G r
P r o a t t s s s s h o
A l l n o a g t t y o m
R e
y p
L a p o r r t t b

Introduction page 3
Summary of pathological finding page 3
Atherosclerosis and Associated Complications page 5
Pacemaker page 8
Total Knee Arthroplasty
Laminectomy page 11 page 14
Direct Inguinal Hernia
Right Kidney Hypoplasia and Renal Failure
Cause of Death and Conclusions
Credits
References page 17 page 19 page 23 page 24 page 25
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Robert was a 6’0” 88-year-old white male who died on the 20 th
of June 2001. The reported cause of death is renal failure. His body number is C-135-01. The body was not well fixed in spots, probably due in part to his arteriole disease. This made dissections of deep portions of both the lower pelvis and buttocks very difficult. Soft tissues of the anal and urogenital triangles were similarly affected.
Robert had a robust build, especially considering his age. Well-defined muscles were discovered upon dissection of the upper and lower limbs. This allowed for greater ease in identifying muscular structures. He was moderately overweight and dissection showed the characteristic male distribution of excess fat in the neck, upper arms/axilla, lower back, and abdomen/pelvis. The appearance and condition of the skin and hair for a male of this age were unremarkable.
This report begins with a brief summary of major pathological findings. The report then discusses specific pathological states and diseases in greater detail. Atherosclerosis and associated complications, pacemaker, total knee arthroplasty, laminectomy, direct inguinal hernia, and renal disorders will be covered.
External Examination


No significant abnormalities except for an enlarged left scrotum
Scar along the medial surface of the left leg from a great saphenous vein harvest
 Navy anchor tattoo over lateral aspect of the right upper arm
Body Cavities


Thoracic inspection revealed slight, dispersed pleural adhesions
20-30 ml fluid found in both left and right pleural cavities (embalming fluid)
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 Direct inguinal hernia composed of fatty tissue found on the right body wall within
Hesselbach’s triangle
Musculoskeletal


Dissection of the lumbar spine exposed a laminectomy of the L1 vertebra
Joints unremarkable except for a right total knee replacement
Heart



Cardiomegaly—largely due to left ventricular hypertrophy
Coronary artery bypass grafts—three vessels originating from anterior ascending aorta terminating at anterior & posterior interventricular sulci with the third bypassing the left circumflex branch of the LCA
Pacemaker was imbedded on the left pectoralis major muscle with two leads—one terminating at the right atrium, possible at the SA node, the other terminating at the apex of the right ventricle piercing the endocardium
Major Blood Vessels
 Moderate aortic atherosclerosis with large atheromatous plaques
 Abdominal aortic aneurysm, along with a large plaque, found at the origin of inferior mesenteric artery
Respiratory System
 Both left and right lung parenchyma possessed a mottled black appearance—however, lungs were relatively healthy with no signs of chronic smoking. Dr. Hunter stated this represents typical exposure throughout life to dust and other airborne particles
GI Tract and Digestive Organs


No significant abnormalities found
Appendix was removed
Genito-Urinary System
 Atrophied kidneys—normal for an 88-year-old man



Retention cysts found on both kidneys with the largest being 12mm in diameter
Possible renal artery stenosis, nephrosclerosis, pyelonephritis, and other kidney disorders
Lipoma (fatty growth) in left spermatic cord. Dr. Dreyer mentioned this is a common finding in the cord
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Brain




Enlarged sulci (shrunken gyri) of the left and right frontal lobes—possibly indicative of mild dementia
Normal ventricles and substantia nigra throughout
Occluded or narrow left and right lentriculostriate arteries
Large soft spot deep in the right parietal lobe due to no blood flow through the middle cerebral artery. Dr. Bruce mentioned this happened near the time of death
We concluded Robert had advanced atherosclerosis upon death due to anatomical observations and pathology findings. The thickened arterial walls, especially the abdominal aorta, and the abdominal aortic aneurysm (AAA) coupled with the findings of multiple coronary artery bypass grafts (CABG) support this deduction. Atherosclerosis is the dominant presentation of a variety of vascular diseases causing hardening of the arteries, known collectively as arteriosclerotic diseases. It is the number one killer in industrialized societies claiming close to half of all deaths in the U.S. Risk factors include age, sex (male more prone), genetics (most likely polygenic), hyperlipidemia, cigarettes, diabetes mellitus, and other chemical and lifestyle factors (e.g., homocysteine or lack of exercise). Robert appeared not to be a chronic or recent smoker because his lungs were relatively healthy for his advanced age. The diagnostic characteristic of atherosclerosis is the presence of atheromas—also termed fibrous, fibro-fatty, lipid, or fibro-lipid plaques with the term atheromatous plaques being commonly used.
Atheromatous plaques are lesions of the arterial cell wall intima that progressively develop over many years.
The lesions begin as localized fatty streaks occupying a patchy distribution within the circulatory system, often originating at points of turbulence in vessels such as bifurcations and branching points. Repetitive endothelial injury, whether hemodynamic, immune, chemical, etc.,
5

alters normal function and allows for increased permeability and white blood cell adhesion. Lowdensity lipoprotein (LDL), and very-low-density lipoproteins, invade and congregate within the intimal layer. Monocyte infiltration with subsequent phagocytosis of fats and other components, especially oxidized LDL, further expand the lesion by occupying space as stationary foam cells.
Monocytes release inflammatory factors that attract platelets and additional monocytes. A major process that aids the conversion of a fatty streak into an atheromatous plaque is smooth muscle cell infiltration and proliferation. These cells lay down extracellular matrix moieties that further harden and entrap components of the lesion. If high cholesterol levels are left unattended, LDLs will continue to coalesce within the lipid debris. These processes occur over long periods and progressively worsen as one ages.
Macroscopic inspection of Robert's vessels showed evidence of these whitish yellow plaques, with a firm white fibrous cap overlying the friable, intimal-layer center. These were found predominantly in the abdominal aorta wall. Of clinical concern is that vessel lumen narrowing leads to hypoperfusion of tissues and possible ischemia. Therefore, it is not surprising to learn that atherosclerosis affects all parts of the body and leads to a variety of organ failures, most notably heart (ischemia/MI), brain (strokes), and kidneys (renal failure). Advanced or
"complicated" lesions become considerably calcified leading to increased brittleness.
Unfortunately rupture may occur, discharging microemboli into the blood stream that can block arteries. Superimposed thrombosis can occur at sites causing partial or complete lumen occlusion. Coronary artery stenosis and occlusion by means of atheromatous plaques account for over 90% of myocardial ischemia cases and therefore play a major role in myocardial infarction
(Cotran et al. 1999).
6

We concluded Robert must have experienced myocardial ischemia or infarction to some extent because of his multiple CABG. Three vessels were found originating from the anterior base of the ascending aorta. It appeared the anterior interventricular branch and the circumflex branch of the LCA were bypassed. One vessel traversed the right atrium and then dispersed around the posterior interventricular branch of the RCA. CABG surgery is one of the most common surgical procedures in the U.S. (Cotran et al. 1999). In this procedure a vessel is harvested, occasionally the great saphenous vein or internal mammary artery, and placed as a detour around a highly atherosclerotic section of a coronary artery. The great saphenous vein is particularly useful due to its similar diameter, easy dissection, and lengthy valveless sections, although less effective at maintaining patency as the mammary artery (Moore 1999; Robbins
1999). An alternative course being exploited is the connection of the internal thoracic arteries to the coronary arteries (Barner 1999). Procedures have been developed and perfected that seek to limit post-operative complications, such as off-pump bypass, minimally invasive bypass conducted through a keyhole incision, and the innovative trans-myocardial laser revascularization procedure where a laser creates pinholes in heart muscle that play a role in promoting new vessel growth (Singh 2001). The re-routing of blood allows for proper tissue perfusion of the heart and has contributed to a decrease in deaths from ischemic heart disease
(IHD) (Cotran et al. 1999).
We believe Robert's condition may be considered chronic ischemic heart disease (CIHD).
This is often found in the elderly who have continual myocardial ischemia having experienced previous infarcts and CABG surgery. The heart is often hypertrophied due to increased workload, with inefficient pumping, aortic stenosis, and often systemic hypertension. These cells
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are in additional danger because of the increased oxygen demand from an already precarious circulation network. Robert did have cardiomegaly and other symptoms of CIHD.
In addition to the heart findings, a large abdominal aortic aneurysm was discovered
(AAA) at the origin of the inferior mesenteric artery. It was somewhat of a fusiform aneurysm that narrowed the vessel lumen to under 3 cm. One major cause of AAAs is atheromatous plaques at the site. The abdominal aorta is the most common site of aneurysm followed by the common iliac arteries, the arch of the aorta, and the thoracic aorta (Cotran et al. 1999). Coronary artery aneurysms can occur as well. The underlying cause is weakening of the vessel wall through lesion growth and destruction of the intima and media wall layers. The lumen of the inferior mesenteric artery at its origin appeared to be quite narrow. A thick whitish yellow plaque occupied a significant space. Those at greatest risk for AAAs are people over 65 years old with peripheral atherosclerotic vascular disease, as was Robert (O'Conner 2001). Treatment consists of the surgical placement of a prosthetic graft in advanced cases. Due to the surgical risks, a physician must be careful not to misdiagnose an AAA. Patients may present with normal vital signs despite an AAA rupture, because of retroperitoneal containment. A pulsatile mass, often diagnostic of AAA, is not easily appreciated. In fact, a pulsatile mass was not palpable by surgeons in 25% of pre-op patients known to have an aneurysm (O'Conner 2001). Legal battles have been fought because patients sent home eventually had an AAA rupture and subsequent morbidity or mortality.
During dissection of the left pectoral region, a small (approximately 3 cm x 4 cm) white object implanted subcutaneously was discovered. Two leads were running from it, which
8

penetrated the chest wall through two small plastic shunts imbedded in the pectoralis major muscle. Upon removal of the device, The white plastic shell was stripped and discovered to be an implanted pacemaker.
In a normal heart, the SA node fires an electrical impulse that spreads across the right atrium and to the left atrium by the Bachman's bundle so that both atria may contract at the same time. The impulse then travels to the atrioventricular (AV) node, which acts as a delay line to slow the action potential. The action potential then travels from the AV node to the Purkinje fibers, which are arranged in two bundles—one bundle branching to the right ventricle and the other branching to the left ventricle. The action potential moves through these fibers very rapidly and spreads throughout the ventricles. If any of the conductive pathways of the heart are blocked, a patient may develop a heart block. In a typical heart block, a patient’s ventricles contract at a rate independent of the atria—almost always slower than the atria (Moore & Dalley 1999).
The conductive system of the heart is commonly damaged by coronary artery disease, which can cause ischemic attacks and subsequent cell death of either node or of the conductive fibers. This is the likely cause of Robert’s inability to maintain a proper cardiac rhythm, as indicated by his advanced heart disease and multiple coronary artery bypasses.
9

Robert’s pacemaker was a Medtronic device, model Preva DR 7088, which according to the Medtronic website is dual chambered and rate responsive. Dual chamber refers to the fact that it supplies pacing for both the right atrium and right ventricle. This allows for independent control of the contraction of the atrium and ventricle to more closely resemble the natural beating of the heart.
A dual chambered pacemaker consists of three general parts:

Generator (Pacemaker)

2 Leads (1 Atrial and 1 Ventricular)

Electrodes
The electrodes are threaded or equipped with tines or barbs so that they can be securely fastened to the myocardium.
(Source: www.heartcenteronline.com/myheartdr/ common/articles.cfm?Artid=185)
10
Minor surgery is required to implant a permanent pacemaker. This procedure is usually performed while the patient is in the hospital for a related heart condition (e.g., following a heart attack). A catheter is inserted into the left subclavian vein, through which leads are threaded down the superior vena cava, into the right atrium, through the tricuspid valve and into the right ventricle.
The lead is then attached to the trabeculae carneae using small screws or tines. To verify that the electrode(s) are in the correct position(s), a chest X-ray may be taken or the whole procedure could be observed real-time using a fluoroscope (Moore & Dalley 1999).

One item of particularly interest is pacemaker “checkups” which take place over the telephone through transtelephonic monitoring. With the help of a special device, information from the implanted pacemaker can be sent via phone lines. These transtelephonic checks are scheduled every two to three months. If programming adjustments are needed or battery replacement is necessary, a medical appointment may be made.
Patients typically experience a significant increase in their quality of life after having a pacemaker implanted. Batteries may last up to 10 years before replacements need to be implanted.
While investigating the ligaments of Robert’s knees, a prosthetic joint was found in the right knee (Figure 1). The femoral condyles had been replaced by a rounded component made of shiny chrome-alloy. A polyethylene disc cemented to a metal component, which had been embedded in the bone itself, covers the proximal end of the tibia. A prosthetic knee joins both femoral and tibial components and is the product of a total knee arthroplasty, or total knee replacement. The menisci and anterior cruciate ligament are missing in this knee, but the posterior cruciate ligament is present.
The patella was also present and left intact.
Although some knee fractures or other disorders may require joint replacement, the most
Figure 1.
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common cause of knee damage requiring knee arthroplasty is osteoarthritis, or degenerative joint disease (“knee joint replacement”). This disease is characterized by a progressive breakdown of articular cartilage due to intrinsic changes in biochemical and metabolic processes (Cotran et al.
1999). Primary osteoarthritis usually affects only a few joints and appears idiopathic regardless of age. Trauma or other diseases, such as diabetes, may instigate secondary osteoarthritis in one or several predisposed joints. Osteoarthritis is highly prevalent, with as much as 80-90% of the population showing evidence of the disease by age 65 (Cotran et al. 1999). Thus, it is likely that
Robert, who was 88 at time of death, would have been affected by osteoarthritis. No evidence of osteoarthritis was found in Robert’s other joints nor was it determined if the replaced right knee was subject to primary or secondary osteoarthritis.
Osteoarthritis has a gradual onset of symptoms that usually do not occur until a patient is in his or her fifties. Diseased joints develop deep pains that worsen with use and stiffen after sleep or inactivity leading to limited range of motion and may emit crackling sounds when moved (crepitis). The hips, knees, and lower lumbar/cervical vertebrae are among the joints commonly affected by osteoarthritis (Cotran et al. 1999). The pain and limited movement of diseased joints may become greatly debilitating.
Treatment for osteoarthritis involves controlling the pain and attempting to maintain function. There is no known way to prevent developing primary osteoarthritis or halting its progression. Exercise can maintain healthy cartilage, increase a joint’s range of motion, and strengthen surrounding muscles so they absorb shock better. Physical therapy can also relieve pain and stabilize joints during painful activities. A nonsteroidal anti-inflammatory drug
(NSAID), such as aspirin, can be taken to alleviate pain and swelling. Corticosteroid injections into inflamed joints may provide short-term relief. When these treatment modalities have failed
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to bring relief, joint replacement surgery is a very successful method to improve function and reduce pain in a diseased knee or hip (“osteoarthritis”).
Patients undergoing knee replacement surgery often are sedated and given regional anesthesia via an epidural instead of general anesthesia. Access to the knee is gained through an incision down the front of the mid-thigh to below the knee (“Total knee replacement” 2000). The end of the femur and top of the tibia are sliced off with a saw and the menisci and anterior cruciate ligament are resected (Figure 2). The posterior cruciate ligament may be spared, as it was in Robert, in order to increase stability of the joint in the future (Ishii, et. al. 1998). The patella is either resurfaced or left intact, depending on the prosthesis being used. Knee replacements come in separate components to allow the surgeon to fit the device to the individual knee. The curved femoral component is cemented to the end of the femur to replace the condyles and is usually made of a shiny chrome alloy, as observed in Robert’s right knee.
The metal tibial component has a flat top and a two-inch spike on the bottom that insert into a hole drilled in the tibia. A polyethylene disc is cemented to this flat top and will articulate with the chrome femoral component (“Total knee replacement” 2000).
Figure 2.
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Some of the risks involved with a total knee arthroplasty include venous thromboembolism, infections of the joint and fractures around the prosthesis. Venous embolisms are more likely to form if the blood is not returned promptly; this constitutes the major cause of postoperative death following a knee arthroplasty and should be minimized with elastic stockings and anti-coagulants (Thomas 2001). Joint infections may necessitate removal of the joint and are often avoided by administering prophylactic antibiotics for any invasive medical or dental procedures (“Knee joint replacement”). Femoral or tibial fractures directly above or below the knee may occur due to weakened bone and are typically repaired surgically (Gaddis 2001). No further complications were found in Robert’s knee.
Despite its potential risks, total knee arthroplasty is considered a very successful surgery.
According to some studies, total knee replacements have survival rates of 85% at 13 years
(Moran & Horton 2000). As new techniques and materials become available, total knee replacements are lasting longer with greater patient satisfaction. In “low demand” people who lead sedentary lives, the metal on plastic joint mimics the natural bone on cartilage joint. In more active people, however, the bone cement junctions may gradually loosen, requiring further surgery (Moore & Dalley 1999). Total knee replacement allows patients to lead a normal lifestyle without the knee pain and limited motion that may have previously disabled them.
After exposing the thoracic and lumbar vertebrae, the lamina and spinous process of the first lumbar vertebrae (L1) was missing. This pathologic feature indicated Robert underwent a laminectomy.
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A laminectomy is a surgical procedure that removes the lamina of the affected vertebrae in order to relieve pressure on the spinal nerve roots being compressed below the lamina. This pressure on the spinal roots is often referred to as nerve root compression or a “pinched” nerve
(“Laminectomy” 2000).
There are several reasons why nerve compression may occur. Intervertebral disc herniation, spondylosis, and lumbar spinal stenosis are three causes of nerve root compression that make an individual a candidate for laminectomy. Herniation of the nucleus pulposus (inner nucleus of vertebral disc) can exert direct pressure on the nerve root, which causes pain along the dermatome of the nerve root (see Figures 3 and 4). Herniation commonly occurs between L4 and L5, which usually cause compression of the fifth lumbar nerve root.
Figure 3. Superior View of Disc. Figure 4. Herniated Disc.
Each disc has a spongy center (nucleus) surrounded by outer layers that support and cushion the spine.
A herniated disc occurs when disc material migrates out through the outer layers of the disc.
( Source : http://www.nwinspine.com/anatomy.htm)
The spinal nerve root typically entrapped is the lower of the two roots proximal to a herniated intervertebral disc (J. Yee, class lecture, September 19, 2001). Symptoms commonly associated with disc herniation between L4 and L5 are: 1) the inability to dorsiflex the foot, and
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2) referred pain in the buttocks, lateral side of thigh and knee, anterior side of leg, and spaces between the first three toes (J. Yee, class lecture, September 19, 2001). If there is motor nerve compression, muscle atrophy and weakness may result.
Spondylosis and spinal stenosis are also causes of nerve compression. Spondylosis refers to deterioration of intervertebral discs with bony spur formation impinging on spinal nerve roots
(“Laminectomy” 2000). With lumbar spinal stenosis (LSS), there is an abnormal narrowing of the spinal canal. Consequently, areas of nerve compression result. Here too a laminectomy can be performed to reduce pressure on the spinal cord. The majority of patients with LSS acquire the disease after age 60. However, LSS occasionally occurs congenitally in patients with symptoms presenting in their thirties and forties (“Decompressive lumbar …” 1998). Bone fractures, scar tissue, and growths such as tumors also entrap spinal nerve roots.
Ultimately, the goal of a laminectomy is to alleviate spinal nerve root compression. After removing the lamina (or portion of the lamina) from one or more vertebra, the surgeon will be able to locate the point(s) of nerve entrapment. After the lamina is removed, a cut in the ligamentum flavum is made to reach the spinal canal, with the ligamentum flavum is retracted
(see Figure 5). At this point, the source of pressure can be identified (i.e. herniated disc, bone
Figure 5.
(Source: http://www.espine.com/diagnosis_ll02.html#operation)
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spur formation, scar tissue, etc.) and removed. Once the source of pressure is removed, the compressed spinal nerve can begin to heal (“The operation”). Hopefully, Robert’s laminectomy was successful in alleviating his spinal root compression.
After dissection of the abdominal muscles, a protrusion was noticed in the peritoneum on
Robert’s left side. This protrusion was medial to the inferior epigastric vessels and located in the inguinal (Hesselbach) triangle, suggesting a left-sided direct inguinal hernia. The protrusion was medial to both the medial umbilical ligament and spermatic cord.
In an inguinal hernia, the parietal peritoneum and a loop of intestine or abdominal contents (e.g., fat), protrude through an opening in the lower abdominal wall. There are two types of inguinal hernias: direct and indirect. Robert’s direct hernia is the least common of the two. Only one-third of all inguinal hernias are direct (Moore & Dalley 1999). As opposed to indirect inguinal hernias, which can be congenital, direct hernias are acquired. Additionally, direct inguinal hernias leave the abdominal cavity medial to the epigastric vessels, while indirect hernias leave the abdominal cavity lateral to the inferior epigastric vessels.
In a direct inguinal hernia, the posterior wall of the inguinal canal may be a relatively weak area. The hernial sac is comprised of transversalis fascia, and this fascia may become stretched and thin out on the posterior wall of the inguinal canal. Obesity, heavy lifting, straining to pass stool, and chronic coughing can strain the abdominal wall, tearing it and allowing part of the intestine to protrude through (Grinsted 2000). The herniating loop of intestine then travels medially to the inferior epigastric vessels, protruding through the peritoneum and transversalis fascia in the inguinal triangle to enter the inguinal canal. The aforementioned inguinal
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(Hesselbach) triangle is bordered inferiorly by the inguinal ligament, medially by the rectus abdominis muscle, and superolaterally by the inferior epigastric artery.
The direct inguinal hernia does not pass through the entire inguinal canal, only at its most medial portion near the superficial inguinal ring. After the hernia protrudes through the conjoint tendon (inguinal falx), it gathers external spermatic fascia at the superficial ring inside or parallel to that on the spermatic cord. The external spermatic fascia is derived from the external oblique aponeurosis. The hernia rarely enters the scrotum, and if so, it travels lateral to the spermatic cord. It should be noted that inguinal hernias are rare in women. If they exist, they are mostly direct and found along the track line of the round ligament, which extends from the lower abdomen to the labia of the vagina (Perper & Weston).
It is important to know that most hernias are reducible. The surgical repair of an inguinal hernia, herniorrhaphy, is a relatively uncomplicated procedure. In conventional surgery, an incision is made approximately 3-4 inches long where the abdomen and thigh meet. The intestine and fascia in the hernial sac are placed back into the abdominal cavity, while the excess sac that has been stretched is either removed or tied off (Jones). Now, the bulge is absent and the abdominal wall is sutured, and a supportive synthetic mesh is patched to the abdominal wall. The surgery requires local, general, or spinal anesthesia and typically is an outpatient procedure.
Many physicians prefer laparoscopic surgery as an alternative to traditional therapy.
Laparoscopic surgery is preferred because less damage is made to the abdominal wall than in conventional surgery in which a larger incision is made (“Inguinal hernia”).
In laparoscopic hernia repair, three or four one-half inch incisions are made next to the umbilicus. After a space is created with a balloon, the abdominal wall is insufflated with carbon dioxide. Next, a metal tube is inserted in one of the incisions. The laparoscope, an endoscopic
18

video camera with a light source, can then be inserted. Two cannulas are also introduced through other incisions. Through these hollow sheaths, other surgical instruments and the synthetic piece of mesh can be inserted (Jones). Once the hernia is identified, it is placed back into the abdominal cavity, and the defect in the abdominal wall can be patched with the synthetic mesh
(Ballantyne 1996). The abdomen is deflated, and the fascia is closed with a suture. The skin incisions are closed with dissolving sutures.
In conclusion, Robert possessed a left-sided direct inguinal hernia in which the transversalis fascia on the posterior wall of the inguinal canal was over-stressed. He did not have his hernia surgically repaired. It is possible that Robert did not experience much discomfort, as is the case with some individuals with inguinal hernias. Robert’s direct inguinal hernia protruded through the peritoneum and transversalis fascia in the inguinal triangle and reached the superficial inguinal ring of the inguinal canal, but it did not traverse further into the scrotum.
Human kidneys convert more than 1700 liters of blood per day into about 1 liter of urine.
As part of this process the kidneys excrete the waste products of metabolism, regulate the body’s concentration of salt and water, help maintain the pH of plasma, and serve the endocrine function of secreting such hormones as renin, erythropoietin and prostaglandins. The adult kidney typically weighs 150 grams.
With respect to pathology, the kidney can be divided into four components: glomeruli, tubules, interstitium, and blood vessels. There is a tendency for all forms of chronic renal disease to ultimately destroy all four of these kidney components, resulting in chronic renal failure
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(characterized by prolonged symptoms and signs of uremia) and what is termed end-stage kidneys.
With some exceptions, the progression from normal renal function to end-stage kidneys and renal failure goes through four semi-overlapping stages:
1) Diminished renal reserve : glomerular filtration rate (GFR) is about 50% of normal.
Serum blood urea nitrogen (BUN) and creatinine levels are normal. The patient is asymptomatic.
2) Renal insufficiency : GFR is 20 – 50% of normal. Polyurea and nocturia occur. Stress may cause uremia.
3) Renal failure : GFR is 5 – 20% of normal. Patient may develop edema and metabolic acidosis. Uremia ensues with associated gastrointestinal, cardiovascular and neurologic complications.
4) End-stage renal disease : GFR less than 5%. Terminal stage of uremia (Robbins 1994).
Changes in renal anatomy and physiology occur during normal human aging. These changes are unique from the renal effects of diseases linked to aging which require specific diagnosis and therapy. Age associated changes are slow and mild; with no metabolic consequences even for those at 80 years of age. However, in hospitalized patients, acute renal failure is frequent and occurs during inflammatory disorders, dehydration, or drug combinations affecting glomerular filtration (Richard-Harston et al. 2000).
Older patients are susceptible to acute renal failure due to functional impairments of the kidneys secondary to diseases like hypertension, arteriosclerosis, and heart failure. To prevent failure of the kidneys, patients who suffer a large fluid loss should be rehydrated to avoid volume depletion. Blood pressure should be maintained. GFR should be considered when determining
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the dose of nephrotoxic antibiotics. Preparations of saline should be given before radiocontrast dye injections (Murray 1995).
After dissecting through the perirenal fat on both sides of the body, the right kidney (8cm vertical axis

5 cm horizontal

2 cm deep axis) was noticeably smaller than the left (11 cm

5.5 cm

2.5 cm) (see figure 6). The cortex of the right kidney also had two 2-4 mm round pink cysts on the anterior surface of the superior pole. There was also a 12 mm round pink cyst on the medial surface of the inferior pole. (see attached necropsy protocol page XI). figure 6.
Separate pyramid section, and overlying cortical section biopsies were taken from both kidneys and delivered to Dr. W. Hunter in the St. Joseph’s Hospital Pathology Department. All four samples were sectioned and mounted on glass slides, and then hematoxylin and eosin (H &
E) stained to examine cell nuclei and cytoplasm respectively.
Paradoxically, looking under the microscope, Dr. Hunter said he could find little wrong with these sections. Unusual, considering they were from an 88 year old patient who had died of renal failure. He mentioned he had seen worse renal disease in patients 60 years old, and that he would not consider these biopsies to be from end-stage kidneys. Pyramids and cortices from both
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kidneys appeared normal. Dr. Hunter did mention that arterioles running in the kidneys showed signs of having cholesterol emboli and atherosclerotic plaques. Dr. Hunter and I observed renal cortices having significant fat lining the lumen of arterioles.
Dr. Hunter further mentioned the three renal retention cysts (nephrocystosis) Robert had in his right kidney were not unusual for his age, and that for a kidney to be considered diseased, it would have to have about 50 or more cysts and / or the cyst diameter be much greater.
In regards to why the right kidney was smaller than the left, Dr. Hunter speculated that often a renal artery will become occluded in elderly, overweight people, with the kidney slowly becoming hypoplastic, usually with little clinical significance, until a renal stress or challenge is presented.
Additionally, renal hypoplasia is most commonly encountered as a unilateral defect, with cases presenting with scarring due to infectious, vascular or other diseases, rather than a developmental failure (Cotran et al. 1994).
Although, recent longitudinal studies indicate that morphological and functional renal changes of aging tend to be less marked than previously thought. The culmination of these changes results in a decrease in renal reserve, and subsequently a decrease in the kidney’s ability to respond to challenges. While these changes don’t generate clinical consequences under normal conditions, they attain clinical significance when residual renal function is challenged by the superposition of an acute illness. Therefore, elderly patients may suffer from comorbid conditions, such as heart disease, and hypertension that are additive to age associated changes, and thereby amplify renal abnormalities (Epstein 1996).
In light of the normal renal biopsies, Dr. Hunter thought that since the cause of death was renal failure, what caused Robert’s death was probably insufficient arterial throughput. In other
22

words, the kidneys were working fine, just not enough blood was reaching them due to blocked or occluded renal arteries, particularly in the right kidney. Therefore, Robert probably showed high levels of urea and creatinine in his blood indicative of end-stage kidneys, but the problem was most likely in the plumbing (renal arteries / arterioles) and not in the filter (kidney).
Robert’s reported cause of death was renal failure. However, his advanced atherosclerosis may have played an important underlying role in his death, through atherosclerotic renovascular disease (ARVD). Vascular diseases have profound effects on the kidneys because they receive about one-fourth of the cardiac output. The most common cause of renal artery stenosis is occlusion by an atheromatous plaque (Cotran et al. 1999). This can result in poor renal perfusion, with possible ischemia, and an even greater increase in blood pressure (further aggravating the vessels) through increased vasoconstriction (through renin/angiotensin II release) and less kidney fluid filtration and excretion. Renal ischemia, atherosclerotic nephropathy, and atheroembolic damage contribute greatly to renal destruction (Wright, et al. 2001; Main 2001).
Rates of MI and stroke are 5 to 10 times greater in atherosclerotic patients with end state renal disease (ESRD). (Kes 2000). A recent study found death may be attributed to a high uremic state that accelerates plaque expansion through lipoprotein binding and complement activation of
C-reactive protein (Arici 2001). Although, as mentioned previously, the biopsies suggest Robert did not have ESRD, although his right kidney was hypoplasic.
We know next to nothing about Robert’s life, and can only speculate on his health status and life-style from the anatomy and pathology discovered in lab. His strong muscles and bones, particularly in his arms and hands suggests his occupation involved manual labor such as that
23

found in farming, auto repair, or construction. His being moderately overweight suggests he ate a
(typical USA) moderate to high calorie diet, with little regular exercise besides work. Overall,
Robert’s anatomical and pathological condition for an 88 year old male living in 20 th
century
America is typical.
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
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

Table Five would like to especially thank the following for instruction and assisting in dissections:


Dr. T. Quinn
The gracious T.A.’s
Dr. J. Yee
Dr. B. Fritzsch

Dr. P. Brauer
Dr. D. Nichols

Dr. W. Hunter for greatly assisting in the pathology of submitted biopsies.
Joe Torcia for logistical support and material services
And other individuals who tutored us, including fourth-year medical students
And most importantly—Robert, for giving of himself, so that we as physicians may give to others.
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