rare tumors that can be seen using medical microscopes, accounting for approximately 0.1 to 1.5% of all esophageal

tumors. They present with the symptom of dysphagia, which does not differ from the dysphagia associated with the

more common epithelial carcinoma. Tumors located within the cervical or high thoracic esophagus can cause symptoms

of pulmonary aspiration secondary to esophageal obstruction. Large tumors originating at the level of the tracheal

bifurcation can produce symptoms of airway obstruction and syn­cope by direct compression of the tracheobronchial

tree and heart. The duration of dysphagia and age of the patients af­fected with these tumors are similar to those

with carcinoma of the esophagus.

style="font-size: 10pt; font-family: Arial">

A barium swallow usually shows a large polypoid

intialuminal esophageal mass, causing partial obstruction and dilatation of the esophagus proximal to the tumor.

The smooth polypoid nature of the lesion, seen through a medical microscope, although not diagnostic, is

distinctive enough to suggest the presence of a sarcoma rather than the more common ulcerating, stenosing

carcinoma.

Esophagoscopy commonly shows an intraluminal necrotic mass. When biopsy is attempted and

the tissue examined under a medical microscope, it is important to remove the necrotic tis­sue until bleeding is

seen on the tumor’s surface. When this is not done, the biopsy specimen will show only tissue necrosis when it is

examined under a microscope. Even when viable tumor is obtained on biopsy, it has been observed that it cannot be

definitively identified as carcinoma, sar­coma, or carcinosarcoma on the basis of the histology of the portion

biopsied. Biopsy results cannot be totally relied on to identify the presence of sarcoma, and it is often the

polypoid nature of the le­sion, which arouses suspicion that it may be something other than

carcinoma.

Polypoid sarcomas of the esophagus, in contrast to infiltrating carcinomas, remain

superficial to the muscularis propria and are less likely to metastasize to regional lymph nodes. In one series of

14 patients, local extension or tumor metastasis would have pre­vented a potentially curative resection in only

five. Thus the pres­ence of a large polypoid tumor should not deter the surgeon from resecting the

lesion.

Sarcomatous lesions of the esophagus can be divided into epi­dermoid carcinomas

with spindle cell features, such as carcinosar­coma, and true sarcomas that arise from mesenchymal tissue, such as

leiomyosarcoma, fibrosarcoma, and rhabdomyosarcoma. Based on current histologic criteria for diagnosis,

fibrosarcoma and rhab­domyosarcoma of the esophagus are extremely rare lesions and may not in fact

exist.

Surgical resection of polypoid sarcoma of the esophagus is the treatment of choice,

since radiation therapy has little success and the tumor remain superficial, with local invasion or distant

metastases occurring late in the course of the disease. As with carcinoma, the absence of both wall penetration and

lymph node metastases is nec­essary for curative treatment. Surgical resection is consequently responsible for the

majority of the reported 5-year survivals. Re­section also provides an excellent means of alleviating the

patient’s symptoms. The surgical technique for resection and the subsequent restoration of the gastrointestinal

continuity is similar to that de­scribed for carcinoma.

style="text-align: justify">It was observed that four of the

eight patients with carci­nosarcoma survived for 5 years or longer. Even though this number is small, it suggests

that resection produces better results in ep­ithelial carcinoma with spindle cell features than in squamous cell

carcinoma of the esophagus. Similarly, with leiomyosarcoma of the esophagus, the same scattered reports exist with

little information on survival. Of seven patients with leimyosarcoma, two died from their disease-one in 3 months

and the other 4 years and 7 months after resection. The other five patients were reported to have survived more

than 5 years.

style="font-size: 10pt; font-family: Arial">It is difficult to evaluate the benefits of resection for leiomyo­

blastoma of the esophagus, due to the small number of reported patients with tumors in this location. Most

leiomyoblastomas occur in the stomach, and 38% of these patients succumb to the cancer in 3 years. Fifty-five

percent of patients with extragastric leiomy­oblastoma also die from the disease, within an average of 3 years.

Consequently, leiomyoblastoma should be considered a malignant lesion and apt to behave like a leiomyosarcoma. The

presence of nuclear hyperchromatism, increased mitotic figures, tumor size larger than 10 cm, and clinical symptoms

of longer than 6 months’ duration are associated with a poor prognosis.

class="MsoNormal" style="text-align: justify">

justify">Plummer-Vinson

Syndrome

style="font-size: 10pt; font-family: Arial; letter-spacing: 0.1pt">

style="text-align: justify">This uncommon

clinical syndrome is characterized by dysphagia as­sociated with atrophic oral mucosa, spoon-shaped fingers with

brit­tle nails, and chronic anemia. It characteristically occurs in middle-aged edentulous women. Because iron-

deficiency anemia is a common finding, another name for this condition is sideropenic dys­phagia. The syndrome is

more common in the Scandinavian coun­tries than in the United

States, and its presentation is variable. Not all patients exhibit the classic

syndrome; some lack iron-deficiency anemia and others have the typical clinical stigmata, but lack dys­phagia or

the presence of an esophageal web.

style="font-size: 10pt; font-family: Arial; letter-spacing: 0.1pt">

style="text-align: justify">Clinical

observation with the use of medical microscopes suggests that the esophageal web once thought to be a component of

the syndrome in some patients may actually be a drug-induced lesion, caused by ingestion of ferrous sulfate, a drug

commonly prescribed in cases of iron-deficiency anemia. Ferrous sulfate is known to cause esophageal injury, and a

number of patients may have had a drug-induced esophageal in­jury develop at the site where the web is commonly

observed. Not knowing the cause of the esophageal abnormality, early observers reported the web as part of the

syndrome. Malignant lesions of the oral mucosa, hypopharynx, and esophagus that were studied with the use of

medical microscopes have been noted to occur in up to 100% of patients when followed long-

term.

Videoradiographic studies, as

well as endoscopic findings, have demonstrated a fibrous web just below the cricopharyngeus mus­cle as the cause

of dysphagia in these patients. Treatment consists of dilation of the web and iron therapy to correct the

nutritional deficiency.

style="font-size: 10pt; font-family: Arial; letter-spacing: 0.1pt">

class="MsoNormal" style="text-align: justify">Schatzki’s ring

style="font-size: 10pt; font-family: Arial; letter-spacing: 0.1pt">

style="text-align: justify">Schatzki’s

ring is a thin submucosal circumferential ring in the lower esophagus at the squamocolumnar junction, often

associated with a hiatal hernia. Its significance and pathogenesis are unclear. Templeton first noted the ring, but

Schatzki and Gary defined it as a distinct entity in 1953. Its prevalence varies from 0.2 to 14% in the general

population, depending on the tech­nique of diagnosis and the criteria used. Stiennon believed the ring to be a

pleat of mucosa formed by infolding of redundant esophageal mucosa due to shortening of the esophagus. Others

believe the ring to be congenital, and still others suggest it is an early stricture result­ing from inflammation

of the esophageal mucosa caused by chronic reflux.

class="MsoNormal" style="text-align: justify">Schatzki’s ring is a distinct clinical entity having different symptoms, upper gastrointestinal function

studies, and response to treatment when compared with

patients with a hiatal hernia, but without a ring. Twenty-four-hour esophageal pH monitoring has shown that

patients with a Schatzki’s ring have a lower incidence of reflux than hiatal hernia controls. They also have

better LES func­tion. This, together with the presence of a ring, as observed using medical microscopes, could

represent a protective mechanism to prevent gastroesophageal reflux.

style="text-align: justify">

class="MsoNormal" style="text-align: justify">Symptoms associated

with Schatzki’s ring are brief episodes of dysphagia during hurried ingestion of solid foods. Its treatment has

varied from dilation alone to dilation with antireflux measures, antireflux procedure alone, incision, and even

excision of the ring. Little is known about the natural progression of Schatzki’s rings. Using radiologic

techniques, Chen and colleagues showed progres­sive stenosis of rings in 59% of patients, whereas Schatzki found

that the rings decreased in diameter in 29% of patients and remained unchanged in the

rest.

Symptoms in patients with a ring are caused more by the pres­ence of the ring than by

gastroesophageal reflux. Most patients with a ring but without proven reflux respond to a single dilation, while

most patients with proven reflux require repeated dilations. It is through these findings that the majority of

Schatzki’s ring patients without proven reflux have a history of ingestion of drugs known to be damaging to the

esophageal mucosa. Bonavina and associates have suggested drug-induced injury as the cause of stenosis in patients

with a ring, but without a history of reflux. Since rings also occur in patients with proven reflux, it is likely

that gastroesophageal reflux also plays a part. This is supported by the fact that there is less drug ingestion in

the history of these patients. Schatzki’s ring is probably an acquired lesion that can lead to stenosis from

chemical-induced injury by pill lodgment in the distal esophagus, or from reflux-induced injury to the lower

esophageal mucosa.

style="font-size: 10pt; font-family: Arial">The best form of treatment of a symptomatic Schatzki’s ring in

patients who do not have reflux consists of esophageal dilation for relief of the obstructive symptoms. In patients

with a ring who have proven reflux and a mechanically defective sphincter, an antireflux procedure is necessary to

obtain relief and avoid repeated dilation.

class="MsoNormal" style="text-align: justify">Mallory-

weiss syndrome

style="font-size: 10pt; font-family: Arial">

In 1929, Mallory and Weiss described four patients with

acute upper gastrointestinal bleeding who were found at autopsy using medical microscopes to have mucosal tears at

the gastroesophageal junction. This syndrome, characterized by acute upper gastrointestinal bleeding following

repeated vomiting is considered to be the cause of up to 15% of all severe upper gastrointestinal

bleeds. The mechanism is similar to spontaneous esophageal perforation: an acute increase in intra-abdominal

pressure against a closed glottis in a patient with a hiatal hernia.

style="text-align: justify">

class="MsoNormal" style="text-align: justify">Mallory-Weiss tears

are characterized by arterial bleeding, which may be massive. Vomiting is not an obligatory

factor, as there may be other causes of an acute increase in infra-abdominal pressure, such as paroxysmal coughing,

seizures, and retching. The diagnosis requires a high index of suspicion, particularly in the patient who develops

upper gastrointestinal bleeding following prolonged vomiting or retching. The use of upper endoscopy and medical

microscopes confirms the suspicion by identifying one or more longitudinal fissures in the mucosa

of the herniated stomach as the source of bleeding.

style="text-align: justify">For the majority of patients, the

bleeding will stop spontaneously with no operative management. In addition to blood replacement, the stomach should

be decompressed and antiemetics administered. A distended stomach and continued vomiting aggravate further

bleeding. A Sengstaken-Blakemore tube will not stop the bleeding, as the pressure in the balloon

is not sufficient to overcome arterial pressure.

style="text-align: justify">Surgery is required occasionally to

stop blood loss. The procedure consists of laparotomy and high gastrotomy with over sewing of the linear tear.

Mortality is uncommon and recurrence is rare.

class="MsoNormal" style="text-align: justify">Scleroderma

style="font-size: 10pt; font-family: Arial">

Scleroderma is a systemic disease accompanied by

esophageal ab­normalities in approximately 80% of patients. In most cases, the disease follows a prolonged course.

Renal involvement occurs in a small percentage of patients and signals a poor prognosis. The onset of the disease

is usually in the third or fourth decade of life, occurring twice as frequently in women as in

men.

Small vessel inflammation, as observed using medical microscopes, appears to be an

initiating event, with subsequent perivascular deposition of normal collagen, which may lead to vascular

compromise. In the gastrointestinal tract, the pre­dominant feature is smooth muscle atrophy. Whether the atrophy

in the esophageal musculature is a primary effect or occurs secondary to a neurogenic disorder is unknown. The

results of pharmacologic and hormonal manipulation, with agents that act either indirectly via neural mechanisms or

directly on the muscle, suggest that sclero­derma is a primary neurogenic disorder. Methacholine, which acts

directly on smooth muscle receptors, causes a similar increase in LES pressure in normal controls and in patients

with scleroderma. Edrophonium, a cholinesterase inhibitor that enhances the effect of acetylcholine when given to

patients with scleroderma, causes an increase in LES pressure that is less marked in these patients than in normal

controls, suggesting a neurogenic rather than myogenic etiology. Muscle ischemia due to perivascular compression

has been suggested as a possible mechanism for the motility abnormality in scleroderma. Others have observed that

in the early stage of the dis­ease, the manometric abnormalities may be reversed by reserpine, an agent that

depletes catecholamines from the adrenergic system. This suggests that in early scleroderma an adrenergic

overactivity may be present that causes a parasympathetic inhibition, supporting a neurogenic mechanism for the

disease. In advanced disease mani­fested by smooth muscle atrophy and collagen deposition, reserpine no longer

produces this reversal. Consequently, from a clinical per­spective, the patient can be described as having a poor

esophageal pump and a poor valve.

style="font-size: 10pt; font-family: Arial">

The diagnosis of scleroderma can be made manometrically

by the observation of normal peristalsis in the proximal striated esoph­agus, with absent peristalsis in the

distal smooth muscle portion. The LES pressure is progressively weakened as the disease advances. Because many of

the systemic sequelae of the dis­ease may be nondiagnostic, the motility pattern is frequently used as a specific

diagnostic indicator. Gastroesophageal reflux commonly occurs in patients with scleroderma, since they have both

hypoten­sive sphincters and poor esophageal clearance. This combined defect can lead to severe esophagitis and

stricture formation. The typical barium swallow shows a dilated, barium-filled esophagus, stomach, and duodenum, or

a hiatal hernia with distal esophageal stricture and proximal dilatation.

class="MsoNormal" style="text-align: justify">

Traditionally, esophageal symptoms have been treated with medications such as H2 blockers, antacids,

elevation of the head of the bed, and multiple di­lations for strictures, with generally unsatisfactory results.

The de­gree of esophagitis is usually severe and leads to marked esophageal shortening. Consequently a Collis

gastroplasty in combination with a Belsey antireflux repair is the usual procedure for the surgical management of

this problem. Surgery reduces esophageal acid ex­posure, but does not return it to normal because of the poor

clearance function of the body of the esophagus. Only 50% of the patients have a good-to-excellent result. If the

esophagitis is severe, or there has been a previous failed antireflux procedure and the disease is associated with

delayed gastric emptying, a gastric resection with Roux-en-Y esophagojejunostomy and a Hunt-Lawrence pouch has

proved the best option.

must follow a carefully prescribed procedure to ensure valid results. Laboratory testing of urine generally falls

under three categories, example, chemical, bacteriologic, and microscopic examination. There are also three kinds

of collection for urine specimens, first random, second timed, and third 24-hour total volume. Random specimens may

be collected any time, but a first morning voided aliquot is optimal for constituent concentration. Laboratory

results from a random urine collection are expressed per unit volume if the result is a quantitative analysis.

Result reporting of a random collection is expressed as positive or negative, indicating the presence or absence of

a particular constituent, such as glucose. Random urine specimens should be collected in a chemically clean

receptacle, either glass or plastic. A clean-catch midstream specimen is most desirable for bacteriologic

examinations using medical microscopes. The vessel is tightly sealed, labeled with the patient’s name

and date of collection, and submitted for analysis. A first morning urine specimen is generally the most

concentrated and considered a better specimen for evaluation. Timed specimens are obtained at designated intervals,

starting from time zero, and are noted on each subsequent container time of collection. Urine specimens for a 24-

hour total volume collection are most difficult to obtain and require cooperation from the patient. Incomplete

collection is the major problem.

In some instances, over collection occurs. Because in-hospital collection

is usually under the supervision of the nursing staff, it is more reliable than outpatient collections. Collection

of urine specimens from pediatric patients requires special attention to avoid contamination from the stool. One

can avoid problems by giving patients complete written and verbal instructions with a warning that the test can be

invalidated by incorrect collection technique. If specimen is to be collected on an outpatient basis, exercise care

and instruct patient’s parents to keep the specimen out of the reach of children, especially if concentrated acid

is used as a preservative. An unbreakable, 4 L approximately plastic, chemically clean container with the correct

preservative already added is preferred. One should remind the patient to discard the first morning specimen,

record the time, and collect every subsequent voiding for the next 24 hours, with the last to be 24 hours after

timing commenced. Over collection occurs if the first morning specimen is included in this routine. Measure the

total volume collected, record the information on the request form, thoroughly mix the entire 24-hour collection,

and submit for analysis. A 40-mL aliquot is adequate for this purpose. Completeness of collection is difficult to

determine.

If results appear clinically invalid when examined under a medical microscope, this is cause for

suspicion. Because creatinine excretion is based on muscle mass, and because a patient’s muscle mass is relatively

constant, creatinine excretion is also reasonably constant. Therefore, one should measure creatinine on several 24

-hour collections and keep this as part of the patient’s record. Another approach is to express results relative

to the concentration of creatinine when collecting a specimen other than a 24-hour one. One and two-hour timed

collection specimens may suffice in some instances.

SPECIAL URINE COLLECTION

TECHNIQUES

Catheterization of the bladder may cause infection but is necessary in some patients.

Catheterization also is used for urine collection when patients are unable to void or control micturition.

Suprapubic aspiration is performed with a syringe and needle above the symphysis pubis, through the abdominal wall,

into a full bladder. This method is used to obtain otherwise problematic anaerobic cultures. Ureteral catheters are

inserted via a cystoscope into the ureter. Bladder urine is collected first, followed by a bladder washing.

Ureteral urine specimens are useful in differentiating bladder from kidney infection or for differential ureteral

analysis using medical microscopes, and may be obtained separately from each kidney pelvis labeled left and right.

First morning urine samples for cytologic examination are optimal.

ready access to the patient circulation, eliminating multiple phlebotomies, and are especially useful in critical

care and surgical situations. Arterial catheters most often are placed in the radial artery. Indwelling catheters

are surgically inserted in the cephalic vein or internal jugular, subclavian, or femoral veins and positioned. They

are especially useful in selected patients for drawing venous blood, administering drugs or blood products, and

providing total parenteral nutrition. Continuous, real-time intra-arterial monitoring of blood gases and acid-base

status using fiberoptic channels containing fluorescent and absorbent chemical analyses has been used

successfully.

Placement of indwelling catheters, although not a routine laboratory function, is

of primary concern to the laboratorian blood specimens drawn from catheters may be contaminated with whatever was

administered or infused via the catheter. The solution, usually heparin used to maintain patency of the vein must

also be cleared. Sufficient blood minimum of 2 to 3 mL must be withdrawn to clear the line so laboratory data are

reliable. To obtain a blood specimen from the indwelling catheter, first draw 6 mL of intravenous fluid from the

line and discard. In a separate syringe, withdraw the amount of blood required for requested laboratory procedures.

Follow strict aseptic technique to avoid site or catheter contamination or both. Coagulation measurements

prothrombin time, activated partial thromboplastin time, and thrombin time are extremely sensitive to heparin

interference, so that even larger volumes of presample blood must be withdrawn before the laboratory results are

acceptable. The appropriate volume to be discarded should be established by each laboratory when performing

prothrombin times PT and activated partial thromboplastin times APTT, a minimum of 5.3 mL discard volume should be

used. The laboratory is sometimes asked to perform blood culture studies, using medical microscopes, on blood drawn

from indwelling catheters. This procedure is not recommended since, when viewed under a medical microscope, the

organisms that grow on the walls of the catheter can contaminate the blood specimen.

SPECIMEN

INTERFERENCES

The collection of specimens depends on proper identification of the patient, the appropriate

collecting method to procure the specimen, and the correct collection tubes. Timed collections must be verified to

ensure accuracy in generating laboratory data that will be used in the diagnosis or management of a patient. The

site of collection is generally not critical except for glucose tolerance test, in which it has been reported that

capillary glucose is 10 to 30 percent higher than venous blood glucose. Additionally, blood specimens collected

from an extremity with any type of catheter delivering parenteral solutions can generate artefactual results. If

this type of collection cannot be avoided, the venipuncture must be performed distal to the intravenous needle

site, with the tourniquet between the two. Blood-drawing equipment must be void of any residual detergents,

plasticizers, or other material that may interfere with laboratory determinations. Examples include specimens for

lead analysis, which must be collected in acid-washed, lead-free containers, and contamination from tissue

thromboplastin that may interfere with specific coagulation assays if a double-syringe technique first 5 mL of

blood is discarded is not used.

Lysis of red blood cells during the collection process or after phlebotomy,

before analysis is performed using medical microscopes, can contaminate the serum or plasma and alter results in

vitro hemolysis. Overzealous mixing of blood in collection tubes, residual alcohol left when cleansing skin,

prolonged exposure of tubes to heat or extreme cold freezing, and inadequate removal of red cells during

centrifugation may cause hemolysis. Even small amounts of lysed erythrocytes may have a significant impact on blood

plasma and serum analyte concentrations. In vitro hemolysis results may show increased levels of serum acid

phosphatase, zinc, magnesium, albumin, potassium, bilirubin spectrophometrically determined, and CK. Thrombolysis

can result in elevated serum potassium, magnesium, acid phosphatase, and aldolase. Granulocytosis releases

muramidase lysozyme, phosphohexose isomerase, arginase, glucose-6-phosphatase G6PD, and glutamate dehydrogenase.

Hemolysis may alter spectrophometric readings, such as those used in coagulation studies or hemoglobin

evaluations.

Lumbar punctures

LPs are performed to collect cerebrospinal fluid CSF that may be evaluated in the laboratory to establish a

diagnosis of infection bacterial, fungal, mycobacterial, or amebic meningitis, malignancy, subarachnoid hemorrhage,

multiple sclerosis, or demyelinating disorders using medical microscopes. A serious complication of an LP is

cerebellar tonsillar herniation in patients with elevated intracranial pressure and should be avoided unless CSF

findings are expected to improve treatment or outcome. Patients with spinal cord tumors with paresis may progress

to paralysis following LP. To avoid introduction of infection, patients with sepsis in the lumbar region

skin infection, cellulitis, or epidural abscess should not have an LP performed to avoid introduction of infection.

Other complications of lumbar puncture include asphyxiation in infants due to hyper extending the head forward,

thus occluding the trachea, paresthesia, headache, and rarely, hematomas.
Before collection of CSF begins, the

pressure, measured by allowing fluid to rise in a sterile, graduated manometer, should be between 90 and 180 mmHg.

Breath holding, abdominal compression, congestive heart failure, inflammation of the meninges, obstruction of

intracranial venous sinuses, mass lesions, and cerebral edema may cause the pressure to be elevated above 180 mm

Hg. Initially, only 1 to 2 mL of CSF should be removed. A marked decrease in pressure following this procedure

suggests cerebellax herniation or spinal cord compression, thus no additional CSF should be collected. Patients

with partial or complete spinal block may have low pressure less than 80 mm Hg, falling to zero after removal of

only 1 mL. Again, no additional fluid should be removed. If pressure is normal and does not fall after several

milliliters are removed, additional fluid may be taken. Three aliquots are generally collected in separate, sterile

tubes labeled appropriately with name, date, and sequential tube collection number aid distributed for chemical and

immunologic studies, microbiologic studies second, and cell count and differential third. Closing pressure of 40 to

90 mm Hg is common after 10 to 20 mL of CSF has been removed.

SYNOVIAL FLUID

Synovial fluid is produced by dialysis of plasma across the synovial membrane and secretion of a

hyaluronate-protein complex. This fluid is collected using careful, aseptic technique, avoiding aspiration from

patients with bacteremia or extra-articular soft tissue infection. Collection of synovial fluid arthrocentesis

should be performed after six hours of fasting into a syringe containing about 25 units of heparin per milliliter

of synovial fluid collected. Generally, less than 2.0 mL of fluid is collected unless an effusion is present and

therapeutic collection is continued. Using additional syringes, larger amounts may be collected when appropriate

for microbiologic and other studies using various types of microscopes like a medical

microscope.

PLEURAL FLUID, PERICARDIAL FLUID, AND PERITONEAL FLUID

The lubricating

fluids found between potential spaces of pleura, from the pericardial sac, or from the peritoneum, may accumulate

excessively. Thoracentesis is a surgical procedure that is performed to drain accumulated fluids effusions from the

thoracic cavity and is helpful in the diagnosis of inflammation or neoplastic diseases in the lung or pleura.

Likewise, pericardiocentesis and peritoneocentesis refer to the collection of fluid from the pericardium and the

peritoneal cavities, respectively.

The patient, sitting in an upright position, with arms and head extended

on an overbed table, is prepared with a local anesthetic after appropriate cleansing of the site. A 50-mL syringe

is fitted with a stopcock and rubber tubing to assist in the aseptic collection process. Specimens are obtained for

chemical, microbiological, and cylologie examination and measurements using medical microscopes and are transferred

to collecting tubes with appropriate additives. For most chemical evaluations, no additive is used and specimen is

allowed to clot. Bacteriologic and cytologic specimens may be collected in EDTA or sterile sodium heparin without

preservatives. Special studies for Mycobacterium, anaerobie bacteria, or viruses may require special handling

procedures, which are planned and reviewed prior to collection.