Medical anatomical knowledge center

Anatomical relations of the kidney

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<span style="color: blue;"><b>Anatomical relations of the kidney.</b></span> The axis of each <a href="http://imedicalcenter.blogspot.com/2015/07/anatomical-relations-of-kidney.html">kidney</a> is such that its lower pole lies farther from the midline and more anterior than its upper pole, causing the renal vessels and pelvis to exit the hilum in a relatively anterior direction. Anteriorly the right kidney lies behind the liver, separated from it by a reflection of peritoneum except for a small bare area of contact at the upper pole. This peritoneum forms the hepatorenal and the hepatocolic ligaments and excessive traction upon them during mobilization can produce hepatic tears. The duodenum is a direct medial relation of the right kidney and hilum; the hepatic flexure of the colon crosses its lower pole. See later section for the relationship to the adrenal glands.<br /> </div>
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The tail of the pancreas and the splenic vessels are anterior to the upper and middle portion and the hilum of the left kidney. Superiorly the left kidney is covered by the peritoneum of the lesser sac and the posterior gastric wall. Medially it is covered by the peritoneum of the great sac and the jejunum. The lower pole is crossed by the splenic flexure of the colon. Again the peritoneum in this region forms the splenorenal (linenorenal) and splenocolic ligament e traction upon which during operative mobilization can cause splenic bleeding. Both kidneys and associated suprarenal glands are surrounded by perirenal fat and are loosely enclosed by the renal fascia e Gerota’s fascia e which is an important anatomic and pathologic barrier. The anterior and posterior leaves of Gerota’s fascia extend anterior and posterior to the kidney to fuse<br />laterally, medially (where they extend across the midline and fuse densely to great vessels) and superiorly (where they fuse nd disappear over the inferior diaphragmatic surface). Inferiorly they do not fuse and there remains an open potential space containing the ureter and gonadal vessels on either side whichthins and is continuous with the retroperitoneal fascia. </div>
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Vasculature </div>
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The vascular pedicle composed of the posteriorly sited renal artery and more anteriorly sited renal vein enters the kidney via the renal hilum medially. The renal pelvis and ureter lie anterior to both in the hilum.<br />Arterial<br />The renal arteries leave the aorta at the level of the 2nd lumbar vertebral body. The right renal artery is longer than the left and travels posteroinferiorly behind the inferior vena cava to the lower right kidney. The shorter left artery passes horizontally and slightly posteriorly to reach the left kidney. The renal arteries provide small superior branches to the suprarenal glands and small inferior branches to the renal pelvis and upper ureter. The main renal artery divides into five segmental arteries, one posterior and four anterior; posterior, apical, upper, middle and lower. The posterior branch exits before the hilum and supplies a large posterior segment whilst the remaining anterior branches are given off in the hilum. All five are end arteries, without anastomosis or collaterals. These segmental arteries pass through the renal sinus and branch into the lobar and then interlobar arteries.<br /> </div>
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Venous<br />The venous drainage mirrors the arteries e with interlobar and lobar veins uniting to become segmental veins. These in turn unite in the region of the sinus to become the renal veins. The right renal vein is shorter and drains in the inferior vena cava. The longer left renal vein receives the right gonadal and suprarenal veins (and in some cases the ascending lumbar vein) before passing anterior to the aorta to drain in the inferior vena cava.<br /> </div>
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Lymphatic<br />The principal lymph drainage for the left kidney is to the left paraaortic lymph nodes and on the right to the right interaortocaval and paracaval lymph nodes. Suprarenal (adrenal) glands<br />Function<br />The adrenal glands are subdivided into a medulla that forms part of the sympathetic nervous system and secretes adrenaline (epinephrine) and noradrenaline (norepinephrine), and a cortex which secretes androgens and corticosteroids.<br /> </div>
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Microscopic anatomy<br />Each suprarenal gland is subdivided into two glands. They have a yellow external appearance with the mesodermal cortex enveloping the neural crest derived medulla.<br /> </div>
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Gross anatomy<br />These are paired glands situated superomedial to the kidneys e surrounded by perirenal fat and contained within Gerota’s fascia. They are attached to the diaphragmatic crura. The right suprarenal gland is tetrahedral and lies between the superior pole of the right kidney and the inferior vena cava and the left suprarenal gland is crescent shaped and lies on the superomedial border of the left kidney.<br /> </div>
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Vasculature<br />Arterial: the blood supply to both glands is from branches of the renal arteries, the inferior phrenic arteries and the aorta. Venous: the left suprarenal vein drains into the left renal vein whilst the right suprarenal vein drains directly into the inferior vena cava. Lymphatic: there are copious lymph vessels from the suprarenal glands e draining to the lumbar lymph nodes. </div>
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Ureters<br />Function<br />The ureters are paired hollow smooth muscular conduits for the active transport of urine into the bladder.<br />Microscopic anatomy. They are lined by transitional epithelium, outside this are two muscle layers (inner longitudinal and outer circular) continuous with that of the renal pelvis and calyces.<br />Gross anatomy<br />They descend bilaterally from the pelvi-ureteric junction in the retroperitoneum of the posterior abdominal wall on psoas major to the pelvic brim where they cross the bifurcation of the common iliac artery over the sacroiliac joint into the pelvis. In the pelvis the ureter runs over the external iliac artery and then continues down the pelvic sidewall anterior to the internal iliac artery. It turns anteriorly at the level of the ischial spine above the pelvic floor to enter the base of the bladder. In the male the ureter is crossed anteriorly by the vas deferens and in the female by the uterine artery.<br />There are three important narrowings of the ureteric lumen e at the pelvi-ureteric junction, crossing the iliac vessels and at the vesico-ureteric junction. Instrumentation and stones may get held up at these sites.<br /> </div>
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Vasculature<br />Arterial: for the proximal ureter is from the ureteric branch of the renal artery; the distal ureter gains its arterial supply from branches of the inferior and superior vesical arteries whilst the mid portion is supplied by an anastomosis of the gonadal artery with branches from the common iliac. Venous: drainage follows arterial supply. Lymphatic: upper e joins that of the kidneys or lumbar nodes, middle drains to the common iliac lymph nodes, the lower third drains to the common, internal or external iliac lymph nodes.<br />Nerve supply and pain<br />There is a sympathetic supply to the kidney from the 8th thoracic to 2nd lumbar nerves. The autonomic supply to the ureter is less clear. Pain signals travel with the sympathetic nerves leading to visceral pain (T8 to L2) distribution. This pain is referred along the genitofemoral nerve, ilioinguinal, iliohypogastric and subcostal<br />nerves and explains the flank, groin and scrotal pain of ureteric colic.</div>

Anatomical relations of the kidney. The axis of each kidney is such that its lower pole lies farther from the midline and more anterior than its upper pole, causing the renal vessels and pelvis to exit the hilum in a relatively a…

Surgical anatomy of the kidney and ureters

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Position and function<br />
<span style="color: blue;"><b><a href="http://imedicalcenter.blogspot.com/2015/07/surgical-anatomy-of-kidney-and-ureters.html">The kidneys</a> are paired solid organs </b></span>(11 cm 6 cm 3 cm) usually situated within the retroperitoneum on either side of the spine. They are responsible for:</div>
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<li>    urinary excretion</li>
<li>    fluid, electrolyte and acidebase balance</li>
<li>    vitamin D metabolism</li>
<li>    renin and erythropoietin production.</li>
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<b>Embryology</b><br />
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Three sets of structures appear and then regress in succession; the pronephros, the mesonephros and the metanephros e which persists to form the definitive kidney. In the male the persistent longitudinal collecting duct of the mesonephros e the mesonephric (or Wolffian) duct forms; the duct of the epididymis, the vas deferens and the ejaculatory duct, the efferent ductules of the testis, the superior and inferior aberrant ductules and the appendix of the epididymis.<br />
The mesonephric duct also gives rise to the ureteric bud in both sexes. Inferiorly this is absorbed into the bladder to become the trigone and part of the urethra, whilst superiorly it forms the ureter, the pelvis of the ureter, the major and minor calyces and the collecting ducts.<br />
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The metanephros is initially a pelvic organ, from weeks 6 to 9 of gestation there is progressive development and the kidneys ‘ascend’ the posterior abdominal wall e secondary to the relative growth of the body in the lumbosacral regions and the straightening of its curvature.  The ureter elongates as this ‘ascent’ occurs. The ‘ascending’ kidneys receive successive blood supply from lateral splanchnic arteries from the aorta until it reaches its final position opposite L2 vertebrae. Fusion of the lower poles of metanephric tissue results in a horseshoe kidney and alters the ascent and rotation of the developed kidneys. Failure of development or interaction between the ureteric bud and metanephros have been implicated in congenital anomalies such as renal dysplasia and multicystic dysplastic kidneys.<br />
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Microscopic anatomy<br />
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The outer cortex appears lighter and the inner medulla darker. The medulla is composed of the renal pyramids, each with a rounded apex, which points centrally into the renal sinus where it is cupped by an individual minor calyx (a renal lobe). The renal cortex covers the pyramids peripherally and extends between the pyramids to the renal sinus (the columns of Bertin).<br />
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<b>Gross anatomy</b><br />
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The gross anatomy of the kidney is shown in Figure 1. The renal capsule surrounds each kidney; it is a thin fibroelastic structure that encases the meat (parenchyma) and holds sutures whilst the parenchyma is very friable and will not. There is a depression (the hilum) on the medial surface of each kidney, which opens into the renal sinus e a central space surrounded by the renal parenchyma that contains the urinary collecting structures and renal vessels which exit the kidney via the hilum medially and varying amounts of fat. The kidneys are mobile and their position changes during respiration. The right kidney generally lies lower than the left due to the mass of the liver. The upper pole of the left kidney lies at the level of the 12th thoracic vertebrae and its lower pole at the 3rd lumbar vertebrae. The upper pole of the right kidney lies at the level of the 1st lumbar vertebrae and its lower pole at the bottom of the 3rd lumbar vertebrae.<br />
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Posteriorly the diaphragm (and the pleural reflection) covers the upper pole/third of each kidney. The 12th rib crosses on both sides at the lower edge of the diaphragm. The upper border of the left kidney extends to the upper border of the 11th rib. Any direct approach to the upper pole of either kidney risks entering the pleural space and this should be minded with all supracostal approaches. The medial portions of the lower two-thirds of both kidneys (with their associated renal vessels and pelvis) lie against the psoas muscle, whilst quadratus lumborum and the aponeurosis of transversus abdominus sit behind both kidneys.</div>

Position and function The kidneys are paired solid organs (11 cm 6 cm 3 cm) usually situated within the retroperitoneum on either side of the spine. They are responsible for: urinary excretion fluid, electrolyte and acide…

The Visual System Pathways to the Brain

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<span style="color: blue;"><b>The Visual System Pathways to the Brain.</b></span> The neural signals initially processed by the retina travel via the axons of the ganglion cells through the optic nerves, dividing and partially crossing over into the optic chiasm and then travelling via the optic tracts to the lateral geniculate nucleus (LGN). From the LGN, the signals continue to the <a href="http://imedicalcenter.blogspot.com/2015/06/the-visual-system-pathways-to-brain.html">primary visual cortex</a>, where further visual processing takes place.<br /> </div>
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<b>The optic nerves and optic tracts</b><br />The optic nerve of each eye consists of a bundle of approximately 1 million retinal ganglion cell axons. The nerve connects to the posterior aspect of the eye in a position that is about 15° nasal to the macula. The connection is referred to as the optic nerve head and is visible when looking into the eye using an ophthalmoscope. The optic nerve head is approximately 1.8 mm (0.07 in) in diameter. Since there are no photoreceptors (rods or cones) overlying the optic nerve head, there is a small blind spot or “scotoma” of approximately 5° in size about 15° temporal to fixation in the visual field of each eye. When both eyes are open, the blind spot of each eye is “filled in” by the visual field of the other eye. The optic nerves of each eye continue posteriorly and then meet at the optic chiasm. It is here that axons of neurons from the nasal retina (temporal visual field) cross to the opposite or “contralateral” optic tract (e.g. axons from the right eye temporal visual field cross to the optic tract on the left side of the brain). Axons of neurons from the temporal retina (nasal visual field) continue along the same side or “ipsilateral” optic tract (same side of the brain). This means that visual signals from the right side of the visual field are traveling to the brain via the left optic tract and signals from the left visual field are traveling via the right optic tract. Each optic tract terminates at its LGN.<br /><br /><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjSAb7o4E7bGKR_MmJCUWQfgtsEz0ilVLoCfJGoAVaT6haOOecjNBTrup5M5Lr4TrXhuifs45uXe1RF-jq3cg4DnWhJTQhhPs_ZgfNeFKyVLMYG5a8uNShgGXJlXYvg-r0zsj7uBSrQRek/s1600/the-visual-system-pathways-to-brain.jpg" style="margin-left: 1em; margin-right: 1em;"></a><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjSAb7o4E7bGKR_MmJCUWQfgtsEz0ilVLoCfJGoAVaT6haOOecjNBTrup5M5Lr4TrXhuifs45uXe1RF-jq3cg4DnWhJTQhhPs_ZgfNeFKyVLMYG5a8uNShgGXJlXYvg-r0zsj7uBSrQRek/s1600/the-visual-system-pathways-to-brain.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjSAb7o4E7bGKR_MmJCUWQfgtsEz0ilVLoCfJGoAVaT6haOOecjNBTrup5M5Lr4TrXhuifs45uXe1RF-jq3cg4DnWhJTQhhPs_ZgfNeFKyVLMYG5a8uNShgGXJlXYvg-r0zsj7uBSrQRek/s1600/the-visual-system-pathways-to-brain.jpg" /></a><br /><br />If a stroke, aneurism or tumor causes damage along the visual pathway, it is often possible to diagnose the exact location of the insult by measuring the visual field. For instance, a pituitary tumor would appear near the<br />optic chiasm and the impact on the visual field would be on the fibers that are crossing to the other side of the<br />brain. Since these fibers are from the nasal retina of each eye, the loss of vision would be in both temporal visual fields or a bitemporal visual field defect. Whereas an insult to one of the optic tracts would result in a loss of vision to the opposite or contralateral side of the visual field. For instance, a defect to the right optic tract would cause a loss of the left visual field of both eyes (the temporal visual field of the left eye and the nasal visual field of the right eye).<br /> </div>
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<b>The lateral geniculate nucleus (LGN)</b><br />The LGN is a paired structure located at the dorsal thalamus. It is here that visual information to the brain, specifically the visual cortex, appears to be regulated and the first stage of coordinating vision from both eyes<br />begins. Each LGN has six layers, three receiving input from the right eye and three receiving input from the left eye. Because of the way the retinal ganglion cell axons are distributed through the chiasm and on to the optic tracts, the information processed in any one layer of the LGN represents specific areas of the visual field for one eye. Four of the layers are composed of the Parvocellular (small) ganglion cells from the retina that are primarily from the fovea. These cells are most sensitive to color and fine detail. Two of the layers are composed of the Magnocellular (large) ganglion cells from the retina. These cells are mostly from the perifoveal and more peripheral retina and are largely responsible for the processing of motion. The LGN then sends forward neurons via the optic radiations to the primary visual cortex.<br /> </div>
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<b>The Visual Cortex</b><br />The visual cortex in the occipital lobe of the brain is where the final processing of the neural signals from the retina takes place and “vision” occurs. The occipital lobe is at the most posterior portion of the brain. There are a total of six separate areas in the visual cortex, known as the V1, V2, V3, V3a, V4 and V5.<br />The primary visual cortex or V1 is the first structure in the visual cortex where the neurons from the LGN synapse. In V1, the neural signals are interpreted in terms of visual space, including the form, color and orientation of objects. V1 dedicates most of its area to the interpretation of information from the fovea. This mapping is known as “cortical magnification” and is typical in primates and animals that rely on information from the fovea for survival. The signals then pass through to V2 where color perception occurs and form is further interpreted.<br />As the neural signals continue further into other areas of the visual cortex, more associative processes take place. In the portions of the visual cortex that make up the parietal visual cortical areas, motion of objects, motion of self through the world and spatial reasoning occur. In the temporal visual cortical areas, including the middle temporal (V5) area, recognition of objects through interpretation of complex forms and patterns occurs. The final psychological and perceptual experience of vision also includes aspects of memory, expectation/prediction and interpolation subserved by other apparently non-visual areas of the brain.</div>

The Visual System Pathways to the Brain. The neural signals initially processed by the retina travel via the axons of the ganglion cells through the optic nerves, dividing and partially crossing over into the optic chiasm and the…

The crystalline lens and ciliary muscle

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<span style="color: blue;"><b>The crystalline lens and ciliary muscle</b></span>. Like the cornea, the crystalline lens is a transparent structure. Unlike the cornea, it has the ability to change its shape in order to increase or decrease the amount of refracting power applied to light coming into the eye. Transparency is maintained by the regularity of elongated fiber cells within the lens. These cells originate at the equator of the lens and lay down across the surface of other fiber cells while growing toward the anterior portion of the lens and the posterior portion of the lens until they meet at the central sutures. During elongation they pick up crystallins, hence the name “<a href="http://imedicalcenter.blogspot.com/2015/06/the-crystalline-lens-and-ciliary-muscle.html">crystalline lens</a>.” It is these crystallins that give the lens a higher index of refraction than the aqueous and vitreous humors. The gradient index of refraction of the lens ranges from about 1.406 through the center to about 1.386 through the more peripheral portions of the lens (Hecht, 2002). This isdue to the fiber cells near the surface having a lower index of refraction than deeper cells, which results in a decrease in spherical aberrations and therefore a more refined quality of focus. The lens is surrounded by an elastic extracellular matrix known as the “capsule.” The capsule not only provides a smooth optical surface, but it provides an anchor for the suspension of the lens within the eye. A meshwork of nonelastic microfibrils or “zonules” anchor into the capsule near the equator of the lens and, much like a suspension system around a trampoline, connect into the ciliary muscle. When the ciliary muscle is relaxed, the tension on the zonules is highest and the lens is “pulled” to its flattest curvature. This generally results in focus for a distant object when the eye is emmetropic (e.g. does not have any refractive errors, such as myopia or hyperopia). When the ciliary muscle contracts, it moves slightly forward, but mostly inward towards the center line of the eye. This releases the tension on the zonules and allows the lens to take up its preferred shape, which is more rounded and thereby more powerful. This increases the focal power of the eye to focus on nearby objects.</div>
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Since the lens continues to lay down fiber cells throughout life, it becomes denser and less flexible resulting in</div>
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a loss of the ability to change focus for near objects with age. This process called presbyopia will be covered in a later chapter. A cataract is a condition in which the crystalline lens starts to develop opacities or lose its</div>
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transparency. Cataracts can be associated with environmental factors such as smoking, health conditions such as diabetes, or the use of certain medications such as corticosteroids (Delcourt et al., 2000; Rowe et al., 2000). The effect of cataracts on vision is generally a reduction in contrast sensitivity, an increase in glare and halos at night and some shift in color sensitivity due to the “yellowing” of the lens.</div>
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The Posterior Segment of the Eye The retina lines the interior of the posterior portion of the globe and is where images are formed. Initial processing of the image occurs at this highly specialized sensory tissue. Vitreous is the clear gel that fills the posterior segment and serves to provide for light transmission through the eye and to protect the retina.</div>
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<u><b>The retina</b></u></div>
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The retina is a mostly transparent thin tissue designed to capture photons of light and initiate processing of the</div>
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image by the brain. The average thickness of the retina is 250 μm and it consists of 10 layers. From the surface of the retina to the back of the eye the layers are the inner limiting membrane, the nerve fiber layer</div>
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(axons of the ganglion cells), the ganglion cell layer, the inner plexiform layer (synapses between ganglion and</div>
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bipolar or amacrine cells), the inner nuclear layer (horizontal, bipolar amacrine and interplexiform cells, along</div>
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with the retina spanning glial cells), the outer plexiform layer (synapses between bipolar, horizontal and photoreceptor cells), the outer nuclear layer (photoreceptor cells), the outer limiting membrane, the receptor layer (outer and inner segments of the photoreceptor cells) to the retinal pigment epithelium (RPE). The RPE is the outmost layer of the retina and serves as the primary metabolic support for the outer segment of the receptor cells and also acts as the final light sink for incoming photons that reduces intraocular glare. Its light absorbing pigmentation is why the pupil appears black.</div>
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The fact that the receptor layer is deep within the retina means that photons of light actually must pass through most layers of the retina before reaching the receptors. The receptors absorb and convert photons to neural signals, which are than processed through the network of bipolar, horizontal, amacrine and ganglion cells. The output axons of the ganglion cells form the nerve fiber layer that collects at the optic nerve to exit the eye. It’s the intricate interconnections of the various neural cells in the retina that complete the first processing of the visual information being sent to the brain. There are two types of receptors in the receptor layer, rods and cones, essentially named for their shape. The outer segment of the receptor cells contain the light sensitive visual pigment molecules called “opsins” in stacked disks (rods) or invaginations (cones). There are approximately 5 million cones and 92 million rods in the normal adult retina. Cones provide the ability to discern color and the ability to see fine detail and are more concentrated in the central retina. Rods are mainly responsible for peripheral vision, vision under low light conditions and are more prevalent in the mid-peripheral and peripheral retina.</div>
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At the most posterior aspect of the retina, where most of the light that the eye receives is focused, is a region</div>
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called the macula lutea. The macula is an area approximately 5 to 6 mm in diameter which has a greater density of pigments (lutein and zeaxanthine). These pigments help to protect the retinal neural cells against oxidative stress. Within the macular area is the fovea centralis, the small region at the center of the retina where vision is most acute. In this small 1.5 mm (0.06 in) diameter area there are no rods, only cones and the overlying neural layers are effectively swept away so that there is a depression in the retina. The average thickness of the retina drops to around 185 ìm in this “foveal pit.” The area immediately outside the fovea is called the parafoveal region and is where there is a transition from cone-dominated to rod-dominated retina.</div>
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The retina receives its nourishment from two sources, the retinal vasculature serves the inner layers of the retina and the choroidal vasculature, which lies between the RPE and the sclera, serves the metabolically active RPE and outer layers of the retina. In order to maximize photon capture in the central retina, the retinal capillary system does not extend in to the fovea centralis, an area known as the foveal avascular zone. This area depends on the blood supply provided by the choriocapillaris.</div>
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One of the most common conditions that can affect the retina is age-related macular degeneration (ARMD), in which there is a loss of vision in the center of the visual field (Klein et al., 2004; Nicolas et al., 2003; van</div>
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Leeuwen et al., 2003). In ARMD, the ability of the retinal pigment epithelium to remove the waste produced by the photoreceptor cells after processing light coming into the eye is reduced. As a result, waste builds up in the form of “drusen.” These drusen further disrupt the metabolic process and eventually the retina starts to deteriorate. If blood vessels from the choriocapillaris break through (“wet ARMD”) the condition can become significantly worse. ARMD is generally hereditary and early signs are detectable through routine eye exams.<br />
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<b>The vitreous humor</b><br />The vitreous body is a gel-like structure that fills the posterior portion of the globe. Vitreous humor is comprised of collagen fibrils in a network of hyaluronic acid and is a clear gel (Kaufman and Alm [eds.], 2003). The vitreous body is loosely attached to the retina around the optic nerve head and the macula and more firmly attached to the retina at the ora serrata just posterior to the ciliary body. The connections at the anterior portion of the vitreous body help to keep the anterior and posterior chamber fluids separated. The connections around the optic nerve and macula help to hold the vitreous body against the retina.<br />With aging, the vitreous starts to liquefy and shrink. When this happens, aqueous from the anterior chamber can get into the posterior chamber of the eye. Additionally, there can be increased tugging at the attachment points on the retina causing a release of cells that the individual sees as “floaters.” If there is significant traction at the attachment points, the retina can be pulled away from the inner globe and a retinal tear or detachment can result. </div>

The crystalline lens and ciliary muscle. Like the cornea, the crystalline lens is a transparent structure. Unlike the cornea, it has the ability to change its shape in order to increase or decrease the amount of refracting power …

The aqueous humor

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<tr><td class="tr-caption" style="text-align: center;">The aqueous humor</td></tr>
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<span style="color: blue;"><b>The aqueous humor.</b></span> The fluid that fills the anterior chamber of the eye, that area between the cornea and the front surface of the crystalline lens, is called the aqueous humor. Aqueous is produced by the ciliary body that is just posterior to the root of the iris and extends backwards along the inner globe to the anterior aspect of the retina.. Aqueous finds its way into the anterior chamber by flowing between the crystalline lens and the iris through the pupil. Aqueous has two functions; it provides nutrients to the cornea and is part of the optical pathway of the eye. <a href="http://imedicalcenter.blogspot.com/2015/06/the-aqueous-humor.html">Aqueous humor</a> is basically a fortified blood plasma that circulates in the anterior chamber, providing nutrients to the cornea and the crystalline lens. It is a transparent fluid with an index of refraction of 1.333, which is slightly less than the index of refraction of the cornea (1.376) and less than the index of refraction of the lens (gradient index of 1.406 to 1.386). As is discussed in another chapter, it is these differences in index of refraction between media coupled with the curvature of the various optical surface interfaces that result in the bending of light at each interface.<br /> </div>
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As nutrients are drawn from the aqueous into the cornea by the endothelium, the aqueous fluid is circulated out of the eye and replaced by newly produced aqueous produced. To move out of the anterior chamber, it flows out of the eye primarily through the trabecular meshwork, a “drainage” system that lies behind the limbus in the angle between the cornea and the anterior iris. There is some resistance to outflow of aqueous at the trabecular meshwork that serves to maintain a pressure within the eye of approximately 15 mmHg. If there were no resistance, the eye would lose its shape and therefore its optical integrity. If there is too much resistance (or too much production of aqueous), the pressure in the eye may exceed the eye’s tolerance and damage to the optic nerve may occur, a condition known as “glaucoma.” Glaucoma generally results in a loss of mid-peripheral vision with sparing of central vision until the condition has progressed significantly. It is most commonly hereditary with a higher prevalence in certain ethnic groups (Friedman et al., 2004; Leske, 2007; Rivera, Bell, and Feldman, 2008; Wadhwa and Higginbotham, 2005); however, it may occur in individuals without a family history of glaucoma or may result secondarily to blunt trauma to the eye Cavallini et al., 2003; Kenney and Fanciullo, 2005; Sihota, Sood, and Agarwal, 1995).<br /> </div>
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Glaucoma can be slowly progressive, as in the case of primary open angle glaucoma (POAG) or low tension<br />glaucoma (LTG), and the loss of vision may be initially barely noticeable. A third type of glaucoma, angle closure glaucoma (ACG), is more acute and may or may not be accompanied by pain in and around the eye when it occurs (Ang and Ang, 2008; Congdon and Friedman, 2003). During routine eye exams, measurement of intraocular pressure and assessment of visual fields are essential for early detection of glaucoma.<br /> </div>
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<b>The iris</b><br />The iris is visible through the cornea and is what gives the eye its “color.” All irides have a dark pigmented posterior layer; it is the amount of pigment in the anterior or stromal layer that produces different colors. A “blue” eye results from the selective absorption of long wavelength light by the stroma of the iris and the reflection of short wavelength (blue) light by the posterior pigmented layer. In a “brown” eye almost all visible wavelengths are absorbed by the iris stroma and very little light is left to reflect out of the eye.<br /> </div>
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<tr><td class="tr-caption" style="text-align: center;">The Iris, Cornea and Lens</td></tr>
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The main purpose of the iris, however, is to block excess light from entering the eye and to control the iris aperture or “pupil” for differing amounts of ambient light (Figure 6-2). There are two opposing muscles in the iris; the sphincter muscles that serve to constrict the pupil and the dilator muscles that serve to dilate the pupil. Parasympathetic nerves innervate the sphincter muscles and sympathetic nerves innervate the dilator muscles. It’s because the sympathetic system is heightened relative to the parasympathetic system during “fight or flight” situations that pupils dilate when danger is sensed. Most pupil responses are controlled by a complex set of signals sent through the midbrain (specifically the Edinger-Westphal nucleus) in response to the amount of light striking the retina or as part of the accommodative triad (discussed in Chapter 7, Visual Function). There are very few conditions that affect the iris directly; however, changes in the normal response of the pupil to light or accommodation can result from lesions in the neural pathways or direct trauma to the iris. If the iris does not constrict in response to light, likely the parasympathetic system has been affected by such conditions known as Adie’s tonic pupil or third nerve palsy. This lack of constriction may also occur in response to anticholinergic drugs, such as found in scopolamine patches, or adrenergic drugs, such as found in some eye drops used for “red eye.” If the iris fails to dilate under low light conditions, likely the sympathetic system has been affected by a condition known as <i>Horner’s syndrome</i>.</div>

The aqueous humor The aqueous humor. The fluid that fills the anterior chamber of the eye, that area between the cornea and the front surface of the crystalline lens, is called the aqueous humor. Aqueous is produced by the ciliar…

The Protective Structures of the Eye

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<span style="color: blue;"><b>The Protective Structures of the Eye.</b></span> The two orbits, sometimes referred to as “sockets,” that protect the human eyes are situated at the front of the skull, each with a wider opening to the front narrowing to a small opening at the rear where the optic nerve exits to connect through the visual pathways and the brain. The orbits are angled outward approximately 23° with respect to the midline of the skull. The human eye itself is approximately 24 millimeters (mm) (0.94 inches [in]) in diameter and occupies about 25% of the volume of the orbit, allowing for the extraocular muscles, blood vessels, nerves, orbital fat and connective tissue that surround and support the eye (Figure 6-1). The orbit surrounds and supports most of the human eye, while the cornea and part of the anterior globe extend somewhat beyond the orbital rims. These structures are protected by the eyelids.</div>
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<tr><td class="tr-caption" style="text-align: center;">Figure 6-1. The position f the eye in its socket (Wolff, 1933).</td></tr>
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The upper and lower eyelids form an aperture that is generally 30 mm (1.2 in) wide and 10 to 12 mm (0.4 to 0.5 in) high when the eye is “open.” The lids themselves have cartilage-like tarsal plates within their structure that provide shape to the lids and additional strength for protection of the eye. Each lid has a row of cilia or eyelashes that are very sensitive to touch or particles near the eye, which when stimulated bring on the blink reflex. The lids also contain the glands responsible for maintenance of the tear layer. The globe itself is predominately formed of and protected by the sclera that extends from the edges of the clear<br />
cornea at the front of the eye (the “limbus”) to the optic nerve at the back of the eye. The sclera is a thick, opaque white tissue that covers 95% of the surface area of the eye. It is approximately 530 microns (μm) in thickness at the limbus, thinning to about 390 μm near the equator of the globe and then thickening to near 1 mm (0.04 in) at the optic nerve. At the posterior aspect of the eye, the sclera forms a netlike structure or “lamina cribrosa” through which the optic nerve passes. The sclera also serves as the anchor tissue for the extraocular muscles.<br />
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<b>The Anterior Segment of the Eye</b></div>
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The portion of the eye visible to the observer without special instrumentation is considered the anterior (or<br />
“front”) segment of the eye. Most of the structures responsible for focusing images onto the <a href="http://imedicalcenter.blogspot.com/2015/06/the-protective-structures-of-eye.html">retina of the eye</a> are here. The cornea is the primary focusing structure, providing about 75% of the focusing power of the eye. The crystalline lens provides the remaining variable focusing power and serves to further refine the focus, allowing the eye to focus objects at different distances from the eye. The iris controls the aperture or pupil of the eye for different light levels. The iris is actually an extension of the ciliary body, a structure that has multiple functions in the anterior segment, from production of the fluid that fills the anterior segment (aqueous humor) to suspension and control of the shape of the crystalline lens of the eye. Figure 6-2 shows most of the major structures of the human eye, including the components of the anterior segment, the protective sclera and the posterior segment (described in the next section).<br />
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<b>The cornea</b><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg1vqQFmBWB-TwGS7kApRn4JnphymH3lwa02Oe-1q_9QmJEQDoHyc4It6W36pyKAl_mX3drP4B9BzL6GvB8kEcA_TBfzuzNaRBdRwaIyv-_PpAuF1oDmrvDjqP5r65Gnebegde_y5N6BFw/s1600/cornea-structure.jpg" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg1vqQFmBWB-TwGS7kApRn4JnphymH3lwa02Oe-1q_9QmJEQDoHyc4It6W36pyKAl_mX3drP4B9BzL6GvB8kEcA_TBfzuzNaRBdRwaIyv-_PpAuF1oDmrvDjqP5r65Gnebegde_y5N6BFw/s1600/cornea-structure.jpg" /></a>The cornea is a unique biological tissue that is transparent to light and contains no blood vessels. This small transparent dome at the front of the eye is approximately 11 mm (0.43 in) in diameter and 500 μm thick in the center, thickening to around 700 μm at the periphery. At the very edge of the cornea, transparency is slowly lost over a 1-mm (0.04-in) range in an area known as the “limbus”, which is where the cornea integrates into the opaque sclera. The cornea is more curved than the rest of the globe with an average radius of curvature of 7.7 mm (0.3 in), while the radius of curvature of the globe is approximately 12 mm (0.5 in).</div>
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<tr><td class="tr-caption" style="text-align: center;">Figure 6-2. Cross-sectional view of the eye (http://www.gimbeleyecentre.com/images/<br />
Cross_Section_Labelled.gif).</td></tr>
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With the primary function of transmitting and focusing light into the eye, all the structures of the cornea are very specifically arranged (Figure 6-3). About 90% of the cornea is made up of evenly spaced collagen fibrils arranged in sections that crisscross to cover the entire extent of the cornea. This layer is known as the “stroma” and it provides not only transparency, but strength. Four more layers make up the remaining 10% of the cornea, the epithelium and Bowman’s layer at the front of the cornea and Descemet’s membrane and the endothelium at the back of the cornea. The epithelium of the cornea, much like the epithelium of the skin, serves as a barrier to bacteria or other pathogens.<br />
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Additionally, the epithelium helps to maintain the stroma at a proper level of hydration by preventing fluid from entering the stroma through its tight cell junctions and the pumping of a small portion of fluid out of the stroma. Bowman’s layer is a very thin (12 μm) membrane right beneath the epithelium and, in mammals, is only found in primates. Its purpose is not entirely known, although it may aid in protection of the stroma. At the back or posterior aspect of the cornea is another very thin membrane called Descemet’s membrane that is between 10 to 15 μm thick. It also is felt to have some protective function. The endothelium is a single layer of cells at the very posterior aspect of the cornea. The endothelium is in direct contact with the aqueous humor, the fluid that fills the anterior chamber of the eye. The endothelium pumps nutrients, such as glucose, from the aqueous humor into the cornea while actively pumping fluid out of the cornea. The hydration balance maintained by the endothelium and somewhat assisted by the epithelium is important to the transparency of the cornea, since excess fluid would disturb the regularity of the corneal fibrils and result in increased light scatter. In mild cases of edema, such as may occur when contact lenses are worn too long or under hypoxic conditions, the cornea may become slightly cloudy (Jones and Jones, 2001; Liesegang, 2002; Morris et al., 2007). Under more extreme conditions, such as anoxic conditions, or in cases of endothelial dystrophies, the swelling of the stroma could result in complete opacity of the cornea. </div>

The Protective Structures of the Eye. The two orbits, sometimes referred to as “sockets,” that protect the human eyes are situated at the front of the skull, each with a wider opening to the front narrowing to a small opening at …

Basic Anatomy And Physiology Of The Human Visual System (Eye Anatomy)

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<span style="color: blue;"><b>Basic Anatomy And Physiology Of The Human Visual System (Eye Anatomy). </b></span>The human eye is a complex structure designed to gather a significant amount of information about the environment around us. It is the sensor used by the Warfighter in the visually-rich battlespace. In designing a head/helmet-mounted display (HMD) system for the <a href="http://imedicalcenter.blogspot.com/2015/06/basic-anatomy-and-physiology-of-human.html">Warfighter, the human visual system</a> (which begins with the eyes) could be considered as an integral component of the HMD and not as a separate and different system that subsequently is mated with the HMD. It is therefore important that HMD designers have an understanding of both anatomy and function of the human eye itself.<br />
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The functional operations of the human eye, its pointing and tracking mechanisms and the integration into a binocular visual system will be described. In this chapter, the goal is to provide the HMD designer with a basic understanding of the anatomy and physiology of this critical element of the human visual system. This chapter provides a brief overview of the visual system (inclusive of the eye organ itself), beginning at the front surface of the eye and progressing to the primary visual cortex at the back of the brain. Topics include:<br />
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• The Protective Structures of the Eye<br />
<ul>
<li>The Orbit</li>
<li>The Lids</li>
<li>The Sclera</li>
</ul>
• The Anterior Segment of the Eye<br />
<ul>
<li>The Cornea</li>
<li>The Aqueous Humor</li>
<li>The Iris</li>
<li>The Crystalline Lens and Ciliary Muscle</li>
</ul>
• The Posterior Segment of the Eye<br />
<ul>
<li>The Retina</li>
<li>The Vitreous Humor</li>
</ul>
• The Visual System Pathways to the Brain<br />
<ul>
<li>The Optic Nerves and Optic Tracts</li>
<li>The Lateral Geniculate Nucleus</li>
<li>The Visual Cortex</li>
</ul>
For more detailed discussions of the human eye’s anatomy and physiology, the reader should refer to the large volumes of texts available, e.g., Adler’s Physiology of the Eye (Kaufman and Alm [Eds.], 2003).</div>

Basic Anatomy And Physiology Of The Human Visual System (Eye Anatomy). The human eye is a complex structure designed to gather a significant amount of information about the environment around us. It is the sensor used by the Warf…

Biomechanics of the Lateral Side of the Knee

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<a href="http://imedicalcenter.blogspot.com/2015/06/biomechanics-of-lateral-side-of-knee.html"><b><span style="color: blue;">BIOMECHANICS</span></b></a>. The primary function of the structures of the lateral and posterolateral knee are to resist varus rotation, external tibial rotation, and, to a lesser extent, posterior tibial translation. Several biomechanical studies have shown the FCL, popliteus tendon, and popliteofibular ligament to be the most important stabilizing structures of the posterolateral knee.12,17,22–25  The posterolateral structures act in concert with the PCL in providing overall stability of the knee. The complex anatomy of the knee does not allow pure rotational or translational motions to occur.  Normal biomechanics of the knee, and abnormal pathomechanics, are the result of complex coupled rotations and translations. This section discusses posterolateral biomechanics, including anterior-posterior translation, varus-valgus rotation, and internal-external rotation. In addition, the role of intra-articular pressures, osseous configurations, and meniscal configurations will also be addressed.<br />
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<b>OSSEOUS AND MENISCI</b><br />
In the majority of the population, the normal mechanical axis of the lower extremity lies slightly medial to the center of the knee. To achieve balance in the stance phase of gait, compressive forces are transmitted through the medial compartment of the knee whereas the lateral structures are under significant tension. During the normal gait cycle, the lateral ligamentous structures of the knee are subjected to greater forces than the medial ligamentous structures and are appropriately more substantial and stronger.11<br />
Likewise, the bony anatomy of the lateral compartment of the knee is quite different from the medial compartment. The medial femoral-tibial compartment has an inherently stable ‘‘cup’’ formation. The convex medial femoral condyle rests in the concavity of the medial tibial plateau. On the contrary, the lateral compartment of the knee is inherently unstable as the convex lateral femoral condyle articulates with a convex lateral tibial plateau. Without additional support these 2 convex surfaces would have minimal surface contact, high contact stresses, and very little stability. The inherently unstable bony geometry of the lateral compartment allows greater motion than the medial compartment, but relies on the posterolateral soft tissue structures to provide the required stability. The roles of the medial and lateral menisci parallel the roles of the medial and lateral osseous compartments. Both menisci add stability to their respective compartments, but the lateral meniscus must do so when accommodating the relatively greater range of motion of the lateral compartment. The lateral meniscus contributes to lateral knee stability by adding concavity to the lateral tibial plateau. To preserve its increased motion across the tibial plateau, it has less restraining static meniscotibial attachments than the medial meniscus, and is dynamically stabilized by a branch of the popliteus tendon. <br />
Because the lateral meniscus is less restrained, it is also less stable than the medial meniscus. This permits it more motion across the tibial plateau with flexion and extension of the knee. The increased excursion of the lateral meniscus limits its ability to compensate for the unstable bony geometry of the lateral tibiofemoral compartment. Therefore, the remaining soft tissues of the PLC must provide significant stability to the lateral side of the knee.25<br />
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<b>ANTERIOR-POSTERIOR TRANSLATION</b><br />
The primary restraint to anterior translation of the tibia relative to the femur is the ACL. It accounts for about 86% of the total resistance to anterior tibial translation.11 Although the posterior horn of the medial meniscus provides some support to this role, especially in the ACL-deficient knee, it is easily injured when the ACL<br />
is compromised. This indicates the minimal amount of support the ACL receives in this role and the necessity of reconstructing it when it is deficient. Several studies have demonstrated that the posterolateral structures do not prevent primary anterior tibial translation.26,27 However, like the posterior horn of the medial meniscus, the PLC helps prevent anterior tibial translation in the ACL-deficient knee. The role of the PLC seems to be more prominent near extension, whereas the role of the posterior horn of the medial meniscus is<br />
more noticeable in flexion. This can be demonstrated on physical examination. Typically, an ACL-deficient knee, with an intact posterior horn of the medial meniscus and a torn PLC, will have a markedly positive Lachman test (greater than +2) and a subtle (grade 1) anterior drawer. Conversely, an ACL-deficient knee, with a torn posterior horn of the medial meniscus and an intact PLC, will have a positive anterior drawer and positive Lachman test. However, in the later example, the Lachman test may not be as prominent. Clinically, if an ACL is reconstructed in a knee with a PLC injury, the reconstructed graft will be at higher risk of failure unless the PLC injury is addressed. This underscores the need to thoroughly exam the PLC in all ACL-deficient knees, before reconstruction.</div>
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Resistance to posterior tibial translation is far more complex. The stout and centrally located PCL is the primary static stabilizer of the knee and plays a strong role in resisting posterior tibial translation. It provides<br />
95% of the total restraint to posterior tibial displacement forces at all flexion angles.11,22 With the knee in near full extension, isolated sectioning of the posterolateral structures results in increased posterior translation of the lateral tibial plateau. As the knee is flexed to 90 degrees, there is minimal posterior translation. In PCL-deficient knees with transected posterolateral structures, posterior tibial translation of the medial and lateral tibial plateaus is appreciated at 30 and 90 degrees of flexion. Thus, the posterolateral structures are important in resisting posterior tibial translation at small flexion angles (eg, 30 degrees). The PCL and PLC structures work in concert, and injury to both of these structures results in a significant increase in posterior translation of the knee at all flexion angles.23,24<br />
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The popliteus is a dynamic stabilizer that assists the PCL by resisting posterior tibial translation. In the intact knee, loading the popliteus has been shown to reduce the in situ forces in the PCL by 9% and 36%, at 90 and 30 degrees of flexion, respectively.28 In the PCL-deficient knee, loading the popliteus has been shown to reduce posterior tibial translation by up to 36%. This amounts to a reduction of posterior translation by approximately 2 to 3 mm. The results of this study confirm that the popliteus muscle complements the PCL in resisting posterior tibial loads and can contribute to knee stability when the ligament in absent.27,28 In a combined PCL and PLC injury model, Harner et al29 demonstrated that a deficiency of the PLC increased posterior tibial translation, in the PCL reconstructed knee, by 4.6 to 6.0 mm. They found a corresponding increase in the in situ forces in the PCL graft of 22% to 150%, if the posterolateral structures were not<br />
repaired or reconstructed. These results demonstrate that an isolated PCL graft reconstruction is rendered ineffective and may be overloaded if the posterolateral structures are deficient. Although the PCL provides the greatest contribution to resisting posterior tibial translation, both biomechanical and clinical studies have shown that it cannot function appropriately in a knee with a deficient PLC. Conversely, clinical studies have demonstrated that many individuals can function with an isolated rupture of the PCL, although their biomechanics may not be identical to that of a healthy knee. These studies demonstrate the importance of a fully functional PLC in resisting posterior tibial translation, and the necessity of repairing or reconstructing the PLC when it is compromised.<br />
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VARUS-VALGUS ROTATION<br />The FCL is the primary restraint to varus stress at all flexion angles of the knee. LaPrade et al30 found that varus forces on the FCL had loading responses from 0 to 90 degrees of flexion, with the greatest being at 30 degrees (12 N/J). Although other soft tissues provide additional support in this function, the FCL receives the least support at 30 degrees of flexion. This makes the FCL most susceptible to injury at 30 degrees of flexion. It has been shown that approximately 300N of force is required to cause failure of this ligament.17 The PCL is considered a secondary restraint to varus rotation; however, sectioning of this structure with an intact FCL does not affect varus rotation. Conversely, when the PLC is deficient and the PCL is intact, the PCL will provide some resistance to varus stress, but it is not as effective in this role as an intact PLC. In a combined PCL and PLC injury model, Harner et al29 demonstrated that a deficiency of the posterolateral structures after PCL reconstruction increased varus rotation up to 7 degrees. Grood et al23 and Veltri et al31 reported that an increase in varus rotation (as much as 19 degrees) can be appreciated with the combined sectioning of the PCL and posterolateral structures. This varus rotation occurred throughout all angles of knee flexion, with the maximal increase observed at 60 degrees. The posterolateral structures act as the primary restraint to varus rotation especially at lesser degrees of knee flexion (maximal restraint at 30 degrees). The PCL acts as secondary restraint that is most noticeable when the PLC is compromised. The PCL is more effective at resisting varus stresses at greater degrees of knee flexion (60 degrees). To a lesser degree, dynamic resistance to varus rotation is provided by the iliotibial band, biceps femoris muscle tendon complex, and lateral gastrocnemius.9<br /><br />INTERNAL-EXTERNAL ROTATION<br />The popliteus complex is usually considered the primary restraint to external rotation of the knee. However, recent studies have shown that this function is shared by the FCL. In selective cutting studies, several authors have demonstrated that sectioning of the FCL, popliteus tendon, and deep ligaments of the lateral knee created increases in external rotation at all angles of knee flexion.22,28 Further studies have identified the specific roles of the FCL and the popliteus complex in resisting external rotation. In a recent cadaveric study, LaPrade et al30 found that the FCL resisted greater external rotation forces in the early range of knee flexion (0 to 30 degrees) when compared to the popliteus complex. The external rotation moment responses for the FCL were fairly constant from 0 to 60 degrees of knee flexion, averaging approximately 10 N/J. The mean load response peaked at 30 degrees of flexion (20 N/J) before falling to 8.1 N/J at 90 degrees of flexion. The popliteus tendon and popliteofibular ligament became more highly loaded by an external rotation torque with higher amounts of knee flexion. The popliteus tendon and the popliteofibular ligament had similar loading patterns to an external rotation torque, from 0 to 90 degrees of knee flexion. Their mean load response generally increased with increasing knee flexion, peaking to approximately 13 N/J at 60 degrees of knee flexion (FCL 10 N/J) before slightly declining to 10 N/J at 90 degrees.30 Therefore, the FCL is the primary restraint to external rotation from 0 to 30 degrees, whereas the popliteus complex (popliteus tendon and popliteofibular ligament) assumes a more important primary role in resisting external rotation at knee flexion angles greater than 60 degrees. The PCL is a secondary stabilizer in resisting external rotation of the tibia. Isolated sectioning of the PCL does not increase external tibial rotation when the PLC is intact. The role of the PCL as a secondary stabilizer becomes significant when the PLC is compromised. In a PCL-intact knee, isolated sectioning of the posterolateral structures increased external rotation of the lateral tibial plateau, with maximal external rotation (average 13 degrees) demonstrated at 30 degrees of knee flexion. At 90 degrees of flexion, a smaller amount (average 5.3 degrees) of external rotation was observed. Combined sectioning of the PLC and the PCL results in an increase in external rotation of the lateral tibial plateau at all angles of knee flexion, with a maximal increase noted at 90 degrees. As much as 20 degrees of increased external rotation can be appreciated at this degree of knee flexion.22,23 This is the basic science behind the external<br />tibial rotation test (or Dial test) commonly used to distinguish between isolated PLC injuries and combined PCL/PLC injuries.<br /><br />
Thus, the fibular collateral ligament is the primary restraint to external rotation at small degrees of knee flexion (30 degrees) and the popliteus complex is the primary restraint against external rotation at greater degrees of knee flexion (60 degrees). The PCL serves as a secondary restraint when the PLC is injured and is most effective at knee flexion angles of 90 degrees. These basic science studies have important clinical applications. Because isolated sectioning of the PCL does not increase external tibial rotation, any increased tibial external rotation should make a clinician suspicious of a PLC injury. In a combined PCL and PLC injury model, Harner et al29 biomechanically demonstrated that a deficiency of the posterolateral structures after PCL reconstruction increased external rotation up to 14 degrees. If the PLC is not reconstructed when the PCL is reconstructed, this resulting increased external rotation places the patient at increased risk of reinjury. Therefore, it is important to reconstruct the posterolateral complex in addition to the PCL to restore normal external tibial rotation restraints. The posterolateral structures play a small role in preventing primary internal rotation of the knee.31 Because there is a large amount of variability in internal rotation changes within ACL-intact and ACL-deficient knees, this particular knee instability has not demonstrated much clinical significance.<br /><br />ARTICULAR CONTACT PRESSURES<br />The structures of the PLC are important in maintaining joint stability, which can have significant effects on articular contact pressures. Abnormal joint loading patterns and contact pressures can predispose a joint to degeneration. Sectioning the PCL and posterolateral structures has been shown to increase medial, lateral, and patellofemoral compartment contact pressures. 32 In a cadaveric biomechanical model of the knee, Skyhar et al,32 demonstrated that sequentially sectioning the PCL and then the posterolateral structures resulted in a significant increase in patellofemoral contact pressure at all angles of flexion. This finding is a result of 2 interrelated factors. First, with the loss of these structures, posterior tibial translation increases, thus, diminishing the moment arm of the patellar tendon. The angle between the quadriceps and patellar tendon decreases and creates an increase in the reaction force of the patellofemoral joint. This phenomenon is known as the ‘‘reverse Maquet’’ effect. Second, the quadriceps must exert a greater force because it is acting through a diminished lever arm. This increases articular contact pressures even more. The loss of ligamentous support creates instability so that the pressure is less likely to be distributed over the articular surface in a normal pattern. A combined PCL and PLC injury induces external rotation of the tibia on the femur, which creates aberrant medial and lateral contact pressures that are already elevated owing to the increase in quadriceps force. Several authors have postulated that this combined injury shifts the center of rotation further into the medial compartment, increasing shear and/or changing contact areas within these compartments during knee motion, ultimately, resulting in a varus-thrust gait pattern.32,33 The abnormal contact pressures seen in this combined injury may lead to premature degeneration of the joint and underscore the importance of the PLC in maintaining a healthy knee.<br /><br />GRAFT RECONSTRUCTIONS<br />From a clinical standpoint, the PLC can have a significant effect on the survival of the native ACL and PCL. Studies have shown that sectioning of the FCL and surrounding posterolateral structures resulted in increased<br />stresses on the ACL with internal rotation and on the PCL with external rotation.24 Similar to the native ACL or PCL, the reconstructed ACL or PCL is at increased risk of failure in a knee with a deficient PLC. Studies have shown that sectioning the FCL and surrounding posterolateral structures results in increased<br />stresses on reconstructed ACL and PCL grafts.34,35 LaPrade et al34,35 have shown that coupled loading of varus and internal moments, at 0 and 30 degrees of flexion, significantly increased ACL graft forces. Furthermore, significantly increased forces were demonstrated within PCL grafts with varus and/or coupled external rotation at 30, 60, and 90 degrees of flexion. These studies affirm the recommendation to reconstruct the PLC in both isolated and combined injuries.</div>

BIOMECHANICS. The primary function of the structures of the lateral and posterolateral knee are to resist varus rotation, external tibial rotation, and, to a lesser extent, posterior tibial translation. Several biomechanical stud…

Lateral Gastrocnemius Tendon

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<span style="color: blue;"><b>Lateral Gastrocnemius Tendon.</b></span> The lateral gastrocnemius tendon originates at or near the supracondylar process of the distal femur. In this region, this tendon can be easily identified by blunt dissection medial and distal to the long head of the biceps femoris in the interval between the lateral gastrocnemius and the soleus muscle. On average, it attaches 13.8mm posterior to the FCL, 28.4mm posterior to the popliteus <a href="http://imedicalcenter.blogspot.com/2015/06/lateral-gastrocnemius-tendon.html">tendon insertion</a>, and is nearly inseparable from the meniscofemoral portion of the posterior capsule. At the level of the fibular styloid, the lateral head of the gastrocnemius blends with the popliteofibular ligament, providing varying degrees of additional posterolateral stability.9<br />
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JOINT CAPSULE/MIDTHIRD LATERAL CAPSULAR LIGAMENT<br />
The joint capsule can be divided into superficial and deep laminae. The 2 laminae become confluent anterior to the overlying iliotibial band. The inferior lateral geniculate artery, traveling through an anterior truncated space between the deep and superficial laminae, always separates these 2 capsular structures.10<br />
The superficial lamina, which is the original capsule embryologically, encompasses the FCL and ends posteriorly at the fabellofibular ligament. The deep capsular lamina is phylogenetically younger and is a result of the fibula receding from the lateral femur. It extends posterolaterally and forms the coronary ligament and the hiatus for the popliteus tendon. </div>
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<tr><td class="tr-caption" style="text-align: center;">FIGURE 7. Attachment sites of the anterior (AD) and posterior (PD) (over surgical pickups) divisions of the popliteofibular ligament (PFL) at the popliteus musculotendinous junction (medially) and the medial aspect of the fibular head and the fibular styloid process (laterally) (posterior view of the right knee). FCL, fibular collateral ligament; PLT, popliteus tendon. Reprinted with permission.23</td></tr>
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The deep lamina travels along the lateral meniscus and spans from the junction of the popliteus muscle and tendon to its termination at the popliteofibular ligament. In the cranial to caudal direction, it extends from the femur to the fibula. An in vivo anatomic and magnetic resonance imaging study demonstrated that the most inferior extent of the capsular reflection of the knee is along the posterior fibula. The most extensive capsular reflection was less than 14mm inferior to the subchondral bone of the proximal tibia. This anatomic finding has lent credence to the recommendation of placing fine wires for circular fixators no closer than 15mm inferior to the articular surface to minimize the incidence of iatrogenic knee sepsis secondary to pin tract infection.19<br />
The joint capsule of the knee can be divided into 3 sections in the anterior to posterior direction: anterior, lateral, and posterior. The anterior section extends from the patella tendon to the anterior border of the popliteus tendon’s insertion on the femur. It is adherent to the patellar fat pad, intermeniscal ligament, and anterior horn of the lateral meniscus. The lateral capsule extends from the anterior border of the popliteus tendon’s insertion on the femur to the lateral gastrocnemius attachment. The posterior capsule is attached to the femur, proximal to the articular margin of the lateral femoral condyle.7,10,20<br />
From medial to lateral, the posterior capsule is covered by the muscular origins of the plantaris and lateral gastrocnemius muscle and tendon. Distally, it blends with the musculotendinous junction of the popliteus and the posterior division of the popliteofibularligament. The midthird lateral capsular ligament is a thickening of the lateral capsule of the knee. It is divided into 2 components: the meniscofemoral and meniscotibial components. It is thought to be homologous to the deep medial collateral ligament on the medial aspect of the knee. The meniscofemoral component extends from the femur down to the meniscus and the mensicotibial component extends up from the tibia to the meniscus.<br />
Anterior to the popliteal hiatus, the lateral meniscus is stabilized by the meniscotibial portion of the midthird lateral ligament. Biomechanically, this structure is thought to be an important secondary stabilizer to varus instability.4,5<br />
CORONARY LIGAMENT OF THE LATERAL MENISCUS<br />The coronary ligament of the lateral meniscus lies posterior to the midthird lateral capsular ligament. It is the meniscotibial portion of the posterior joint capsule extending from the anterior margin of the popliteal hiatus to the lateral aspect of the posterioinferior popliteomeniscal fascicle. It secures the posterior horn of the lateral meniscus to the tibia. The coronary ligament is important clinically in providing resistance to hyperextension and posterolateral rotation of the tibia.5<br /><br />OBLIQUE POPLITEAL LIGAMENT<br />The oblique popliteal ligament (or ligament of Winslow) is formed by the coalescence of the oblique popliteal expansion of the semimembranosus and the capsular arm of the posterior oblique ligament. These 2 structures originate from the medial side of the knee, merge anterior to the medial head of the gastrocnemius, and form the oblique popliteal ligament. This ligament crosses the midsagittal plane of the knee at the level of the tibial insertion of the PCL and attaches to the inferomedial edge of the fabella and the lateral capsule.5,10,20,21<br /><br />FABELLOFIBULAR LIGAMENT<br />The fabellofibular ligament is the most distal edge of the capsular arm of the short head of the biceps femoris.4 It spans from the lateral edge of the fabella, distally and laterally, to attach to the fibular head just posterior to the attachment of the posterior division of the popliteofibular ligament. If no osseous fabella is present, the ligament’s fibers blend with the anterior fibers of the lateral gastrocnemius tendon, on the posterior aspect of the supracondylar process of the femur, becoming part of the superficial capsular layer. In a cadaveric study, LaPrade et al4 found an ossified fabella in 5 of 30 (20%) specimens. In the absence of a bony fabella, some authors have named the structure the short lateral ligament.10,20 The fabellofibular ligament is in the greatest tension when the knee is in full extension and is often difficult to identify as it relaxes with knee flexion.5,21 Therefore, the clinical significance seems to be important for providing stability of the knee close to full extension. However, biomechanical studies specifically on the fabellofibular ligament have not been performed. </div>

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Popliteus Muscle/Popliteus Complex

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<span style="color: blue;"><b>Popliteus Muscle/Popliteus Complex. </b></span>The popliteus is an obliquely oriented muscle that originates from the postero-medial aspect of the proximal tibia. It forms the floor of the inferior part of the popliteal fossa and is innervated by the tibial nerve. The muscle gives rise to the popliteus tendon at the lateral one-third of the popliteal fossa in the PLC. The average length of the popliteus tendon is 54.5 mm.5 The tendon continues proximally, through the popliteal hiatus in the coronary ligament, at which point it becomes intra-articular, and inserts onto the lateral femoral condyle. This popliteal hiatus is also known as the ‘‘bare area of the lateral mensicus.’’10<br />The <a href="http://imedicalcenter.blogspot.com/2015/06/popliteus-musclepopliteus-complex.html">popliteus</a> is a dynamic internal rotator of the tibia and is believed to contribute to the dynamic stability of the lateral meniscus. To facilitate these functions, it has multiple insertions on the posterolateral aspect of the knee. The popliteus muscle-tendon unit and its multiple ligamentous connections from the tendon to the fibula, tibia, and meniscus are known as the popliteus complex.11 Each of these ligamentous connections have been further clarified. The ligamentous insertion on the fibula is comprised of the anterior and posterior popliteofibular ligaments. Historically, these 2 ligaments were collectively known as the arcuate ligament. The popliteal insertion onto the tibia is known as the muscular aponeurotic attachment. The popliteal connections to the lateral meniscus are known as the 3 popliteomeniscal fascicles. This complex provides dynamic and static stability to the knee primarily in response to external tibial rotation.5,9</div>
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<tr><td class="tr-caption" style="text-align: center;">FIGURE 4. A and B, Photograph (A) and illustration (B) demonstrating<br />the isolated fibular collateral ligament, popliteus tendon, popliteofibular ligament, and lateral<br />gastrocnemius tendon (lateral view of a right knee). Reprinted with permission.23</td></tr>
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The femoral insertion of the popliteus tendon is intra-articular and requires an arthrotomy for clear identification. During a surgical approach, the arthrotomy should begin just distal to the lateral epicondyle, run parallel to the FCL, and end at around the level of the lateral meniscus. The popliteus should be easily identified in the popliteal sulcus of the femur. The insertion of the popliteus is consistently found at the most anterior 1/5 and proximal 1/2 of the sulcus. The average crosssectional area of the popliteus sulcus is 3.4 cm2; 0.59 cm2 of the popliteal sulcus is used for the footprint of the popliteus tendon.9<br />Numerous researchers have found that the popliteus tendon insertion site was consistently anterior to the FCL along the lateral aspect of the lateral femoral condyle9,12–14 (Fig. 4). Specifically, LaPrade et al9 located the popliteus insertion site 18.5mm distal and anterior to the femoral insertion of the FCL, and 15.8mm distal and anterior to the lateral epicondyle of the femur (Fig. 5). Furthermore, they noted that the popliteus tendon did not completely enter the confines of the popliteal sulcus until the knee was flexed to an average of 112 degrees. In knee flexion less than 112 degrees, the tendon subluxed anteriorly out of the sulcus (Fig. 6). As the popliteus tendon courses proximal and laterally, it gives off 3 branches which contribute to the dynamic stability of the lateral meniscus. These are known as the popliteomeniscal fascicles.4,14<br /> </div>
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<tr><td class="tr-caption" style="text-align: center;">FIGURE 5. Attachment sites of the fibular collateral ligament<br />(FCL) on the femur and fibula and the popliteus tendon (PLT)<br />in the popliteus sulcus of the femur (lateral view of a right<br />knee). In addition, the average distance between the femoral<br />attachment sites is noted. Reprinted with permission.23</td></tr>
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The first meniscal fascicle is the popliteus muscle’s aponeurotic attachment. This meniscal aponeurosis is an attachment of the popliteus muscle to the posterior capsule and lateral meniscus. This structure, initially described by Last,15 was termed the posteroinferior popliteomensical fascicle by Staubli and Birrer.14 Located medial to the popliteus tendon, this popliteomeniscal fascicle provides a posterior tibial attachment for the lateral meniscus. The postero-superior popliteomeniscal fascicle arises from the medial superior surface of the popliteus tendon as it penetrates the posterior capsule. It blends into the posterior horn of the lateral meniscus and the meniscofemoral portion of the posterior capsule of the joint.4,14<br />The postero-inferior popliteomeniscal fascicle forms from the popliteus muscle aponeurosis, just medial to the tendon, whereas the postero-superior popliteomensical fascicle forms from the popliteus tendon. The ligament of Wrisberg bisects these 2 posterior popliteomeniscal fasicles as it connects the posterior horn of the lateral meniscus to the medial femoral condyle, providing additional stability to the lateral meniscus.5 The last fascicle, the antero-inferior popliteomeniscal fascicle, originates the furthest distally along the popliteus tendon. From the anterior edge of the popliteus tendon, it blends into the middle third of the lateral meniscus forming the anterior boundary of the popliteal hiatus.4,5,14<br />The biomechanical significance of each of the 3 individual popliteomeniscal fascicles is not completely understood. However, it is known that together they stabilize the lateral meniscus and prevent medial entrapment of the meniscus during varus forces on the knees.16 These functions are complicated by the need to permit the large excursion of the lateral meniscus over the chondral surfaces.</div>
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<tr><td class="tr-caption" style="text-align: center;">FIGURE 6. The position of the popliteus tendon (PLT) to the<br />popliteus sulcus with the knee in full extension and at an<br />average of 112 degrees of knee flexion (ghosted view) (lateral<br />view of the right knee). PFL, popliteofibular ligament.<br />Reprinted with permission.23</td></tr>
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The popliteofibular ligament is the second most prominent structure in the PLC, with the most prominent being the popliteus tendon. The anatomy and function of the popliteofibular ligament is becoming more defined. The popliteofibular ligament consists of anterior and posterior divisions. These divisions originate from the popliteus tendon at its musculotendinous junction.9 They form a ‘‘Y’’ configuration, providing a firm connection between the popliteus tendon and fibula (Fig. 7).<br />The anterior division, attached to the proximallateral musculotendinous junction, inserts just anterior to the posterior division and medial to the FCL. On average, it attaches 2.8mm distal to the anteromedial aspect of the tip of the fibular styloid process.9 The stouter posterior division of the popliteofibular ligament, which is typically reconstructed in PLC injuries, originates from the popliteus tendon and inserts 1.6mm distal to the tip of the fibular styloid process on its posterior medial downslope.9 A small longitudinal groove may be palpated on this downslope, identifying its course. It inserts on the fibular styloid just anterior to the fabellofibular ligament.<br />The popliteofibular ligament is a static stabilizer of the lateral and posterolateral knee, resisting varus, external rotation, and posterior tibial translation.4,11 A force of 298N is required to cause failure of this structure.17 Alternatively, rather than an intrasubstance tear, the posterior division may avulse a fragment of the fibular head in what is known as an arcuate fracture. Arcuate fractures are often associated with cruciate ligament injuries.18 Due to their roles as both static and dynamic restraints, the popliteus and popliteofibular ligaments are vital components of any posterolateral reconstructive procedure. Directly posterior to the popliteofibular ligament courses the inferior lateral geniculate artery. This artery originates off the popliteal artery and courses along the posterior joint capsule just proximal to the superior aspect of the lateral meniscus. As it courses laterally, it bisects the popliteofibular ligament and the fabellofibular ligament (capsular arm of the short head of the biceps femoris) as they attach to the fibular styloid. The popliteofibular ligament lies anterior and the fabellofibular ligament lies posterior to the inferior lateral geniculate artery where it crosses the posterior aspect of the fibular styloid.7,10<br />The final component of the popliteus complex is its popliteotibial insertion. This is a direct attachment extending from the anterior surface of the popliteus muscle to an area just lateral to the fovea of the posterior cruciate ligament (PCL). It inserts on the inferior surface of the lateral meniscus and on the posterior capsule. The insertion on the posterior capsule lies medial to the popliteal tendon, an area devoid of a coronary ligament attachment.4,9</div>

Popliteus Muscle/Popliteus Complex. The popliteus is an obliquely oriented muscle that originates from the postero-medial aspect of the proximal tibia. It forms the floor of the inferior part of the popliteal fossa and is innerva…