat ankle.
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