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Skandalakis’ Surgical Anatomy > Chapter 27. Adrenal (Suprarenal) Glands >

History

The anatomic and surgical history of the adrenal glands is shown in Table 27-1.

Table 27-1. The History of Anatomy and Surgery of the Adrenal Glands

Eustachius 1522 Discovered the adrenals. Reported his findings in 1563.
Spigelius 1627 Described the adrenals as “capsulae renales”
Riolan 1629 Described the adrenals as supra-renal capsules
Valsalva (1666-1732)   Argued that the adrenal arteries were ducts running from the “glandula renalis” to the epididymis
Bartholinus (Bartolin) 1656 Described the adrenals as “capsulae atrabilariae” because he observed that they were filled with black fluid. This was later misconstrued to mean they were filled with black bile.
Diemerbroek 1694 Called the adrenals “deputy kidneys”
Winslow 1732 Provided a detailed and accurate description of the adrenals
Bordeau 1775 Reported his belief that the adrenals distribute substances into the blood
Schmidt 1785 Stated that the adrenals secreted substances that helped the action of the heart
J.F. Meckel (“The Younger Meckel”) 1805 Reported on the form, color, and weight of the adrenals in 30 species of animals
Cuvier 1805 Studied the adrenals of the human fetus, claiming that they were large during embryological growth
Henle 1843 Stated that the adrenals could be extirpated with impunity “without sensation or motion suffering in the least”
Ecker 1846 Provided a detailed description of the microscopic anatomy of the adrenal glands
Remak 1847 Postulated that the adrenal medulla originates from sympathetic ganglia
Addison 1849 & 1855 Described the effects of diseases of the adrenals, including primary adrenocortical insufficiency (Addison’s disease)
Vulpian 1856 Reported that the adrenal medulla developed a green color when in contact with ferric chloride
Brown-Séquard 1856 Established that the adrenals were essential for life
Gerlach and Welcher 1857 First to stain the adrenals
Harley 1858 Used carmine stain to provide a histological description of the adrenals. Stated that the removal of the adrenals prolonged life in some species.
Henle 1865 Used chromium salts to develop a brown-yellow color in the medulla (thus the term pheochrome, or “dark color”) 
Arnold 1866 Presented a classification of the adrenal cortex based on three zonae (glomerulosa, fasciculata, and reticularis)
Leydig 1866 Claimed that the adrenal gland is part of the nervous system rather than a blood gland, with the medulla functioning like a nervous ganglion
Frey 1875 Noted the presence of a rich blood supply in the adrenals
Gottschau 1883 Grouped the zona reticularis and the medulla together as the zona consuptiva. Stated that the cells of the cortex grew inward toward the medulla.
Frankel 1886 Described what is now known as pheochromocytoma
Tizzoni 1889 Showed that removing the adrenals caused changes in the brain and in the nervous system
Thorton 1889 Removed a tumor that “reminded the observer of the structure of an adrenal” when studied microscopically
Stilling 1890 Noted that accessory cortical bodies caused differing results after bilateral adrenalectomy
Oliver and Schafer 1894-1895 Found that a rise in blood pressure occurred after administration of an extract from the medulla, which they called adrenalin
Osler 1896 Administered an adrenal extract to temporarily treat Addison’s disease
Abel 1897 Referred to Oliver and Schafer’s extract called “adrenalin” (see above) as “epinephrine”
Takamine and Aldrich 1901 Working independently, they both isolated epinephrine/adrenalin 
Blum 1901 Found that adrenal extracts caused glycosuria
Kohn 1902 Demonstrated that the cells of the adrenal medulla, the carotid body, the abdominal paraganglia, and the organ of Zuckerkandl contained cells positive to chromaffin; described the “chromaffin system”
Stolz 1904 Synthesized epinephrine and norepinephrine 
Pick 1912 First used the term pheochromocytoma
Cushing 1912-1932 Described the syndrome of pituitary basophilism (Cushing’s syndrome) and connected it with pituitary-adrenal hyperactivity
Elliot 1913 Described the association of the adrenal medulla with the sympathetic nervous system
Sargent 1914 Removed a 1,025-gram adrenal tumor
Rogoff and Stewart 1921 Wrote a series of reports on the removal of the adrenal glands
Vaquez and Donzelot 1926 Made the first clinical diagnosis of pheochromocytoma
Roux (Switzerland) 1926 Independently extirpated pheochromocytomas
Mayo (U.S.)
Hartman, Dean and McArthur 1928 Purified adrenocortical extracts and published a paper about this new isolate which prolonged life in adrenalectomized animals
Pincoffs 1929 First to preoperatively diagnose pheochromocytoma
Rabin 1929-1930 Identified an epinephrine-type substance in a pheochromocytoma 
Crile 1932 Surgically denervated an adrenal gland
Broster 1933 Used a transthoracic approach during surgery of the adrenals
Walters 1934 Used a lateral lumbar approach during surgery of the adrenals
Kendall 1934 Isolated cortisone 
Young 1936 Noted the importance of direct observation of both adrenals. Recommended bilateral subtotal adrenalectomy to treat bilateral hyperplasia.
Holtz, Credner and Kronenberg 1945 Rediscovered norepinephrine 
Roth and Kwale 1945 Introduced the histamine provocative test
Huggins and Scott 1945 Attempted to treat advanced prostatic cancer with a bilateral total adrenalectomy
Von Euler 1946 Reported that norepinephrine can be found in sympathetic nerve endings 
Holtz 1947 Found norepinephrine in the adrenal medulla 
Langino 1949 Introduced the Regitine (phentolamine) test 
Thorn and Forsham 1949 Used cortisone acetate to treat Addison’s disease 
Wendlet 1950 Synthesized cortisol
Priestley 1951 With his colleagues at the Mayo Clinic, reported 29 patients who underwent subtotal adrenalectomy to treat Cushing’s disease, noting that perioperative cortisol treatment greatly decreased postoperative complications
Patiño 1951 Successful transplantation of human fetal adrenal cortical tissue in patient with Addison’s disease
Grundy and Reichstein 1952 Isolated aldosterone
Conn 1955 Described primary aldosteronism (Conn’s syndrome)
Liddle 1961 Labeled hydrocortisone as the most important hormone in the adrenal cortex, noting its secretion after ACTH stimulation 
Bartter 1962 Reported sodium-wasting condition (Bartter’s syndrome)
Pearce 1968-1978 Described APUD (amine precursor uptake decarboxylation) system, including cells that produced peptide hormones of neural crest or neuroectodermal origin
Vingerhoeds et al. 1976 Described primary cortisol and glucocorticoid resistance
Viveros et al. 1979 Discovered enkephalins in the chromaffin vesicle
Forest et al. 1982 Studied (and discounted) relationship between adrenarche and gonadarche
Hricak & Williams 1984 Studied normal and pathologic adrenal anatomy with MRI
Madrazo et al. 1987 Autologous transplation of medullary tissue to treat Parkinson’s disease
Counts et al. 1987 Studied (and discounted) relationship between adrenarche and gonadarche

History table compiled by David A. McClusky III and John E. Skandalakis.

Recommended Reading (History):

Bourne GH. The Mammalian Adrenal Gland. Oxford: Clarendon Press, 1949, pp. 1-28.

DeGroot LJ (ed). Endocrinology (3rd ed). Vol. II Part VI. Adrenal Cortex. Philadelphia: WB Saunders, 1995, pp. 1627-1880.

Hughes S, Lynn J. Surgical anatomy and surgery of the adrenal glands. In: Lynn J, Bloom SR (eds). Surgical Endocrinology. London: Butterworth Heinemann, 1993, pp. 458-467.

Scott HW. Surgery of the Adrenal Glands. Philadelphia: J.B. Lippincott Company, 1990, pp. 1-16.

Note to readers: We have used the term “adrenal” rather than “suprarenal” in this text because in spoken language such lengthy terms as “suprarenalectomy” are so cumbersome they are not used.

Embryogenesis

Normal Development

The adrenal glands form from two separate primordia: the neuroectodermal component develops into the adrenal medulla, and the mesodermal component becomes the adrenal cortex. The cells of the future medulla are identified by the 21st to the 22nd day, and are among the wide variety of cells that migrate out of the neural crest (neuroectoderm) in the sixth and seventh weeks2 (Fig. 27-1). These cells travel along the nerves of the 6th to 12th segments into the developing cortical primordia.

Fig. 27-1.

Formation of neural tube and origin of cells of neural crest from neuroectoderm. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Within the cortical tissue, the migrating cells proliferate and differentiate into chromaffin cells at around the third month of gestation. This process is not complete until 12 to 18 months after birth. Some cells do not reach the adrenal organs, but differentiate into chromaffin cells along the aorta. They form nodules of extraadrenal medullary tissue.

The mesodermal component of the cortex is visible as early as the fourth week. The first indication of the cortex is increased division among the peritoneal epithelial cells of the posterior abdominal wall in the groove between the mesentery and the cranial end of the mesonephric ridge (Fig. 27-2). From this epithelium, cords of cells invade the mesenchyme, while surface cells form a cap over the region (Fig. 27-3A). This epithelial cap represents the future zona glomerulosa of the permanent cortex (Fig. 27-3B). Other derivatives of the neural crest cells such as chromaffin cells of the adrenal medulla and the aortic bodies are shown in Fig. 27-4 and Table 27-2.

Table 27-2. Derivatives of the Neural Crest Cells

Dorsal root ganglion cells
Sympathetic trunk ganglia
Parasympathetic ganglia
Schwann cells
Ultimobranchial bodies
Epidermal pigment cells
Glial cells of peripheral ganglia (the satellite or capsule cells)
Leptomeninx
Parts of all the cranial nerve ganglia (except olfactory), connective tissue surrounding the eye and the ciliary muscle
All derivatives of the pharyngeal arches (except skeletal muscles), dermis, and hypodermis of the face and neck, and truncoconal septum (heart outflow tracts)

Fig. 27-2.

Mesothelial cells from mesenteric root differentiate to form cortex. (Modified from Sadler TW. Langman’s Medical Embryology (8th ed). Baltimore: Lippincott, Williams & Wilkins, 2000; with permission.)

Fig. 27-3.

Migration of neural crest cells into mesodermal components of adrenal gland during the sixth week (A) and seventh week (B). (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Fig. 27-4.

Derivatives of neural crest. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Differentiation of cortical zones begins in the eighth week. The outer layer will become the adult zona glomerulosa. Beneath this is the proportionally large “fetal cortex” (Fig. 27-5A), which will decrease in relative size and form the zona fasciculata and the zona reticularis of the adult. These zones may be distinguished at birth (Fig. 27-5B), although they do not appear in the final adult form until the fourth year of postnatal life (Fig. 27-5C).

Fig. 27-5.

Relative proportions of components of adrenal gland: A, fifth month of gestation; B, at birth; C, adult. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw Hill, 1983; with permission. Data from Sucheston ME, Cannon MS. Development of zonular patterns in the human adrenal gland. J Morphol 1968;126:477.)

In the words of Sucheston and Cannon,3 the adult zones appear to be established by “proliferation of the permanent cortex, maturation of the fetal cortex and growth of the medulla,” and are finally completed by 11 to 15 years of age. However, some writers disagree with that view, and believe that shortly after birth, the fetal cortex degenerates and is replaced or reorganized,4 or that the fetal zone cells remodel and reduce in size.5

Due to the large size of the fetal cortex, the volume of the adrenal glands of the human fetus is 20 times larger than that of the adult gland in relation to the weight of the body. The adrenal medulla, however, is small, and enlarges slightly after birth.

At birth, the volume of the adrenals is about 40 ml. Two months after birth, the volume has decreased to about 10 ml, owing to regression and replacement of the fetal cortex (by whatever means). Growth begins again in the second year of postnatal life and accelerates after puberty. Final adult size (40 ml) is reached by age 17.6

Bocian-Sobkowska7 studied the adrenal gland in the first postnatal year:

The postnatal decrease in adrenal volume was caused mainly by a rapid fall of fetal zone volume (from 70% to 3% of total adrenal volume) that can be divided into two phases: rapid phase (from birth to the end of the second week) and a slow phase from the 3rd week on. Involution was accompanied by increase of zona glomerulosa (from 10% to 25% of total adrenal volume), zona fasciculata (from 10% to 38%) and zona reticularis volume (from 1% to 23%). During the whole investigated period the volume of medulla remained constant. The volume fraction of stroma (connective tissue and blood vessels) was highest at the beginning of the first postnatal week and then decreased rapidly at the end of the 2nd week, with the most pronounced changes in the fetal zone and medulla.

The adrenal glands maintain their position in the abdomen, neither ascending with the kidney, nor descending with the testis. Their arterial supply is from segmental mesonephric arteries, greatly altered in their arrangement.

Congenital Anomalies

Congenital anomalies of the adrenal glands are shown in Table 27-3 and Figure 27-6.

Table 27-3. Anomalies of the Adrenal Glands

Anomaly Prenatal Age at Onset First Appearance (or Other Diagnostic Clues) Sex Chiefly Affected Relative Frequency Remarks
Agenesis of the adrenals 4th week None, when unilateral ? Uncommon Associated with absence of kidney on the same side
Fusion of the adrenals 6th week None Male Rare Associated with fused kidneys
Hypoplasia of the adrenals Probably late in gestation At birth Male Very rare, except in anencephalic infants Usually lethal in infancy
Heterotopia of the adrenals 8th week None ? Uncommon Usually found within the capsule of the liver or the kidney
Accessory adrenal glands 4th-6th weeks None Probably equal Common Rarely contain medullary tissue
Adrenal gland hemorrhage At birth Hypovolemic shock or corticosteroid deficiency at birth ? Rare; second most common source of hemoperitoneum in newborn  
Neuroblastoma Approximately 4-5 weeks (?) (Originates in neural crest) 2-5 years of age Males slightly more than females In up to 1:7000 children; most frequent solid tumor in children It has been noted to occur with other congenital syndromes

Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994, p. 726. Used with permission.

Fig. 27-6.

Chief congenital anomalies of adrenal glands. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994; with permission.)

Agenesis of the Adrenal Glands

Unilateral adrenal agenesis is almost always associated with renal agenesis on the same side, but in 90 percent of patients with unilateral renal agenesis, the adrenal gland is present. Absence of the kidney is usually the result of defective ureteric bud development, which does not affect the adrenal gland. Only a failure of formation of the entire nephrogenic ridge results in the absence of both the kidney and the adrenal gland.

Fusion of the Adrenal Glands

Fusion of the adrenal glands behind the aorta may accompany fusion of the kidneys (horseshoe kidney).8

Hypoplasia of the Adrenal Glands

Adrenal hypoplasia is represented by two types: anencephalic and the type in which the marginal fetal cortex does not exist. According to Kerenyi,9 Winquist,10 and others all patients survived no longer than a few months.

Adrenal Heterotopia

Occasionally, the adrenal gland is in its normal location but is also beneath the capsule of the kidney (adrenorenal heterotopia) or that of the liver (adrenohepatic heterotopia) (Fig. 27-7A). Renal tubules or bile ducts may be intermingled with adrenal cells in the area of fusion of the organs. Such fusion renders adrenalectomy more difficult.

Fig. 27-7.

Sites of heterotopic adrenal glands and nodules of cortical tissue (A), and chromaffin tissue (B). Masses (colored black) on and near aorta are retroperitoneal extraadrenal paraganglia. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Accessory Adrenal Tissue

Small nodules of adrenal tissue may be found throughout the abdomen (Figs. 27-8 and 27-9). The largest may contain both cortical and medullary tissue.11 These are true accessory adrenal glands. They are usually found near the aorta, between the origin of the celiac axis and that of the superior mesenteric artery.

Fig. 27-8.

Reported locations of adrenocortical and medullary tissue. (Modified from Fonkalsrud EW. The adrenal glands. In: O’Neill JA, Rowe MI, Grosfeld JL, Fonkalsrud EW, Coran AG (eds). Pediatric Surgery, 5th ed. St. Louis: Mosby, 1998, pp. 1155-1574; with permission.)

Fig. 27-9.

Most frequent location of accessory gland (shaded area) on aorta between celiac and superior mesenteric arteries. (Modified from Graham LS. Celiac accessory suprarenal glands. Cancer 1953;6:149-152.)

Accessory cortical tissue alone is not rare. Most such cortical nodules are under the renal capsule, in the broad ligament in the female or in the spermatic cord of the male.12,13 These sites have surgical significance when the suspected lesion is not found within the substance of the normally situated adrenal glands. All these cortical structures are as susceptible to adenomas as is the normal adrenal gland (Fig. 27-7A).

Chromaffin tissue distributed around the aorta near the origin of the inferior mesenteric artery, in the lumbar sympathetic chain, and in and about the celiac plexus is normal (Fig. 27-7B). Such tissue represents chromaffin cells from the neural crest that were not incorporated into the adrenal medulla. The largest of these are the paraaortic bodies (organs of Zuckerkandl); they regress in size with age.14

These structures may be sites of pheochromocytomas in childhood. They may also be sites of “nonfunctioning” paragangliomas with no clinical evidence of hormonal activity.15 Medullary (chromaffin) tissue outside the normal adrenal gland is much more frequently found than is cortical tissue, and is more frequently associated with hyperfunction than is cortical tissue. O’Riordain et al.16 studied extraadrenal functional paragangliomas and their locations (Fig. 27-10).

Fig. 27-10.

Anatomic location of extraadrenal tumors. Numbers indicate number of patients with tumors in particular location. (Note: patients with multiple tumors are counted more than once if they had tumors at different locations.) (Modified from O’Riordain DS, Young WF Jr, Grant CS, Carney JA, van Heerden JA. Clinical spectrum and outcome of functional extraadrenal paraganglioma. World J Surg 1996;20:916-922.)

Pheochromocytoma

Pheochromocytoma is a benign or malignant medullary tumor. “Functioning” tumors produce catecholamines, either epinephrine, norepinephrine, or both. Hypertension, tachycardia, sudoresis, and anxiety reaction result from the hormonal excess.17

Lo et al.18 stated that “[a]drenal pheochromocytoma is potentially lethal if undetected and is associated with long-term morbidity.” They cited the results of studies in which pheochromocytoma was diagnosed in 4 of 8486 autopsies (0.05%); in 3 of these cases, it was the immediate cause of death.

Ito et al.19 stated that parenchymal degeneration of pheochromocytomas produces paroxysmal hypertension in most cases. Pheochromocytoma is a rare tumor that is found in only 0.1% of patients with diastolic hypertension, according to Favia et al.20 They presented 55 patients with pheochromocytoma as a rare cause of hypertension.

Adrenal Gland Hemorrhage

Adrenal gland hemorrhage is the second most common source of hemoperitoneum in newborns. The right side is involved in 70% of cases, the left in 25%; the condition is bilateral in 5%.21 This phenomenon has several etiologic factors. The large size of the neonatal adrenal gland makes it vulnerable to traumatic injury. Involution of the inner fetal cortical zone leaves central vessels unsupported.

Neuroblastoma

Neuroblastoma is the second most common tumor of infancy, and the most common abdominal tumor of infancy. Fifty percent of the tumors originate in the adrenal gland; the remainder originate in the sympathetic chain. Genetic basis, autosomal dominance, autosomal recessive inheritance patterns, and chromosomal abnormalities are probably all responsible for the genesis of neuroblastoma.

We quote Alexander22:

Neuroblastoma is a malignant tumor of neural crest origin that may arise anywhere along the sympathetic ganglia or within the adrenal medulla. The median age of diagnosis is 2 years; however occurrence is skewed toward younger children, with nearly 35% of cases occurring under 1 year of age and the remainder under 10 years of age. Seventy-five percent of neuroblastomas originate within the abdomen or pelvis, and half of these occur within the adrenal medulla, whereas 20% originate within the posterior mediastinum and 5% within the neck.

Adrenal Cyst

Dermoid cyst of the adrenal gland has been reported.23

Surgical Anatomy

Topography and Morphology

The adult adrenal gland weighs 4 to 8 g and measures 4 x 3 x 1 cm. It is larger in women than in men. The adrenal glands are composed of two distinct parts, with differing functions and embryonic origins (see “Embryogenesis”). The volume of the larger portion, the cortex, is 8 to 20 times that of the medulla.6

The adrenal glands lie on the anteromedial surface of the kidneys near the superior poles; both the glands and the kidneys are retroperitoneal. The two glands differ in shape. The left is more flattened and has more extensive contact with the kidney. It is crescentic or semilunar in form, and may extend on the medial surface of the kidney almost to the hilum. The right gland is more triangular or pyramidal and lies higher on the kidney. This positioning is the reverse of that of the kidneys, in that the left kidney is higher. Each gland is capsulelike, covered by a thin connective tissue stroma.

Each adrenal gland, together with the associated kidney, is enclosed in the renal fascia (of Gerota) and is surrounded by fat, although the adrenal gland is separated from the kidney by a partition of connective tissue. The perirenal fat is more yellow and of a firmer consistency than fat elsewhere in the abdomen.

The adrenal glands are firmly attached to the fascia, which is in turn firmly attached to the abdominal wall and to the diaphragm. The inferior phrenic arteries pass superior to the adrenals to reach the diaphragm. The inferior phrenic arteries give off a series of branches, the superior adrenal arteries, like teeth of a comb. These, their associated connective tissue, and other adrenal arteries and veins assist in holding the adrenal glands in situ.

A layer of loose connective tissue separates the capsule of the adrenal gland from that of the kidney. Because the kidney and the adrenal gland are thus separated, the kidney can be ectopic or ptotic without a corresponding displacement of the gland. Fusion of the kidneys, however, is often accompanied by fusion of the adrenal glands.8

Occasionally, the adrenal gland is fused with the kidney so that separation is almost impossible. Davie24 found six such cases in 1,500 autopsies. A partial or total nephrectomy in such individuals would require a coincidental adrenalectomy.

Normal adrenal glands can be visualized with computed tomography. They appear as triangular shadows, 2 cm in width, with their bases over the upper poles of the kidneys.25 Linos and Stylopoulos26 reported that computed tomography underestimates the actual size of adrenal tumors; even when corrected, the size of the tumor cannot predict its clinical behavior.

Anand et al.27 reported that “[t]he commonest shape of the [adrenal] glands on the left side was semilunar but on the right side it was highly variable: triangular, tetrahedral, inverted Y or V shaped. On comparison of the gross measurements with available ultrasound and CT scan data it was found that both the length and thickness in the population studied were greater than reported in the literature. A knowledge of these variations is very important in diagnosis of abnormalities of the [adrenal] gland, of which tumoral enlargement is rather common.”

Relations

Each adrenal gland has only an anterior and posterior surface. Their relationships to other structures are as follows: (Figs. 27-11 and 27-12)

 

Right adrenal gland:

 

– Anterior surface:

 

Superior: “bare area” of the liver

Medial: inferior vena cava

Lateral: “bare area” of the right lobe of the liver

Inferior: peritoneum (very rarely, if ever) and first part of the duodenum (occasionally)

– Posterior surface:

 

Superior: diaphragm

Inferior: anteromedial aspect of the right kidney

Left adrenal gland:

 

– Anterior surface:

 

Superior: peritoneum (posterior wall of the omental bursa) and the stomach

Inferior: body of the pancreas

– Posterior surface:

 

Medial: left crus of the diaphragm

Lateral: medial aspect of the left kidney

Fig. 27-11

. Relations of adrenal glands from anterior approach. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Fig. 27-12.

Anatomy of adrenal glands. Ao, Aorta (Modified from Hughes S, Lynn J. Surgical anatomy and surgery of the suprarenal glands. In: Lynn J, Bloom SR (eds). Surgical Endocrinology. Oxford: Butterworth Heinemann, 1993, pp. 458-467; with permission.)

The medial borders of the right and left adrenal glands are about 4.5 cm apart. In this space, from right to left, are the inferior vena cava, the right crus of the diaphragm, part of the celiac ganglion, the celiac trunk, the superior mesenteric artery, the other part of the celiac ganglion, and the left crus of the diaphragm.

Remember

 

The right adrenal gland is located posterior to the duodenum and the right lobe of the liver.

In many cases, the medial part of the right adrenal gland is related to the inferior vena cava.

The right adrenal gland may be closely related to the right hepatic vein as it passes to drain into the inferior vena cava.

The right adrenal vein is short, and is difficult to ligate.

The right adrenal gland is anterior to the diaphragmatic and pleural reflections.

The left adrenal gland is located posterior to the stomach and pancreas and medial to the splenic porta.

The left adrenal gland is located in front of the reflections of the diaphragm and the pleura.

The left adrenal gland is related to the medial aspect of the upper pole of the left kidney, occasionally extending to the left renal porta.

Adrenal Zones

The outer portion of the adrenal gland, the adrenal cortex, is composed of three zonae: glomerulosa, fasciculata, and reticularis. The innermost region of the adrenal gland is the medulla. Figs. 27-4 and 27-7 demonstrate chromaffin cells of the adrenal medulla and of heterotopic adrenal glands.

To help the student remember the layers of the adrenal gland, every year in our clinical and surgical anatomy classes we repeat the mnemonic “Good For Reason Mother” (Fig. 27-13). Another mnemonic device which is currently popular with medical students relates the architecture of the cortical region of the adrenal gland and its regulatory functions: Great fat rats: salt, sugar, sex.

Fig. 27-13.

Summary of embryology, anatomy, physiology, and pathology of adrenal glands. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994.)

Vascular Supply

Arterial Supply

The adrenal glands and the thyroid gland are the viscera having the greatest blood supply per gram of tissue. As many as 60 arterial twigs may enter the adrenal gland. The arterial supply of the adrenal glands arises, in most cases, from three sources (Fig. 27-14):

 

The superior adrenal arteries. A group of six to eight arteries arises separately from the inferior phrenic arteries. One artery may be larger than the others, or all may be of similar size.

The middle adrenal artery arises from the aorta just proximal to the origin of the renal artery. It can be single, multiple, or absent. It supplies the perirenal fat only.

One or more inferior adrenal arteries arise from the renal artery, an accessory renal artery, or a superior polar artery. Small twigs may arise from the upper ureteric artery.

Fig. 27-14.

Arterial supply and venous drainage of adrenal glands. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

All these arteries branch freely before entering the adrenal gland, so 50-60 arteries penetrate the capsule over the entire surface.28 It is possible that this branching of arteries before entering the adult adrenal gland indicates the outline of the surface of the much larger gland of the embryonic period, when the fetal cortex was present.

The sources of arterial supply to the adrenal gland are subject to variation.29-31 In 61 percent of individuals, the supply by middle or inferior adrenal arteries may be lacking; the superior adrenals are absent in only about 2 percent of cases. In about 5 percent of individuals, the arterial supply is derived wholly from one source — a singular vessel supplying the superior, middle, and inferior branches.

Venous Drainage

The adrenal venous drainage does not accompany the arterial supply, and is much simpler (Fig. 27-14). A single vein drains the adrenal gland, emerging at the hilum. The left vein passes downward over the anterior surface of the gland. This vein is joined by the left inferior phrenic vein before entering the left renal vein.

The right vein is typically very short; it may be 0.5 cm long, or even less. The right adrenal vein passes obliquely to open into the posterior side of the inferior vena cava. The right adrenal vein does not usually have any tributaries other than from the adrenal gland. If the adrenal gland must be mobilized or removed, it is wise to ligate the right adrenal vein first, then divide and ligate the arteries later, because the right vein is so easily torn from the inferior vena cava.

The right adrenal vein may drain into the right hepatic vein, close to the junction of the hepatic vein with the inferior vena cava.32 Occasionally there are two veins: one having a normal course, and an accessory vein entering the inferior phrenic vein.33 In his 40 years in the dissecting room, the senior author of this chapter (JES) has encountered accessory veins several times. Some variations of the venous drainage are shown in Fig. 27-15.

Fig. 27-15.

Venous drainage of adrenals. HV, hepatic vein; Rt. RV, right renal vein; Inf. VC, inferior vena cava; TV, testicular vein; Lt. RV, left renal vein; OV, ovarian vein; Sp. V, suprarenal vein. (Modified from Johnstone FRC. The surgical anatomy of the suprarenal glands with particular reference to the suprarenal vein. Surg Clin North Am 1964;44: 1315-1385; with permission.)

When using the posterior approach to the adrenal gland, the left adrenal vein is found on the anterior surface of the gland. The right adrenal vein is found between the inferior vena cava and the gland. Careful mobilization of the gland is necessary for good ligation of the vein.

In the early studies of Dobbie and Symington,34 it was observed that the adrenal gland appeared to be divisible into three regions: the head, the body, and the tail. The head region, in which the medullary tissue was most prominent, was that part closest to the emergence of the adrenal vein from the gland. The tail, where medulla was almost absent, was the most lateral part. The ventral surface of the gland was characterized by an anterior groove. The dorsal surface possessed a ridgelike elevation, the crest, which increased in prominence near the lateral tip of the gland. The crest is flanked by two alar parts.

The central adrenal vein carries with it a cuff of cortical tissue into the substance of the gland. The vein is characterized by unique longitudinal muscle fibers, especially thick on its dorsal surface, which may be related to effective closure of its tributaries upon contraction. Shortly after entering the adrenal gland, the central vein receives a large muscular branch which curves backwards and drains the head of the gland. Several other main tributaries enter the main vein from the body and tail region.

In the studies of Monkhouse and Khalique,35 in almost all cases venous interconnections were found between the adrenal venous system and the azygos, hemiazygos, and lumbar veins, in addition to accessory connections with the renal veins. The study was initiated by the finding (in a patient with a left-sided pheochromocytoma) of high levels of catecholamines in the superior vena cava and right atrium, rather than in the inferior vena cava, as one would normally expect.

Lymphatic Drainage

The lymphatics of the adrenal gland are usually said to consist of a profuse subcapsular plexus that drains with the arteries and a medullary plexus that drains with the adrenal veins. Merklin36 could find no evidence of lymphatic vessels within the parenchyma of the adrenal glands.

Drainage is to renal hilar nodes, lateral aortic nodes, and to nodes of the posterior mediastinum above the diaphragm by way of the diaphragmatic orifices for the splanchnic nerves (Fig. 27-16). Rouvière37 stated that lymphatics from the upper pole of the right adrenal gland may enter the liver. The majority of capsular lymphatic vessels pass directly to the thoracic duct without the intervention of lymph nodes.36

Fig. 27-16.

Lymphatics of adrenal glands. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Innervation

The adrenal cortex appears to have only vasomotor innervation. Most of the fibers reaching the gland from the splanchnic nerves, the lumbar sympathetic chain, the celiac ganglion, and the celiac plexus enter the medulla (Fig. 27-17). These fibers are preganglionic38 and end on the medullary chromaffin cells. This arrangement is not as anomalous as it might appear; chromaffin cells arise from the same embryonic source as do the postganglionic neurons elsewhere. Most of these preganglionic fibers in humans are nonmyelinated.39

Fig. 27-17.

Nerve supply to adrenal glands. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Histology

Adrenal Cortex

The vascularity of the adrenal cortex is among the greatest in the entire body. The adrenal cortex is composed of three zones: the zona glomerulosa, the zona fasciculata, and the zona reticularis. In all three zones, all cells produce steroids.

In the zona glomerulosa (the outermost layer), small cells are arranged in roughly spherical groups. This zone secretes the mineralocorticoid aldosterone.

In the zona fasciculata, larger cells are arranged in columns which are oriented radially. The carbohydrate-active steroid, cortisol, and the adrenal sex steroids are produced here. Vitamin C is abundant in these cells.

In the third layer, the zona reticularis, small cells are arranged in strands forming an irregular network. These cells secrete cortisol, androgens, and estrogens. Cholesterol is present as a precursor to the genesis of the steroids.

Adrenal Medulla

The cells in the adrenal medulla are large and pale. They secrete epinephrine and have a chromaffin reaction. These cells are called chromaffin cells, or pheochromocytes. Distributed throughout the medulla, but few in number, are postganglionic sympathetic neurons.

Most medullary cells secrete epinephrine, but some secrete norepinephrine instead.

An abundance of round or oval secretory granules is located within the cellular cytoplasm of the adrenal medulla.

Physiology

As mentioned above, the following corticosteroid hormones are secreted by the adrenal cortex:40

 

aldosterone (in the zona glomerulosa)

cortisol

carbohydrate-active cortisol and androgens (in the zonae fasciculata and reticularis)

Secretion of aldosterone is controlled by angiotensin II, serum potassium, and the adrenocorticotropic hormone (ACTH) (Fig. 27-18).

Fig. 27-18.

Relations of renin, angiotensin I, angiotensin II, and their anatomic sites of production and enzymatic conversion. ACTH, adrenocorticotropic hormone. (Modified from Newsome HH. Suprarenal glands. In: Greenfield LJ (ed). Surgery: Scientific Principles and Practice. Philadelphia: JB Lippincott, 1993, pp. 1209-1223; with permission.)

Cortisol secretion is controlled by ACTH from the anterior pituitary gland (Fig. 27-19).

Fig. 27-19.

Feedback relations between adrenal gland, hypothalamus, and anterior pituitary. CRH, corticotropin-releasing hormone; ACTH, adrenocorticotropic hormone. (Modified from Newsome HH. Suprarenal glands. In: Greenfield LJ (ed). Surgery: Scientific Principles and Practice. Philadelphia: JB Lippincott, 1993, pp. 1209-1223; with permission.)

An excess of androgenic sex steroids almost always arises from carcinoma. Enzymatic defects (Fig. 27-20) are responsible for congenital adrenal hyperplasia with sexual ambiguity.41 By blocking the adrenal production of cortisol, the defects result in the loss of negative feedback to the hypothalamus. There is continued stimulation and excess production of androgens and possibly mineralocorticoids. The result is congenital adrenal hyperplasia syndrome. The most common enzymatic deficiencies are 21-hydroxylase, 11--hydroxylase and 3--hydroxysteroid dehydrogenase.

Fig. 27-20.

Adrenal production of cortisol blocked by heritable enzymatic defects. CRH, corticotropin-releasing hormone; ACTH, adrenocorticotropic hormone. (Modified from Newsome HH. Suprarenal glands. In: Greenfield LJ (ed). Surgery: Scientific Principles and Practice. Philadelphia: JB Lippincott, 1993, pp. 1209-1223; with permission.)

In the adrenal medulla, sympathetic stimulation is responsible for the secretion of epinephrine and norepinephrine.

An excellent paper by Hiatt and Hiatt42 presents the triumphal conquest of Addison’s disease. It includes the discovery of the glands, identification of their hormonal products, use of the hormones for therapy, and biosynthesis for pharmacologic applications. We recommend it to all our readers.

Ito et al.43 reported that the assay for urine metanephrine and normetanephrine is an effective test for the diagnosis of pheochromocytoma and management of incidentaloma.

We present Del Rio44 verbatim:

The sympathoadrenal system (SAS) represents a major contributor to body homeostasis, regulating blood pressure, heart rate, energy balance and inter-mediary metabolism. Thus, it is not unexpected that in the last decades a consistent literature has been focused on the possible role of the sympathoadrenal system in the pathogenesis of human obesity. There are, however, many factors confounding a compar-ison of sympathoadrenal system activity between lean and obese subjects. Among these, one should be aware that SAS should be functionally separated into sympathetic nervous system (SNS) and adrenal medulla (AM), and that each of these two systems can be activated independently from the other by distinct physiological stimuli; this phenomenon in fact underlies the discordant pattern of findings for adrenomedullary and sympathetic activity in human obesity. While, in fact, obese subjects often display an increased basal SNS activity, there are numerous reports of blunted AM function in the obese. Recent evidence suggests that this reduced adrenaline secretion is an acquired feature of human obesity, a finding that fits in well with the hypothesis that the hormonal milieu, particularly sex steroids and cortisol, plays a role in the determination of blunted AM activity. Catecholamines have been recently demonstrated to play a role also in the regulation of the whole energy balance. Adrenaline in fact acutely reduces both leptin mRNA as well as circulating leptin in human obese subjects, suggesting that catecholamines may influence the cross-talk between energy stores and the centrally mediated modulation of food intake.

Surgical Applications

…it should be recognized that the surgical approach and exposure to the suprarenal gland will be tailored to the underlying disease process…—Richard Bihrie and John P. Donahue45

Surgery is the treatment of choice for all benign functioning or malignant adrenal tumors. Stratakis and Chrousos46 summarized several studies of adrenal cancer, which showed these neoplasias accounting for 0.05-0.2% of all cancers and occurring at every age:

A bimodal age distribution has been reported, with the first peak occurring before the age of 5 years and the second in the fourth to fifth decade. In all published series, females predominate, accounting for 65% to 90% of the reported cases. Several studies have shown a left-sided prevalence in adrenal cancer, whereas others have reported a right-sided preponderance. In approximately 2% to 10% of patients, adrenal cancer is found bilaterally.

Khorram-Manesh et al.47 reported the rarity of adrenocortical carcinoma and the need for better treatment alternatives. Though surgery is the treatment of choice, its role in advanced disease has been questioned.

Cook and Christie48 reminded us that a unilateral adrenal mass may be secondary to Mycobacterium kansasii in patients with AIDS. The only conservative treatment applies to congenital adrenal hyperplasia with adrenal hyperfunction syndromes.

The adrenal glands may be approached by three open methods. These are: anterior, posterior, and lateral (transthoracic).

Harrison et al.49 reported that the prognosis of adrenocortical carcinomas after curative resection depends on tumor size, hemorrhage, and mitotic count.

Paul et al.50 advocated adrenalectomy for isolated adrenal metastases for selected patients presenting with long disease-free intervals and favorable tumor biology. Tsui et al.51 provided a thoughtful analysis of the role of adrenalectomy in radical nephrectomy:

With a low incidence of 0.6%, adrenal involvement is not likely in patients with localized, early stage renal cancer cell carcinoma and adrenalectomy is unnecessary, particularly when CT is negative. In contrast, the 8.1% incidence of adrenal involvement with advanced renal cell carcinoma supports the need for adrenalectomy. Careful review of preoperative imaging is required to determine the need for adrenalectomy in patients at increased risk with high stage lesions, renal vein thrombus and upper pole or multifocal intrarenal tumors. With a negative predictive value of 99.4%, negative CT should decrease the need for adrenalectomy. In contrast, positive findings are less reliable…[and] may not necessarily indicate adrenalectomy….

Anterior Approach for Left Adrenalectomy

The anterior approach is preferred when

 

Adrenal disease is bilateral (10 percent of patients)52

Tumor is over 10 cm in size

Adrenal tumor has invaded surrounding structures

The anterior approach has the advantage of enabling the surgeon to inspect, palpate, and biopsy both glands. The incision chosen for an anterior approach may be vertical, midline or paramedian, transverse, or chevron. The chevron transabdominal incision provides bilateral exposure (Fig. 27-21).

Fig. 27-21.

Incisions for anterior exposure of adrenal glands. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Exposure and Mobilization of Left Adrenal Gland

Exposure of the left adrenal gland begins with the incision of the posterior parietal peritoneum lateral to the left colon. The incision is carried upward, dividing the splenorenal ligament (Fig. 27-22). Care must be taken to avoid injury to the spleen, the splenic capsule, or the splenic vessels and the tail of the pancreas. The latter are enveloped by the splenorenal ligament.

Fig. 27-22.

Incision of parietal peritoneum lateral to left colon. Incision divides splenorenal ligament. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Another approach to the left adrenal gland is by opening the lesser sac through the gastrocolic omentum, which may be incised longitudinally outside the gastroepiploic arcade (Fig. 27-23). In this approach, care must be taken to avoid traction on the spleen or the splenocolic ligament. The ligament may contain tortuous or aberrant inferior polar renal vessels or a left gastroepiploic artery.

Fig. 27-23.

Approach to the left adrenal through the gastrocolic omentum by opening the lesser sac. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Following either approach, the peritoneum under the lower border of the pancreas should be incised halfway along the tail; the incision should be extended laterally for about 10 cm. The pancreas can be gently retracted upward, avoiding injury. This maneuver will expose the left adrenal gland on the superior pole of the left kidney; both the gland and the kidney are covered with renal fascia (of Gerota). The adrenal gland will be lateral to the aorta, about 2 cm cranial to the left renal vein. Incision of the renal fascia exposes the adrenal gland completely, and permits access to the adrenal vein. If the operation is for pheochromocytoma, the adrenal vein should be ligated at once to prevent the release of catecholamines into the circulation during subsequent manipulation of the gland.

A retractor must be placed gently to avoid tearing the inferior mesenteric vein from the splenic vein. Although the inferior mesenteric vein may be ligated without sequelae, it is prudent to refrain from the use of retractors in this area if possible.

A third approach, useful in patients whose left adrenal lesion is anterior, is exposure of the gland by an oblique incision of the left mesocolon (Fig. 27-24). The arcuate vessels can be divided and the marginal artery can be sectioned, but the major branches of the middle and left colic arteries must be preserved. Care to avoid excessive retraction will prevent injury to the wall of the left colon.

Fig. 27-24.

Approach to the adrenal by incision of the left mesocolon near the splenic flexure. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

In some lesions, such as primary aldosteronism, the adrenal gland is hypervascular and friable; meticulous attention to hemostasis is essential. Adenoma can be disguised or mimicked by hematomas from operative trauma.53 The surgeon can use a part of the adjacent periadrenal fascia to handle the gland. Manipulation should be with fine forceps only. Hemostasis from the numerous arteries can be maintained by clips, ligatures, or by electrocoagulation.

Dissection should start at the inferolateral aspect of the left adrenal gland and should proceed superiorly (Fig. 27-25). The surgeon should keep in mind the possible presence of a superior renal polar artery. The gland can be retracted superiorly. Remember that the left adrenal gland extends downward, close to the left renal artery and vein.

Fig. 27-25.

The left adrenal gland exposed by an upward dissection. Note position of left adrenal vein. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

After removal of the adrenal gland, its bed should be inspected for bleeding points. Surrounding organs, especially the spleen, should be inspected for injury. Splenic injury can be repaired with sutures over a piece of retroperitoneal fat, Gelfoam, or Avitene. More severe injury may require partial or even total splenectomy.

Anterior Approach for Right Adrenalectomy

Exposure and Mobilization of Right Adrenal Gland

On the right, the anterior approach to the adrenal gland begins with the mobilization of the hepatic flexure of the colon. Sharp dissection is necessary to divide posterior adhesions of the liver to the peritoneum. Remember that medial attachments can contain hepatic veins.

Mobilization of the colon will expose the duodenum. The second portion of the duodenum is freed by incision of its lateral avascular peritoneal reflection. It can now be separated from retroperitoneal structures and reflected forward and to the left (Kocher maneuver). This maneuver will expose the vena cava, the right adrenal gland, and the upper pole of the right kidney (Fig. 27-26). The surgeon must remember that the common bile duct and the gastroduodenal artery are in this area.

Fig. 27-26.

Right adrenal gland and upper pole of right kidney are exposed following Kocher maneuver. Note position of right adrenal vein. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw- Hill, 1983; with permission.)

Unlike the left adrenal gland, the right gland rarely extends downward to the renal pedicle. The right adrenal vein usually leaves the gland on its anterior surface close to the cranial margin, and enters the vena cava on its posterior surface (Fig. 27-26). To prevent the release of catecholamines and to avoid stretching the vein, hemostatic clips should be placed as soon as both borders of the vein are visible. Stretching the vein invites hemorrhage from the vena cava.

Tominaga et al.54 advised resection of pheochromocytoma by completely isolating the IVC and using extracorporeal charcoal hemoperfusion, thereby preventing systemic distribution of catecholamines during manipulation of the tumor.

Posterior Approach for Adrenalectomy

Exposure and Mobilization

In spite of the advantage of being able to inspect, palpate, or biopsy both glands by using the anterior approach, improvements in preoperative diagnosis (such as computed tomography and selective adrenal angiography) have increased the use of the posterior approach.55 The posterior approach can be used for any adrenalectomy except that in which a large or ectopic tumor is a strong possibility.

Nagesser et al.56 have different parameters for surgery: “Although laparoscopic adrenalectomy is the treatment of choice for small and benign adrenal lesions, larger lesions and/or adrenal malignancy require open adrenalectomy. In these cases the retroperitoneal approach is the preferred route.”

With the patient prone, a curvilinear incision is made through the latissimus dorsi muscle to the posterior lamella of the thoracolumbar fascia (Fig. 27-27). This will expose the erector spinae muscle. Lumbar cutaneous vessels must be ligated or cauterized. The surgeon must be sure to be over the 12th, not the 11th, rib. Dissection of the pleural fold at the 11th rib can result in pneumothorax. Remove the 12th rib on the left, and the 11th rib on the right.57

Fig. 27-27.

Incisions for posterior approach to adrenal glands. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw- Hill, 1983; with permission.)

The erector spinae muscle attachments to the dorsal aspect of the 12th rib should be detached, exposing the rib. The rib must be removed subperiosteally to avoid damaging the underlying pleura. Periosteum should be stripped on the superior surface from medial to lateral and on the inferior surface from lateral to medial. Avoid injury to the 12th intercostal nerve bundle at the inferior angle of the rib. The nerve is separate from, but parallel with, the blood vessels. The vessels can be ligated if necessary.

The pleura must be separated from the upper surface of the diaphragm, and the diaphragm should be incised from lateral to medial. The fascia can be opened, and the upper pole of the kidney identified. Inferior retraction of the kidney will usually bring the adrenal gland into the field. Care must be taken to avoid tearing the renal capsule or stretching a possible superior polar artery.

Dissection of the left adrenal gland should begin on the medial aspect, with clips for the arteries encountered. Remember that the pancreas lies just beneath the gland; it is easily injured. In this approach, the last step is to identify the left adrenal vein, which usually emerges from the medial aspect of the gland and courses obliquely downward to enter the left renal vein. Undue traction on the gland can tear the renal vein.

The right adrenal gland is approached by retracting the superior pole of the right kidney inferiorly; the posterior surface of the adrenal gland can then be dissected free from fatty tissue. The liver must be retracted upward as the apex of the gland is reached. The lateral borders are freed up, leaving only the medial margins attached.

The right adrenal gland should be retracted laterally. Branches from the inferior phrenic artery, aorta, and right renal artery to the gland should be ligated. The right adrenal vein, also, should be ligated (Fig. 27-26). We recommend freeing the vena cava far enough to ensure room for an angle clamp should hemorrhage from the vena cava or the adrenal vein require it. After removing the gland, carefully inspect for air leaks and bleeding before closing the incision.

Thoracoabdominal Approach for Adrenalectomy

Exposure and Mobilization

The thoracoabdominal approach provides a better exposure for large tumors of a single adrenal gland.58 It will permit removal of the spleen and the distal pancreas, should they be involved with the adrenal tumor.59

The incision starts at the angle of the 8th to the 10th rib. It extends across the midline to the midpoint of the contralateral rectus muscle just above the umbilicus (Fig. 27-28). The 10th rib is removed, the pleura is opened, and the diaphragm is incised from above. The remainder of the procedure is the same as for the anterior approach.

Fig. 27-28.

Incision for thoracoabdominal approach to adrenal gland. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw- Hill, 1983; with permission.)

Laparoscopic Adrenalectomy

Laparoscopic adrenalectomy may be performed by a lateral transabdominal or a posterior retroperitoneal approach. Duh et al.60 reported that both methods are safe. They used the posterior approach for bilateral tumors; for tumors of more than 6 cm, the lateral approach was preferable. Walz et al.61 supported the posterior retroperitoneoscopic approach for adrenalectomy.

Imai et al.62 stated that laparoscopic transperitoneal lateral adrenalectomy is the technique of choice for removing functioning adenomas and adrenal masses less than 6 cm in diameter. They reported that patients undergoing the laparoscopic procedure experience greater comfort, less blood loss, and shorter hospital stays with no increase in cost.

Thompson et al.63 found transabdominal laparoscopic adrenalectomy preferable to open posterior adrenalectomy, despite its greater expense. They reported improved patient comfort and satisfaction, and “dramatically” fewer complications. Rutherford et al.64 presented 67 successful adrenalectomies employing the unilateral transabdominal approach; postoperative bleeding occurred in 1.5% of cases, as did port site herniation.

Basso et al.65 advised that laparoscopic supragastric approach for left adrenalectomy gives a good visualization of the left adrenal, avoiding anatomic complications during mobilization of the spleen, pancreatic tail, and splenic flexure of the colon. Good visualization of the left adrenal vein is also accomplished.

Horgan et al.66 found laparoscopic adrenalectomy safe and effective for benign adrenal tumors. Jossart et al.67 stated “Laparoscopic adrenalectomy can now be considered the standard of care for most adrenal neoplasms.” Using data on pheochromocytoma surgery, Fernández-Cruz et al.68 reached the same conclusion. Walther et al.69 reported the following: “Laparoscopic partial adrenalectomy is technically feasible in patients with a hereditary form of pheochromocytoma, and may preserve adrenocortical function. Laparoscopic ultrasound was necessary to identify 2 of the seven pheochromocytomas removed.”

Shen et al.70 advised laparoscopic adrenalectomy for patients with primary hyperaldosteronism. The authors report that this laparoscopic procedure yields similar results with respect to blood pressure and hypokalemia and is accompanied by lower morbidity than the open procedure. Patients with less severe hypertension and hypokalemia are now undergoing this procedure.

A seven-year study of laparoscopic adrenalectomies by Brunt et al.71 concluded the following:

Laparoscopic adrenalectomy is a safe and effective procedure and has several advantages over open adrenalectomy. Laparoscopic adrenalectomy should become the preferred operative approach for the treatment of patients with small, benign adrenal neoplasms.

In commentary on the Washington University findings, Prinz72 wisely stated that adrenal glands should be removed in toto with their capsule intact. Prinz agreed with Brunt and colleagues that increased tumor size greatly decreased the advisability of laparoscopy. Siperstein et al.73 stated that laparoscopic posterior adrenalectomy should be considered in patients with tumors less than 6 cm. Staren and Prinz74 concluded that more than 60 percent of surgically treatable adrenal disease may be approached laparoscopically.

Walz et al.75 stated that in selected cases subtotal adrenalectomy via posterior approach retroperitoneoscopically is a safe procedure.

Kollmorgen et al.76 compared acute-phase response and wound healing in laparoscopic and open posterior adrenalectomy in 40 pigs. They concluded that laparoscopic adrenalectomy compared favorably enough that study of its use should continue. Ting et al.77 stated that laparoscopic adrenalectomy is replacing posterior adrenalectomy.

Barry et al.78 stated that for small incidentalomas considered benign or nonfunctioning the appropriate treatment is conservative management, rather than laparoscopic removal.

Barresi and Prinz79 stated the following:

Conventional surgical approaches, particularly the transabdominal and thoracoabdominal approaches, will undoubtedly be required to treat certain lesions of the adrenal gland. This is especially true when dealing with larger tumors, and those suspicious for malignancy. Surgeons with an interest in treating patients with adrenal disorders must become proficient in the technique of lapraroscopic adrenalectomy. This will allow them to offer their patients the most appropriate means of operative therapy suitable for their individual problems.

Gill et al.80 provided cautious support for outpatient adrenalectomy, “Ambulatory adrenalectomy is feasible and safe, and results in high patient satisfaction. However, ambulatory adrenalectomy should be restricted to highly select patients and performed by minimally invasive surgeons who have considerable experience with laparoscopic surgery.”

Smith et al.81 have written that “laparoscopic adrenalectomy has become the gold standard for adrenalectomy.”

Anatomic Complications

Anterior Approach for Left Adrenalectomy

Vascular Injury

Inferior Mesenteric Vein

The inferior mesenteric vein can be avulsed by excessive traction at its junction with the splenic vein. Bleeding is difficult to control, and the vessel may have to be ligated.

Middle and Left Colic Arteries

The middle and left colic arteries, or their larger branches, can be severed by sharp dissection through the left mesocolon. A segmental colectomy may be necessary if the blood supply is compromised. Excessive traction on the colon may lead to a tear of the spleen’s capsule due to splenocolic attachment to the inferior pole of the spleen.

Superior Renal Polar Arteries

Superior renal polar arteries are present in about 15 percent of subjects.30 Their position, superior to the renal arteries, renders them vulnerable. They can be ligated if necessary.

Renal Artery and Vein

The left adrenal gland extends down the medial surface of the left kidney almost to the hilum; thus, it is possible to injure the renal vessels while mobilizing the gland. Careful repair is required. If repair is not possible, nephrectomy may be necessary.

Remember, however, that the left kidney can be saved if the left renal vein is ligated proximal to its junction with the adrenal and gonadal veins; this is particularly true when operating on a right kidney tumor with an inferior vena caval thrombus. If ligation must be distal to these tributaries, venous infarction will occur; repair of the vein or nephrectomy is mandatory.

If nephrectomy is performed, ligate the renal and gonadal veins separately. Carlton and Guerriero82 stated that major divisions of the renal vein at the hilum can be ligated with impunity. They believed that intrarenal collateral circulation will compensate for the segmental venous ligation.

Organ Injury

Splenic Capsule and Spleen

Excessive traction on the spleen with tearing of the capsule is the greatest single operative risk in anterior left adrenalectomy. Nash and Robbins83 reported splenic injury requiring splenectomy in up to 20 percent of adrenalectomy patients. We believe that partial splenectomy should be performed whenever possible.

Pancreas

The pancreatic parenchyma can be injured during upward reflection of the organ; this may result in clinical pancreatitis with the formation of a pseudocyst in some cases. Injury to the tail of the pancreas requires resection and drainage. If injury to the inferior border is minor, drain; if major, repair and drain, or resect the entire distal pancreas and drain.

Renal Capsule

Sharp dissection of the inferior medial margin of the left adrenal gland can injure the capsule of the left kidney. Such injury should be repaired.

Left Colon

Incision of the left mesocolon or excessive retraction of the colon could injure the colon wall, or even perforate it. The colon should be prepared with enemas and antibiotics before surgery, in case inadvertent perforation occurs and repair is necessary.

Anterior Approach for Right Adrenalectomy

Vascular Injury

Hepatic Veins

Remember that the medial posterior attachments of the liver contain the hepatic veins. Retract with care. A right hepatic vein can be ligated.84 Hepatic resection after major hepatic vein ligation is necessary in some animals, but not in humans.

Inferior Vena Cava

Avoid aggressive lateral retraction of the adrenal gland. Traction on the right adrenal vein may rupture the vena cava; hemorrhage here is difficult to control, and immediate repair is necessary.

Superior Renal Polar Artery

As on the left, the occasional polar artery lies close to the operative field and can be injured. If injured, it can be ligated.

Gastroduodenal Artery

The gastroduodenal artery should be identified and avoided during the Kocher maneuver. If it is injured, ligation is necessary.

Organ Injury

Liver

Injury to the liver can result from excessive retraction. Pressure, cautery, Gelfoam, or Avitene can be used in repair.

Duodenum

Mobilization and reflection can injure the duodenum and may result in a catastrophic postoperative duodenal fistula. Avoid sharp dissection, and be prepared to repair the defect.

Posterior Approach for Adrenalectomy

Vascular Injury

Superior Renal Polar Arteries

As in other approaches, the superior renal polar arteries, which are inconstant, are vulnerable to inadvertent injury. They can be ligated if necessary.

Left Adrenal Vein

Before mobilizing and clamping the left adrenal vein, the inferior vena cava should be freed up sufficiently to place a clamp on it in case ligation of either vessel should become necessary.

Right Hepatic Vein

The right hepatic vein lies just cephalad to the right adrenal vein. It can be torn by excessive traction. It can be ligated.

Inferior Vena Cava

In a right adrenalectomy, the vena cava can be injured by retraction or sharp dissection. Such injury must be repaired. Remember in retracting the liver that the veins from the caudate lobe often drain directly into the anterior surface of the inferior vena cava. Such veins, like the right adrenal vein, are often very short.

Organ Injury

Pleura

The pleura at the 12th rib must be identified and pushed out of the way. Flint and Bartels58 found 4 cases of perforated pleura among 29 exposures of the adrenal glands.

If perforation occurs, it is necessary to evacuate air from the pleural cavity by catheter, with pulmonary inflation. Repair the pleural defect if possible.

Twelfth Subcostal Nerve

The 12th subcostal nerve should be protected. Its injury will result in hyperesthesia or dysesthesia in the groin.

Renal Capsule

Excessive retraction can tear the renal capsule. Repair it if necessary. The adrenal gland, in some cases, receives inferior adrenal arterial supply from capsular branches of the renal arteries.

Pancreas

Remember that in the posterior approach, the pancreas lies just beneath the left adrenal gland. See details in the “Anterior Approach for Left Adrenalectomy” section.

Thoracoabdominal Approach for Adrenalectomy

Vascular Injury

These injuries are the same as in anterior approaches.

Organ Injury

In the thoracoabdominal approach, the lung and phrenic nerve are at risk in addition to the organs that are subject to injury in an anterior approach to the adrenal glands (splenic capsule and spleen, pancreas, left renal capsule, left colon, liver, duodenum).

If the pleura is entered, there is a possibility of injury to the lung; such injury must be repaired.

Incision of the diaphragm must be planned to avoid sectioning major branches of the phrenic nerve. Fig. 27-29 shows permissible incisions of the diaphragm from above.85

Fig. 27-29.

Schematization showing chief branches of phrenic nerves on cranial surface of diaphragm. Dashed lines indicate location of incisions that will avoid phrenic nerves. A, The diaphragmatic component of a combined abdominothoracic incision extending down into the esophageal hiatus. B, Circumferential incision. C, D, Incisions extending from lateral (midaxillary) and posterior costal areas into the central tendon (from above). (Modified from Merendino KA. The intradiaphragmatic distribution of the phrenic nerve. Surg Clin North Am 1964;44:1217; with permission.)

In a select group of patients with Cushing’s syndrome, bilateral adrenalectomy is necessary and effective. However, this surgery is associated with occasional morbidity and mortality. According to O’Riordain et al.,86 long-term sequelae are not well known.

NOTE: For further reading about the adrenal glands, the authors highly recommend Surgery of the Suprarenal Glands, edited by H. William Scott, Jr.87

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