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Stomach Cancer: StagesWhat does stage of cancer mean?The stage of a cancer is how much and how far the cancer has spread in your body. August 23, 2012Classification of ankle fractures is important in order to estimate the extent of the ligamentous injury and the stability of the joint. The Weber classification focuses on the integrity of the syndesmosis, which holds the ankle mortise together.
Adding the stages of Lauge-Hansen to the Weber system will help you to predict ligamentous injury and instability. This article will help you to correctly stage ankle injuries and to detect fractures, that are not obvious at first sight.
These fractures are identical to the fractures described by Lauge-Hansen as supination-adduction, supination-exorotation and pronation-exorotation.
We will first give a short overview of these fractures and then discuss them in more detail. Once you understand the trauma mechanism as described by Lauge-Hansen and the sequence of events that take place in stages, then you know where to look for fractures and ligamentous injuries. Stage 1 - Tension on the lateral collateral ligaments results in rupture of the ligaments or avulsion of the lateral malleolus below the syndesmosis.
Notice that the fibular fracture is transverse, because it is an avulsion or pull-off fracture. This is a transsyndesmotic fracture with usually partial - and less commonly, total - rupture of the syndesmosis. Weber B and C are more difficult and it is essential to understand the sequence of events in these injuries, which are both exorotation injuries. Another important thing to remember is, that a ligament can rupture or cause an avulsion fracture at the insertion. In daily practice most use the Weber system, which is easy to memorize, while the Lauge-Hansen seems rather difficult at first glance. Combining the simplicity of Weber with the explanation of the trauma mechanism given by Lauge-Hansen has the advantage that you still use a simple system, but now you really know what is going on.
For instance if you see a fracture that is a stage 2 in the Lauge-Hansen system, then you know that there also is a stage 1 injury and you will study the radiographs with a high suspicion for signs of stage 3 and 4.
If you would just report this as - a fracture of the malleolus tertius - you would miss the point.
When we look at the scheme we will notice that a fracture of the malleolus tertius in most cases is part of a Weber B or a Weber C fracture.
On the ankle films there was no sign of an oblique fracture of the lateral malleolus, so we can exclude a Weber B fracture.
At reexamination you notice the subtle avulsion of the medial malleolus (red arrow), which is stage 1. Additional radiographs of the lower extremity were ordered and they demonstrate a high fibular fracture, i.e. The point that I want to make is, that when you understand the sequence of injuries to the ankle, then you know where to look for fractures and soft tissue swelling indicating ligamentous injury. We will now discuss the Weber classification and add the stages of the Lauge-Hansen system. According to Lauge-Hansen the fracture results from an adduction force on the supinated foot.
The lateral side is under extreme tension with stretch on the ligaments which results in an avulsion fracture. This is called a pull off type of fracture in contrast to a push off type, which is seen as an oblique or vertical fracture.
More adduction force results in the medial malleolus being pushed off in a vertical or oblique way. Notice the horizontal orientation of the lateral malleolus fracture and the vertical orientation of the fracture of the medial malleolus. According to Lauge-Hansen the fracture results from an exorotation force on the supinated foot. What we normally see is a stage 2 oblique fracture through the syndesmosis and we have to assume that there is also a rupture of the anterior tibiofibular ligament, which is stage 1.
According to Lauge Hansen the first injury is on the lateral side, which is under maximum tension. In stage 2 the talus exorotates further and since the foot is in supination, the lateral malleolus is held tightly in place by the lateral collateral ligaments. As a result more rotation of the talus will fracture the fibula in an oblique or spiral fashion because the lateral malleolus is pushed off from anteromedially to posterolaterally. The oblique course of the fracture is typical for Weber B and results from the exorotation of the talus that pushes against the fixed lateral malleolus. The malleolar fracture usually starts medially at the level of the talar dome, but can also start a few centimeters above this level. Stage 3 More posterior displacement of the lateral malleolus fragment by the talus results in tension on the posterior syndesmosis with rupture or avulsion of the malleolus tertius. Stage 4 Further posterior movement of the talus will result in extreme tension on the medial side and the deltoid ligament will either rupture or pull off the medial malleolus in the transverse plane.
Immediately after the injury the injured parts may again align, which can make it difficult to detect the injuries. Rupture of the anterior syndesmosis - seen as widening of the space between the distal tibia and fibula (lateral clear space).
Now you start looking for stage 4 and you will notice the subtle lucency in the medial malleolus on the AP view (green arrow). The soft tissue swelling on the medial side is probably a rupture of the medial collateral band , i.e. It is the most difficult fracture to diagnose and the Lauge-Hansen system will help you to understand the fracture-mechanism, as this will be an enormous help. According to Lauge-Hansen the fracture results from an exorotation force on the pronated foot. Stage 1 The first injury will occur on the medial side, which is under maximum tension due to the pronation. It will lead to rupture of the medial collateral ligament or avulsion of the medial malleolus. Now the injury can stop and there will only be a rupture of the medial collateral ligaments or avulsion of the medial malleolus. We can not cathegorize this in the Weber classification, since there is no fibular fracture. The talus rotates externally and moves laterally because it is free from its medial attachment. Due to the pronation, the lateral ligaments are not under tension and the fibula can move away from the tibia.

Continuous force will twist the fibula and displace it distally, while proximally it is fixed to the tibia. Finally the interosseus membrane will rupture up to the point where the fibular shaft fractures. In many cases it is visible on the radiographs of the ankle, but in some cases the fracture is located high and will only be visible on a radiograph of the lower leg. There is an avulsion fracture of the medial malleolus and a fibula fracture above the level of the syndesmosis. According to Lauge-Hansen this is stage 3 pronation exorotation injury and so the anterior syndesmosis (stage 2) must also be ruptured. We do not see a tertius fracture, which would indicate stage 4, but there may be a rupture of the posterior syndesmosis. In fact this is an unstable ankle fracture, since there also must be a rupture of the medial collateral ligament (stage 1) , so the ring is broken in two places leading to instability. Finally the posterior syndesmotic ligament ruptures, or there is an avulsion of the posterior malleolus, also known as malleolus tertius fracture (red arrow). The medial clear space is only slightly widened, but based on the stages of Lauge Hansen there must be a collateral band rupture. The Lauge-Hansen classification will give you the fracture mechanism and the preliminary stage of the ankle injury.
Now re-examine the films to make sure that you do not overlook a higher grade ankle injury.
Describe the number of malleoli involved and whether there are signs of instability or dislocation.
ClassificationNot possible to classify according to Weber, but according to Lauge Hansen a medial avulsion fracture indicates that the foot probably was in pronation at the moment of injury.
You re-examine the x-rays to look for stage 2 (rupture or avulsion of the anterior syndesmosis), stage 3 (high fibular fracture = Weber C) or even stage 4 (rupture or avulsion of posterior syndesmosis). So at second look you notice a subtle widening of the lateral clear space on the original films, which could indicate but is definitely no proof of a syndesmotic rupture.
Although the patient is already in a cast you order additional films to look for a possible stage 3. According to Lauge Hansen the oblique fibular fracture indicates Supination Exorotation injury stage 2 or higher.
Look for stage 3 (posterior syndesmotic rupture or avulsion of the posterior malleolus) and stage 4 (rupture of the deltoid ligament or medial malleolar avulsion). The size of the posterior malleolar fragment is probably less than 25% of the articular AP-diameter and will need no separate repair.
Sometimes CT is needed to get a better impression of the size of the fracture fragment of the posterior malleolus. Fracture of the lateral malleolus starting anteriorly at the level of the joint extending proximally posteriorly. On the lateral view the posterior cortex of the tibia is interrupted indicating a fracture (blue arrow).
There is a widened medial clear space, which indicates a rupture of the medial collateral band, i.e.
Chronic Cholecystitis and Cholelithiasis: Gross natural color opened gallbladder with obviously thickened wall and fill-ed with faceted black calculi. Male hypogonadism is defined as the failure of the testes to produce androgen, sperm, or both.
Testosterone production declines with advancing age; 20% of men older than 60 years and 30% to 40% of men older than 80 years have serum testosterone levels that would be subnormal in their younger adult male counterparts.
Male factor infertility is probably responsible for one third of the 10% to 15% of couples who are unable to conceive within 1 year of unprotected intercourse. The physiologic regulation of the hypothalamic-pituitary-gonadal axis is shown in Figure 1.
Male hypogonadism is caused by a primary (hypergonadotropic) testicular disorder or is secondary (hypo- or normogonadotropic) to hypothalamic-pituitary dysfunction, as illustrated in Figure 3.
Persistent failure of the testes to descend may be an early manifestation of testicular dysfunction. Delayed, arrested, or absent testicular growth and secondary sexual characteristic development are hallmarks of pubertal disorders. The first manifestation of hypogonadism may be a consequence of a large space-occupying intrasellar or parasellar lesion manifested by headaches, bitemporal hemianopia, or extraocular muscle palsy.
Because of the well-known diurnal rhythm of serum testosterone, which appears to be lost with age (>60 years), with values 30% or so higher near 8 am versus the later day trough, a testosterone value should be determined first thing in the morning. If gonadotropin levels are not elevated, despite clearly subnormal testosterone values, anterior pituitary (thyroid-adrenal) function should be determined by measuring free thyroxine and thyroid-stimulating hormone levels, as well as an early morning cortisol level. Androgen replacement therapy is relatively straightforward; see Box 4 for testosterone preparations currently available in the United States. In genuinely hypogonadal men, testosterone administration can be expected to result in improvements in a variety of clinical areas (Box 6). Concerns regarding the use of testosterone have been noted in Box 5 and by Rhoden and Morgentaler.2 There is no evidence that the incidence of prostate cancer is increased by testosterone replacement. The aging man represents a special case and has been the subject of a review.4 There is a well-known decline in testosterone production with aging in otherwise healthy men. The ultimate issue as to whether these changes are normal and physiologic or should be considered pathologic, thus demanding therapy, remains unresolved. The American Association of Clinical Endocrinologists has published 2002 updated guidelines for the evaluation and treatment of hypogonadism in adult male patients.11 This review, geared particularly for endocrinologists, expands on some of the areas reviewed in this chapter and provides a more detailed look into aspects of male infertility.
The Endocrine Society has published clinical practice guidelines12 for testosterone replacement therapy.
Recommend diagnosis of androgen deficiency only in men with consistent symptoms and signs and with unequivocally low serum testosterone levels.
Rhoden EL, Morgentaler A: Risks of testosterone-replacement therapy and recommendations for monitoring. Bremner WJ, Vitiello MV, Prinz PN: Loss of circadian rhythmicity in blood testosterone levels with aging in normal men. Your healthcare provider uses exams and tests to find out the size of the cancer and where it is.
According to Lauge Hansen the oblique fibular fracture indicates that this is a Supination Exorotation injury stage 2 or higher. This apparent physiologic decline in circulating androgen levels is compounded in frequency by permanent disorders of the hypothalamic-pituitary-gonadal axis (see later).
Most of these male-associated cases result from diminished, absent, or faulty spermatogenesis.
In addition, a normally formed but hypotrophic penis may provide a clue to an abnormality of the hypothalamic-pituitary-gonadal axis.

Skeletal proportions may be abnormal (eunuchoid) with more than a 5-cm difference between span and height and between pubis-floor and pubis-vertex dimensions. Perhaps the minor contribution of adrenal androgens (or androgenic precursors) may substitute for testicular deficiency once the target tissues have been fully developed. Typically, the depot esters are administered by the deep intramuscular route once every 2 weeks at a dose of 200 mg in adults. Values are stable within a few days or weeks of the skin patch, gel, or newer buccal preparation. If the patient is truly hypogonadal to begin with, expect a significant rise at the 3-month assessment.
It should be noted that no long- term studies in large numbers of patients (neither young or old) have been performed, so potential risks and benefits need to be individualized. Least predictable are the effects on sexual function, cognitive function, and muscle strength.
The underlying concern is that it might alter the course of an occult malignancy estimated to be present in more than 50% of men older than 50 years. This decline in mean values can be seen in free testosterone levels, beginning in the mid-40s (some clinicians suggest even earlier), as a consequence of increasing SHBG levels, mechanism unknown.
Indeed, it is a situation analogous to the ongoing dilemma of hormone replacement therapy for postmenopausal women, although in this group the hormonal deficiency state is usually more abrupt and symptomatic. In addition to monitoring testosterone levels periodically, prostate screening by digital rectal examination and prostate specific antigen determinations at periodic intervals when the patient is on therapy should be carried out. He or she can also see if the cancer has grown into nearby areas, and if it has spread to other parts of your body.
These include the transient deficiency states associated with acute stressful illnesses, such as surgery and myocardial infarction, and the more chronic deficiency states associated with wasting illnesses, such as cancer and acquired immunodeficiency syndrome. In addition to abnormal sperm production, other conditions, including obstructive ductal disease, epididymal hostility, immunologic disorders, and erectile or ejaculatory dysfunction should be considered.
Some clinicians believe that the bioavailable fraction, the fraction present in the supernatant after ammonium sulfate precipitation, representing testosterone loosely bound predominantly to serum albumin, is more meaningful.
Unexplained osteoporosis or mild anemia sometimes is the clue to an underlying hypogonadal state. An exception to this recommendation is the condition of morbid obesity, in which both total and free testosterone levels are typically low and gonadotropin values not elevated. Greater increments tend to occur more frequently with the intramuscular than with the transdermal preparations. On the other hand, no one would recommend prophylactic castration to prevent prostate cancer so that, in my view, testosterone replacement in the hypogonadal man should not be avoided.
The IMCTA has not recommended a large-scale study to determine whether the risk for prostate cancer would be increased, because the costs of such a study were deemed to be too prohibitive. Measurement of free testosterone levels or bioavailable testosterone levels (performed adequately in select commercial laboratories) may provide additional information, in addition to serum follicle-stimulating hormone, luteinizing hormone, and prolactin levels. Finally, because combined female-male infertility is common, and fertility as well as psychological well-being are ultimate goals, both partners must be assessed from the outset. Hepatic SHBG production rises with aging and thyroid hormone excess and declines in hyperinsulinemic states (obesity and type 2 diabetes), so that free testosterone values may not always be concordant with total testosterone values. Certainly, prolactin excess, testosterone deficiency, or both in men may result in impaired libido and erectile dysfunction.
Although comparable testosterone levels are reached by the patch and the gels, skin reactions at the application site are much more common with the patch. These criteria continue to be revised by our urology colleagues, tending to become more stringent with time. Although there are genuine concerns about worsening of benign prostatic hyperplasia, this may apply only to severe cases with large prostate volumes. The diurnal rhythm, seen in younger men, is lost beyond 60 years.5 Although testicular volume also declines in this age group, spermatogenesis may be well maintained into the 80s or even beyond. The biologic effects of testosterone may be mediated directly by testosterone or by its metabolites 5α-dihydrotestosterone or estradiol (Fig. The yield of finding hyperprolactinemia or testosterone deficiency, or both, in patients presenting with these symptoms is generally considered to be low, usually less than 5%. The subject of androgen deficiency and the aging man is dealt with in greater detail later in this chapter.
Because the acute effect of stressful illness may result in a transient lowering of testosterone levels, a confirmatory early morning specimen should be obtained.
The major disadvantage with the parenteral route is that testosterone levels exhibit a saw-toothed pattern, with high-normal or supranormal levels on days 2 to 4 and low-normal or borderline low trough values before the next injection.
Gonadotropin levels tend to rise after 70 years, indicating that the testosterone deficiency is usually primary.6 Figure 4 schematically presents these hormonal changes with age. Alkylated oral androgens should be viewed as potentially hepatotoxic and should not be used. But it's not in the lymph nodes or other organs.It's in the inner layers of the stomach wall. For example, free testosterone levels may be lower than expected from the total testosterone level as a result of aging and higher than expected in insulin-resistant individuals, such as in obesity.
Useful criteria for selecting preparations for individual patients are summarized in Table 1. It has grown deeper than just the mucosa and has spread to up to one or two lymph nodes very close to the tumor.The cancer is in the inner layers of the stomach wall. In addition, serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin levels should be determined to help delineate the cause of the testosterone-deficient state.
It’s also spread to three to six lymph nodes that are near the tumor.It’s found in the inside layers, but has not grown through all the layers of the stomach wall. Cancer is also found in one or two nearby lymph nodes.The cancer has gone completely through all the layers of the stomach wall, including the lining outside the stomach. But it’s not in other nearby organs or tissues.It’s through the lining of the stomach and in the layer of the stomach wall (subserosa), but it’s not through all the layers to the outside of the stomach. It has spread to three to six nearby lymph nodes.It has penetrated through the inside layers of the stomach wall to the main muscle layer of the stomach. The cancer has spread to seven or more lympph nodes very close to the tumor.It has grown through the inside layers of the stomach wall to the subserosa layer, but it has not grown through all the layers (including the main muscle layer) or the outside lining. It has spread to seven or more nearby lymph nodes.The tumor has penetrated through all the layers of the stomach wall and has spread to nearby organs and tissues. It may come back in your stomach or in another part of the body, such as your liver or lymph nodes.Talking with your healthcare providerOnce your cancer is staged, your healthcare provider will talk with you about what the stage means for your treatment.

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