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386 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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Unless drained, the abscess can become large and invade the breast. An
underlying cancer with secondary infection should be considered.
BREAST SYNDROMES
The Female Breast
Breast masses. Breast masses arise from benign and malignant neoplastic
change in the ductal or acinar epithelium, cystic changes, duct obstruction,
infection, bleeding, inltration by abnormal cells, or accumulation of intra- or
extracellular substances, especially brosis. Some masses retain hormonal control; many do not.
lesions. Cysts are overwhelmingly benign and aspiration of nonbloody uid
with disappearance of the mass is diagnostic. Smooth regular borders and
tenderness suggest an broadenoma. Tenderness is characteristic of inammatory breast disease, with or without infection, but uncommon with cancer.
Histology by aspiration cytology or biopsy is necessary to conrm benignity.
Premalignant and malignant masses. Most malignant neoplasms arise from
the ductal epithelium, some having a strong genetic contribution (BRCA-1,
BRCA-2). Atypical ductal hyperplasia is associated with an increased risk of
subsequent in-situ or invasive ductal carcinoma. Lobular neoplasia, arising in
the acinar lobules, is usually noninvasive but is associated with an increased
risk for invasive ductal carcinoma. Malignant lymphoma may involve the
lymph nodes and other breast tissues. The primary distinctions are between
malignant and nonmalignant masses and invasive and noninvasive malignancies. The virtue in diagnosing a benign breast condition lies in excluding
malignancy, which requires tissue. Discrete dominant lesions require biopsy
for histologic diagnosis. Normal or nondiagnostic mammography must not
prevent biopsy of a clinically suspicious mass. Neither surgeons nor radiologists have the certainty of pathologists. The evaluation of breast masses and
their management is constantly evolving. Expert consultation is advised.
The important distinction is between benign and malignant
Breast cancer. There may be a dominant nontender breast mass in the
breast. Suspensory ligament inltration causes retraction revealed by dimpling, nipple deviation, and xation to the pectoral muscles. Flattening of
the nipple and a bloody or clear discharge indicate disease in the lactiferous tubules. Lymphatic obstruction produces cutaneous edema seen as peau
d’orange (Fig. 8-58). Regional lymphadenopathy suggests lymphatic metastases. A solitary breast mass mandates a diagnostic biopsy. Occasionally, the
presenting sign is a bloody discharge, enlarged lymph axillary nodes, or skin
inammation without a mass.
years of age is 1%, and there is a steady rise with increasing age; it is estimated that 1 in 9–10 women will eventually develop breast cancer. The median
age at which the various pathologic breast abnormalities appear in women is
known, and on that basis, probabilities are estimated. The data in Table 8-5 is
from patients operated on at New York Medical College–Flower Fifth Avenue
Hospitals during the period 1960–1975.
Inammatory breast carcinoma. Breast cancer can present as an acute inammatory disease, especially in the lactating breast. The appearance is
like acute mastitis except that the entire breast is swollen and there is early
DDX: The incidence of cancer in women <30
Breast Syndromes 387
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involvement of the axillary lymph nodes. DDX: In acute mastitis, inammation is usually limited to a single breast quadrant and lymphadenopathy
is uncommon.
Fibrocystic breast disease. This includes a broad spectrum of benign pathologic conditions of the female breast. The specic pathologic diagnosis
depends on the preponderance of one component over others. If the pathology is conned to stromal proliferation, broadenoma, virginal hypertrophy
of the breast, and intracanalicular broadenoma may be diagnosed. When
an abnormal ductal system predominates, micro or macrocystic disease, cystic mastitis, sclerosing adenosis, intraductal papilloma, and ductal ectasia
involving the lactiferous sinus describe the changes. If the main change is in
the terminal ductule and glandular elements, lobular hyperplasia is identied. Finally, myoepithelium hyperplasia leads to a diagnosis of myoepithelial
hyperplasia of Reclus.
Fibroadenoma. Usually found in a young woman with large breasts, the
ovoid or lobulated nodule has a rm, elastic, or rubbery consistency. It can be
the size of a pinhead or quite large. The mass is nontender and freely movable, slipping easily in the breast tissue. It must be distinguished from dysplasia, carcinoma, and cystosarcoma phyllodes.
FIG. 8-58 Peau d’Orange. Cutaneous edema of the breast is indicated by skin that is indented deeply with holes, the
accentuated orifices of the sweat glands, giving the appearance of an orange.
TABLE 8-5 Relationship of Breast Abnormalities and Age.
Diagnosis Age Range (Median)
Fibrocystic disease 20–49 (30)
Fibroadenoma 15–39 (20)
Intraductal papilloma and ductal ectasia 35–55 (40)
Carcinoma 40–71 (54)
388 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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Fluctuant breast mass. Cysts are very common and must be distinguished
from another uctuant mass, e.g., lipoma or abscess. Fluctuance is demonstrated by holding the edges of the mass tightly to the chest wall with one
hand while pressing its center with the ngers of the other hand. Abscess
is often quite tender and has erythema. True lipomas are exceedingly rare,
accounting for <1% of all breast lesions. Transillumination suggesting a cyst
is conrmed by ultrasound or aspiration.
Galactorrhea.
estrogen from the ovaries and placenta support lactation. Milk ejection is
initiated by mechanical nipple stimulation sending afferent impulses to
the hypothalamus, causing release of oxytocin from the posterior pituitary.
Prolactin levels must be checked in patients with galactorrhea or amenorrhea.
Pituitary prolactinomas elevate prolactin levels leading to galactorrhea and
suppressing ovulation. Many physiologic states, clinical disorders, and drugs
are associated with milk secretion.
CLINICAL OCCURRENCE: Endocrine: Pregnancy, adolescence, hypothy-
roidism, hyperthyroidism; Degenerative/Idiopathic: Uterine atrophy with
amenorrhea and lactation (Frommel disease); Infectious: Herpes zoster, postencephalitis; Inammatory/Immune: Mastitis; Mechanical/Traumatic: Mechanical
nipple stimulation, suckling, chest wall trauma, thoracoplasty, pneumonectomy, mammoplasty, irradiation; Metabolic/Toxic: Drugs (phenothiazines,
reserpine, methyldopa, oral contraceptive, tricyclic antidepressants, antihistamines, opiates); Neoplastic: Pituitary prolactinoma.
Fat necrosis. Breast trauma produces a hematoma and fat necrosis resulting in a scar that adheres to the surrounding tissue causing retraction which
suggests carcinoma. Patients commonly attribute masses that turn out to be
malignant to some remote traumatic incident, so a history of trauma should
not deter further evaluation. Even though fat necrosis is inconsequential,
excisional biopsy may be necessary.
Diabetic brous breast disease. Some women with type-1 diabetes develop
diabetic brous breast disease presenting as one or more painless hard
mobile irregular breast masses. Histology shows intralobular and perilobular
B-lymphocyte inammatory nodules with brosis in the breast fat.
Mastitis. In acute suppurative mastitis the breast is ushed, tender, hot, swollen, and indurated, frequently accompanied by chills, fever, and diaphoresis.
Usually a single breast quadrant is involved. Inammation often proceeds to
abscess formation. Approximately two-thirds of cases occur during lactation.
Inammatory carcinoma must be considered, especially in the presence of
nontender axillary lymphadenopathy.
Prolactin from the anterior pituitary and progesterone and
Abscess. Usually a sequel of acute mastitis, there is a localized, hot, exquisitely tender and painful uctuant mass frequently accompanied by chills and
fever with leukocytosis.
Chronic breast abscess. Pus may become enclosed by a thick wall of brous
tissue, presenting a nontender, irregular, rm mass requiring biopsy to exclude carcinoma.
Breast Syndromes 389
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Juvenile mastitis. A tender unilateral rm mass with signs of inammation
occurs beneath the nipple in young boys and in women 20–30 years of age.
The condition is benign and resolves in a few weeks.
The Male Breast
Male breast cancer. Approximately 1% to 2% of breast carcinomas occur in
men. The BRCA2 mutation increases the risk.
because of the paucity of breast tissue. It begins as a painless induration
with nipple retraction and xation to the skin and deep tissues. The mass
does not transilluminate. It must be distinguished from gynecomastia by
ne-needle aspiration biopsy or excision. Mammography in the male is
usually not helpful.
The mass is apparent early
Gynecomastia.
estrogen levels associated with puberty, liver disease, drugs, and endocrine
abnormalities lead to proliferation of breast tissue in men. Gynecomastia is
dened as a transient or permanent noninammatory enlargement of the
male breast. Physical exam reveals a nely lobulated often tender subareolar
mass that is mobile on the chest wall. Increased nipple sensitivity is frequently
noted by the patient. The mass may be small and unilateral. Gynecomastia
developing bilaterally can reach the dimensions of the female breast.
Hard masses or those with skin or chest wall xation must be excised to
exclude carcinoma.
CLINICAL OCCURRENCE: Idiopathic gynecomastia, appearing frequently
at puberty, is usually unilateral. Hormonal stimulation with estrogens
causes bilateral enlargement after castration, and in Cushing syndrome,
hyperthyroidism, and testicular choriocarcinoma. Breast enlargement also
occurs in liver cirrhosis. Refeeding gynecomastia occurs when patients with
severe malnutrition are rst fed. Gynecomastia may occur in association
with leukemia, lymphoma, pulmonary carcinoma, familial lumbosacral
syringomyelia, and Graves disease. Among the drugs occasionally causing
gynecomastia are digitalis, isoniazid, spironolactone, phenothiazine, and
diazepam.
Circulating estrogens control breast development. Increased
390 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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CLINICAL VIGNETTES AND QUESTIONS
CASE 8-1
A 65-year-old man comes to the emergency room (ER) with acute shortness of breath and hypotension. You are told by a medical student that
the patient has pulsus paradoxus.
QUESTIONS:
1. What is pulsus paradoxus?
2. How do you assess for pulsus paradoxus?
3. What is the pathophysiology underlying this sign?
CASE 8-2
A 36-year-old Indian woman with a history of acute rheumatic fever
presents with worsening shortness of breath especially with exertion.
On auscultation she has an accentuated rst heart sound, opening snap,
and low-pitched diastolic murmur heard best with the bell.
QUESTIONS:
1. What is the most likely diagnosis?
2. Explain the physiology of the loud S1, the opening snap, and the
diastolic murmur.
3. How would you estimate the severity of the valve lesion during
physical examination?
4. What is Graham Steell murmur?
A 56-year-old man presents with dyspnea on exertion, orthopnea, and
paroxysmal nocturnal dyspnea. Blood pressure is 140/50 and he has a
bounding pulse. The apical impulse is displaced laterally and inferiorly
and is diffuse and hyperdynamic. You hear a high-pitched, blowing
decrescendo diastolic murmur.
QUESTIONS:
1. What is the diagnosis?
2. Describe physical examination ndings which are associated with
this diagnosis.
3. What is the common clinical presentation and some underlying
causes of acute onset of this valve lesion?
4. What are some chronic conditions leading to this valve lesion?
CASE 8-3
Clinical Vignettes and Questions 391
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CASE 8-4
A 55-year-old man comes for evaluation of worsening shortness of breath
and ankle edema. He has an elevated JVD, bilateral crackles, and an S3
gallop.
QUESTIONS:
1. What causes S3 and S4 heart sounds?
2. Where and how are the S3 and S4 sounds best heard?
3. What is the signicance of these heart sounds?
CASE 8-5
A 55-year-old man is referred to you by your nurse practitioner for evaluation of a heart murmur. You nd a systolic crescendo-decrescendo murmur heard best at the right upper sternal border transmitted equally to
both carotid arteries. An ejection click is heard just after S1. S2 is mufed.
QUESTIONS:
1. What is the most likely diagnosis?
2. What ndings would you expect when examining his carotid arteries?
3. How do you differentiate this murmur from obstructive hypertro-
phic cardiomyopathy?
CASE 8-6
What is the differential diagnosis of:
QUESTIONS:
1. Elevated “a” waves?
2. Cannon “a” waves?
3. Absent “a” waves?
4. Elevated “v” waves?
A 54-year-old man is admitted after a few days of fever, chills, cough, and
shortness of breath. He has had diarrhea and headaches as well. His temperature is 39.4°C and chest examination reveals crackles in the left lower
lobe. Chest X-ray conrms left lower lobe consolidation. His laboratory
workup reveals leucocytosis, mild AST and ALT elevation, hyponatremia, and hypophosphatemia.
QUESTIONS:
1. What are common pathogens responsible for community-acquired
pneumonia?
2. What is the most likely pathogen in this patient?
3. What are some characteristic extrapulmonary features of Myco-
plasma pneumonia infection?
CASE 8-7
392 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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CASE 8-8
A 25-year-old 2 ppd smoker presents to the emergency room with sudden onset of shortness of breath and right-sided pleuritic chest pain.
On examination there is decreased chest excursion, hyperresonance to
percussion, and diminished breath sounds on the right.
QUESTIONS:
1. What is the most likely diagnosis?
2. What are the characteristic signs and symptoms of this condition?
3. Describe the normal physiology and then the pathophysiology of
this condition.
4. What are some causes of this condition?
CASE 8-9
A 30-year-old woman with asthma presents to the ER with signicant
respiratory distress and dramatic inspiratory stridor. She has had three
previous episodes, each triggered by stress, and each lasting about 4
hours. She has dysphonia during these attacks. Albuterol nebulizers
have had no benecial effect. During these episodes stridor is heard,
loudest in the neck, and less so in the chest.
QUESTIONS:
1. What is the pathophysiology of stridor?
2. What is the differential diagnosis of stridor?
3. What is the most likely diagnosis?
A 25-year-old male smoker comes to the ER with sudden shortness of
breath and right-sided pleuritic chest pain. He is tachypneic, tachycardic, and the blood pressure is 90/50 mm Hg. Chest examination
reveals decreased chest excursion on the right, hyperresonance to percussion, and absent breath sounds and fremitus. His trachea is deviated
to the left.
QUESTIONS:
1. What causes hyperresonance to percussion, absent breath sounds
and fremitus?
2. How can physical examination help in your differential diagnosis?
3. What is the most likely diagnosis?
CASE 8-10
CHAPTER 9
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The Abdomen, Perineum, Anus,
and Rectosigmoid
The history and physical exam are the foundation for differential diagnosis and
efcient use of laboratory and imaging studies in evaluating abdominal symptoms. History delineates the character and sequence of symptoms. Knowing
the anatomy and normal and abnormal physiology of the gut and its appended
organs is essential to interpreting abdominal ndings. As a condition evolves,
frequent repetition of the exam yields valuable additional information.
The abdominal cavity is a shallow oval basin with a rigid W-shaped bottom
made up of the vertebral column and back muscles. Heavy ank muscles form
the sides and the diaphragm and pelvic oor muscles close either end. The brim
is formed by the lower rib margins superiorly, and the pubic bones and ilia inferiorly. The anterior abdominal wall muscles and fascia, reinforced by two parallel
rectus muscles attached to the ribs and pelvis, cover the abdominal cavity.
The abdominal viscera are solid or hollow. The solid viscera, the liver,
spleen, kidneys, adrenals, pancreas, ovaries, and uterus, usually retain their
shape and position as they enlarge. The liver, spleen, kidneys, and adrenals
are shielded by the rib cage. The hollow viscera, the stomach, small intestines,
colon, gallbladder, bile ducts, fallopian tubes, ureters, and urinary bladder,
are not palpable unless distended by gas, uid or solid masses.
Two systems are used to describe abdominal topography (Fig. 9-1). We use
the division into quadrants by axial and transverse lines through the umbilicus.
MAJOR SYSTEMS AND THEIR PHYSIOLOGY
Alimentary System: The alimentary system converts ingested food into
absorbable nutrients and fuels, and solid waste. This complex process
includes ingestion, mastication, bulk transport, storage, mechanical disruption, mixing, and digestion of ingested food and absorption of nutrients coordinated with production, storage, transport, and carefully timed release of
digestive enzymes and bile acids. It is a functional barrier to microorganisms,
parasites, and toxic molecules.
The alimentary system starts at the mouth and ends at the anus. Its
intraabdominal portion extends from the diaphragmatic hiatus to the anus.
Normal motility and digestion require coordinated muscular and secretory
activity mediated locally and systemically by neural and endocrine signals. The
bowel is a muscular tube suspended by a mobile mesentery (stomach, small
intestine, cecum, transverse and sigmoid colon) or anchored to the posterior
abdominal wall (duodenum, ascending and descending colon) or pelvic oor
(rectum). It is susceptible to intraluminal obstruction at narrow points (gastroesophageal junction, pylorus, ileocecal valve), to obstruction by extraluminal
393
394 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
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FIG. 9-1 Topographic Divisions of the Abdomen. On the left are the regions of the abdomen as defined
in the Basle Nomina Anatomica terminology. Most of the nine regions are small, so that enlarged viscera and ot her
structures occupy more than one. On the right is a simpler plan with four regions. This is preferred by most clinicians and is employed in this book. Many occasions arise when the quadrant scheme needs supplementing by reference to the
epigastrium, the flanks, or the suprapubic region.
compression, and to twisting or kinking where suspended on a mesentery
(especially the small bowel, cecum, and sigmoid). Symptoms referred to the
abdomen include changes in appetite, pain, nausea, vomiting and altered stool
character and frequency. Physical signs include changes in overall nutrition,
abnormal abdominal contour, altered bowel sounds, solid-organ enlargement,
increased peritoneal uid, localized mass, and tenderness.
Hepatobiliary and Pancreatic System: The liver and pancreas parenchyma
arise from condensation of mesenchymal cells around embryonic gut evaginations that become the biliary and pancreatic ducts. The pancreas releases
bicarbonate, amylase, lipase, and proteinases in response to specic foods
and duodenal contents. The pancreas also contains the islets of Langerhans,
which release insulin, glucagon, and somatostatin in response to blood glucose changes. Portal venous blood from the gut, gallbladder, pancreas, and
spleen percolates from the portal triads through a radial array of sinusoids
to the central vein, hepatic vein and inferior vena cava (IVC). Hepatocytes
process and remove toxic metabolic products and toxins absorbed by the gut
eliminating them via the circulation or bile. They synthesize essential proteins including albumin, coagulation factors, lipoproteins, and transport molecules, and synthesize and secrete the bile salts necessary for fat digestion
and absorption. Kupffer cells within the sinusoids are phagocytic antigenpresenting cells that clear bacteria from the portal circulation releasing cytokines into the systemic circulation.
Liver, biliary, and pancreatic symptoms include changes in food interest,
nausea, vomiting, pain or discomfort associated with meals, and maldigestion altering stool consistency and frequency. Physical signs include changes
in liver size, consistency, and shape, localized tenderness and masses, ascites,
and systemic signs, e.g., jaundice, weight loss and bleeding.
Spleen and Lymphatics: See Chapter 5, page 82 for a discussion of the lymph
nodes.
Supercial Anatomy of the Abdomen and Perineum 395
A. Position of normal kidneys
and adjacent organs
Splenic
Colonic
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Adrenal
Gastric
Pancreatic
Duodenal
Jejunal
LEFTRIGHT
11th
12th
12th
11th
Hepatic
Colonic
B. Surfaces of kidneys
FIG. 9-2 Anatomic Relations of the Normal Kidneys. A. The position of the normal kidneys as viewed
from the anterior surface of the abdomen. Note that the right kidney is lying in front of the twelfth rib, whereas
the slightly higher left kidney is in front of the eleventh and twelfth ribs. B. The anterior surfaces of both kidneys,
showing the regions touched by overlying viscera.
The spleen distributes arterial blood into complex sinusoids where
senescent red blood cells, intracellular inclusions, and red cell membrane
abnormalities are removed. The spleen also clears the blood of encapsulated
bacteria and produces specic antibodies. The abdominal organs are rich in
lymphatics, draining into lymph nodes in the mesentery and the hila of solid
organs. These drain into the para-aortic nodes, mixing with lymph from the
legs and pelvis, and ultimately into the thoracic duct. Few specic symptoms
arise from alterations in these organs. A large spleen produces upper abdominal fullness; retroperitoneal lymph node enlargement or inammation can
present as ank and back pressure or pain. Fever, weight loss, and sweats
may be the only symptoms of intraabdominal lymphoma. Moderate splenomegaly can be detected by physical exam, but intraabdominal lymph nodes
are rarely palpable.
Kidneys, Ureters, and Bladder: See the discussion of urogenital function in
Chapter 10.
The kidneys are in the retroperitoneum under the lower ribs (Fig. 9-2).
The ureters run retroperitoneally along, then over, the psoas muscle, over the
pelvic brim, and into the pelvis before entering the bladder. Obstruction of
the renal pelvis or ureter, produces deep, poorly localized visceral pain in
the abdomen, ank, pelvis, or testicles. Pain is referred to the ank and back
from kidney enlargement or tissue invasion by inammatory, infectious, or
neoplastic processes. Physical signs are palpable kidney and bladder enlargement and pain on deep palpation.
SUPERFICIAL ANATOMY OF THE ABDOMEN AND PERINEUM
The Abdomen: Develop a complete mental image of the location and rela-
tionships of the abdominal organs, the mesentery and its attachments, and
the arterial, venous, and lymphatic supply of each organ. Anchor this picture to supercial landmarks: the spine, ribs and costal margins, umbilicus,
rectus muscle, inguinal ligament, ilia, and pubes. Associate this mental picture with the images presented by plain lms, ultrasonography, CT, and MRI.
This requires studying anatomy texts, reviewing imaging studies with your
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