Surgery-Book_1aim.net

Current Clinical Strategies

Surgery

Sixth Edition

The University of California, Irvine, Manual of
Surgery

Samuel Eric Wilson, MD

Professor and Chairman
Department of Surgery
College of Medicine
University of California, Irvine

Bruce M, Achauer, MD
John A. Butler, MD
David A. Chamberlin, MD
Paul D. Chan, MD
Marianne Cinat, MD
Roger Crumley, MD
Alex Di Stante, MD
C. Garo Gholdoian, MD
Ian L. Gordon, MD, PhD
Joshua Helman, MD
James G. Jakowatz, MD
Fernando Katie, MD
Michael E. Lekawa, MD
I. James Sarfeh, MD
Michelle Schultz, MD
Harry Skinner, MD
Charles Theuer, MD
Russell A. Williams, MD

Current Clinical Strategies Publishing

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Surgical Documentation

S. E. Wilson, MD

Surgical History and Physical
Examination

Identifying Data: Patient's name, age, race, sex;
referring physician.

Chief Compliant: Reason given by patient for seeking
surgical care and the duration of the symptom.
History of Present Illness (HPI): Describe the course of
the patient's illness, including when it began, character of
the symptoms; pain onset (gradual or rapid), precise
character of pain (constant, intermittent, cramping,
stabbing, radiating); other factors associated with pain
(defecation, urination, eating, strenuous activities); loca-
tion where the symptoms began; aggravating or relieving
factors. Vomiting (color, character, blood, coffee-ground
emesis, frequency, associated pain). Change in bowel
habits; rectal bleeding, character of blood (clots, bright or
dark red), trauma; recent weight loss or anorexia; other
related diseases; past diagnostic testing.
Past Medical History (PMH): Previous operations and
indications; dates and types of procedures; serious
injuries, hospitalizations; diabetes, hypertension, peptic
ulcer disease, asthma, heart disease; hernia, gallstones.
Medications: Aspirin, anticoagulants, hypertensive and
cardiac medications, diuretics.
Allergies: Penicillin, codeine, iodine.
Family History: Medical problems in relatives. Family
history of colon cancer, cardiovascular disease.
Social History: Alcohol, smoking, drug usage,
occupation, daily activity.
Review of Systems (ROS):

General: Weight gain or loss; loss of appetite, fever,
fatigue, night sweats. Activity level.
HEENT: Headaches, seizures, sore throat, masses,
dentures.

Respiratory: Cough, sputum, hemoptysis, dyspnea
on exertion, ability to walk up flight of stairs.
Cardiovascular: Chest pain, orthopnea, claudication,
extremity edema.

Gastrointestinal: Dysphagia, vomiting, abdominal
pain, hematemesis, melena (black tarry stools),
hematochezia (bright red blood per rectum), constipa-
tion, change in bowel habits; hernia, hemorrhoids,
gallstones.

Genitourinary: Dysuria, hesitancy, hematuria,
discharge; impotence, prostate problems, urinary
frequency.

Gynecological: Last menstrual period, gravida, para,
abortions, length of regular cycle and periods, birth
control.

Skin: Easy bruising, bleeding tendencies.
Neurological: Stroke, transient ischemic attacks,
weakness.

Surgical Physical Examination

General appearance: Note whether the patient looks

"ill," well, or malnourished.

Vital Signs: Temperature, respirations, heart rate, blood

pressure, weight.

Eyes: Pupils equally round and react to light (PERRL);

extraocular movements intact (EOMI).
Neck: Jugular venous distention (JVD), thyromegaly,

masses, bruits; lymphadenopathy; trachea midline.
Chest: Equal expansion, dullness to percussion; rales,

rhonchi, breath sounds.
Heart: Regular rate and rhythm (RRR), first and second

heart sounds; murmurs (grade 1-6), pulses (graded 0-

2+).
Breast: Skin retractions, erythema, tenderness, masses

(mobile, fixed), nipple discharge, axillary or

supraclavicular node enlargement.
Abdomen: Contour (flat, scaphoid, obese, distended),

scars, bowel sounds, bruits, tenderness, masses, liver

span; splenomegaly, guarding, rebound, percussion

note (dull, tympanic), pulsatile masses, costovertebral

angle tenderness (CVAT), abdominal hernias.
Genitourinary: Inguinal hernias, testicles, varicoceles;

urethral discharge, varicocele.
Extremities: Skin condition, edema (grade 1-4+);

cyanosis, clubbing, pulses (radial, ulnar, femoral,

popliteal, posteriortibial, dorsalis pedis; simultaneous

palpation of radial and femoral pulses). Grading of

pulses: = absent; 1+ weak; 2+ normal; 3+ very

strong (arterial dilation).
Rectal Exam: Masses, tenderness, hemorrhoids,

prostate masses; bimanual palpation, guaiac test for

occult blood.
Neurological: Mental status, cranial nerves, gait,

strength (graded 0-5); tendon reflexes, sensory

testing.
Laboratory Evaluation: Electrolytes (sodium,
potassium, bicarbonate, chloride, BUN, creatinine),
glucose, liver function tests, INR/PTT, CBC with
differential; X-rays, ECG (if older than 35 yrs or
cardiovascular disease), urine analysis.
Assessment (Impression): Assign a number to each
problem and discuss each problem. Begin with most
important problem and rank in order.
Plan: Discuss surgical plansfor each numbered problem,
including preoperative testing, laboratory studies,
medications, antibiotics, endoscopy.

Preoperative Preparation of the
Surgical Patient

1 . Reviewthe patient's history and physical examination,
and write a preoperative note assessing the patient's
overall condition and operative risk.

2. Preoperative laboratory evaluation: Electrolytes,
BUN, creatinine, INR/PTT, CBC, platelet count, UA,
ABG, pulmonary function test. Chest x-ray (>35 yrs
old), EKG (if older then 35 yrs old or if cardiovascular
disease). Type and cross for an appropriate number of
units of blood. No screening laboratory tests are
required in the healthy patient.

3. Skin preparation: Patient to shower and scrub the
operative site with germicidal soap (Hibiclens) on the
night before surgery. On the day of surgery, hair
should be removed with an electric clipper or shaved
just prior to operation.

4. Prophylactic antibiotics or endocarditis
prophylaxis if indicated.

5. Preoperative incentive spirometry on the evening
prior to surgery may be indicated for patients with
pulmonary disease.

6. Thromboembolic prophylaxis should be provided for
selected, high-risk patients.

7. Diet: NPO after midnight.

8. IV and monitoring lines: At least one 1 8-gauge IV for
initiation of anesthesia. Arterial catheter and
pulmonary artery catheters (Swan-Ganz) if indicated.
Patient to void on call to operating room.

9. Medications. Preoperative sedation as ordered by
anesthesiologist. Maintenance medicationsto be given
the morning of surgery with a sip of water. Diabetics
should receive one half of their usual AM insulin dose,
and an insulin drip should be initiated with hourly
glucose monitoring.

10. Bowel preparation

Bowel preparation is required for upper or lower Gl tract

procedures.

Antibiotic Preparation for Colonic Surgery

Mechanical Prep: Day 1 : Clear liquid diet, laxative (milk
of magnesia 30 cc or magnesium citrate 250 cc), tap
water or Fleet enemas until clear. Day 2: Clear liquid
diet, NPO, laxative. Day 3: Operation.

Whole Gut Lavage: Polyethylene glycol electrolyte

solution (GoLytely).

Day 1 : 2 liters PO or per nasogastric tube over 5
hours. Clear liquid diet. Day 2: Operation.

Oral Antibiotic Prep: One day prior to surgery, after
mechanical or whole gut lavage, give neomycin 1
gm and erythromycin 250 mg at 1 p.m., 2 p.m., 11
p.m.

11. Preoperative IV antibiotics: Initiate preoperatively
and give one dose during operation and one dose of
antibiotic postoperatively. Cefotetan (Cefotan), 1 gm
IV q12h, for bowel flora, or cefazolin (Ancef), 1 gm
IVPB q8h x 3 doses, for clean procedures.

12. Anticoagulants: Discontinue Coumadin 5 days
preop and check PT; stop IV heparin 6 hours prior to
surgery.

Admitting and Preoperative Orders

Admit to: Ward, ICU, or preoperative room.

Diagnosis: Intended operation and indication.

Condition: Stable

Vital Signs: Frequency of vital signs; input and output
recording; neurological or vascular checks. Notify
physician if blood pressure <90/60, >160/1 10; pulse
>1 10; pulse <60; temperature >101 .5; urine output
<35 cc/h for >2 hours; respiratory rate >30.

Activity: Bed rest or ambulation; bathroom privileges.

Allergies: No known allergies

Diet: NPO

IV Orders: D5 1/2 NS at 100 cc/hour.

Oxygen: 6 L/min by nasal canula.

Drains: Foley catheter to closed drainage. Nasogastric
tube at low intermittent suction. Other drains, tubes,

dressing changes. Orders for irrigation of tubes.

Medications: Antibiotics to be initiated immediately
preoperatively; additional dose during operation and
1 dose of antibiotic postoperatively. Cefotetan
(Cefotan), 1 gm IV q12h, for bowel flora, or cefazolin
(Ancef) 1 gm IVPB q8h x 3 doses;) for clean
procedures.

Labs and Special X-Rays: Electrolytes, BUN, creatinine,
INR/PTT, CBC, platelet count, UA, ABG, pulmonary
function tests. Chest x-ray (if >35 yrs old), EKG (if
older then 35 yrs old or if cardiovascular disease).
Type and cross for an appropriate number of units of
biood.

Preoperative Note

Preoperative Diagnosis:

Procedure Planned:

Type of Anesthesia Planned:

Laboratory Data: Electrolytes, BUN, creatinine, CBC,

INR/PTT, UA, EKG, chest x-ray; type and screen for

blood or cross match if indicated; liver function tests,

ABG.

Risk Factors: Cardiovascular, pulmonary, hepatic, renal,

coagulopathic, nutritional risk factors.

American Surgical Association (ASA) grading of

surgical risk: 1= normal; 2= mild systemic disease; 3=

severe systemic disease; 4= disease with major threat to

life; 5= not expected to survive.

Consent: Document explanation to patient of risks and

benefits of the procedure and alternative treatments.

Document patient's or guardian's informed consent and

understanding of the procedure. Obtain signed consent

form.

Allergies:

Major Medical Problems:

Medications:

Special Requirements: Signed blood transfusion

consent form; documentation that breast procedure

patients have been given an information brochure.

Brief Operative Note

This note should be written in chart immediately after the

surgical procedure.

Date of the Procedure:

Preoperative Diagnosis:

Postoperative Diagnosis:

Procedure:

Operative Findings:

Names of Surgeon and Assistants:

Anesthesia: General endotracheal, spinal, epidural,

regional or local.

Estimated Blood Loss (EBL):

Fluids and Blood Products Administered During

Procedure:

Urine output:

Specimens: Pathology specimens, cultures, blood

samples.

Intraoperative X-rays:

Drains:

Condition of Patient: Stable

Operative Report

This full report should be dictated at the conclusion of the

surgical procedure.

Identifying Data: Name of patient, medical record

number; name of dictating physician, date of dictation.

Attending Surgeon and Service:

Date of Procedure:

Preoperative Diagnosis:

Postoperative Diagnosis:

Procedure Performed:

Names of Surgeon and Assistants:

Type of Anesthesia Used:

Estimated Blood Loss (EBL):

Fluid and Blood Products Administered During

Operation:

Specimens: Pathology, cultures, blood samples.

Drains and Tubes Placed:

Complications:

Consultations Intraoperatively:

Indications for Surgery: Brief history of patient and

indications for surgery.

Findings: Describe gross findings and frozen section

results relayed to operating room.

Description of Operation: Position of patient; skin prep

and draping; location and types of incisions; details of

procedure from beginning to end, including description of

surgical findings, both normal and abnormal.

Intraoperative studies or x-rays; hemostatic and closure
techniques; dressings applied. Needle and sponge
counts as reported by operative nurse. Patient's condition
and disposition. Send copies of report to surgeons and
referring physicians.

Postoperative Check

A postoperative check should be completed on the
evening after surgery. This check is similar to a daily
progress note.

Example Postoperative Check

Date/time:

Postoperative Check

Subjective: Note any patient complaints, and note

the adequacy of pain relief.

Objective:

General appearance:

Vitals: Maximum temperature in the last 24

hours (T max ), current temperature, pulse,

respiratory rate, blood pressure.

Urine Output: If urine output is less than 30 cc

per hour, more fluids should be infused if the

patient is hypovolemic.

Physical Exam:

Chest and lungs:

Abdomen:

Wound Examination: The wound should be

examined for excessive drainage or bleeding,

skin necrosis, condition of drains.

Drainage Volume: Note the volume and

characteristics of drainage from Jackson-Pratt

drain or other drains.

Labs: Post-operative hematocrit value and
other labs.

Assessment and Plan: Assess the patient's
overall condition and status of wound. Comment on
abnormal labs, and discuss treatment and
discharge plans.

Postoperative Orders

1 . Transfer: From recovery room to surgical ward when
stable.

2. Vital Signs: q4h, l&O q4h x 24h.

3. Activity: Bed rest; ambulate in 6-8 hours if
appropriate. Incentive spirometer q1h while awake.

4. Diet: NPO x 8h, then sips of water. Advance from
clear liquids to regular diet as tolerated.

5. IV Fluids: IV D5 LR or D5 1/2 NS at 125 cc/h (KCL,
20 mEq/L if indicated), Foley to gravity.

6. Medications:

Cefazolin (Ancef) 1 gm IVPB q8h x 3 doses; if
indicated for prophylaxis in clean cases OR

Cefotetan (Cefotan) 1 gm IVq12h x2 doses for clean
contaminated cases.

Meperidine (Demerol) 50 mg IV/IM q3-4h prn pain

Hydroxyzine (Vistaril) 25-50 mg IV/IM q3-4h prn

nausea OR

Prochlorperazine (Compazine) 10 mg IV/IM q4-6h prn
nausea or suppository q 4h prn.

7. Laboratory Evaluation: CBC, SMA7, chest x-ray in
AM if indicated.

Postoperative Surgical Management

I. Postoperative day number 1

A. Assess the patient's level of pain, lungs, cardiac
status, flatulence, and bowel movement. Examine
for distension, tenderness, bowel sounds; wound
drainage, bleeding from incision.

B. Discontinue IV infusion when taking adequate PO
fluids. Discontinue Foley catheter, and use in-and-
out catheterization for urinary retention.

C. Ambulate as tolerated; incentive spirometer,
hematocrit and hemoglobin.

D. Acetaminophen/codeine (Tylenol #3) 1-2 POq4-6h
prn pain.

E. Colace 100 mg PO bid.

F. Consider prophylaxis for deep vein thrombosis.

II. Postoperative day number 2

A. If passing gas or if bowel movement, advance to
regular diet unless bowel resection.

B. Laxatives: Dulcolax suppository prn or Fleet enema
prn or milk of magnesia, 30 cc PO prn constipation.

III. Postoperative day number 3-7

A. Check pathology report.

B. Remove staples and place steri-strips.

C. Consider discharge home on appropriate medica-
tions; follow up in 1 -2 weeks for removal of sutures.

D. Write discharge orders (including prescriptions) in

AM; arrange
for home health care if indicated. Dictate discharge
summary and send copy to surgeon and referring
physician.

Surgical Progress Note

Surgical progress notes are written in "SOAP" format.

Surgical Progress Note

Date/Time:

Post-operative Day Number:

Problem List: Antibiotic day number and

hyperalimentation day number if applicable. List

each surgical problem separately (eg, status-post

appendectomy, hypokalemia).

Subjective: Describe how the patient feels in the

patient's own words, and give observations about

the patient. Indicate any new patient complaints,

note the adequacy of pain relief, and passing of

flatus or bowel movements. Type of food the

patient is tolerating (eg, nothing, clear liquids,

regular diet).

Objective:

Vital Signs: Maximum temperature (T max ) over

the past 24 hours. Current temperature, vital

signs.

Intake and Output: Volume of oral and

intravenous fluids, volume of urine, stools,

drains, and nasogastric output.

Physical Exam:

General appearance: Alert, ambulating.

Heart: Regular rate and rhythm, no murmurs.

Chest: Clear to auscultation.

Abdomen: Bowel sounds present, soft,

nontender.

Wound Condition: Comment on the wound

condition (eg, clean and dry, good

granulation, serosanguinous drainage).

Condition of dressings, purulent drainage,

granulation tissue, erythema; condition of

sutures, dehiscence. Amount and color of

drainage

Lab results: White count, hematocrit, and

electrolytes, chest x-ray
Assessment and Plan: Evaluate each numbered
problem separately. Note the patient's general
condition (eg, improving), pertinent developments,
and plans (eg, advance diet to regular, chest x-
ray). For each numbered problem, discuss any ad-
ditional orders and plans for discharge or transfer.

Procedure Note

A procedure note should be written in the chart when a
procedure is performed. Procedure notes are brief
operative notes.

Procedure Note

Date and time:

Procedure:

Indications:

Patient Consent: Document that the indications,

risks and alternatives to the procedure were

explained to the patient. Note that the patient was

given the opportunity to ask questions and that the

patient consented to the procedure in writing.

Lab tests: Electrolytes, INR, CBC

Anesthesia: Local with 2% lidocaine

Description of Procedure: Briefly describe the

procedure, including sterile prep, anesthesia

method, patient position, devices used, anatomic

location of procedure, and outcome.

Complications and Estimated Blood Loss

(EBL):

Disposition: Describe how the patient tolerated

the procedure.
Specimens: Describe any specimens obtained
and laboratory tests which were ordered.

Discharge Note

The discharge note should be written in the patient's
chart prior to discharge.

Discharge Note

Date/time:

Diagnoses:

Treatment: Briefly describe treatment provided

during hospitalization, including surgical

procedures and antibiotic therapy.

Studies Performed: Electrocardiograms, CT

scans.

Discharge Medications:

Follow-up Arrangements:

Discharge Summary

Patient's Name:
Chart Number:
Date of Admission:
Date of Discharge:
Admitting Diagnosis:
Discharge Diagnosis:
Name of Attending or Ward Service:
Surgical Procedures, Diagnostic Tests, Invasive
Procedures:

Brief History and Pertinent Physical Examination and
Laboratory Data: Describe the course of the patient's
disease up to the time the patient came to the hospital,
and describe the physical exam and pertinent laboratory
data on admission.

Hospital Course: Briefly describe the course of the
patient's illness while in the hospital, including evaluation,
operation, outcome of the operation, and medications
given while in the hospital.

Discharged Condition: Describe improvement or
deterioration of the patient's condition.
Disposition: Describe the situation to which the patient
will be discharged (home, nursing home) and the person
who will provide care.

Discharged Medications: List medications and
instructions and write prescriptions.
Discharged Instructions and Follow-up Care: Date of
return for follow-up care at clinic; diet, exercise
instructions.

Problem List: List all active and past problems.
Copies: Send copies to attending physician, clinic, con-
sultants and referring physician.

Prescription Writing

Patient's name:

Date:

Drug name, dosage form, dose, route, frequency

(include concentration for oral liquids or mg strength for

oral solids): Amoxicillin 125mg/5mL 5 mL PO tid

Quantity to dispense: mL for oral liquids, # of oral solids

Refills: If appropriate

Signature

Clinical Care of the
Surgical Patient

James G. Jakowatz, MD
Marianne Cinat, MD

Radiographic Evaluation of Common
Interventions

I. Central intravenous lines:

A.Central venous catheters should be located well
above the right atrium, and not in a neck vein.
Pneumothorax should be excluded by checking that
the lung markings extend completely to the rib cages
on both sides. An upright, expiratory x-ray may be
helpful. Hemothorax will appear as opacification or
a fluid meniscus on chest x-ray. Mediastinal
widening may indicate great vessel injury.

B. Pulmonary artery catheters should be located
centrally and posteriorly and not more than 3-5 cm
from midline within the mediastinum.

II. Pulmonary tubes

A. Endotracheal tubes: Verify that the tube is located
3 cm below the vocal cords and 2-4 cm above the
carina. The tip of tube should be at the level of aortic
arch.

B. Tracheostomy: Verify by chest x-ray that the tube
is located half way between the stoma and the
carina; the tube should be parallel to the long axis of
the trachea. The tube should be approximately 2/3
of width of the trachea, and the cuff should not cause
bulging of the trachea walls. Check for
subcutaneous air in the neck tissue and for
mediastinal widening secondary to air leakage.

C. Chest tubes: A chest tube for pneumothorax
drainage should be located anteriorly at the mid-
clavicular line at the level of the third intercostal
space or in the anterior axillary line directed toward
the apex at the 4-5th intercostal space. Pleural
effusions should be drained by locating the tube
inferior-posteriorly at or about the level of the eighth
intercostal space and directed posteriorly.

D. Mechanical ventilation: A chest x-ray should be
obtained to rule out pneumothorax, subcutaneous
emphysema, pneumomediastinum or subpleural air
cysts. Lung infiltrates may diminish or disappear
because of increased aeration of the affected lung
lobe.

III. Gastrointestinal tubes

A. Nasogastric tubes: Verify that the tube is in the
stomach and not coiled in the esophagus or trachea.
The tip of the tube should not be near
gastroesophageal junction. The standard size
nasogastric tube is 1 4-1 6 French. Nasogastric tubes
are used to decompress the stomach.

B. Feeding tubes are smaller in size (8-12 Fr) than
nasogastric tubes. They are flexible and are
frequently used for enteral nutrition . They are passed
nasally through the stomach and into the duodenum
or jejunum. The tip is radiopaque, and it should be
located in the distal stomach. The tube may extend
through the pylorus into the duodenum.

Blood Component Therapy

I. Crystalloids solutions: Sodium is the principle
component of crystalloid solutions, which is the most
abundant solute in the extracellular fluid.

A. Hypotonic solutions include 0.45% normal saline
and 0.25% normal saline. Hypotonic solutions are
used as maintenance fluids in adults (0.45% NS)
and infants (0.25% NS).

B. Isotonic solutions include normal saline (0.9%
NaCI; 154 mEq Na and 154 mEq CI) and lactated
Ringers (1 30meq Na, 1 09 mEq CI, 4 mEq K, 3 mEq
Ca, lactate as a buffer). Isotonic solutions are used
for acute resuscitation and volume replacement.
Approximately 3 cc of crystalloid should be given to
replace each 1 cc of blood loss.

C. Hypertonic saline (7.5% NaCI; 1283 mEq Na,
1283 mEq CI) is used to treat symptomatic
hyponatremia. Replacement must be done slowly
to prevent central pontine myelinolysis.

II. Colloid solution therapy is indicated for volume
expansion.

A. Albumin (5% or 25%) is useful for hypovolemia or
to induce diuresis with furosemide in hypervolemic,
hypoproteinemic patients. Salt poor albumin is
used in cirrhosis.

B. Purified protein fraction (Plasmanate) consists of
83% albumin and 17% globulin. It is indicated for
volume expansion as an alternative to albumin.

C. Hetastarch (Hespan) consists of synthetic colloid
(6% hetastarch in saline). Hespan is useful for
volume expansion and raising osmotic pressure.
Maximum dose is 1500 cc per 24 hours.
Hetastarch may prolong the partial thromboplastin
time.

III. Management of acute blood loss - red blood cell
transfusions

A. Hemorrhage should be controlled, and crystalloids
should be infused until packed red blood cells are
available to replace losses. In trauma, bleeding
may require surgical control. If crystalloids fail to
produce hemodynamic stability after more than 2
liters have been administered, packed red blood
cells should be given.

B. If volume replacement and hemostasis stabilize the
patient's hemodynamic status, formal type and
cross match of blood should be completed. In
exigent bleeding, O negative, lowtiter blood or type
specific (ABO matched) Rh compatible blood
should be administered.

IV. Guidelines for blood transfusion in anemia.
Consider blood transfusion when hemoglobin is less
than 8.0 gm/dL and hematocrit is less than 24%. If the
patient has symptoms of anemia, such as chest pain,
dyspnea, mental status changes, transfusion should
be provided.

V. Blood component products

A. Packed red blood cells (PRBCs). Each unit
provides 400 cc of volume, and each unit should
raise hemoglobin by 1 gm/dL and hematocrit by
3%.

B. Platelets are indicated for bleeding due to
thrombocytopenia or thrombopathy. Each unit
should raise the platelet count by 5,000-10,000
cells/mul. Platelets are usually transfused 8-10
units at a time. Dilutional thrombocytopenia occurs
after massive blood transfusions. Therefore,
platelet transfusion should be considered after 8-10
units of blood replacement. ABO typing is not
necessary before platelets are given.

C. Fresh frozen plasma (FFP) is used for bleeding
secondary to liver disease, dilutional coagulopathy
(from multiple blood transfusions), or coagulation
factor deficiencies. ABO typing is required before
administration of FFP, but cross matching is not
required. Improvement of INR/PTT usually requires
2-3 units. One unit of FFP should be administered
for every 4-6 units of PRBCs. FFP contains all
clotting factors except factors V and VII.

D. Cryoprecipitate contains factor VIII, and
fibrinogen. It is given 8-10 units at a time.
Cryoprecipitate may be necessary for massive
transfusions.

E. Autologous blood. The patient donates blood
within 35 days of surgery; frozen blood can be
stored for up to 2 years. Autologous blood is useful
in elective orthopedic, cardiac, and peripheral
vascular procedures.

Fluids and Electrolytes

I. Maintenance fluid guidelines

A. Maintenance fluid requirements consist of 4 cc/kg

for the first 10 kg of body weight, 2 cc/kg for the
second 10 kg, and 1 cc/kg for each additional kg.
B. A 70 mg patient has a maintenance fluid
requirement of approximately 125 mL/hr.
Maintenance fluids used are D5 1/2 NS with 20
mEq KCL/liter and D5 1/4 NS with 20 mEq KCI/liter
in children.

II. Pediatric patients

A. Use D5 1/4 NS with 20 mEq KCL/liter.

B. 24 hour water requirement, kilogram method:
For the first 10 kg body weight: 100 mL/kg/day
PLUS for the second 10 kg body weight: 50
mL/kg/day PLUS for weight above 20 kg: 20
mL/kg/day. Divide by 24 hours to determine hourly
rate.

III. Specific replacement fluids of specific losses

A. Gastric fluid (nasogastric tube, emesis). D5 1/2
NS with 20 mEq/liter KCL; replace equal volume of
lost fluid q6h.

B. Diarrhea. D5LR with 15 mEq/liter KCL. Provide 1
liter replacement for each 1 kg or 2.2 lb of lost body
weight; bicarbonate 45 mEq (1/2 amp) per liter may
be added.

C. Bile. D5LR with 25 mEq/liter (1/2 amp) of
bicarbonate.

D. Pancreatic. D5LR with 50 mEq/liter (1 amp)
bicarbonate.

Evaluation of Postoperative Fever

I. Clinical evaluation

A. History. Fever >1 00.4-1 01 F. Determine the
number of days since operation.

B. Differential diagnosis. Pneumonia, urinary tract
infection, thrombophlebitis, wound infection, drug
reaction. Atelectasis is the most common cause of
fever less than 48 hrs after operation.

C. Dysuria, abdominal pain, cough, sputum,
headache, stiff neck, joint or back pain may be
present.

D. IV catheter infection (central or peripheral) is an
important source of postoperative sepsis.

E. Fever pattern. Check previous day for fever
patterns; spiking fevers indicate abscesses.
Continuous fevers or high fevers indicate vascular
involvement, such as infected prosthetic grafts or
septic phlebitis from central IV lines.

F. Chills or rigors indicate bacteremia. These
symptoms are usually not associated with
atelectasis or drug fevers.

G. Fevers prior to the operation, alcohol use, allergies,
and recent WBC count and differential counts
should be assessed.

II. Physical Exam

A. General. Temperature, fever curve, tachycardia,
hypotension. Examine all vascular access sites
carefully.

B. HEENT. Pharyngeal erythema, neck rigidity.

C. Chest. Rhonchi, crackles, dullness to percussion
(pneumonia), murmurs (endocarditis).

D. Abdomen. Masses, liver tenderness, Murphy's
sign (right upper quadrant tenderness with
inspiration, cholecystitis); ascites. Costovertebral
angle or suprapubic tenderness. Examine wound
for purulence, induration, or tenderness.

E. Extremities. Infected decubitus ulcers or wounds;
IV catheter tenderness (phlebitis); calf tenderness,
joint tenderness (septic arthritis). Cellulitis,
abscesses, perirectal abscess.

F. Genitourinary. Prostate tenderness; rectal
fluctuance. Cervical discharge, cervical motion
tenderness; adnexal tenderness.

III. Laboratory evaluation. CBC, blood C&S X 2, UA,
urine C&S; blood, urine, sputum, wound cultures,
chest x-ray.

IV. Differential diagnosis

A. Wound infection, abscesses, intra-abdominal
abscess, atelectasis, drug fever, pulmonary emboli,
pancreatitis, alcohol withdrawal, deep vein
thrombosis, tuberculosis, cystitis, pyelonephritis,
osteomyelitis; IV catheter phlebitis, sinusitis, otitis
media, upper respiratory infection, pelvic infection,
cellulitis; hepatitis, infected decubitus ulcer,
peritonitis, endocarditis, diverticulitis, cholangitis,
carcinomas.

B. Medications associated with fever: H2 blockers,
penicillins, phenytoin, sulfonamides.

V. Antibiotics should be initiated if there is any
possibility of infection.

Sepsis

About 400,000 cases of sepsis, 200,000 cases of septic
shock, and 100,000 deaths from both occur each year.

I. Pathophysiology

A. Sepsis is defined as the systemic response to
infection. In the absence of infection, it is called
systemic inflammatory response syndrome and is
characterized by at least two of the following:
temperature greater than 38"C or less than 36"C;
heart rate greater than 90 beats per minute;
respiratory rate more than 20/minute or PaC0 2 less
than 32 mm Hg; and an alteration in white blood
cell count (>12,000/mm 3 or <4,000/mm 3 ).

B. Septic shock is defined as sepsis-induced
hypotension that persists despite fluid resuscitation
and is associated with tissue hypoperfusion.

C. The initial cardiovascular response to sepsis
includes decreased systemic vascular resistance
and depressed ventricular function. Low systemic
vascular resistance occurs. If this initial
cardiovascular response is uncompensated,
generalized tissue hypoperfusion results.
Aggressive fluid resuscitation may improve cardiac
output and systemic blood pressure, resulting in the
typical hemodynamic pattern of septic shock (ie,
high cardiac index and low systemic vascular
resistance).

D. Although gram-negative bacteremia is commonly
found in patients with sepsis, gram-positive
infection may affect 30-40% of patients. Fungal,
viral and parasitic infections are usually
encountered in immunocompromised patients.

Defining sepsis and related disorders

Term

Definition

Systemic

inflammatory
response
syndrome
(SIRS)

The systemic inflammatory response to
a severe clinical insult manifested by >2
of the following conditions: Temperature
>38°C or <36°C, heart rate >90
beats/min, respiratory rate >20
breaths/min or PaC0 2 <32 mm Hg,
white blood ceil count >12,000
cells/mm 3 , <4000 cells/mm 3 , or >10%
band cells

Sepsis

The presence of SIRS caused by an
infectious process; sepsis is considered
severe if hypotension or systemic
manifestations of hypoperfusion (lactic
acidosis, oliguria, change in mental
status) is present.

Septic shock

Sepsis-induced hypotension despite
adequate fluid resuscitation, along with
the presence of perfusion abnormalities
that may induce lactic acidosis, oliguria,
or an alteration in mental status.

Multiple organ
dysfunction
syndrome
(MODS)

The presence of altered organ function
in an acutely ill patient such that
homeostasis cannot be maintained
without intervention

E. Sources of bacteremia leading to sepsis include
the urinary, respiratory and Gl tracts, and skin and
soft tissues (including catheter sites). The source
of bacteremia is unknown in 30% of patients.

F. Escherichia coli is the most frequently
encountered gram-negative organism, followed by
Klebsiella, Enterobacter, Serratia, Pseudomonas,
Proteus, Providencia, and Bacteroides species.
Up to 16% of sepsis cases are polymicrobic.

G. Gram-positive organisms, including
Staphylococcus aureus and Staphylococcus
epidermidis, are associated with catheter or line-
related infections.

Diagnosis

A. A patient who is hypotensive and in shock should
be evaluated to identify the site of infection, and
monitorfor end-organ dysfunction. History should
be obtained and a physical examination
performed.

B. The early phases of septic shock may produce
evidence of volume depletion, such as dry
mucous membranes, and cool, clammy skin. After
resuscitation with fluids, however, the clinical
picture resembles hyperdynamic shock, including
tachycardia, bounding pulses with a widened
pulse pressure, a hyperdynamic precordium on
palpation, and warm extremities.

C. Signs of infection include fever, localized
erythema or tenderness, consolidation on chest
examination, abdominal tenderness, and
meningismus. Signs of end-organ hypoperfusion
include tachypnea, oliguria, cyanosis, mottling of

the skin, digital ischemia, abdominal tenderness,
and altered mental status.
, Laboratory studies should include of arterial
blood gases, lactic acid level, electrolytes, renal
function, liver enzyme levels, and chest
radiograph. Cultures of blood, urine, and sputum
should be obtained before antibiotics are
administered. Cultures of pleural, peritoneal, and
cerebrospinal fluid may be appropriate. If
thrombocytopenia or bleeding is present, tests for
disseminated intravascular coagulation should
include fibrinogen, d-dimer assay, platelet count,
peripheral smear for schistocytes, prothrombin
time, and partial thromboplastin time.

Manifestations of Sepsis

Clinical features

Laboratory findings

Temperature instability

Respiratory alkaloses

Tachypnea

Hypoxemia

Hyperventilation

Increased serum lactate

Altered mental status

levels

Oliguria

Leukocytosis and

Tachycardia

increased neutrophil

Peripheral vasodilation

concentration

Eosinopenia

Thrombocytopenia

Anemia

Proteinuria

Mildly elevated serum

bilirubin levels

III. Treatment of septic shock

A. Early management of septic shock is aimed at
restoring mean arterial pressure to 65 to 75 mm
Hg to improve organ perfusion. Clinical clues to
adequate tissue perfusion include skin
temperature, mental status, and urine output.
Urine output should be maintained at >20 to 30
mL/hr. Lactic acid levels should decrease within
24 hours if therapy is effective.

B. Intravenous access and monitoring

1. Intravenous access is most rapidly obtained
through peripheral sites with two 16- to
1 8-gauge catheters. More stable access can be
achieved later with central intravenous access.
Placement of a large-bore introducer catheter in
the right internal jugular or left subclavian vein
allows the most rapid rate of infusion.

2. Arterial lines should be placed to allow for more
reliable monitoring of blood pressure.
Pulmonary artery catheters measure cardiac
output, systemic vascular resistance, pulmonary
artery wedge pressure, and mixed venous
oxygen saturation. These data are useful in
providing rapid assessment of response to
various therapies.

C. Fluids

1. Aggressive volume resuscitation is essential in
treatment of septic shock. Most patients require
4 to 8 L of crystalloid. Fluid should be
administered as a bolus. The mean arterial
pressure should be increased to 65 to 75 mm
Hg and organ perfusion should be improved
within 1 hour of the onset of hypotension.

2. Repeated boluses of crystalloid (isotonic
sodium chloride solution or lactated Ringer's
injection), 500 to 1,000 mL, should be given
intravenously over 5 to 10 minutes, until mean
arterial pressure and tissue perfusion are
adequate (about 4 to 8 L total over 24 hours for
the typical patient). Boluses of 250 mL are
appropriate for patients who are elderly or who
have heart disease or suspected pulmonary
edema. Red blood cells should be reserved for
patients with a hemoglobin value of less than 1
g/dL and either evidence of decreased oxygen
delivery or significant risk from anemia (eg,
coronary artery disease).

D.Vasoactive agents

1. Patients who do not respond to fluid therapy
should receive vasoactive agents. The primary
goal is to increase mean arterial pressure to 65
to 75 mm Hg.

2. Dopamine (Intropin) traditionally has been
used as the initial therapy in hypotension,
primarily because it is thought to increase
systemic blood pressure. However, dopamine is
a relatively weak vasoconstrictor in septic
shock.

3. Norepinephrine (Levophed) is superior to
dopamine in the treatment of hypotension
associated with septic shock. Norepinephrine is
the agent of choice for treatment of hypotension
related to septic shock. Dobutamine (Dobutrex)
should be reserved for patients with a

persistently low cardiac index or underlying left
ventricular dysfunction.

Hemodynamic effects of vasoactive agents

Agent

Dose

Effect

CO

MA
P

SVR

Dopamin

e

(Inotropin

)

5-20

mcg/kg/mi

n

2+

1 +

1 +

Norepin-
ephrine
(Levophe

d)

0.05-5

mcg/kg/mi

n

-101+

2+

2+

Dobutam
ine

(Dobutre
x)

5-20

mcg/kg/mi

n

2+

-101+

Epinephri
ne

0.05-2

mcg/kg/mi

n

2+

2+

2+

Phenylep
hrine
(Neo-Syn
ephrine)

2-10

mcg/kg/mi

n

-10

2+

2+

E. Antibiotics should be administered within 2 hours
of the recognition of sepsis. Use of vancomycin
should be restricted to settings in which the
causative agent is most likely resistant
Enterococcus, methicillin-resistant Staphylococcus
aureus, or high-level penicillin-resistant
Streptococcus pneumoniae.

Recommended Antibiotics in Septic Shock

Suspected
source

Recommended antibiotics

Pneumonia

Second- or third-generation
cephalosporin (cefuroxime, ceftazidime,
cefotaxime, ceftizoxime) plus macrolide
(antipseudomonal beta lactam plus
aminoglycoside if hospital-acquired)

Urinary tract

Ampicillin plus gentamicin (Garamycin)
or third-generation cephalosporin
(ceftazidime, cefotaxime, ceftizoxime)

Skin or soft
tissue

Nafcillin (add metronidazole [Flagyl,
Metro IV, Protostat] or clindamycin if
anaerobic infection suspected)

Meningitis

Third-generation cephalosporin
(ceftazidime, cefotaxime, ceftizoxime)

Intra-abdominal

Third-generation cephalosporin
(ceftazidime, cefotaxime, ceftizoxime)
plus metronidazole or clindamycin

Primary
bacteremia

Ticarcillin/clavulanate (Timentin) or
piperacillin/tazobactam(Zosyn)

Dosages of Antibiotics Used in Sepsis

Agent

Dosage

Ceftizoxime (Cefizox)

2gmlVq8h

Ceftazidime (Fortaz)

2glVq8h

Cefotaxime (Claforan)

2 gm q4-6h

Cefuroxime (Kefurox,
Zinacef)

1.5glVq8h

Cefoxitin (Mefoxin)

2 gm q6h

Cefotetan (Cefotan)

2gmlVq12h

Piperacillin/tazobactam
(Zosyn)

3.375-4.5 gm IV q6h

Ticarcillin/clavulanate (Tim-
entin)

3.1 gmlVq4-6h (200-300
mg/kg/d)

Ampicillin

1-3.0 gm IV q6h

Agent

Dosage

Ampicillin/sulbactam
(Unasyn)

3.0 gm IVq6h

Nafcillin (Nafcil)

2 gm IV q4-6h

Piperacillin, ticarcillin,
mezlocillin

3gmlVq4-6h

Meropenem (Merrem)

1 gm IVq8h

Imipenem/cilastatin
(Primaxin)

1.0gmlVq6h

Gentamicin or tobramycin

2 mg/kg IV loading dose,
then 1.7 mg/kg IVq8h

Amikacin (Amikin)

7.5 mg/kg IV loading dose,
then 5 mg/kg IVq8h

Vancomycin

1 gmlVq12h

Metronidazole (Flagyl)

500 mg IV q6-8h

Clindamycin (Cleocin)

600-900 mg IV q8h

Linezolid (Zyvox)

600mglV/POq12h

Quinupristin/dalfopristin
(Synercid)

7.5 mg/kg IVq8h

1. Initial treatment of life-threatening sepsis
usually consists of a third-generation
cephalosporin (ceftazidime, cefotaxime,
ceftizoxime)orpiperacillin/tazobactam(Zosyn).
An aminoglycoside (gentamicin, tobramycin, or
amikacin) should also be included.
Antipseudomonal coverage is important for
hospital- or institutional-acquired infections.
Appropriate choices include an
antipseudomonal penicillin, cephalosporin, or
an aminoglycoside.

2. Methicillin-resistant staphylococci. If line
sepsis or an infected implanted device is a
possibility, vancomycin should be added to the
regimen to cover for methicillin-resistant Staph
aureus and methicillin-resistant Staph
epidermidis.

3. Vancomycin-resistant enterococcus (VRE):
An increasing number of enterococcal strains
are resistant to ampicillin and gentamicin. The
incidence of vancomycin-resistant
enterococcus (VRE) is rapidly increasing.

a. Linezolid (Zyvox) is an oral or parenteral
agent active against vancomycin-resistant
enterococci, including E. faecium and E.
faecalis. Linezolid is also active against
methicillin-resistant staphylococcus aureus.

b. Quinupristin/dalfopristin (Synercid) is a
parenteral agent active against strains of
vancomycin-resistant enterococcusfaecium,
but not enterococcus faecalis. Most strains
of VRE are enterococcusfaecium.

F. Other therapies

1. Hydrocortisone (100 mg every 8 hours) in
patients with refractory shock significantly
improves hemodynamics and survival rates.
Corticosteroids may be beneficial in patients
with refractory shock.

2. Activated protein C (drotrecogin alfa
[Xigris]) has antithrombotic, profibrinolytic, and
anti-inflammatory properties. Activated protein
C reduces the risk of death by 20%. Activated
protein C is approved for treatment of patients
with severe sepsis who are at high risk of
death. Drotrecogin alfa is administered as 24
mcg/kg/hr for 96 hours. There is a small risk of
bleeding. Contraindications are
thrombocytopenia, coagulopathy, recent
surgery or recent hemorrhage.

References: See page 112.

Nutrition in the Surgical Patient

Nutritional requirements are based on the patient's
nutritional needs, stress and severity of illness.
Requirements are divided into non-protein calories per
kilogram (npc/kg) and grams of protein per kilogram
(gm protein/kg) per 24-hour period.

Nutritional Requirements

Patient

Non-protein
calories/kg

Protein

Well-
nourished,
unstressed

20-25
npc/kg/day

1 gm/kg

Minimal stress
(post-op)

25-30
npc/kg/day

1-1.2 gm/kg

Moderate

stress

(multiple

trauma,

infection)

30-35
npc/kg/day

1.2-1.5 gm/kg

Severe stress
(severe
sepsis, critical
illness)

35-40
npc/kg/day

1.5-2.0 gm/kg

Extreme
stress (burns>
40% body
surface area)

40-45
npc/kg/day

2.0-2.5 gm/kg

A. Sources of non-protein calories

1 . Carbohydrate solutions contain dextrose,
which contains 3.4 kcal/gm

2. Lipid solutions contain 9.1 kcal/gm

B. Protein calories. Amino acid solutions contain
protein in a concentration of 4 kcal/gm

. Enteral nutrition

A. Enteral nutrition is more physiologic and technically
easier to administer than parenteral nutrition.
Enteral nutrition can be administered via
nasogastric, nasoduodenal or nasojejunal tubes, or
gastrostomy or jejunostomy tubes.

B. Continuous enteral infusion

1. Initial enteral solution infusion starts at 30 m/hr.
increase rate by 30 mL at 4-hour intervals as
tolerated until the final rate is achieved.
Residual volume should be measured every 4
hours; hold feedings for 1 hour if the residual is
greater than 2 times the infusion rate.

2. Gastric/duodenal feedings: Start with full
strength formula and increase the rate until the
goal is achieved.

3. Jejunal feedings: Start with 1/4 strength
formula. Increase the rate until the goal is
achieved. Once at goal rate, change to 1/2
strength formula for 4-8 hours, then % strength
formula for 4-8 hours, then full strength formula
for 4-8 hours. This method allows the mucosa of
the distal small bowel to adjust to the increased
osmolarity of enteral formulas.

C. Bolus feedings: Give 50-100 cc enteral nutrition
every 3 hours initially. Increase by 50 cc each
feeding until the goal of 250-300 cc q 3-4 hours is
achieved. Flush tube with 100 cc of water after
each bolus.

D. Promotility agents are given to improve gastric
emptying

1. Metoclopramide (Reglan) 5-10 mg PO/IV q6h
OR

2. Erythromycin 1 25 mg IV or via nasogastric tube
q8h.

E. Antidiarrheal Agents

1. Loperamide (Imodium) 2-4 mg q6h.

2. Diphenoxylate/atropine (Lomotil) 2.5-5.0 mg q4-
6h.

Total Parental Nutrition

Indications for total parenteral nutritions:

Prolonged post-operative ileus, inability to take oral
feedings for more than 5 days, severe malnutrition,
intestinal fistula, pancreatitis. Total parenteral nutrition
should be given via a central catheter because of high
osmolality.

Standard solutions and components
A. Dextrose solutions. Various concentrations are
available. One gram of dextrose yields 3.4 kcal.

Dextrose Solutions

Solution

Concentration

Calories

10%

100 gm/l iter

340 kcal/liter

20%

200 gm/liter

680 kcal/liter

50%

500 gm/liter

1700 kcal/liter

70%

700 gm/liter

2380 kcal/liter

B. Lipid solutions consist of lipid emulsions of long-
chain triglycerides. These are usually given in 500
cc volumes at 32 cc/hour for 16 hours.

Lipid Solutions

Solution

Concentration

Calories

10%

50 gm/500 cc

500 kcal

20%

100gm-500cc

1000 kcal

C.Amino acid solutions supply protein. Various
types of solutions at various concentrations are
available.

Amino Acid Solutions

Solution

Concentration

Indications

Ami nosy n 7%

70 gm/liter

Standard

Aminosyn-HBC*
7%

70 gm/liter

Hypercatabolism

Aminosyn-RF
5.2%

52 gm/liter

Renal Failure

HepatAmine 8%

80 gm/liter

Liver Failure

FreAmine 10%

100 gm/liter

Fluid Overload

(highly

concentrated)

*High-branched chain aminoacid formulas may prevent
muscle breakdown and may prevent hepatic
encephalopathy.

D. Electrolyte requirements should be adjusted daily
based on patient labs.

Electrolyte Requirements

Usual concentration

Range

Sodium 60 (meg/L)

0-150 meq/L

Potassium 20 (meg/L)

0-80 meq/L

Acetate* 50 (meg/L)

50-150 meq/L

Chloride 50 (meg/L)

0-1 50 meq/L

Phosphate 15 (meg/L)

0-30 meq/L

Calcium** 4.5 (meg/L)

0-20 meq/L

Magnesium 5.0 (meg/L)

5-1 5 meq/L

* Acetate is used in addition to chloride to help prevent
hyperchloremic acidosis. One-third to one half of
sodium and potassium should be supplied in the form of
acetate rather than chloride.

** Calcium should be given as calcium gluconate or

calcium chloride. One gram of calcium supplies 4.5 meq
of calcium.

1 . Other additives

a. Multivitamins 1 amp daily

b. Vitamin K 10 mg each week

c. Trace elements chromium, copper,
manganese, zinc, selenium

E. Ordering Total Parenteral Nutrition

1. Step One. Determine the daily non-protein
calories (dextrose and lipid) and grams or protein
(amino acid) that the patient needs.

Non-protein calory requirement/kg/day = wt in kg
x npc requirement/kg/d

Protein requirement = wt in kg x protein

requirement/kg/d

Step Two. Non-protein calories consist of lipids
and carbohydrate (dextrose) solutions. The
amount of each component should be determined .
500cc of 10% Intralipid solution will supply
approximately 500 npc kcal. The patient will
require the remaining non-protein calories from
the dextrose solution. If using D50, the volume of
D50 = npc x 1000 cc/1700 kcal.
Step Three. Protein calories are supplied by
amino acid solutions.

Vol of 7% Aminosyn = gm protein required/dx 100
cc/7 gm

4. Step Four. Combine the above volumes to
determine total volume and rate. The dextrose
and amino acid solutions are mixed together and
given over 24 hours. The lipid solution is infused
separately over 24 hours.

F. Methods of delivery

1 . Continuous infusion of the solutions over 24
hours is the most common method of
administration. The TPN solution should be
initiated slowly at 40 cc/hr for the first 24 hours.
The rate can then be gradually increased by 30
cc/hr every four hours until the goal rate is
reached.

2. Cyclic total parenteral nutrition 12-hour night
schedule. Taper continuous infusion in the
morning by reducing the rate to half of the
original rate for one hour. Further reduce the
rate by half for an additional hour, then
discontinue. Restart TPN in the afternoon.
Taper at the beginning and end of cycle.

G. Laboratory examinations

1. Baseline Labs: CBC, electrolytes, liverfunction
tests, prealbumin, transferrin, triglyceride level,
chest x-ray for line placement

2. DailyLabs: Electrolytes, calcium, phosphorous
until stable; glucometer checks with insulin
sliding scale every 4-6 hours

3. Weekly Labs: CBC, electrolytes, calcium,
phosphorous, liver function tests, triglyceride
level (4-6 hours after completion of lipid infusion;
should be maintained <200 mg/dl)

4. Nutritional Assessment to determine
adequacy of nutritional supplementation:

a. Prealbumin or transferrin weekly

b. 24-hour urine for urine urea nitrogen (to
calculate nitrogen balance

III. Peripheral parenteral nutrition (PPN) can be
delivered via peripheral veins.

A. The goal of PPN is to provide enough non-protein
calories to prevent catabolism and the breakdown
of visceral proteins. Peripheral parenteral nutrition
is not meant to create a positive nitrogen balance
or anabolic state, and it should be used for short-
term support only.

B. PPN usually consists of a 3% amino acid solution
mixed with dextrose 20% or glycerol. Intralipids
(10% or 20%) can also be given peripherally to
supply extra calories.

Central Venous Catheterization

I. Indications for central venous catheter can-
nulation: Monitoring of central venous pressures in
shock or heart failure; management of fluid status;
administration of total parenteral nutrition; prolonged
antimicrobial therapy or chemotherapy.

II. Location of catheterization site

A. The internal jugular approach should not be used
in patients with a carotid bruit, carotid stenosis, or
an aneurysm.

B. The subclavian approach should be avoided in
patients with emphysema or bullae.

C. The external jugular or internal jugular approach by
direct cut-down may be preferable in patients with
coagulopathy or thrombocytopenia.

D. If a chest tube already in place, the catheter should
be placed on the same side as the chest tube.

III. Technique of insertion into the external jugular

vein

A. The external jugular vein courses from the angle of
the mandible to behind the middle of clavicle,
where it joins with the subclavian vein. Place
patient in Trendelenburg's position, and apply
digital pressure to the external jugular vein above
clavicle to distend the vein. Cleanse the skin with
Betadine iodine solution using sterile technique.

Inject 1% lidocaine to produce a skin weal.

B. With an 18-gauge, thin-wall needle, advance the
needle into the vein. Then pass a J-guidewire
through the needle; the wire should advance with-
out resistance. Remove the needle, maintaining
control over the guidewire at all times. Nick the skin
with a No. 1 1 scalpel blade.

C. With guidewire in place, pass the central catheter
over the wire, and remove the guidewire after the
catheter is in place. Cover the catheter hub with a
finger to prevent air embolization.

D. Attach a syringe to the catheter hub, and ensure
that there is free back-flow of dark venous blood.
Attach the catheter to an intravenous infusion at a
keep open rate. Secure the catheter in place with
2-0 silk suture and tape.

E. Obtain a chest x-ray to confirm position and rule
out pneumothorax. The catheter should be remo-
ved and changed within 3-4 days.

IV. Internal jugular vein cannulation. The internal
jugularvein is positioned behind the sternocleidomas-
toid muscle, lateral to the carotid artery. The catheter
should be placed at a location at the upper confluence
of the two bellies of sternocleidomastoid at the level of
cricoid cartilage.

A. Place the patient in Trendelenburg's position, and
turn the patient's head to the contralateral side.
Choose a location on the right or left. If lung
function is symmetrical and no chest tubes are in
place, the right side is preferred because of the
direct path to the superior vena cava. Prepare the
skin with Betadine solution using sterile technique
and drape the area. Infiltrate the skin and deeper
tissues with 1% lidocaine.

B. Palpate the carotid artery. Using a 22-gauge scout
needle and syringe, direct the needle toward the
ipsilateral nipple at a 30 degree angle to the neck.
While aspirating, advance the needle until the vein
is located and blood back flows into the syringe.

C. Remove the scout needle and advance an 18-
gauge, thin wall, catheter-over-needle (with an at-
tached syringe) along the same path as the scout
needle. When back flow of blood is noted into the
syringe, advance the catheter into the vein.
Remove the needle and confirm back flow of blood
through the catheter and into the syringe. Remove
the syringe and cover the catheter hub with a finger
to prevent air embolization.

D. With the catheter in position, advance a guidewire
through the catheter. The guidewire should
advance easily without resistance.

E. With the guidewire in position, remove the catheter
and use a No. 11 scalpel blade to nick the skin.
Place the central vein catheter over the wire, hol-
ding the wire secure at all times. Pass the catheter
into the vein, and suture the catheter to the skin
with O silk suture. Tape the catheter in place, and
connect it to an IV infusion at a keep open rate.

F. Obtain a chest x-ray to rule out pneumothorax and
confirm position.

V. Subclavian vein cannulation

A. The subclavian vein is located in the angle formed
by the medial 1/3 of clavicle and the first rib.

B. Position the patient supine with a rolled towel
located longitudinally between the patient's scap-
ulae, and turn the patient's head towards the con-
tralateral side. Prepare the area with Betadine
iodine solution, and, using sterile technique, drape
the area and infiltrate 1% lidocaine into the skin
and tissues.

C. Use a 16-gauge needle, with syringe attached, to
puncture the mid-point of the clavicle, advancing
until the clavicle bone and needle come in contact.

D. Then slowly probe down until the needle slips
under the clavicle. Advance the needle slowly
towards the vein until the needle enters the vein,
and a back flow of venous blood enters the
syringe. Remove the syringe, and cover the
catheter hub with a finger to prevent air
embolization.

E. With the 16-gauge catheter in position, advance a
0.89 mm x 45 cm guidewire through the catheter.
The guidewire should advance easily without re-
sistance. With the guidewire in position, remove
the catheter, and use a No. 1 1 scalpel blade to nick
the skin. Pass the dilator over the wire.

F. Place the central line catheter over the wire, hol-
ding the wire secure at all times. Pass the catheter
into the vein, and suture the catheter to the skin
with 2-0 silk suture, tape the catheter in place and
connect to IV infusion. Obtain a chest x-ray to
confirm the position of the catheter tip and rule out
pneumothorax.

Pulmonary Artery Catheterization

1 . Cannulate a vein using the technique above, such as
the subclavian vein or internal jugular. Advance a
guidewire through the cannula, and remove the
cannula. Nick the skin with a number 1 1 scalpel blade
adjacent to the guidewire, and pass a number 8
French introducer over the wire and into the vein.
Connect the introducer to an IV fluid infusion at a
keep open rate, and suture introducer to the skin with
2-0 silk.

3. Pass the proximal end of the pulmonary artery
catheter (Swan Ganz) to an assistant for connection
to a continuous flush transducer system.

4. Flush the distal and proximal ports with heparin
solution, removing all bubbles, and check balloon in-
tegrity by inflating 2 cc of air. Check pressure transd-
ucer response by moving the distal tip quickly.

5. Pass the catheter through the introducer into the vein
10-20 cm, then inflate the balloon, and advance the
catheter until the balloon is in or near the right atrium.

6. The correct distance to the entrance of the right atrium
is determined from the site of insertion:

Right antecubital fossa: 35-40 cm.
Left antecubital fossa: 45-50 cm.
Right internal jugular vein: 10-15 cm.
Subclavian vein: 10 cm.
Femoral vein: 35-45 cm.

7. Run a continuous monitoring strip to record pressures
as the PA catheter is advanced. Advance the balloon ,
inflated with 0.8-1.0 cc of air, while monitoring
pressures and wave forms. Advance the catheterthro-
ugh the right ventricle into the main pulmonary artery
until the catheter enters a distal branch of the pul-
monary artery and is stopped by impaction (as
evidenced by a pulmonary wedge pressure wave
form).

8. Do not advance catheterwith balloon deflated, and do
not withdraw the catheter with the balloon inflated.
After placement, obtain a chest x-ray to verify that the
tip of catheter is no farther than 3-5 cm from the
midline, and no pneumothorax is present.

Normal Pulmonary Artery Catheter
Values

Right atrial pressure 1-7mmHg

RVP Systolic 15-25 mmHg

RVP Diastolic 8-15 mmHg

Pulmonary artery pressure

PAP Systolic 15-25 mmHg

PAP Diastolic 8-15 mmHg

PAP Mean 10-20 mmHg

PCWP 6-12 mmHg

Cardiac Output 3.5-5.5 L/min

Cardiac Index 2.0-3.2 L/min/nr

Systemic Vascular Resistance 800-1 200 dyne/-
sec/cm 2

Venous Cutdown

Procedures

1 . Obtain a venous cutdown tray, or a minor procedure
tray and instrument tray with a silk suture (3-0, 4-0)
and a catheter. This procedure will require sterile
gloves, sterile towels/drapes, 4x4 gauze sponges,
povidone-iodine solution, 5 cc syringe, 25 gauge
needle, 1 % lidocaine with epinephrine, adhesive tape,
scissors, needle holder, hemostat, scalpel and blade,
3-0 or 4-0 silk suture.

2. Apply a tourniquet proximal to the site, and identify the
vein. Remove the tourniquet and prep the skin with
povidone-iodine solution and drape the area. Infiltrate
the skin with 1% lidocaine, then incise the skin
transversely.

3. Spread the incision long-wise in the direction of the
vein with a hemostat and dissect adherent tissue from
the vein. Lift the vein and pass two chromic or silk ties
(3-0 or 4-0) behind the vein.

4. Tie off the distal suture, using the upper tie for traction.
Make a transverse nick in the vein. If necessary, use a
catheter introducer to hold the lumen of the vein open.

5. Make a small stab incision in the skin distal to the main
skin incision, and insert a plastic catheter or IV cannula
through the incision, then insert it into vein. Tie the
proximal suture, and attach an infusion of IV fluid.
Release the tourniquet. Suture the skin with silk or
nylon, and apply a dressing.

Arterial Line Placement

Procedure

1. Obtain a 20 gauge, 1 1/2-2 inch, catheter-over-needle
assembly (Angiocath), arterial line setup (transducer,
tubing, pressure bag containing heparinized saline),
armboard, sterile dressing, 1 % lidocaine, 3 cc syringe,
25 gauge needle, and 3-0 silk.

2. The radial artery should be used. Use the Allen test to
verify patency of the radial artery and adequacy of
ulnar artery collaterals. Place the extremity on an
armboard with a gauze roll behind the wrist to
maintain hyperextension.

3. Prep with povidone-iodine and drape the wrist area.
Infiltrate 1% lidocaine using a 25 gauge needle.
Choose a site where the artery is most superficial and
as distal as possible on the wrist.

4. Palpate the artery with the left hand, and use other
hand to advance a 20 gauge catheter-over-needle into
the artery at a 30 degree angle to the skin. When a
flash of blood is seen, hold the needle in place and
advance the catheter into the artery; occlude the
artery with manual pressure while pressure tubing is
connected.

5. If a needle and guide-wire kit is used, advance the
guidewire into the artery, and pass the catheter over
the guide-wire.

6. Suture the catheter in place with 3-0 silk, and apply a
dressing.

Cricothyrotomy

I. Needle cricothyrotomy

A. Obtain a 12-14 gauge, catheter-over-needle
(Angiocath or Jelco), 6-12 mL syringe, 3 mm
pediatric endotracheal tube adapter, oxygen tubing,
and a high flow oxygen source.

B. Locate the cricothyroid membrane (the notch
between the thyroid cartilage and cricoid cartilage).
Cleanse the neck area with povidone-iodine
solution, and inject 2% lidocaine with epinephrine
if the patient is conscious.

C. With a 12 or 14 gauge, catheter-over-needie
assembly on the syringe, advance needle through
the cricothyroid membrane at a 45 degree angle
directed inferiorly. Apply back pressure on the
syringe until air is aspirated.

D. Advance the catheter and remove the needle, then
attach the hub to a 3 mm endotracheal tube
adapter connected to oxygen tubing.

E. Administer oxygen at 15 liters per minute for 1-2
seconds on, then 4 seconds off. Air flow is
controlled with a Y-connector or a hole in the side
of the tubing.

F. The needle cricothyrotomy should be replaced with
oral endotracheal intubation as soon as possible. A
needle cricothyrotomy should not be used for more
than 45 minutes, since exhalation of C0 2 is
inadequate.

II. Surgical cricothyrotomy

A. Obtain a #5-#7 tracheostomy tube; tracheostomy
tube adapter to connect to bag-mask ventilator;
povidone-iodine solution, sterile gauze pads,
scalpel handle, and hemostat.

B. Clean the neck area with povidone-iodine. Locate
the thyroid and cricoid cartilages; the cricothyroid
membrane extends between these two cartilages.

C. Infiltrate the overlying skin with 2% lidocaine with
epinephrine if the patient is conscious. Stabilize the
thyroid cartilage with the left hand, and make a
vertical incision through the skin and subcutaneous
tissues overlying the cricothyroid membrane,
avoiding the large vessels that are located laterally.

D. Make a stab incision inferiorly in the cricothyroid
membrane with the point of the blade. Insert the
knife handle, and rotate the handle 90 degrees to
open the incision; or use a hemostat to dilate the
opening. Gently insert the endotracheal tube and
secure with tape. A tracheostomy tube or an
endotracheal tube may be used.

E. The surgical cricothyrotomy should be replaced
with a formal tracheostomy within 24 hours.

References: See page 112.

Trauma

Michael E. Lekawa, MD

Management of the Trauma Patient

I. Primary Survey of the Trauma Patient: The primary
survey should identify immediate life threatening
injuries.

A = Assess airway maintenance with cervical

spine protection.
B = Assess breathing and administer assisted

ventilation if required; rule out tension

pneumothorax.
C = Assess circulation and control hemorrhage.
D = Assess disability and neurologic status

(determine the level of consciousness with

Glasgow Coma Scale).
E = Exposure: Completely undress the patient

and prevent hypothermia.

II. Resuscitation phase: The primary survey and
resuscitation of the patient should be done
simultaneously.

A. Assess airway and alleviate obstruction. Establish
a definitive airway for patients with a GCS of less
than 8 or hemodynamic instability. Protect the
cervical spine until fractures have been excluded.

B. Give oxygen and manage tension pneumothorax
with needle or tube thoracostomy.

C. Control hemorrhage by direct pressure or by
surgical ligation. At least 2 large bore IVs should be
places, and infuse 2-3 liters of warm Ringer's
lactate solution (LR) as needed. Administer type
specific or O-negative blood if the response to LR
is inadequate. Send blood for type and cross and
hemoglobin.

D. If the patient has a decreased level of
consciousness, treat hypoxemia and shock, and
evaluate for intracranial space-occupying lesion.

E. Give warm fluids, keep the room warm, and cover
the patient with warm blankets. Small doses of
short acting narcotics (Fentanyl) or
benzodiazepines may be given as needed.

III. Ongoing assessment and treatment

A. Change to cross matched blood when available.

B. Monitor for coagulopathy. The PT/PTT and
fibrinogen level should be monitored, and fresh
frozen plasma, cryoprecipitate or platelets should
be administered as indicated.

C. A nasogastric tube should be placed for
decompression of the stomach (caution if facial
fracture or unstable cervical spine).

D. Shock

1. A Foley catheter should be placed to evaluate
urine output. Adequate resuscitation is
suggested by improvement in physiologic
parameters such as heart rate, systolic
pressure, ventilatory rate, distal perfusion and
capillary refill, pulse oximetry, arterial blood gas,
and urine output.

2. Reassess ABCs prior to beginning secondary
survey.

IV. Secondary survey

A. Obtain an abbreviated history, including allergies,
medications, past illness, last meal,
event/mechanism (AMPLE history).

B. Evaluate the completely undressed patient, front
and back, and from head to toe. Evaluate each
system (head and neck, chest, abdomen,
perineum, musculoskeletal, vascular and
neurologic).

C. Obtain x-rays of the chest, cervical spine, and
pelvis. Perform peritoneal lavage, and/or CT-scan
as needed. Unstable patients should not be sent to
the radiology department.

D. Laboratory studies: Send type and cross for six
units or more of packed red blood cells; complete
blood count, platelet count, creatinine, glucose,
ethanol level, pregnancy test, arterial blood
gasses, UA, and urine toxicology screens.

V. Treatment of shock

A. Maintain airway, breathing, and circulation
(ABCs). Rapid exsanguinating injuries take
precedence over other injuries, including head
injuries.

B. Initial stabilization: Control external bleeding with
direct external pressure. Place two 14 or 16 gauge
intravenous lines and type and cross for packed
red blood cells. If there is insufficient time to cross
match, give type O-negative blood. Type specific
blood should be given if time permits.

C. For hypotensive patients, give an initial fluid
challenge of 2 liters of LR over 5-10 min or 20

ml/kg in children over 5-10 min. Assess response

to initial fluid challenge by checking blood pressure

and heart rate. Patients who respond with only a

transient increase in blood pressure should be

rechallenged with LR or blood transfusion. Blood

loss may be continuing in these patients.

D. Patients who do not respond to initial fluid

challenge may have had either extensive blood

loss or continuing bleeding, which must be

identified (chest, abdomen, extremities, pelvis).

Surgical intervention should be initiated. Other

causes of hypotension include tension

pneumothorax and cardiac tamponade.

VI. Empiric management of coagulopathy. Consider

empiric administration of 1 unit FFP for every 4 units

of packed red blood cells, and consider 10 units

platelets (or 1 unit of single donor platelets) per 6 units

PRBC.

Penetrating Abdominal Trauma

I. Gun shot wounds

A. All abdominal gun shot wounds require exploratory
laparotomy. Tangential wounds that do not
penetrate the peritoneal cavity may be assessed by
peritoneal lavage or laparoscopy if the wound is
located on the anterior abdominal wall.

II. Stab wounds and other penetrating abdominal
trauma

A. Exploratory laparotomy is required if an acute
abdomen is present or if signs of visceral injury,
shock, hypertension, upper or lower Gl bleeding,
evisceration or pneumoperitoneum is present.

B. If the patient is stable and the abdominal fascia has
been penetrated or if disruption cannot be ruled out
by local exploration, diagnostic peritoneal lavage
(DPL) or 24 hours of serial exams should be
completed.

C. Consider tetanus prophylaxis as indicated.

Blunt Abdominal Trauma

I. Physical findings of peritonitis or pneumoperitoneum
on x-ray require exploratory laparotomy.

II. If the patient has a non-acute abdomen

A. If the patient is stable with a clinically evaluable
abdomen who does not undergo exploratory
laparotomy, serial abdominal exams should be
performed. If significant tenderness or peritoneal
signs are noted, the patient should be evaluated by
diagnostic peritoneal lavage, CT, or laparotomy.

B. If the clinical evaluation is inadequate, perform
diagnostic peritoneal lavage or CT-scan to rule out
intra-abdominal injury.

C. If the patient is not stable (systolic blood pressure
<100 mmHg, HR >100, decreasing hemoglobin)
and abdominal injury is possible, diagnostic
peritoneal lavage should be done rather than CT-
scan. If lavage is positive, laparotomy is required.

D. If a CT-scan shows isolated splenic or liver injury,
and the patient remains stable, the patient may be
observed in the ICU. Other injuries should be
assessed with laparotomy. CT-scan is less
sensitive for intestinal or diaphragmatic injury.

E. If there is a significant head injury, intoxication, or
distracting injury (eg, multiple rib fractures, pelvic
fracture, extremity fracture), the abdominal exam is
unreliable. These patients must be evaluated by
diagnostic peritoneal lavage or CT-scan.

F. If the patient is to undergo a prolonged orthopedic
or neurosurgical procedure, the abdomen should
be evaluated with diagnostic peritoneal lavage or
CT-scan before the procedure. A diagnostic
peritoneal lavage can be done in the operating
room.

III. Diagnostic peritoneal lavage

A. Insert a nasogastric tube and Foley catheter to
decompress the stomach and the bladder. Restrain
or sedate the patient if necessary. Prep and drape
the periumbilical region with Betadine solution and
sterile towels. A site should be selected above or
below umbilicus. If the patient has a pelvic fracture
or if pregnant, the site should be located above the
umbilicus.

B. Infiltrate the skin and subcutaneous tissue with 1%
lidocaine with epinephrine. Incise the skin with a
1 .5 cm vertical incision through the subcutaneous
tissue down to fascia. Use a No. 1 1 scalpel blade
to make a 2-3 mm stab incision into the fascia.
Apply traction to both sides of fascial incision with
towel clips. An assistant should apply strong
upward traction on clips. Dissect bluntly with a

small hemostat to the peritoneum, then grasp and
incise the peritoneum, and introduce a lavage
catheter into the pelvis.

C. Aspirate with a 12 cc syringe. If 10 cc of blood is
returned, the lavage should be considered "grossly
positive" which mandates an immediate
laparotomy. If the aspirate is negative, instill 1 liter
of LR or saline from a pressure bag. Periodically
agitate the abdomen. When only a small amount of
fluid remains in the bag, drop bag to the floor, and
drain the fluid by siphon action.

D. During the procedure, keep a sponge packed in the
wound and hold the catheter in place. After at least
400 cc of fluid have been removed, clamp the
tubing and withdrawthe catheter. Close the fascial
defect with heavy absorbable suture, and staple
the skin.

E. Previous abdominal surgery, morbid obesity and
advanced cirrhosis are relative contraindication to
diagnostic peritoneal lavage. If diagnostic
peritoneal lavage is indicated, it should be done by
open, rather than the closed, Seldinger technique.

IV. Criteria for a positive peritoneal lavage

A. Gross blood; red blood cell count <100,000
cells/mm 3 (or 5-10,000 cells/mm 3 ) white blood cell
count >500 cells/mm 3 . Presence of food particles,
bile, feces, or bacteria on Gram stain. Exit of
lavage fluid via a chest tube or bladder catheter.

B. Amylase >20 IU/L; alkaline phosphates >3 IU.

Head Trauma

I. Initial management of head trauma

A. Support airway, breathing, and circulation (ABCs).
A cervical spine injury should be considered to be
present in any patient with multisystem trauma.

B. Intravenous resuscitation solutions should consist
of isotonic Ringer's lactate (LR) or normal saline
(NS). Fluids should be infused until the patient is
euvolemic.

C. Make an initial assessment of the patient during the
primary survey (alert, voice, pain, unresponsive).

D. Perform a mini-neurologic examination and repeat
frequently (GCS, motor/lateralizing signs).

E. A history, including the mechanism of injury, past
medical history, drug intake, should be completed.

Glasgow Coma Scale Assessment of Level of
Consciousness

Eye Opening

Points

Spontaneous

4

To speech

3

To pain

2

None

1

Verbal Response

Oriented

5

Confused

4

Inappropriate words

3

Incomprehensible sounds

2

None

1

Best Motor Response

Obeys

6

Localities

5

Withdraws

4

Flexion

3

Extension

2

None

1

Examine the skull depressed skull fractures,
Battle's sign (blood in the ear canal or ecchymosis
over mastoid process), Raccoon's eyes (periorbital
ecchymosis), or rhinorrhea. If any of these signs
are present, the patient requires admission and a
neurosurgical consult. Nasogastric and
nasotracheal intubation are contraindicated in

patients with significant facial trauma because a
cribriform plate fracture may be present.

II. Secondary management of head trauma

A. All patients with significant head trauma should be
admitted for at least 24 hours of serial neurological
exams unless Glasgow coma scale is 1 5 and there
is only brief amnesia of events, without loss of
consciousness. Such patients may be discharged
with instructions if reliable observation is ensured.

B. If the Glasgow coma scale is 14 or less, or if loss of
consciousness was for more than a few seconds,
a head CT-scan should be obtained.

C. If the mechanism of injury was significantly violent
(rollover of vehicle) or if massive upper torso
trauma, or if any lateralizing neurologic deficits, a
head CT-scan should be obtained.

D. If the Glasgow coma scale is less than 8 or if
unequal pupils, lateralizing deficits, or open head
injury, there is a high probability of a subdural,
epidural, or intracerebral bleed or diffuse axonal
injury. This patient requires ICU admission after
obtaining a CT-scan of the head and a
neurosurgical consultation.

III. Ongoing management of head trauma

A. Continually reassess ABCs, ECG, systolic blood
pressure, heart rate, and pulse oximeter. Serial
hemoglobin or hematocrit should be obtained.

B. Isolated head injuries rarely cause hypotension. If
hypotension is present, the cause should be
vigorously sought. Secondary causes of brain
injury, such as hypoxia and hypotension, should be
managed immediately.

C. Stress ulcer prophylaxis with H 2 -blockers
(ranitidine, cimetidine) or sucralfate should be
administered.

D. Sequential compression stockings should be
applied if the Glasgow coma scale is less than 13,
or if spinal cord injury or pharmacologic paralysis is
present.

E. Mannitol 1 gm/kg is used to treat elevated
intracranial pressure, especially in normotensive
patients with pupillary abnormalities, or lateralizing
signs. Steroids are not indicated in acute head
injuries. Hyperventilation may be used for short
periods in select patients.

F. Open head wounds should be cleaned and
repaired.

G. Tetanus prophylaxis should be given with 0.5 cc
tetanus toxoid IM, with or without tetanus Ig 250 IU,
IM, as indicated.

H. Patients with an abnormal head CT-scan,
neurologic deficit or a sustained Glasgow coma
scale less than 14 require early neurosurgery
consultation.

Thoracic Trauma

I. Management of traumatic pneumothorax

A. Give high-flow oxygen and immediately insert a
chest tube. Aggressive hemodynamic and
respiratory resuscitation should be initiated.

B. Tension pneumothorax should be treated
immediately with a needle thoracostomy, followed
by insertion of a chest tube.

II. Technique of chest tube insertion

A. The patient should be placed in the supine
position, with involved side elevated 10-20
degrees. The arm should be abducted at 90
degrees. The usual site of insertion is the anterior
axillary line at the level of the fourth intercostal
space (nipple line). Cleanse the skin with Betadine
iodine solution and drape the field. The
intrathoracic tube distance can be estimated by the
distance between the lateral chest wall and the
apex of the lung. The intrathoracic tube distance
should be marked with a clamp.

B. Infiltrate 1% lidocaine into the skin, subcutaneous
tissues, intercostal muscles, periosteum, and
pleura using a 25-gauge needle. Use a scalpel to
make a transverse skin incision, 2 centimeters
wide, located over the rib just inferior to the
interspace where the tube will penetrate the chest
wall.

C. A Kelly clamp should be used to bluntly dissect a
subcutaneous tunnel from the skin incision,
extending just over the superior margin of the rib.
The nerve, artery, and vein located just below each
rib should be avoided.

D. Bluntly dissect over the rib and penetrate the
pleura with the clamp, and open the pleura 1
centimeter.

E. With a gloved finger, explore the subcutaneous
tunnel, and palpitate the lung medially. Exclude
possible abdominal penetration, and verify correct

location within the pleural space, use a finger to
remove any local pleural adhesions.

F. Use the Kelly clamp to grasp the tip of the
thoracostomy tube (36 F, Argyle, internal diameter
12 mm), and direct it into the pleural space in a
posterior, superior direction for pneumothorax
evacuation. Guide the tube into the pleural space
until the last hole is inside the pleural space.

G. Attach the tube to 20 cm H 2 of suction. Suture the
tube to the skin of the chest wall using O silk. An
untied, vertical, mattress suture may be placed to
close the skin when the chest tube is removed in a
few days.

H. Apply Vaseline gauze, 4x4 gauze sponges, and
elastic tape. Obtain a chest x-ray to verify correct
tube placement and to evaluate re-expansion of
the lung.
III. Indications for thoracotomy after trauma

A. >1500 mL blood from chest tube on insertion.

B. >200mL blood/hour from chest tube thereafter (for
2-4 hours).

C. Massive air leak such that lung will not re-expand
after a properly placed and functioning chest tube
has been inserted.

Tension Pneumothorax

I. Clinical signs

A. Tension pneumothorax will manifest as severe
hemodynamic and respiratory compromise, a
contralateral^ deviated trachea, and decreased or
absent breath sounds on the involved side.

B. Signs of tension pneumothorax may include
hyperresonance to percussion on the affected side;
jugular venous distention, and asymmetrical chest
wall motion with respiration.

II. Radiographic findings. Loss of lung markings of
ipsilateral side is common ly seen. Flattening or
inversion of the ipsilateral hemidiaphragm and
contralateral shifting of the mediastinum are usually
present. Flattening of the cardiomediastinal contour,
and spreading of the ribs on the ipsilateral side may
be apparent.

III. Acute management of tension pneumothorax.
Place a chest tube as described above. A temporary
large-bore IV catheter may be inserted at the level of
the second intercostal space at the mid-clavicular line
into the pleural space, until the chest tube is placed.

Flail Chest

I. Clinical evaluation

A. Flail chest occurs after two or more adjacent ribs
become fractured in two locations. Flail chest
usually occurs secondary to severe, blunt chest
injury. The fractured ribs allow a rib segment,
without bony continuity with the chest wall, to move
freely during breathing. Hypoxia may result from
underlying pulmonary contusion.

B. Arterial blood gases should be measured if
respiratory compromise is significant. If the fracture
is in the left lower rib cage, splenic injury should be
excluded with CT-scan.

II. Management of flail chest

A. Aggressive pulmonary suctioning and close
observation for any signs of respiratory
insufficiency or hypoxemia are recommended.
Endotracheal intubation and positive-pressure
ventilation is indicated for significant cases of flail
chest if oxygenation is inadequate. Associated
injuries, such as pneumothorax and hemothorax,
should be treated with tube thoracostomy.

B. Pain control with epidural or intercostal blockade
may eliminate the need for intubation. Intubation is
required if there are significant injuries with
massive pulmonary contusion or poor pulmonary
reserve.

C. If mechanical ventilation is required, the ventilator
should be set to assist control mode to put the flail
segment at rest for several days. Thereafter, a trial
of low rate, intermittent, mandatory ventilation may
be attempted to check for return of flail, prior to
attempting extubation.

Massive Hemothorax

I. Clinical evaluation

A. Massive hemothorax is defined as greater than
1500 mL of blood lost into the thoracic cavity. It
most commonly occurs secondary to penetrating
injuries.

B. Signs of massive hemothorax include absence of
breath sounds and dullness to percussion on the
ipsilateral side and signs of hypovolemic shock.

Management

A. Volume deficit should be replaced. The chest cavity
should be decompressed with a chest tube. Two
large-bore intravenous lines or a central venous
line should be inserted. A cardiothoracic surgeon
should be consulted as soon as possible.

B. A chest tube should be inserted. The site of
insertion should be at the level of the fifth or sixth
intercostal space, along the midaxillary line,
ipsilateral to the hemothorax. The chest tube
should be inserted in a location away from the
injury.

C. Penetrating wounds should be cleaned and closed.
The wound should be covered with Vaseline
impregnated gauze to decrease the likelihood of
tension pneumothorax.

D. A thoracotomy is indicated if blood loss continues
through the chest tube at a rate greater than 200
mL/hr for 2-3 consecutive hours. If the site of
wound penetration is medial to the nipple anteriorly
or medial to the scapula posteriorly, it has a higher
probability of being associated with injury to the
myocardium and the great vessels. If the wound is
belowthe fourth intercostal space, abdominal injury
should be excluded.

E. Consider tetanus prophylaxis and empirical
antibiotic coverage.

Cardiac Tamponade

Clinical evaluation

A. Cardiac tamponade most commonly occurs
secondary to penetrating injuries. Cardiac
tamponade can also occur when a central line
penetrates the wall of the right atrium.

B. Cardiac tamponade is often manifested by Beck's
triad of venous pressure elevation, drop in the
arterial pressure, and muffled heart sounds.

C. Other signs include hypovolemic shock, pulseless
electrical activity (electromechanical dissociation),
low voltage ECG, and enlarged cardiac silhouette
on chest x-ray.

D. Kussmaul's sign, rise in venous pressure with
inspiration, may be present. Pulsus paradoxus or
elevated venous pressure may be present.

Management

A. Pericardiocentesis or placement of a pericardial
window is indicated if the patient is unresponsive to
fluid resuscitation measures for hypovolemic
shock.

B. All patients who have a positive pericardiocentesis
(recovery of non-clotting blood) due to trauma
require open thoracotomy with inspection of the
myocardium and the great vessels. Cardiothoracic
surgery should be consulted.

C. Intravenous fluids or blood should be given as
temporizing measures on the way to the operating
room.

D. Other causes of hemodynamic instability or
electromechanical dissociation that may mimic
cardiac tamponade include tension pneumothorax,
massive pulmonary embolism, or hypovolemic
shock.

E. Subxiphoid pericardial window is an equally rapid
and safer procedure than pericardiocentesis if
equipment and experienced surgical personnel are
available.

Other Life-Threatening Trauma
Emergencies

I. Cardiac contusions

A. Arrhythmias are the most common consequence of
cardiac contusions. Pump failure can also occur.

B. Treatment. The patient should receive cardiac
monitoring for 24 hours or longer if arrhythmias are
present. If pump failure is suspected, cardiac
function should be assessed with an
echocardiogram or Swan Ganz catheter. Inotropic
support should be provided.

II. Pulmonary contusions

A. Pulmonary contusions are the most common
potentially fatal chest injuries. Respiratory failure
and hypoxemia may develop gradually over
several hours. The clinical severity of hypoxia does
not correlate well with chest x-ray, however, a
contusion visible the initial CHEST X-RAY predicts
a need for mechanical ventilation.

B. If pulmonary compromise is mild and there is no

other injury, patients can be managed without
intubation.
C. Treatment of severe contusions, especially with
multiple injuries consists of intubation, positive
pressure ventilation, and PEEP.

III. Traumatic aortic transection

A. Diagnosis of traumatic aortic transection requires
a high index of suspicion after severe chest
trauma.

B. The chest x-ray may showa widened mediastinum,
obscured aortic knob, and a left pleural cap. The
diagnostic standard remains aortogram, although
transesophageal echocardiogram and spiral CT-
scan are also useful. Management consists of
immediate surgical repair.

IV. Pelvic fracture

A. Fracture of the pelvis can produce exsanguinating
hemorrhage. Diagnosis is by physical examination,
plain x-ray films, and CT-scan.

B. Hemorrhage is often difficult or impossible to
control at laparotomy. Most bleeding is venous,
and may be decreased by external fixation of the
pelvis. Arterial bleeding sometimes occurs, and
requires angiographic embolization.

C. Pelvic fractures are often associated with
abdominal injury. Diagnostic peritoneal lavage can
be utilized to establish the presence of internal
hemorrhage, although CT-scan is preferred.
Associated bladder or urethral injuries are also
common.

V. Traumatic esophageal injuries

A. Clinical evaluation

1. Esophageal injuries are usually caused by
penetrating chest injuries, severe blunt trauma
to the abdomen, nasogastric tube placement,
endoscopy, or by repeated vomiting
(Boerhaave's syndrome).

2. After rupture, esophageal contents leak into the
mediastinum, followed by immediate or delayed
rupture into the pleural space (usually on left),
with resulting empyema.

3. A high index of suspicion is required in
transthoracic penetrating injuries.
Transmediastinal penetrating injuries mandate
a search for great vessel, tracheobronchial, and
esophageal injuries.

B. Treatment of esophageal injuries. Surgical
therapy consists of primary surgical repair of the
esophagus, with drainage, or esophageal diversion
in the neck and a gastrostomy. Perforated tumors
should be resected. Empiric broad spectrum
antibiotic therapy should be initiated.

References: See page 112.

Burns

Bruce M. Achauer, MD

Over 50,000 people are hospitalized every year for burn
injuries, and more than one million people are burned
each year in the US. Burn injuries cause over 5000

deaths each year in the US.

I. Initial assessment

A. An evaluation of the Airway, Breathing, and
Circulation (the ABCs) should receive first priority.
The history should include the time, location and
circumstances of the injury, where the patient was
found, and their condition. Past medical and social
history, current medication usage, drug allergies,
and tetanus status should be rapidly determined.

B. Smoke inhalation causes more than 50% of fire-
related deaths. Patients sustaining an inhalation
injury may require aggressive airway intervention.
Most injuries result from the inhalation of toxic
smoke; however, super-heated air may rarely
cause direct thermal injury to the upper respiratory
tract.

C. Patients who are breathing spontaneously and at
risk for inhalation injury should be placed on high-
flow humidified oxygen. Patients trapped in
buildings or those caught in an explosion are at
higher risk for inhalation injury. These patients may
have facial burns, singeing of the eyebrows and
nasal hair, pharyngeal bums, carbonaceous
sputum, or impaired mentation. A change in voice
quality, striderous respirations, orwheezing may be
noted. The upper airway may be visualized by
laryngoscopy, and the tracheobronchial tree should
be evaluated by bronchoscopy. Chest radiography
is not sensitive for detecting inhalation injury.

D. Patients who have suffered an inhalation injury are
also at risk for carbon monoxide (CO) poisoning.
The pulse oximeter is not accurate in patients with

CO poisoning because only oxyhemoglobin and
deoxyhemoglobin are detected. CO-oximetry
measurements are necessary to confirm the
diagnosis of CO poisoning. Patients exposed to CO
should receive 100% oxygen using a
nonrebreather face mask. Hyperbaric oxygen
(HBO) therapy reduces the half-life of CO to 23
minutes.
II. Burn assessment

A. After completion of the primary survey, a
secondary survey should assess the depth and
total body surface area (TBSA) burned.

B. First-degree burns involve the epidermis layer of
the skin, but not the dermal layer. These injuries
are characterized by pain, erythema, and lack of
blisters. First-degree burns are not considered in
calculation of the TBSA burned.

C. Second-degree burns are subdivided into
superficial and deep partial-thickness burns.

1. Superficial partial-thickness burn injury
involves the papillary dermis, containing pain-
sensitive nerve endings. Blisters or bullae may
be present, and the burns usually appear pink
and moist.

2. Deep partial-thickness burn injury damages
both the papillary and reticular dermis. These
injuries may not be painful and often appear
white or mottled pink.

D. Full-thickness or third-degree burns involve all
layers of the epidermis and dermis. They appear
white or charred. These burns usually are painless
because of destruction of nerve endings, but the
surrounding areas are extremely painful. Third-
degree burns are treated with skin grafting to limit
scarring.

E. Fourth-degree burns involve structures beneath
the subcutaneous fat, including muscle and bone.

F. Estimation of total body surface area burn is based
upon the "rule of nines."

Assessment of Percentage of Burn Area

Head

9%

Anterior Torso

18%

Posterior Torso

18%

Each Leg

18%

Each Arm

9%

Genitalia/perineum

1%

Classification of Burns

Less than 15% TBSA burns in adults or less than 10%
TBSA burns in children or the elderly with less than 2%
full-thickness injury

Partial- and full-thickness burns of 15-25% TBSA in
young adults, 10-20% in children younger than 10 and
adults older than 40

Full-thickness burns less than 10% TBSA, not involving
special care area.

Major Burns

Greater than 25% TBSA burns in young adults or

greater than 20% TBSA in children younger than 10 and

adults older than 40.

Full-thickness burns of 10% or greater. All burns of

special care areas that are likely to result in either

functional or cosmetic impairment (ie, face, hands, ears,

or perineum).

All burns complicated by inhalation injury, high-voltage

electrical injury, or associated major trauma. High-risk

patients include infants, the elderly, and patients with

complicated medical problems.

III. Management of moderate to severe burns

A. Initial fluid resuscitation-The Parkland Formula

1. Initiation of fluid resuscitation should precede
initial wound care. In adults, IV fluid
resuscitation is usually necessary in second- or
third-degree burns involving greater than 20%
TBSA. In pediatric patients, fluid resuscitation
should be initiated in all infants with burns of
10% or greater TBSA and in older children with
burns greater than 15% or greater TBSA.

2. Two large-bore IV lines should be placed.

Lactated Ringer's solution is the most commonly
used fluid for burn resuscitation.

3. The Parkland formula is used to guide initial
fluid resuscitation during the first 24 hours. The
formula calls for 4 cc/kg/TBSA burn (second and
third degree) of lactated Ringer's solution over
the fast 24 hours. Half of the fluid should be
administered over the first eight hours post
burn, and the remaining half should be
administered over the next 16 hours. The
volume of fluid given is based on the time
elapsed since the burn.

4. A urine output of 0.5-1.0 mL/kg/h should be
maintained. Patients with significant burns
should have a Foley catheter inserted in order
to monitor urine output.

B. A nasogastric (NG) tube should be placed in
patients with burns involving 20% or more TBSA in
order to prevent gastric distention and emesis
associated with a paralytic ileus.

C. Antibiotics is not generally recommended for
initial management of burns but may be considered
in the young child with suspected streptococcal
infection.

D. Laboratory studies should include a complete
blood count, electrolytes, serum glucose, BUN, and
creatinine. Additional laboratory studies may
include an ABG, CO HB level, urinalysis, urine
myoglobin, coagulation studies, blood type and
screen, toxicology screen, serum ethanol level, and
serum protein. Patients with known heart disease
or patients at risk for cardiac complications require
a baseline ECG. A chest x-ray and other
radiographs should be obtained as indicated.

E. Pain control. After completion of the primary and
secondary survey, priority should be given to pain
management. Morphine 0.1 mg/kg IV or
meperidine (Demerol) 1 -2 mg/kg IV should be used
on an hourly basis.

F. Complications associated with eschar formation
may occur in circumferential, deep partial- or full-
thickness burns. Emergent escharotomy can
relieve life- or limb-threatening constrictions
caused by circumferential burns.

G. Tetanus toxoid (0.5 cc) should be administered as
indicated. If the wound is >50% of the body surface
area, 250 units of tetanus immune globulin should
also be administered.

H. Burn center transfer. Most burn patients require
only outpatient care. Most moderate burns and all
major burns require hospitalization. Burns involving
more than 15% of the total body surface area in
adults, or more than 10% in children, should be
transferred to a burn center. Patients with other
severe injuries, extremes of age or inhalation injury
should also be admitted to a burn center.
IV. Management of minor burns

A. Home wound care, pain medication, and active
range-of-motion exercises should be prescribed.
Some patients require physical therapy.

B. Tetanus status should be assessed. The burn
wound should be cleansed with a mild soap and
water or saline. Devitalized tissue or ruptured
blisters should be debrided using aseptic tech-
nique. Unruptured blisters should be left intact.

C. Most outpatient burns are managed with closed
dressings applied with topical antibiotics. A thin
layer of sulfadiazine 1 % (Silvadene) cream can be
applied to a sterile gauze using a tongue blade,
and then the gauze should be applied to the burn.
Dressings are changed daily or twice daily and can
be removed under running water.

D. Silver sulfadiazine should be avoided in patients
with allergies to sulfonamides, pregnant women
approaching or at term, or in newborn infants
during the first two months of life. Silvadene
therapy may rarely cause a transient leukopenia
and staining of sun-exposed skin.

References: See page 112.

Pulmonary Disorders

Charles F. Chandler, MD

Airway Management and Intubation

Orotracheal Intubation:

Endotracheal tube size (Interior diameter):
Women 7.0-9.0 mm
Men 8.0 -10.0 mm.

1. Prepare functioning suction apparatus. Have bag
and mask apparatus

setup with 100% oxygen; and ensure that the patient
can be adequately bag ventilated and that suction
apparatus is available.

2. If sedation and/or paralysis is required, consider

rapid sequence induction as follows:

-Fentanyl (Sublimaze) 50 meg increments IV (1

meg/kg) with:
-Midazolam hydrochloride (Versed) 1 mg IV q2-3
min, max 0.1-0.15 mg/kg; 2-5 mg IV doses q1-
4h prn followed by:
-Succinylcholine (Anectine) 0.6-1.0 mg/kg, at
appropriate intervals.
Note: These drugs may cause vomiting; therefore,
cricoid cartilage pressure should be applied during
intubation (Sellick maneuver).

3. Position the patient's head in "sniffing" position
with head flexed at neck and extended. If necessary
elevate the head with a small pillow.

4. Ventilate the patient with a bag mask apparatus and
hyperoxygenate with 100% oxygen.

5. Hold endoscope handle with left hand, and use
right hand to open the patient's mouth. Insert blade
along the right side of mouth to the base of tongue,
and push the tongue to the left. If using curved blade,
advance to the vallecula (superior to epiglottis), and
lift anteriorly, being careful not to exert pressure on
the teeth. If using a straight blade, place it beneath the
epiglottis and lift anteriorly.

6. Place endotracheal tube (ETT) into right corner of
mouth and pass it through the vocal cords; stop just
after the cuff disappears behind the vocal cords. If
unsuccessful after 30 seconds, stop and resume bag
and mask ventilation before reattempting. If
necessary, use stilette to maintain the shape of the
ETT; remove stilette after intubation. Application of
lubricant jelly at the balloon facilitates passage
through the vocal cords.

7. Inflate cuff with syringe, keeping cuff pressure <20
cm H 2 and attach the tube to an Ambu bag or
ventilator. Confirm bilateral, equal expansion of the
chest and equal bilateral breath sounds. Auscultate
the abdomen to confirm that the ETT is not in the
esophagus. If there is any question about proper ETT
location, repeat laryngoscopy with tube in place to be
sure it is located endotracheal; remove tube
immediately if there is any doubt about proper
location. Secure the tube with tape and note
centimeter mark at the mouth. Suction the oropharynx
and trachea.

8. Confirm proper tube placement with a chest X-ray.
The tip of the ETT should be between the carina and
thoracic inlet, or level with the top of the aortic notch.

Ventilator Management

I. Indications for Ventilatory Support: Respirations
>35, vital capacity <15 mL/kg, negative inspiratory
force <-25, p02 <60 on 50% O,, pH <7.2, pCO, >55,
severe, hypercapnia, hypoxia, severe metabolic
acidosis.

II. Initiation of ventilatory support

A. Intubation

1. Prepare suction apparatus, laryngoscope,
endotracheal tube. Clear airway and place oral
airway, then hyperventilate with bag and mask
attached to high flow oxygen.

2. Midazolam (Versed) 1-2 mg IV boluses until
sedated. 2-5 mg IV doses q1-4h prn.

3. Intubate, inflate cuff, ventilate with bag,
auscultate chest, and suction trachea.

B. Initial orders. FiO, = 100%, PEEP = 3-5 cm H 2 0,
assist control 8-14 breaths/min, tidal volume = 800
mL (10-15 mL/kg ideal body weight), set rate so
that minute ventilation (VE) is approximately 10
L/min. Alternatively, use intermittent mandatory
ventilation mode with tidal volume and rate to
achieve near-total ventilatory support. Consider
pressure support in addition to IMV at 5-15 cm
H,C\

. ABG should be obtained in 30 min, CHEST X-RAY
for tube placement, measure cuff pressure q8h
(maintain <20 mmHg), pulse oximeter, arterial line,
or monitor end tidal CO,. Maintain oxygen
saturation >90-95%.

. Ventilator management

1. Decreased minute ventilation. Evaluate
patient and rule out complications (endotracheal
tube malposition, cuff leak, excessive
secretions, bronchospasms, pneumothorax,
worsening pulmonary disease, sedative drugs,
pulmonary infection). Readjust ventilator rate to
maintain mechanically assisted minute
ventilation of 10 L/min. If peak airway pressure
(AWP) is >45 cm H 2 0, decrease tidal volume to
7-8 mL/kg (with increase in rate if necessary) or
decrease ventilator flow rate.

2. Arterial saturation >94% and pO z >100,
reduce FI0 2 (each 1 % decrease in FIO, reduces
pO, by 7 mmHg); once FIO, is <60%, PEEP
may be reduced by increments of 2 cm H 2 until
PEEP is 3-5 cm H 2 0. Maintain O, saturation of
>90% (pO, >60).

3. Arterial saturation <90% and p02 <60,
increase FI0 2 up to 60-100%, then consider
increasing PEEP by increments of 3-5 cm H 2
(PEEP >10 requires a PA catheter). Add
additional PEEP until oxygenation is adequate
with an FI0 2 of <60%.

4. Excessively low pH, (pH <7.33): Increase rate
and/or tidal volume. Keep peak airway pressure
<40-50 cm H 2 if possible.

5. Excessively high pH (>7.48): Reduce rate
and/or tidal volume to lessen hyperventilation. If
patient is breathing rapidly above ventilator rate,
sedate patient.

6. Patient "fighting" ventilator: Consider
intermittent mandatory ventilation or
spontaneous intermittent mandatory ventilation
mode, or add sedation with or without paralysis
(exclude complications or other causes of
agitation). Paralytic agents should not be used
without concurrent amnesia and/or sedation.

7. Sedation

a. Midazolam (Versed) 0.05 mg/kg IVP x1 , then
0.02-0.1 mg/kg/hr IV infusion. Titrate in
increments of 25-50%.

b. Lorazepam (Ativan) 1-2 mg IV ql-2h pm
sedation or 0.005 mg/kg IVP x1 , then 0.025-
0.2 mg/kg/hr IV infusion. Titrate in increments
of 25-50%.

c. Morphine sulfate 2-5 mg IV q5min, max dose
20-30 mg OR 0.03-0.05 mg/kg/h IV infusion
(50-100 mg in 500 mL D5W) titrated OR

d. Propofol (Diprivan): 50 mcg/kg bolus over 5
min. then 5-50 mcg/kg/min. Titrate in
increments of 5 mcg/kg/min.

8. Paralysis

a. Pancuronium (Pavulon) is the agent of
choice in most settings. This agent should be
avoided in patients with a history of asthma
(causes mast cell degranulation) and heart
disease (vagolytic). Load with 0.08 mg/kg,
then start a continuous infusion of 0.02-0.03
mg/kg/hr.

b. Vecuronium (Norcuron) is an analog of
pancuronium that does not cause
hypertension or mast cell degranulation. It is
the agent of choice with cardiac disease or
hemodynamic instability. However, it has the
highest incidence of post-neuromuscular
blockade paralysis. Load with 0.1 mg/kg,
then start a continuous infusion of 0.06
mg/kg/hr.

c. Cisatracurium (Nimbex) is an isomer of
atracurium with less histamine release and
hypotension. It has no hepatic or renal
excretion. The dosage is 0.15 mg/kg IV, then
0.3 mcg/kg/min IV infusion; titrate between
0.5-1.0 mcg/kg/min.

d. All patients on neuromuscular blocking
agents should be continuously monitored for
degree of blockade with a peripheral nerve
stimulator to a train of four of 90-95%.

9. Loss of tidal volume: If a difference between
the tidal volume setting and the delivered
volume occurs, check for a leak in the ventilator
or inspiratory line. Check for a poor seal
between the endotracheal tube cuff or
malposition of the cuff in the subglottic area. If a
chest tube is present, check for air leak.

10. Weaning from mechanical ventilation

a. Consider extubation in patients with
cardiovascular stability, a high Pa0 2 /Fi0 2
ratios (>200) on low PEEP, and those able to

protect their airway.

The most common weaning method is the
daily trial of spontaneous breathing. While at
the bedside, the patient is placed on CPAP
and allowed to breath on his own. If the
respiratory rate/tidal volume ratio is <100,
patients are rested on the previous settings
until the next day.

If they fail the T-tube trial, or their respiratory
rate to tidal volume ratio is >100, they are
rested on the previous settings until the next
day.

Epistaxis

Roger Crumley, MD

Almost all persons have experienced a nosebleed at
some time, and most nosebleeds resolve without
requiring medical attention. Prolonged epistaxis,
however, can be life-threatening, especially in the elderly
or debilitated.

I. Pathophysiology

A. Anterior epistaxis, in the anterior two thirds of the
nose, is usually visible on the septum and is the
most common type of epistaxis. The anterior
portion of the septum has a rich vascular supply
known as Kiesselbach's plexus or Little's area, and
most epistaxis originates in this region. Anterior
bleeding can often be stopped by pinching the
cartilaginous part of the nose.

B. Posterior epistaxis from the posterior third of the
nose accounts for 10% of nosebleeds. Bleeding is
profuse because of the larger vessels in that
location. It usually occurs in older patients, who
have fragile vessels because of hypertension,
atherosclerosis, coagulopathies, or weakened tis-
sue. Posterior bleeds require aggressive treatment
and hospitalization.

II. Causes of epistaxis

A. Trauma. Nose picking, nose blowing, or sneezing
can tear or abrade the mucosa and cause bleed-
ing. Other forms of trauma include nasal fracture
and nasogastric and nasotracheal intubation.

B. Desiccation. Cold, dry air and dry heat contribute
to an increased incidence of epistaxis during the
winter.

C. Irritation. Upper respiratory infections, sinusitis,
allergies, topical decongestants, and cocaine
sniffing may cause bleeding.

D. Less common causes of anterior epistaxis include
Wegener's granulomatosis, mid-line destructive
disease, tuberculosis, syphilis, and tumors.
Epistaxis is exacerbated by coagulopathy, blood
dyscrasia, thrombocytopenia, or anticoagulant
medication (NSAIDs, warfarin), hepatic cirrhosis,
and renal failure.

E. Hypertension complicates active bleeding by
promoting rigid arteries, and arteriosclerosis
weakens vessels.

III. Clinical evaluation of epistaxis

A. The airway, breathing and circulation should be
maintained. Hemodynamic evaluation for
tachycardia, hypotension, or light-headedness
should be completed immediately. Hypovolemic
patients should be resuscitated with fluids and
packed red blood cells. Oxygen should be
administered and intravenous access established.
When inserting the intravenous line, it is convenient
to obtain blood for complete blood count and, if
clinically indicated, type and screen, coagulation
profile, and electrolytes.

B. After stabilization, the site, cause, and amount of
bleeding should be determined. Most patients do
not require resuscitation. Posterior epistaxis in an
elderly and debilitated patient can be life-
threatening.

C. Determine the side of bleeding. Unilateral nose
bleeding suggests anterior epistaxis in
Kiesselbach's plexus. Bilateral bleeding suggests
posterior epistaxis caused by overflow around the
posterior septum.

D. Determine whether epistaxis is anterior or pos-
terior: When the patient is upright, blood drains
primarily from the anterior part of the nose in
anterior bleeding, or it drains from the nasopharynx
in posterior bleeding.

E. Assess the duration of the nosebleed and any
inciting incident (eg, trauma). Swallowed blood
from epistaxis may cause melena. Hypertension,
bleeding disorders, diabetes, alcoholism, liver
disease, pulmonary disease, cardiac disease and
arteriosclerosis should be assessed.

F. Medications including aspirin, NSAIDs, warfarin,
nasal sprays, and oxygen via nasal cannula should
be sought.

G. Blood tests. Hematologic tests include CBC,
platelet count, INR, partial thromboplastin time, and
blood for type and cross. The hematocrit does not
immediately drop in acute hemorrhage.

IV. Localization of the site of bleeding

A. Sedation. When sedation is required, midazolam
(Versed), 1-2 mg IV in adults and 0.035-0.2 mg/kg
IV in children is recommended; overmedication
may threaten the cough reflex which protects the
airway.

B. Drape the patient, and furnish an emesis basin.
Keep the patient sitting upright or leaning forward.
A gown, gloves, mask, and protective eyewear
should be worn because patients may inadvertently
cough blood.

C. A nasal speculum and a suction apparatus with a
#10 Frazier tip are used to aspirate blood from the
nose and oropharynx. A bright headlight should be
used.

D. Anesthesia and vasoconstriction: A cotton-
tipped applicator or cotton pledget is used to apply
a topical anesthetic (eg, 1% tetracaine or 4%
lidocaine) and a topical vasoconstrictor (eg, 1%
ephedrine, 1% phenylephrine, or 0.05%
oxymetazoline) to the entire nasal mucosa. If a
bleeding site isobserved, press the vasoconstrictor
applicator directly to that site.

E. Visualization of bleeding site

1. The nasal speculum should be used to localize
active bleeding. Kiesselbach's plexus and the
inferior turbinate are the most frequent sites of
bleeding.

2. Posterior bleeding may be located by applying
suction; when the suction tip is at the site of
bleeding, blood will no longer well up.

V. Management of hemorrhage

A. Anterior septal hemorrhage can sometimes be
stopped by nose pinching alone and by having the
patient sit upright. If bleeding continues, application
of the topical anesthetic and vasoconstrictor may
stop it.

B. Cauterization

1 . Bleeding sites that can be visualized should be
cauterized with silver nitrate sticks; they work
best in a dry field.

2. The septum should not be cauterized bilaterally
at the same level because cartilaginous
necrosis and septal perforation may result.

C. Hemostatic agents. Application of a hemostatic
material (eg, microfibrillar collagen or oxidized
regenerated cellulose) to the bleeding site may be
useful. These products do not require removal
because they dissolve in the nose after several
days. The patient should lubricate the nose
regularly with saline nasal spray and to use
bacitracin ointment tid.

D. Packing. Gauze packing or a sponge pack applied
to the anterior portion of the nose may be used as
a tamponade for uncontrolled bleeding sites. These
packs stay in place for 5 days.

E. Anterior nasal pack

1. The pack consists of 72 inches of half-inch
gauze impregnated with antibiotic ointment.
Topical anesthesia is necessary.

2. Use the nasal speculum to open the vestibule
vertically. With the bayonet forceps, grasp the
gauze approximately 10 cm from the end; place
layers along the floor of the nose all the way
back to the nasopharynx.

3. An oral broad-spectrum antibiotic, such as
cephalexin (Keflex), 500 mg orally every 6
hours, is given while the pack is in place to
prevent secondary sinusitis or toxic shock
syndrome. The pack is removed after 5 days.

F. Sponge pack

1. This dry, compressed sponge is lubricated with
an antibiotic ointment, then placed into the nasal
cavity.

2. Once moistened with blood or saline, the
sponge expands, filling the nasal cavity and
exerting gentle pressure on the bleeding site.

G. Posterior pack

1. Posterior bleeding requires a posterior pack,
and the patient should be admitted to the
hospital. The posterior pack requires a
sphenopalatine block and topical anesthetic.

2. The posterior pack is made by sewing together
two tonsil tampons with 0-silk, leaving two 8-inch
tails, and lubricating the tampons with antibiotic
ointment.

3. Place a tight anterior gauze pack, and tie the
tails around one or two dental rolls to stabilize

the tampons.
H. Balloon pack

1. An effective alternative to the tampon posterior
pack is a 14-French, 30-mL balloon Foley
catheter.

2. Use the same anesthetic as for the tampon
posterior pack, and cover the balloon with
antibiotic ointment, and insert it through the
nostril until the tip can be seen in the
nasopharynx.

References: See page 112.

Disorders of the Alimen-
tary Tract

Russell A. Williams, MD
I. James Sarfeh, MD
S.E. Wilson, MD

Acute Abdomen

I. Clinical evaluation of abdominal pain

A. Onset and duration of the pain

1. The duration, acuity, and progression of pain
should be assessed, and the exact location of
maximal pain at onset and at present should be
determined. The pain should be characterized
as diffuse or localized. The time course of the
pain should be characterized as either constant,
intermittent, decreasing, or increasing.

2. Acute exacerbation of longstanding pain
suggests a complication of chronic disease,
such as peptic ulcer disease, inflammatory
bowel disease, or cancer. Sudden, intense pain
often represents an intraabdominal catastrophe
(eg, ruptured aneurysm, mesenteric infarction,
or intestinal perforation). Colicky abdominal pain
of intestinal or ureteral obstruction tendsto have
a gradual onset.

B. Pain character

1 . Intermittent pain is associated with spasmodic
increases in pressure within hollow organs.

2. Bowel ischemia initially causes diffuse crampy
pain due to spasmodic contractions of the
bowel. The pain becomes constant and more
intense with bowel necrosis, causing pain out of
proportion to physical findings. A history of
intestinal angina can be elicited in some
patients.

3. Constant pain. Biliary colic from cystic or
common bile duct obstruction usually is
constant. Chronic pancreatitis causes constant
pain. Constant pain also suggests parietal
peritoneal inflammation, mucosal inflammatory
conditions, or neoplasms.

4. Appendicitis initially causes intermittent
periumbilical pain. Gradually the pain becomes
constant in the right lower quadrant as
peritoneal inflammation develops.

C. Associated symptoms

1. Constitutional symptoms (eg, fatigue, weight
loss) suggests underlying chronic disease.

2. Gastrointestinal symptoms

a. Anorexia, nausea and vomiting are
commonly associated with acute abdominal
disorders. The frequency, character, and
timing of these symptoms in relation to pain
and time of the last flatus or stool should be
determined.

b. Constipation, obstipation, crampy pain
and distention usually predominate in distal
small-bowel and colonic obstruction.
Paralytic ileus causes constipation and
distention.

c. Diarrhea is suggestive of gastroenteritis or
colitis but may also be seen in partial small-
bowel obstruction or fecal impaction.

d. Small amounts of bleeding may
accompany esophagitis, diverticulitis,
inflammatory bowel disease, and left colon
cancer. Right colon cancers usually present
with occult blood loss. Severe abdominal
pain accompanied by melena or
hematochezia suggests ischemic bowel.

e. Jaundice with abdominal pain usually is
caused by biliary stones. Obstruction of the
common bile duct by cancer may also cause
pain and jaundice.

3. Urinary symptoms. Urinary tract infections may
cause pain in the lower abdomen (cystitis) or
flanks (pyelonephritis). Urinary tract infections
are characterized by dysuria, frequency, and
cloudy urine.

4. Recent menstrual and sexual history should
be determined in women with acute abdominal
pain.

a. Menstrual cycle. Lower abdominal pain and
a missed or irregular menses in a young
woman suggests ectopic pregnancy. Pelvic
inflammatory disease tendsto cause bilateral
lower abdominal pain. Ovarian torsion may
cause intense, acute pain and vomiting.
Chronic pain at the onset of menses
suggests endometriosis.

b. Pregnancy. Ectopic pregnancy occurs in the
first trimester. Threatened abortion, ovarian
torsion, or degeneration of a uterine fibroid
also may cause acute pain in women.

D. Medications

1. Nonsteroidal anti-inflammatory drugs
predispose to ulcer disease.

2. Antibiotic therapy may obscure the signs of
peritonitis. Patients with abdominal pain and
diarrhea who have received antibiotics may
have pseudomembranous colitis.

3. Anticoagulants. Warfarin therapy predisposes
to retroperitoneal or intramural intestinal
hemorrhage.

4. Thiazide diuretics may rarely cause
pancreatitis.

E. Surgical history. Small bowel obstruction is often
caused by postoperative adhesions.

II. Physical examination

A. General appearance. Peritonitis is suggested by
shallow, rapid breathing and the patient often will
lie still with knees flexed to minimize peritoneal
stimulation. Patients may be pale or diaphoretic.
Cachexia may indicate malignancy or chronic
illness.

B. Fever suggests an inflammatory or infectious
etiology. Tachycardia and tachypnea may be
caused by pain, hypovolemia, or sepsis.
Hypothermia and hypotension often suggest an
infectious process. Pneumonia and myocardial
infarction may occasionally cause pain that is felt in
the abdomen.

C. Abdominal examination

1. Inspection. Surgical scars should be noted.
Distention suggests obstruction, ileus, or
ascites. Venous engorgement of the abdominal
wall suggests portal hypertension. Masses or
peristaltic waves may be visible.
Hemoperitoneum may cause bluish
discoloration of the umbilicus (Cullen's sign).
Retroperitoneal bleeding (eg, from hemorrhagic
pancreatitis) can cause flank ecchymoses
(Turner's sign).

2. Auscultation. Borborygmi may be heard with
obstruction. A quiet, rigid tender abdomen may
occur with generalized peritonitis. A tender,
pulsatile mass suggests an aortic aneurysm
rupture.

3. Palpation

a. Palpation should be gently started at a point
remote from the pain. Muscle spasm,
tympany or dullness, masses and hernias
should be sought.

b. Peritoneal signs. Rigidity is caused by reflex
spasm of the abdominal wall musculature
from underlying inflamed parietal peritoneum.
Stretch and release of inflamed parietal
peritoneum causes rebound tenderness.

c. Common signs

(1) Murphy's sign. Inspiratory arrest from
palpation in the right upper quadrant
occurs when an inflamed gallbladder
descends to meet the examiner's
fingers.

(2) Obturator sign. Suprapubic tenderness
on internal rotation of the hip joint with
the knee and hip flexed results from
inflammation adjacent to the obturator
internus muscle.

(3) Iliopsoas sign. Extension of the hip
elicits tenderness in inflammatory
disorders of the retroperitoneum.

(4) Rovsing's sign. Referred, rebound
tenderness in the left lower quadrant
suggests appendicitis.

D. Rectal and pelvic examination

1. Digital examination of the rectum may detect
cancer, fecal impaction, or pelvic appendicitis.
Stool should be checked for gross or occult
blood.

2. Pelvic examination. Vaginal discharge should
be noted and cultured. Masses and tenderness
should be sought bimanually. Adnexal or
cervical motion tenderness indicate pelvic
inflammatory disease.

III. Laboratory evaluation

A. Leukocytosis or a left shift on differential cell
count are non-specific findings for infection.
Leukopenia may be present in sepsis. The
hematocrit can detect anemia due to occult blood
loss from cancer. The hematocrit may be elevated
with plasma volume deficits.

B. Electrolytes. Metabolic alkalosis occurs after
persistent vomiting. Metabolic acidosis occurs with
severe hypovolemia or sepsis.

C. Urinalysis. Bacteriuria, pyuria, or positive
leukocyte esterase suggest urinary tract infection.
Hematuria suggests urolithiasis.

D. Liver function tests. High transaminases with mild
to moderate elevations of alkaline phosphatase
and bilirubin suggests acute hepatitis. High alkaline
phosphatase and bilirubin and mild elevations of
transaminases suggests biliary obstruction.

E. Pancreatic enzymes. Elevated amylase and
lipase indicates acute pancreatitis.
Hyperamylasemia also may occur in bowel
infarction and perforated ulcer.

F. Serum beta-human chorionic gonadotropin is
required in women of childbearing age with
abdominal pain to exclude ectopic gestation.

IV. Radiography

A. Plain abdominal films

1 . Acute abdomen series includes an upright PA
chest, plain abdominal film ("flat plate"), upright
film, and a left lateral decubitus view of the
abdomen.

2. Bowel obstruction

a. Small bowel obstruction may cause
multiple air-fluid levels with dilated loops of
small intestine, associated with minimal
colonic gas.

b. Colonic obstruction causes colonic dilation
which can be distinguished from small
intestine by the presence of haustral
markings and absence of valvulae
conniventes.

3. Free air is seen on the upright chest x-ray
under the hemidiaphragms. Intestinal
perforation is the most common cause of free
air. A recent laparotomy may also cause free
air.

4. Stones and calcifications. Ninety percent of
urinary stones are radiopaque. Only 15% of
gallstones are visible on plain film. A fecalith in
the right lower quadrant may suggest
appendicitis. Vascular calcification may be
visible in abdominal aneurysm.

B. Ultrasonography is useful for evaluation of biliary
colic, cholecystitis, or female reproductive system
disorders.

C. Computed tomography with or without oral
and/or rectal contrast may help in evaluating the
acute abdomen in the following situations:

1. Unobtainable or highly atypical history or
physical examination

2. History of intraabdominal cancer

3. Abdominal pain and fever in the immediate
postiaparotomy period

4. Acute pain superimposed on a history of chronic
abdominal complaints

5. A stable patient with suspected leaking
abdominal aneurysm

References: See page 112.

Appendicitis

About 10% of the population will develop acute
appendicitis during their lifetime. The disorder most
commonly develops in the teens and twenties.
Appendicitis is caused by appendiceal obstruction,
mucosal ischemia, infection, and perforation.

I. Diagnosis of appendicitis

A. Clinical presentation. Early appendicitis is
characterized by progressive midabdominal
discomfort, unrelieved by the passage of stool or
flatus. Ninety percent of patients are anorexic, 70%
have nausea and vomiting, and 1 0% have diarrhea.
The pain migrates to the right lower quadrant after
4-6 hours. Peritoneal irritation is associated with
pain on movement.

B. Physical examination

1. Mild fever and tachycardia are common in
appendicitis.

2. Abdominal palpation should begin away from the
right lower quadrant. Point tenderness over the
right lower quadrant is the most definitive
finding. Pain in the right lower quadrant during
palpation of the left lower quadrant (Rovsing's
sign) indicates peritoneal irritation. The degree
of direct tenderness and rebound tenderness
should be assessed. The degree of muscular
resistance to palpation reflects the severity of
inflammation. Cutaneous hyperesthesia often
overlies the region of maximal tenderness.

3. Psoas sign. With the patient lying on the left
side, slow extension of the right hip causes local
irritation and pain. A positive psoas sign
indicates retroperitoneal inflammation.

4. Obturator sign. With the patient supine, passive
internally rotation of the flexed right hip causes
hypogastric pain.

5. Rectal examination should evaluate the pres-
ence of localized tenderness or an inflammatory
mass in the pelvis.

6. Pelvic examination, in women, should be
completed to assess cervical motion tenderness
and to evaluate the presence of adnexal
tenderness.

7. The appendix usually is found at McBurney's
point (two-thirds of the distance from the
umbilicus to the anterior superior iliac spine).

8. Diarrhea, urinary frequency, pyuria, or
microscopic hematuria may suggest a retrocecal
appendix, causing irritation of adjacent
structures.

C. Laboratory evaluation

1. Leukocyte count greater than 11,000 cells/ul
with polymorphonuclear cell predominance is
common in children and young adults.

2. Urinalysis is abnormal in 25% of patients with
appendicitis. Pyuria, albuminuria, and hematuria
are common. Bacteria suggest urinary tract
infection. Hematuria suggests urolithiasis.

3. Serum pregnancy test should be performed in
women of childbearing age. A positive test
suggests an ectopic pregnancy.

D. Radiologic evaluation

1. Abdominal x-rays. An appendicolith can be
seen in only one-third of children and one-fifth of
adults with appendicitis. An appendiceal mass
can indent the cecum, and tissue edema can
cause loss of peritoneal fat planes around the
psoas muscle and kidney.

2. Ultrasonography. Findings associated with
appendicitis include wall thickening, luminal
distention, lack of compressibility, abscess
formation, and free intraperitoneal fluid.

II. Differential diagnosis

A. Gastrointestinal diseases

1. Gastroenteritis is characterized by nausea,
emesis prior to the onset of abdominal pain,
malaise, fever, and poorly localized abdominal
pain and tenderness. The WBC count is less
frequently elevated.

2. Meckel's diverticulitis may mimic appendicitis.

3. Perforated peptic ulcer disease, diverticulitis,
and cholecystitis can present similarly to
appendicitis.

B. Urologic diseases

1. Pyelonephritis is associated with high fever,
rigors, and costovertebral pain and tenderness.
Diagnosis is confirmed by urinalysis.

2. Ureteral colic. Renal stones cause flank pain
radiating into the groin. Tenderness is usually
minimal and hematuria is present. The
intravenous pyelogram is diagnostic.

C. Gynecologic diseases

1. Pelvic inflammatory disease (PID). The onset
of pain in PID usually occurs within 7 days of
menstruation. Cervical motion tenderness, a
white vaginal discharge, and bilateral adnexal
tenderness suggest PID. Ultrasound can help
distinguish PID from appendicitis

2. Ectopic pregnancy. A pregnancy test should be
performed in all female patients of childbearing
age presenting with abdominal pain.
Ultrasonography is diagnostic.

3. Ovarian cysts can cause sudden pain by
enlarging or rupturing. The cysts are detected by
transvaginal ultrasonography.

4. Ovarian torsion. The ischemic ovary often can
be palpated on bimanual pelvic examination.
The diagnosis is confirmed by ultrasonography.

References: See page 112.

Appendectomy Surgical Technique

I. Preoperative preparation

A. Intravenous isotonic fluid replacement should be
initiated to achieve good urinary output and to
correct electrolyte abnormalities. Nasogastric
suction should be initiated if the patient is vomiting
or if peritonitis is present.

B. Fever is treated with acetaminophen. Broad-
spectrum antibiotic coverage is initiated
preoperatively. Antibiotic therapy should cover
gram-negative and anaerobic organisms (Cefotan
orZosyn).

II. Surgical technique

A. After induction of anesthesia, place an incision
over any appendiceal mass if palpable. If no mass
is present, make a transverse skin incision over

McBurney's point, located two thirds of the way
between the umbilicus and anterior superior iliac
spine. A transverse incision allows easy extension
medially for greater exposure. Diffuse peritonitis
should be explored through a midline incision.

B. Incise the subcutaneous tissues in the line of the
transverse incision, and incise the external oblique
aponeurosis in the direction of its muscle fibers.
Spread the muscle with a Peon hemostat.

C. Incise the internal oblique fascia and spread the
incision in the direction of its fibers. Sharply incise
the transversus abdominis muscle, transversalis
fascia, and peritoneum. Note the presence and
characteristics of peritoneal fluid, and send
purulent fluid for Gram's stain and aerobic and
anaerobic culture.

D. Identify the base of the cecum by the converging
taeniae coli, and raise the cecum, exposing the
base of the appendix. Hook an index finger around
the appendix, and gently break down any adhe-
sions to adjacent tissues. Use gauze packing to
isolate the inflamed appendix, and stabilize the
appendix with a Babcock forceps.

E. Apply two clamps to the mesoappendix, then divide
the mesoappendix between the clamps, then firmly
ligate belowthe clamps with 000 silk or polyglycolic
acid sutures. Apply an encircling purse-string
suture of 000 silk at the end of the cecum about 0.8
cm from the base of the appendix. Place a
hemostat at the proximal base of the appendix, and
crush the appendix. Remove the hemostat and
reapply it to the appendix distal to the crush. Use
an chromic catgut suture to ligate the crushed
area belowthe hemostat.

F. Transect the appendix against the clamp. Invertthe
stump into the cecum with the purse-string suture,
and tie the purse-string suture, burying the stump.
Irrigate the peritoneum with normal saline, and
examine the mesoappendix and abdominal wall for
hemostasis. Close the peritoneum with continuous
000 catgut suture.

G. Close the internal oblique and transversus
abdominis with interrupted O chromic catgut. Close
the external oblique as a separate layer. Close the
skin and subcutaneous tissues. A soft rubber
Penrose drain should be placed if perforation has
occurred. It should be brought out through a stab
incision in the lateral abdominal wall or through the
lateral end of the incision.

H. If the appendix is normal on inspection (5-20% of
explorations), it should be removed, and alternative
diagnoses should be investigated. The cecum,
sigmoid colon, and ileum should be inspected, and
mesenteric lymphadenopathy should be sought.
Ovaries and fallopian tubes should be inspected for
PID, ruptured cysts, or ectopic pregnancy. Bilious
peritoneal fluid suggests perforation of a peptic
ulcer or the gallbladder.
III. Intravenous antibiotics

A. Antibiotic prophylaxis should include coverage for
bowel flora, including aerobes and anaerobes.
Cefotetan (Cefotan), 1 gm IV q12h, or
piperacillin/tazobactam (Zosyn), 4.5 gm IV q6h,
should be given before the operation and
discontinued after two doses postoperatively.

B. If perforation has occurred, IV antibiotics should be
continued for 5-10 days. Check culture on the third
postoperative day and change antimicrobials if a
resistant organism is present.

References: See page 112.

Hernias

A hernia is an abnormal opening in the abdominal wall,
with or without protrusion of an intraabdominal structure.
A hernia develops in 5% of men during their lifetime. The
most common groin hernia in males or females is the
indirect inguinal hernia. Femoral hernias are more
common in females than in males.

I. Inguinal hernias

A. Indirect hernia sacs pass through the internal
inguinal ring lateral to the inferior epigastric vessels
and lie within the spermatic cord. Two-thirds of
inguinal hernias are indirect

B. Direct hernias occur when viscera protrude
through a weak area in the posterior inguinal wall.
The base of the hernia sac lies medial to the inferior
epigastric vessels, through Hesselbach's triangle,
which is formed by the inferior epigastric artery, the
lateral edge of the rectus sheath, and the inguinal
ligament.

C. Combined (pantaloon) hernias occur when direct
and indirect hernias occur simultaneously.

. Sliding hernias occur when part of the wall of the
sac is formed by a viscera (bladder, colon).
Richter's hernias occur when part of the bowel
(rather than the entire circumference) becomes
trapped. Only a "knuckle" of bowel enters the hernia
sac.

. Incarcerated hernias cannot be reduced into the
abdominal cavity. Strangulated hernias are hernias
with incarcerated contents and a compromised
blood supply; intense pain indicates intestinal
ischemia.
Inguinal anatomy

1. Layers of abdominal wall: Skin, subcutaneous
fat, Scarpa's fascia, external oblique, internal
oblique, transversus abdominous, transversalis
fascia, peritoneum.

2. Hesselbach's triangle: A triangle formed by the
lateral edge of rectus sheath, the inferior
epigastric vessels, and the inguinal ligament.

3. Inguinal ligament: Ligament running from
anterior superior iliac spine to the pubic tubercle.

4. Lacunar ligament: Reflection of inguinal
ligament from the pubic tubercle onto the
iliopectineal line of the pubic ramus.

5. Cooper's ligament: Strong, fibrous band
located on the iliopectineal line of the superior
public ramus.

6. External inguinal ring: Opening in the external
oblique aponeurosis; the ring contains the
ilioinguinal nerve and spermatic cord or round
ligament.

7. Internal ring: Bordered superiorly by internal
oblique muscle and inferomedially by the inferior
epigastric vessels and the transversalis fascia.

8. Processus vaginalis: A diverticulum of
peritoneum which descends with the testicle and
lies adjacent to the spermatic cord. The
processus vaginalis may enlarge to become the
sac of an indirect inguinal hernia.

9. Femoral canal: Formed by the borders of the
inguinal ligament, lacunar ligament, Cooper's
ligament, and femoral sheath.

. Clinical evaluation

1. Inguinal hernias usually present as an
intermittent mass in the groin. The symptoms
can usually be reproduced by a purposeful
Valsalva maneuver. A bowel obstruction may
rarely be the first manifestation of a hernia.

2. Physical examination. An inguinal bulge with a
smooth, rounded surface is usually palpable.
The bulge may become largerwith straining. The
hernia sac can be assessed by invaginating the
hemiscrotum with an index finger passed
through the external inguinal ring.

3. Radiologic evaluation. X-ray studies are not
usually needed. Ultrasonography or CT scanning
may be necessary to evaluate small hernias,
particularly in the obese patient.

. Differential diagnosis. Inguinal hernias are
distinguished from femoral hernias by the fact that
femoral hernias originate below the inguinal
ligament. Inguinal adenopathy, lipomas, dilatation
of the saphenous vein, and psoas abscesses may
present as inguinal masses.
Treatment

1. Preoperative evaluation and preparation.
Hernias should be treated surgically. If
incarceration or strangulation has occurred,
broad-spectrum antibiotics and nasogastric
suction should be initiated.

2. Reduction. In uncomplicated cases, the hernia
should be reduced by placing the patient in
Trendelenburg's position or by gentle pressure
applied over the hernia. Strangulated hernias
should not be reduced because reduction may
cause peritoneal contamination by a necrotic
bowel loop and release of vasoactive agents
from infarcted tissue.

3. Surgical repair

a. Indirect inguinal hernias. The aponeurosis
of the external oblique muscle should be
opened, then the cremaster muscle is
opened, and the contents of the cord
identified. The hernia sac is separated from
the cord structures and transected. The neck
should then be ligated, and the posterior
abdominal wall should be repaired.

b. Direct inguinal hernias. The external
oblique should be opened and the cord
structures should be separated from the
hernia sac, then the sac should be inverted.
The posterior abdominal wall is repaired by
approximating the inferior arch of the
transversus muscle (conjoint tendon) to the
iliopubic tract (Bassini repair).

c. Lichtenstein (Tension-Free) Repair. A
mesh plug or patch is often used to produce
a "tension free" repair.

II. Femoral hernias

A. Femoral hernias account for 5% of all hernias, and
84% of femoral hernias occur in women.
Incarceration or strangulation occur in 25% of
femoral hernias.

B. In femoral hernias, the abdominal viscera and
peritoneum protrude through the femoral ring into
the upper thigh. The femoral ring is limited medially
by the lacunar ligament of Gimbernat, laterally by
the femoral vein, anteriorly and proximally by the
inguinal ligament, and posteriorly and distally by
Cooper's ligament.

C. Clinical evaluation

1. Femoral hernias may present as a tender groin
mass, and small-bowel obstruction may
sometimes occur.

2. Physical examination. The hernia sac
manifests clinically as a mass in the upper thigh,
curving craniad over the inguinal region. It may
appear while the patient is standing or straining
and may disappear in the supine position.

D. Treatment. A Cooper's ligament repair (McVey)
through the inguinal approach is recommended.

III. Abdominal wall hernias

A. Incisional hernias occur at sites of previous
incisions. Hernias occur after 14% of abdominal
operations.

B. Umbilical hernias are congenital defects. Most
newborn umbilical hernias close spontaneously by
the second year of life. Patients with ascites have a
high incidence of umbilical hernias.

C. Epigastric hernias occur in the linea alba above
the umbilicus.

D. Spigelian hernias protrude near the termination of
the transversus abdominis muscle at the lateral
edge of the rectus abdominis muscle.

E. Lumbar hernias occur superior to the iliac crest or
below the last rib.

F. Obturator hernias pass through the obturator
foramen and present with bowel obstruction and
focal tenderness on rectal examination.

Inguinal Hernia Repair Technique

I. Indirect hernia

A. Prep and draped the skin of the abdomen, inguinal
region, upper thigh, and external genitalia. Place
the incision 1 cm above and parallel to the inguinal
ligament. Begin the incision at a point just above,
and medial to, the pubic tubercle, and extend it to
a point two-thirds the distance to the anterior iliac
spine. Incise the subcutaneous fat in the length of
the incision down to the external oblique
aponeurosis. Clear the external oblique muscle of
overlying fat and identify the external inguinal ring.
Incise the aponeurosis of the external oblique,
beginning laterally and splitting the aponeurosis in
the direction of its fibers, taking care not to injure
the underlying ilioinguinal nerve. Expose the
inguinal canal in which the spermatic cord and the
indirect inguinal hernia are located.

B. Use blunt dissection to mobilize the spermatic cord
and the associated hernia up to the level of the
pubic tubercle. Lift these structures up from the
floor of the inguinal canal, and encircle with a
Penrose drain. Retract the drain anteriorly, and
free the remainder of the cord from the floor of the
canal. Use sharp and blunt dissection to incise the
anterior muscular and fascial investments of the
cord.

C. Sharply incise the internal spermatic fascia, and
locate the hernial sac; identify the spermatic artery,
venous plexus, and vas deferens before opening
the sac.

D. Incise the indirect hernial sac anteriorly along its
long axis. Place an index finger inside the hernial
sac, and separate the sac from surrounding cord
structures, using sharp and blunt dissection. Carry
the dissection proximally to the internal inguinal
ring.

E. Close the sac with a circumferential purse-string
suture on an atraumatic, gastrointestinal needle.
Tie this suture, being careful that no abdominal
organs are within the purse string. Reinforce this
ligation by placing another transfixion suture
through the sac 1 mm distal to the purse-string
suture. Transect the sac a few millimeters below
the second suture, and cut both sutures and allow
sac to retract into the retroperitoneum. Remove the
sac. Inspect the floor of the inguinal canal. If there
is only minimal dilation of the internal ring, the

hernia repair can be completed by placing a few
interrupted sutures at the medial border of the
internal ring and completing a Bassini repair.

F. If the hernia is moderately sized, use a
modification of the Bassini repair. Place a series of
interrupted sutures in the transversalis fascia,
beginning medially at the level of the pubic
tubercle. Carry the sutures laterally as far as the
medial border of the internal ring. Incorporate the
posterior fibers of the conjoint tendon or use the
posterior fascia of the transversalis abdominous
muscle with some of the muscular fibers of the
internal oblique muscle.

G. Begin suturing medially at Cooper's ligament, and
transition at the femoral sheath to Poupart's liga-
ment. Place the sutures 1 cm apart, and use
nonabsorbable monofilament 00 suture. Tie the
sutures to reinforce the floor of the inguinal canal.

H. Replace the ilioinguinal nerve and the spermatic
cord in the inguinal canal, and reapproximate the
external oblique aponeurosis over the cord with
interrupted, nonabsorbable, 000 sutures.

I. Close the subcutaneous tissues with interrupted,
fine, absorbable sutures in Scarpa's fascia, and
close the skin with staples or subcuticular sutures.
Apply a sterile dressing.

II. Repair of direct inguinal hernias

A. The skin incision is the same as for repair of the
indirect inguinal hernia. The direct inguinal hernia
appears as a diffuse bulge in the area of
Hesselbach's triangle, appreciated by palpating
with a fingertip. Reduce the direct inguinal hernia
with a series of interrupted, inverting, 00,
nonabsorbable sutures placed in the redundant
preperitoneal tissue.

B. The fascial defect in Hesselbach's triangle is
repaired with a Cooper's ligament or modified
McVay-type repair. Sharp and blunt dissection of
the floor of the inferior portion of the inguinal canal
should be used to expose the lacunar ligament and
Cooper's ligament. Dissect laterally along Cooper's
ligament as far as the medial aspect of the femoral
vein. A relaxing incision should be made in the
deep portion of the anterior rectus sheath, then
grasp the medial and superior edge of the defect in
Hesselbach's triangle with Allis clamps.

C. A series of interrupted sutures is placed, beginning
medially at the pubic tubercle, and carried laterally
as far as the femoral vein. Check the appropriate
snugness of the deep inguinal ring. When all
sutures are placed, tie the sutures medial to lateral.
Replace the cord and the ilioinguinal nerve in the
bed of the inguinal canal, and reapproximate the
external oblique aponeurosis overthese structures.

III. Lichtenstein (Tension-Free) Repair

A. One of the most commonly performed open
herniorrhaphy techniques is the tension-free
(Lichtenstein) repair. A tension-free hernioplasty
performed with mesh reinforcement of the inguinal
floor significantly decreases the recurrence rate.

B. The Lichtenstein repair is routinely performed in an
outpatient setting with local anesthesia. A Marlex
mesh patch is sutured to the aponeurotic tissue
overlying the pubic bone, with continuation of this
suture along the edge of the inguinal (Poupart's)
ligament to a point lateral to the internal inguinal
ring.

C. The lateral edge of the mesh is slit to allow
passage of the spermatic cord between the split
limbs of the mesh. The cephalad edge of the mesh
is sutured to the conjoined tendon, with the internal
oblique edge overlapped by 2 cm. The two tails of
the lateral aspect of the mesh are sutured together,
incorporating the margin of the inguinal ligament.

References: See page 112.

Upper Gastrointestinal Bleeding

When bleeding is believed to be caused by a source
proximal to the ligament of Treitz or the source of
bleeding is indeterminant, flexible upper gastrointestinal
endoscopy is indicated after initial resuscitation and
stabilization.

I. Clinical evaluation

A. Initial evaluation of upper Gl bleeding should
estimate the severity, duration, location, and cause
of bleeding. A history of bleeding occurring after
forceful vomiting suggests Mallory-Weiss
Syndrome.

B. Abdominal pain, melena, hematochezia (bright red
blood per rectum), history of peptic ulcer, cirrhosis
or prior bleeding episodes may be present.

C. Precipitating factors. Use of aspirin, nonsteroidal
anti-inflammatory drugs, alcohol, or anticoagulants
should be sought.

II. Physical examination

A. General: Pallor and shallow, rapid respirations
may be present; tachycardia indicates a 1 0% blood
volume loss. Postural hypotension (increase in
pulse of 20 and a systolic blood pressure fall of 10-
15 mmHg), indicates a 20-30% loss.

B. Skin: Delayed capillary refill and stigmata of liver
disease (jaundice, spider angiomas, parotid gland
hypertrophy) should be sought.

C. Abdomen: Scars, tenderness, masses, hepato-
megaly, and dilated abdominal veins should be
evaluated. Stool occult blood should be checked.

III. Laboratory evaluation: CBC, SMA 12, liver function
tests, amylase, INR/PTT, type and cross for pRBC,
ECG.

IV. Differential diagnosis of upper bleeding: Peptic
ulcer, gastritis, esophageal varices, Mallory-Weiss
tear, esophagitis, swallowed blood from epistaxis,
malignancy (esophageal, gastric), angiodysplasias,
aorto-enteric fistula, hematobilia.

V. Management of upper gastrointestinal bleeding

A. If the bleeding appears to have stopped or has
significantly slowed, medical therapy with H2
blockers and saline lavage is usually all that is
required.

B. Two 14- to16-gauge IV lines should be placed.
Normal saline solution should be infused until
blood is ready, then transfuse 2-6 units of pRBCs
as fast as possible.

C. A large bore nasogastric tube should be placed,
followed by lavage with 2 L of room temperature
tap water. The tube should then be connected to
low intermittent suction, and the lavage should be
repeated hourly. The NG tube may be removed
when bleeding is no longer active.

D. Oxygen is administered by nasal cannula. Urine
output should be monitored.

E. Serial hematocrits should be checked and
maintained greater than 30%. Coagulopathy
should be assessed and corrected with fresh
frozen plasma, vitamin K, cryoprecipitate, and
platelets.

F. Definitive diagnosis requires upper endoscopy, at
which time electrocoagulation, banding, and/or
local injection of vasoconstrictors at bleeding sites
may be completed. Surgical consultation should
be requested in unstable patients or patients who
require more than 6 units of pRBCs.

Clinical Indicators of Gastrointestinal Bleeding
and Probable Source

Clinical
Indicator

Probability of
Upper

Gastrointestin
al source

Probability of
Lower

Gastrointestin
al Source

Hematemesis

Almost certain

Rare

Melena

Probable

Possible

Hematochezia

Possible

Probable

Blood-streaked
stool

Rare

Almost certain

Occult blood in
stool

Possible

Possible

VI. Peptic Ulcer Disease

A. Peptic ulcer disease is the commonest cause of
upper gastrointestinal bleeding, responsible for 27-
40% of all upper gastrointestinal bleeding episodes.
Duodenal ulcer is more frequent than gastric ulcer.
Three fourths of all peptic ulcer hemorrhages
subside spontaneously.

B. Upper gastrointestinal endoscopy is the most
effective diagnostic technique for peptic ulcer
disease. Endoscopic therapy is the method of
choice for controlling active ulcer hemorrhage.

C. Proton-pump inhibitor administration is effective
in decreasing rebleeding rateswith bleeding ulcers.
Therapy consists of intravenous omeprazole.

1. Omeprazole (Prilosec) dosage is 80 mg IV,
followed by continuous infusion with 8 mg/hrfor
72 hrs and 20-mg per day PO.

2. Twice daily dosing of oral proton pump inhibitors
may be a reasonable alternative when
intravenous formulations are not available. Oral
omeprazole (Prilosec) for duodenal ulcer: 20 mg
qd for 4-8 weeks. Gastric ulcers: 20 mg bid.
Lansoprazole (Prevacid), 15 mg qd.
Esomeprazole (Nexium) 20-40 mg qd.

D. Indications for surgical operation include (1)
severe hemorrhage unresponsive to initial
resuscitative measures; (2) failure of endoscopic or
other nonsurgical therapies; and (3) perforation,
obstruction, or suspicion of malignancy.

E. Duodenal ulcer hemorrhage. Suture ligation of
the ulcer-associated bleeding artery combined with
a vagotomy is indicated for duodenal ulcer
hemorrhage that does not respond to medical
therapy. Truncal vagotomy and pyloroplasty is
widely used because it is rapidly and easily
accomplished.

F. Gastric ulcer hemorrhage is most often managed
by truncal vagotomy and pyloroplasty with wedge
excision of ulcer.

G. Transcatheter angiographic embolization of the
bleeding artery responsible for ulcer hemorrhage is
recommended in patients who fail endoscopic
attempts at control and who are poor surgical
candidates.

VII. Hemorrhagic Gastritis

A. The diffuse mucosal inflammation of gastritis rarely
manifest as severe or life-threatening hemorrhage.
Hemorrhagic gastritis accounts for 4% of upper
gastrointestinal hemorrhage. The bleeding is
usually miid and self-limited. When coagulopathy
accompanies cirrhosis and portal hypertension,
however, gastric mucosal bleeding can be brisk
and refractory.

B. Endoscopic therapy can be effective for multiple
punctate bleeding sites, but when diffuse mucosal
hemorrhage is present, selective intra-arterial
infusion of vasopressin may control bleeding. For
the rare case in which surgical intervention is
required, total gastrectomy is the most effective
procedure.

VIM. Mallory-Weiss syndrome

A. This disorder is defined as a mucosal tear at the
gastroesophageal junction following forceful
retching and vomiting.

B. Treatment is supportive, and the majority of
patients stop bleeding spontaneously. Endoscopic
coagulation or operative suturing may rarely be
necessary.

References: See page 112.

Esophageal Varices

Esophageal varices eventually develop in most patients
with cirrhosis, but variceal bleeding occurs in only one
third of them. The initiating event in the development of
portal hypertension is increased resistance to portal
outflow.

Causes of Portal Hypertension

Presinusoidal

Extrahepatic causes

Portal vein thrombosis

Extrinsic compression of the portal vein

Cavernous transformation of the portal vein

Intrahepatic causes

Sarcoidosis

Primary biliary cirrhosis

Hepatoportal sclerosis

Schistosomiasis
Sinusoidal: Cirrhosis, alcoholic hepatitis
Postsinusoidal

Budd-Chiari syndrome (hepatic vein thrombosis)

Veno-occlusive disease

Severe congestive heart failure

Restrictive heart disease

I. Pathophysiology

A. Varices develop annually in 5% to 15% of patients
with cirrhosis, and varices enlarge by 4% to 10%
each year. Each episode of variceal hemorrhage
carries a 20% to 30% risk of death.

B. After an acute variceal hemorrhage, bleeding
resolves spontaneously in 50% of patients.
Bleeding is least likely to stop in patients with large
varices and a Child-Pugh class C cirrhotic liver.

II. Management of variceal hemorrhage

A. Primary prophylaxis

LAN patients with cirrhosis should undergo
endoscopy to screen for varices every 2 to 3
years.

2. Propranolol (Inderal) and nadolol (Corgard)
reduce portal pressure through beta, blockade.
Beta-blockade reduces the risk of bleeding by
45% and bleeding-related death by 50%. The
beta-blocker dose is adjusted to decrease the
resting heart rate by 25% from its baseline, but
not to less than 55 to 60 beats/min.

3. Propranolol (Inderal) is given at 10 to 480 mg
daily, in divided doses, or nadolol (Corgard) 40
to 320 mg daily in a single dose.

B. Treatment of acute hemorrhage

1. Variceal bleeding should be considered in any
patient who presents with significant upper
gastrointestinal bleeding. Signs of cirrhosis may
include spider angiomas, palmar erythema,
leukonychia, clubbing, parotid enlargement, and
Dupuytren's contracture. Jaundice, lower
extremity edema and ascites are indicative of
decompensated liver disease.

2. The severity of the bleeding episode can be
assessed on the basis of orthostatic changes
(eg, resting tachycardia, postural hypotension),
which indicates one-third or more of blood
volume loss.

3. Blood should be replaced as soon as possible.
While blood for transfusion is being made
available, intravascular volume should be
replenished with normal saline solution. Once
euvolemia is established, the intravenous
infusion should be changed to solutions with a
lower sodium content (5% dextrose with 1/2 or
1/4 normal saline). Blood should be transfused
to maintain a hematocrit of at least 30%. Serial
hematocrit estimations should be obtained
during continued bleeding.

4. Fresh frozen plasma is administered to patients
who have been given massive transfusions.
Each 3 units of PRBC should be accompanied
by CaCL 2 1 gm IV over 30 min. Clotting factors
should be assessed. Platelet transfusions are
reserved for counts below 50,000/mL in an
actively bleeding patient.

5. If the patient's sensorium is altered because of
hepatic encephalopathy, the risk of aspiration
mandates endotracheal intubation. Placement of
a large-caliber nasogastric tube (22 F or 24 F)
permits tap water lavage for removal of blood
and clots in preparation for endoscopy.

6. Octreotide acetate (Sandostatin) is a
synthetic, analogue of somatostatin, which
causes splanchnic vasoconstriction. Octreotide
is the drug of choice in the pharmacologic
management of acute variceal bleeding.
Octreotide infusion should be started with a
loading dose of 50 micrograms, followed by an
infusion of 50 micrograms/hr. Treatment is
continued through the fifth hospital day.
Definitive endoscopic therapy is performed
shortly after hemostasis is achieved.

7. Endoscopic therapy

a. A sclerosant (eg, morrhuate [Scleromate]) is
injected into each varix. Complications
include bleeding ulcers, dysphagia due to
strictures, and pleural effusions.

b. Endoscopic variceal ligation with elastic
bands is an alternative to sclerotherapy
because of fewer complications and similar
efficacy.

c. If bleeding persists (or recurs within 48 hours
of the initial episode) despite pharmacologic
therapy and two endoscopic therapeutic
attempts at least 24 hours apart, patients
should be considered for salvage therapy
with TIPS or surgical treatment (transection
of esophageal varices and devascularization
of the stomach, portacaval shunt, or liver
transplantation).

8. Transjugular intrahepatic portosystemic

shunt (TIPS) consists of the angiographic
creation of a shunt between hepatic and portal
veins which is kept open by a fenestrated metal
stent. It decompresses the portal system,
controlling active variceal bleeding over 90% of
the time. Complications include secondary
bleeding, worsening encephalopathy in 20%,
and stent thrombosis or stenosis.
C. Secondary prophylaxis

1.A patient who has survived an episode of
variceal hemorrhage has an overall risk of
rebleeding that approaches 70% at 1 year.
2. Endoscopic sclerotherapy decreases the risk
of rebleeding (50% versus 70%) and death
(30% to 60% versus 50% to 75%). Endoscopic
variceal ligation is superior to sclerotherapy.
Banding is carried out every 2 to 3 weeks until
obliteration.
References: See page 112.

Peptic Ulcer Disease

Peptic ulcer disease is diagnosed in 500,000 patients
each year. Patients with peptic ulcer disease should be
treated as having an infectious illness caused by the
bacterium Helicobacter pylori. Peptic ulcer disease due
to H pylori infection can be cured with a combination of
antimicrobial and antisecretory drugs.

I. Pathophysiology

A. Helicobacter pylori (HP), a spiral-shaped,
flagellated organism, is the most frequent cause of
peptic ulcer disease (PUD). Nonsteroidal anti-
inflammatory drugs (NSAIDs) and pathologically
high acid-secreting states (Zollinger-Ellison
syndrome) are less common causes. More than
90% of ulcers are associated with H. pylori.
Eradication of the organism cures and prevents
relapses of gastroduodenal ulcers.

B. Complications of peptic ulcer disease include
bleeding, duodenal or gastric perforation, and
gastric outlet obstruction (due to inflammation or
strictures).

II. Clinical evaluation

A. Symptoms of PUD include recurrent upper
abdominal pain and discomfort. The pain of
duodenal ulceration is often relieved by food and
antacids and worsened when the stomach is empty
(eg, at nighttime). In gastric ulceration, the pain
may be exacerbated by eating.

B. Nausea and vomiting are common in PUD.
Hematemesis ("coffee ground" emesis) or melena
(black tarry stools) are indicative of bleeding.

C. Physical examination. Tenderness to deep
palpation is often present in the epigastrium, and
the stool is often guaiac-positive.

Presentation of Uncomplicated Peptic Ulcer
Disease

Epigastric pain (burning, vague abdominal

discomfort, nausea)
Often nocturnal

Occurs with hunger or hours after meals
Usually temporarily relieved by meals or antacids
Persistence or recurrence over months to years
History of self-medication and intermittent relief

D. NSAID-related gastrointestinal complications.

NSAID use and H pylori infection are independent
risk factors for peptic ulcer disease. The risk is 5 to
20 times higher in persons who use NSAIDs than
in the general population. Misoprostol (Cytotec)
has been shown to prevent both NSAID ulcers and
related complications. The minimum effective
dosage is 200 micrograms twice daily; total daily
doses of 600 micrograms or 800 micrograms are
significantly more effective.
III. Laboratory and diagnostic testing

A. Alarm signs and symptoms that suggest gastric
cancer are indications for early endoscopy or
upper gastrointestinal radiology studies.

Indications for early endoscopy

Anorexia

Presence of a mass

Dysphagia

Unexplained anemia

Gastrointestinal bleeding

Unexplained weight loss

(gross or occult)

Vomiting (severe)

New-onset symptoms in

persons >45 yr of age

B. Noninvasive testing for H pylori

1. In the absence of alarm symptoms for gastric
cancer, most patients with dyspepsia should
undergo evaluation for H pylori infection with
serologic testing for H pylori antigens.

2. Serologic testing to detect H pylori antibodies
isthe preferred testing method. Serologic testing
is highly sensitive, but it cannot be used for
follow-up after therapy because antibody titers
may remain elevated for a year or longer. Rapid
office-based serologic kits have a sensitivity of
90% and a specificity of 85%.

3. Urea breath tests measure the carbon dioxide
produced when H pylori urease metabolizes
urea labeled with radioactive carbon (13C or
14C). The 13C test does not involve a
radioactive isotope and, unlike the 14C test, can
be used in children and pregnant women. With
the 13C test, exhaled breath samples are
usually sent to a central testing facility. The 1 4C
test, which exposes the patient to a small dose
of radiation, can be analyzed in a hospital's
nuclear medicine laboratory. Urea breath tests
have a sensitivity and specificity of 90-99%. The
urea breath test is the best method of
confirmation of care.

4. Stool testing for H pylori antigens has an
accuracy for pretreatment testing of H pylori that
is similar to that of other available tests.

5. Biopsy-based testing performed at endoscopy
can provide valuable information via histologic
testing, rapid urease tests, and culture.
Sensitivity of the tests for H pylori ranges from
80% to 100%, and specificity exceeds 95%.

Triple therapies for peptic ulcer disease

BMT therapy:

Bismuth subsalicylate (Pepto-Bismol), 2 tablets with meals

and at bedtime for 14 days

and

Metronidazole (Flagyl), 250 mg with meals and at bedtime

(total daily dose, 1 ,000 mg) for 14 days

and

Tetracycline, 500 mg with meals and at bedtime (total daily

dose, 2 g) for 1 4 days

or

A prepackaged triple-therapy agent (Helidac), to be taken

qid for 14 days, consists of 525 mg bismuth subsalicylate,

250 mg metronidazole, and 500 mg tetracycline; an H 2 -

blocker or proton pump inhibitor should be added

(Omeprazole [Prilosec], 20 mg qd or lansoprazole [Prevacid],

15 mg qd).

Ranitidine bismuth citrate (Tritec), 1 tablet (400 mg) bid for

14 days

and

Tetracycline, 500 mg bid for 14 daysandClarithromycin

(Biaxin) or metronidazole (Flagyl), 500 mg bid for 14 days

Omeprazoie (Prilosec), 20 mg bid, or lansoprazole

(Prevacid), 30 mg bid

and

Clarithromycin (Biaxin), 250 or 500 mg bid for 14 days

and

Metronidazole (Flagyl), 500 mg bid, or amoxicillin, 1 g bid for

14 days

or

A prepackaged triple-therapy agent (Prevpac), to be

taken bid for 14 days, consists of 30 mg lansoprazole, 1 g

amoxicillin, and 500 mg clarithromycin.

IV. Treatment of peptic ulcer disease

A. Combination therapy

1 . Dual therapy is not recommended because cure
rates for all regimens are less than 85%.
Recommended triple therapies consist of a
bismuth preparation or proton pump inhibitor or
H2 receptor antagonist plus two antibiotics.

2. The H pylori eradication rate is 96% for patients
who take more than 60% of their medication.

B. Confirmation of cure of H pylori infection

1 . Confirmation of cure of H pylori infection is
always necessary. About 75% of patients
presumed to have uncomplicated peptic ulcer
disease due to H pylori infection are cured after
one course of therapy.

2. The urea breath test is the best method for
assessing the effectiveness of therapy. The
stool antigen test is only slightly less accurate,
and its use should be considered when breath
testing is not available.

3. Confirmation of cure must be delayed until at
least 4 to 6 weeks after completion of
antimicrobial therapy. Treatment with proton
pump inhibitors must be discontinued at least 1
week before urea breath testing to confirm cure.
H2-receptor antagonists have no effect on the
urea breath test and need not be discontinued

before confirmation testing.
C. Treatment of NSAID-related ulcers

1 . When the ulcer is caused by NSAID use, healing
of the ulcer is greatly facilitated by discontinuing
the NSAID. Acid antisecretory therapy with an
H2-blocker or proton pump inhibitor speeds
ulcer healing. Proton pump inhibitors are more
effective in inhibiting gastric acid production and
are often used to heal ulcers in patients who
require continuing NSAID treatment.

2. If serologic or endoscopic testing for H pylori is
positive, antibiotic treatment is necessary.

3. Acute H 2 -blocker therapy

a. Ranitidine (Zantac), 150 mg bid or 300 mg
qhs.

b. Famotidine (Pepcid), 20 mg bid or 40 mg
qhs.

c. Nizatidine (Axid Pulvules), 150 mg bid or
300 mg qhs.

d. Cimetidine (Tagamet), 400 mg bid or 800
mg qhs.

4. Proton pump inhibitors

a. Omeprazole (Prilosec), 20 mg qd.

b. Lansoprazole (Prevacid), 15 mg before
breakfast qd.

c. Esomeprazole (Nexium) 20-40 mg qd.
V. Surgical treatment of peptic ulcer disease

A. Indications for surgery include exsanguinating
hemorrhage, >5 units transfusion in 24 hours,
rebleeding during same hospitalization,
intractability, perforation, gastric outlet obstruction,
and endoscopic signs of rebleeding.

B, Unstable patients should receive a truncal
vagotomy, oversewing of bleeding ulcer bed, and
pyloroplasty.

References: See page 112.

Lower Gastrointestinal Bleeding

H.L. Daneschvar, WID
S.E. Wilson, MD

The spontaneous remission rates for lower
gastrointestinal bleeding is 80 percent. No source of
bleeding can be identified in 12 percent of patients, and
bleeding is recurrent in 25 percent. Bleeding has usually
ceased by the time the patient presents to the emergency

Clinical evaluation

A. The severity of blood loss and hemodynamic status
should be assessed immediately. Initial
management consists of resuscitation with
crystalloid solutions (lactated Ringers) and blood
products if necessary.

B. The duration and quantity of bleeding should be
assessed; however, the duration of bleeding is
often underestimated.

C. Risk factors that may have contributed to the
bleeding include nonsteroidal anti-inflammatory
drugs, anticoagulants, colonic diverticulitis, renal
failure, coagulopathy, colonic polyps, and
hemorrhoids. Patients may have a prior history of
hemorrhoids, diverticulosis, inflammatory bowel
disease, peptic ulcer, gastritis, cirrhosis, or
esophageal varices.

D. Hematochezia. Bright red or maroon output per
rectum suggests a lower Gl source; however, 12 to
20% of patients with an upper Gl bleed may have
hematochezia as a result of rapid blood loss.

E. Melena. Sticky, black, foul-smelling stools suggest
a source proximal to the ligament of Treitz, but
Melena can also result from bleeding in the small
intestine or proximal colon.

F. Clinical findings

1. Abdominal pain may result from ischemic
bowel, inflammatory bowel disease, or a
ruptured aneurysm.

2. Painless massive bleeding suggests vascular
bleeding from diverticula, angiodysplasia, or
hemorrhoids.

3. Bloody diarrhea suggests inflammatory bowel
disease or an infectious origin.

4. Bleeding with rectal pain is seen with anal
fissures, hemorrhoids, and rectal ulcers.

5. Chronic constipation suggests hemorrhoidal
bleeding. Newonset of constipation orthin stools
suggests a left sided colonic malignancy.

6. Blood on the toilet paper or dripping into the
toilet water suggests a perianal source of
bleeding, such as hemorrhoids or an anal
fissure.

7. Blood coating the outside of stools suggests a
lesion in the anal canal.

8. Blood streaking or mixed in with the stool may
results from polyps or a malignancy in the
descending colon.

9. Maroon colored stools often indicate small
bowel and proximal colon bleeding.

II. Physical examination

A. Postural hypotension indicates a 20% blood
volume loss, whereas, overt signs of shock (pallor,
hypotension, tachycardia) indicates a 30 to 40
percent blood loss.

B. The skin may be cool and pale with delayed refill if
bleeding has been significant.

C. Stigmata of liver disease, including jaundice,
caput medusae, gynecomastia and palmar
erythema, should be sought because patients with
these findings frequently have Gl bleeding.

III. Differential diagnosis of lower Gl bleeding

A. Angiodysplasia and diverticular disease of the
right colon accounts for the vast majority of
episodes of acute lower Gl bleeding. Most acute
lower Gl bleeding originates from the colon
however 1 5 to 20 percent of episodes arise from
the small intestine and the upper Gl tract.

B. Elderly patients. Diverticulosisand angiodysplasia
are the most common causes of lower Gl bleeding.

C. Younger patients. Hemorrhoids, anal fissures and
inflammatory bowel disease are most common
causes of lower Gl bleeding.

Clinical Indicators of Gastrointestinal Bleeding
and Probable Source

Clinical Indicator

Probability of
Upper

Gastrointestinal
source

Probability of
Lower

Gastrointestinal
Source

Hematemesis

Almost certain

Rare

Melena

Probable

Possible

Hematochezia

Possible

Probable

Blood-streaked
stool

Rare

Almost certain

Occult blood in
stool

Possible

Possible

IV. Diagnosis and management of lower
gastrointestinal bleeding

A. Rapid clinical evaluation and resuscitation

should precede diagnostic studies. Intravenous
fluids (1 to 2 liters) should be infused over 10- 20
minutes to restore intravascular volume, and blood
should be transfused if there is rapid ongoing blood
loss or if hypotension or tachycardia are present.
Coagulopathy is corrected with fresh frozen plasma,
platelets, and cryoprecipitate.

B. When small amounts of bright red blood are passed
per rectum, then lower Gl tract can be assumed to
be the source. In patients with large volume maroon
stools, nasogastric tube aspiration should be
performed to exclude massive upper
gastrointestinal hemorrhage.

C. If the nasogastric aspirate contains no blood then
anoscopy and sigmoidoscopy should be performed
to determine weather a colonic mucosal
abnormality (ischemic or infectious colitis) or
hemorrhoids might be the cause of bleeding.

D. Colonoscopy in a patient with massive lower Gl
bleeding is often nondiagnostic, but it can detect
ulcerative colitis, antibiotic-associated colitis, or
ischemic colon.

E. Polyethylene glycol-electrolyte solution (CoLyte
or GoLytely) should be administered by means of a
nasogastric tube (Four liters of solution is given
over a 2-3 hour period), allowing for diagnostic and
therapeutic colonoscopy.

V. Definitive management of lower gastrointestinal
bleeding

A. Colonoscopy

1. Colonoscopy is the procedure of choice for
diagnosing colonic causes of Gl bleeding. It
should be performed after adequate preparation
of the bowel. If the bowel cannot be adequately
prepared because of persistent, acute bleeding,
a bleeding scan or angiography is preferable.

2. If colonoscopy fails to reveal the source of the
bleeding, the patient should be observed
because, in 80% of cases, bleeding ceases
spontaneously.

B. Radionuclide scan or bleeding scan.
Technetium- labeled (tagged) red blood cell
bleeding scans can detect bleeding sites when
bleeding is intermittent. Localization may not he a

precise enough to allow segmental colon resection.

C. Angiography. Selective mesenteric angiography
detects arterial bleeding that occurs at rates of 0.5
mL/per minute or faster. Diverticular bleeding
causes pooling of contrast medium within a
diverticulum. Bleeding angiodysplastic lesions
appear as abnormal vasculature. When active
bleeding is seen with diverticular disease or
angiodysplasia, selective arterial infusion of
vasopressin may be effective.

D. Surgery

1. If bleeding continues and no source can be
found, surgical intervention is usually warranted.
Surgical resection may be indicated for patients
with recurrent diverticular bleeding, or for
patients who have had persistent bleeding from
colonic angiodysplasia and have required blood
transfusions.

2. Surgical management of lower gastrointestinal
bleeding is ideally undertaken with a secure
knowledge of the location and cause of the
bleeding lesion. A segmental bowel resection to
include the lesion and followed by a primary
anastomosis is usually safe and appropriate in
all but the most unstable patients.

VI.Diverticulosis

A. Diverticulosis of the colon is present in more than
50% of the population by age 60 years. Bleeding
from diverticula is relatively rare, affecting only 4%
to 1 7% of patients at risk.

B. In most cases, bleeding ceases spontaneously, but
in 10% to 20% of cases, the bleeding continues.
The risk of rebleeding after an episode of bleeding
is 25%. Right-sided colonic diverticula occur less
frequently than left-sided or sigmoid diverticula but
are responsible for a disproportionate incidence of
diverticular bleeding.

C. Operative management of diverticular bleeding is
indicated when bleeding continues and is not
amenable to angiographic or endoscopic therapy.
It also should be considered in patients with
recurrent bleeding in the same colonic segment.
The operation usually consists of a segmental
bowel resection (usually a right colectomy or
sigmoid colectomy) followed by a primary
anastomosis.

VII. Arteriovenous malformations

A. AVMs or angiodysplasias are vascular lesions that
occur primarily in the distal ileum, cecum, and
ascending colon of elderly patients. The
arteriographic criteria for identification of an AVM
include a cluster of small arteries, visualization of a
vascular tuft, and early and prolonged filling of the
draining vein.

B. The typical pattern of bleeding of an AVM is
recurrent and episodic, with most individual
bleeding episodes being self-limited. Anemia is
frequent, and continued massive bleeding is
distinctly uncommon. After nondiagnostic
colonoscopy, enteroscopy should be considered.

C. Endoscopic therapy for AVMs may include heater
probe, laser, bipolar electrocoagulation, or argon
beam coagulation. Operative management is
usually reserved for patients with continued
bleeding, anemia, repetitive transfusion
requirements, and failure of endoscopic
management. Surgical management consists of
segmental bowel resection with primary
anastomosis.

VIII. Inflammatory bowel disease

A. Ulcerative colitis and, less frequently, Crohn'scolitis
or enteritis may present with major or massive
lower gastrointestinal bleeding. Infectious colitis can
also manifest with bleeding, although it is rarely
massive.

B. When the bleeding is minor to moderate, therapy
directed at the inflammatory condition is
appropriate. When the bleeding is major and
causes hemodynamic instability, surgical
intervention is usually required. When operative
intervention is indicated, the patient is explored
through a midline laparotomy, and a total abdominal
colectomy with end ileostomy and oversewing of
the distal rectal stump is the preferred procedure.

IX. Tumors of the colon and rectum

A. Colon and rectal tumors account for 5% to 10% of
all hospitalizations for lower gastrointestinal
bleeding. Visible bleeding from a benign colonic or
rectal polyp is distinctly unusual. Major or massive
hemorrhage rarely is caused by a colorectal
neoplasm; however, chronic bleeding is common.
When the neoplasm is in the right colon, bleeding is
often occult and manifests as weakness or anemia.

B. More distal neoplasms are often initially confused
with hemorrhoidal bleeding. For this reason, the
treatment of hemorrhoids should always be
preceded by flexible sigmoidoscopy in patients
older than age 40 or 50 years. In younger patients,
treatment of hemorrhoids without further
investigation may be appropriate if there are no risk
factors for neoplasm, there is a consistent clinical
history, and there is anoscopic evidence of recent
bleeding from enlarged internal hemorrhoids.

X. Anorectal disease

A. When bleeding occurs only with bowel movements
and is visible on the toilet tissue or the surface of
the stool, it is designated outlet bleeding. Outlet
bleeding is most often associated with internal
hemorrhoids or anal fissures.

B. Anal fissures are most commonly seen in young
patients and are associated with severe pain during
and after defecation. Other benign anorectal
bleeding sources are proctitis secondary to
inflammatory bowel disease, infection, or radiation
injury. Additionally, stercoral ulcers can develop in
patients with chronic constipation.

C. Surgery for anorectal problems is typically
undertaken only after failure of conservative
medical therapy with high-fiber diets, stool
softeners, and/or hemorrhoidectomy.

XI. Ischemic colitis

A. Ischemic colitis is seen in elderly patients with
known vascular disease. The abdomen pain may
be postprandial and associated with bloody
diarrhea or rectal bleeding. Severe blood loss is
unusual but can occur.

B. Abdominal films may reveal "thumb-printing"
caused by submucosal edema. Colonoscopy
reveals a well-demarcated area of hyperemia,
edema and mucosal ulcerations. The splenic
flexure and descending colon are the most common
sites. Most episodes resolve spontaneously,
however, vascular bypass or resection may be
required.

References: See page 112.

Anorectal Disorders

I. Hemorrhoids

A. Hemorrhoids are dilated veins located beneath the
lining of the anal canal. Internal hemorrhoids are
located in the upper anal canal. External
hemorrhoids are located in the lower anal canal.

B. The most common symptom of internal hemor-
rhoids is painless rectal bleeding, which is usually
bright red and ranges from a few drops to a spatter-
ing stream at the end of defecation. If internal
hemorrhoids remain prolapsed, a dull aching may
occur. Blood and mucus stains may appear on
underwear, and itching in the perianal region is
common.

Classification of Internal Hemorrhoids

Gr

ad
e

Description

Symptoms

1

Non-prolapsing

Minimal bleeding

2

Prolapse with straining,
reduce when spontan-
eously prolapsed

Bleeding, discomfort,
pruritus

3

Prolapse with straining,
manual reduction
required when
prolapsed

Bleeding, discomfort,
pruritus

4

Cannot be reduced
when prolapsed

Bleeding, discomfort,
pruritus

C. Management of internal hemorrhoids

1. Grade 1 and uncomplicated grade 2
hemorrhoids are treated with dietary
modification (increased fiber and fluids).

2. Symptomatic grade 2 and grade 3
hemorrhoids. Treatment consists of

hemorrhoid banding with an anoscope. Major
complications are rare and consist of excessive
pain, bleeding, and infection. Surgical
hemorrhoidectomy may sometimes be
necessary.
3. Grade 4 hemorrhoids require surgical
hemorrhoidectomy.
D. External hemorrhoids

1 . External hemorrhoids occur most often in young
and middle-aged adults, becoming symptomatic
only when they become thrombosed.

2. External hemorrhoids are characterized by rapid
onset of constant burning or throbbing pain,
accompanying a new rectal lump. Bluish skin-
covered lumps are visible at the anal verge.

3. Management of external hemorrhoids

a. If patients are seen in the first 48 hours, the
entire lesion can be excised in the office. Local
anesthetic is infiltrated, and the thrombus and
overlying skin are excised with scissors. The
resulting wound heals by secondary intention.

b. If thrombosis occurred more than 48 hours
prior, spontaneous resolution should be
permitted to occur.

II. Anal fissures

A. An anal fissure is a longitudinal tear in the distal
anal canal, usually in the posterior or anterior
midline. Patients with anal fissures complain of
perirectal pain which is sharp, searing or burning
and is associated with defecation. Bleeding from
anal fissures is bright red and not mixed with the
stool.

B. Anal fissures may be associated with secondary
changes such as a sentinel tag, hypertrophied anal
papilla, induration of the edge of the fissure, and
anal stenosis. Crohn's disease should be
considered if the patient has multiple fissures, or
whose fissure is not in the midline.

C. Anal fissures are caused by spasm of the internal
anal sphincter. Risk factors include a low-fiber diet
and previous anal surgery.

D. Treatment of anal fissures

1. High-fiber foods, warm sitz baths, stool
softeners (if necessary), and daily application of
1% hydrocortisone cream to the fissure should
be initiated. These simple measures may heal
acute anal fissures within 3 weeks in 90% of
patients.

2. Lateral partial internal sphincterotomy is
indicated when 4 weeks of medical therapy fails.
The procedure consists of surgical division of a
portion of the internal sphincter, and it is highly
effective. Adverse effects include incontinence
to flatus and stool.

III. Levator ani syndrome and proctalgia fugax

A. Levator ani syndrome refers to chronic or recurrent
rectal pain, with episodes lasting 20 minutes or
longer. Proctalgia fugax is characterized by anal or
rectal pain, lasting for seconds to minutes and then
disappearing for days to months.

B. Levator ani syndrome and proctalgia fugax are
more common in patients under age 45, and
psychological factors are not always present.

C. Levator ani syndrome is caused by chronic tension
of the levator muscle. Proctalgia fugax is caused
by rectal muscle spasm. Stressful events may
trigger attacks of proctalgia fugax and levator ani
syndrome.

D. Diagnosis and clinical features

1. Levator ani syndrome is characterized by a
vague, indefinite rectal discomfort or pain. The
pain is felt high in the rectum and is sometimes
associated with a sensation of pressure.

2. Proctalgia fugax causes pain that is brief and
self limited. Patients with proctalgia fugax
complain of sudden onset of intense, sharp,
stabbing or cramping pain in the anorectum.

3. In patients with levator ani syndrome, palpation
of the levator muscle during digital rectal
examination usually reproduces the pain.

E. Treatment

1. Levator ani syndrome. Treatment with hot
baths, nonsteroidal anti-inflammatory drugs,
muscle relaxants, or levator muscle massage is
recommended. EMG-based biofeedback may
provide improvement in pain.

2. Proctalgia fugax. For patients with frequent
attacks, physical modalities such as hot packs
or direct anal pressure with a finger or closed
fist may alleviate the pain. Diltiazem and
clonidine may provided relief.

IV. Pruritus ani

A. Pruritus ani is characterized by the intense desire
to scratch the skin around the anal orifice. It occurs
in 1 % of the population. Pruritus ani may be related

to fecal leakage.

B. Patients report an escalating pattern of itching and
scratching in the perianal region. These symptoms
may be worse at night. Anal hygiene and dietary
habits, fecal soiling, and associated medical
conditions should be sought.

C. Examination reveals perianal maceration,
erythema, excoriation, and lichenification. A digital
rectal examination and anoscopy should be
performed to assess the sphincter tone and look
for secondary causes of pruritus. Patients who fail
to respond to 3 or 4 weeks of conservative
treatment should undergo further investigations
such as skin biopsy and sigmoidoscopy or
colonoscopy.

D. Treatment and patient education

1. Patients should clean the perianal area with
water following defecation, but avoid soaps and
vigorous rubbing. Following this, the patient
should dry the anus with a hair dryer or by
patting gently with cotton. Between bowel
movements a thin cotton pledget dusted with
unscented cornstarch should be placed against
the anus. A high fiber diet is recommended to
regulate bowel movements and absorb excess
liquid. All foods and beverages that exacerbate
the itching should be eliminated.

2. Topical medications are not recommended
because they may cause further irritation. If
used, a bland cream such as zinc oxide or 1%
hydrocortisone cream should be applied
sparingly two to three times a day.

3. Diphenhydramine (Benadryl) or hydroxyzine
(Vistaril) may relieve the itching and allow the
patient to sleep.

. Perianal abscess

A. The anal glands, located in the base of the anal
crypts at the level of the dentate line, are the most
common source of perianal infection. Acute infec-
tion causes an abscess, and chronic infection
results in a fistula.

B. The most common symptoms of perianal abscess
are swelling and pain. Fevers and chills may occur.
Perianal abscess is common in diabetic and
immunosuppressed patients, and there is often a
history of chronic constipation. A tender mass with
fluctuant characteristics or induration is apparent
on rectal exam.

C. Management of perianal abscess. Perianal
abscesses are treated with incision and drainage
using a local anesthetic. Large abscesses require
regional or general anesthesia. A cruciate incision
is made close to the anal verge and the corners
are excised to create an elliptical opening which
promotes drainage. An antibiotic, such as Zosyn,
Timentin, or Cefotetan, is administered.

D. About half of patients with anorectal abscesses will
develop a fistula tract between the anal glands and
the perianal mucosa, known as a fistula-in-ano.
This complication manifests as either incomplete
healing of the drainage site or recurrence. Healing
of a fistula-in-ano requires a surgical fistulotomy.

Fistula-in-Ano

A fistula-in-ano develops when an anorectal abscess
forms a fistula between the anal canal and the perianal
skin. The fistula may develop after an anorectal abscess
has been drained operatively, or the fistula may develop
spontaneously.

I. Clinical evaluation

A. The fistula is characterized by persistent purulent
or feculent drainage, soiling the underwear.

B. The fistula orifice can be seen just outside the anal
verge. Complex fistulae may have multiple tracts
with multiple orifices.

II. Treatment of fistula-in-ano

A. Fistulae will not resolvewithoutdefinitivetreatment.
The more common type of fistula, located at the
anorectal junction, has an external opening where
it can be drained operatively. The entire
epithelialized tract must be found and obliterated.

B. Goodsall's rule predicts the course of fistulae that
exit the skin within 3 cm of the anal verge. Anterior
fistulae go straight toward the anorectal junction;
posterior fistulae curve toward the posterior midline
and enter the anorectal junction.

C. A pilonidal cyst-sinus (coccygeal region) can be
difficult to distinguish from a fistula-in-ano. Probing
the tract under anesthesia usually will reveal its
origin.

D. Fistulotomy. For fistulae that do not cross both
internal and external sphincters, the tract should be

unroofed and curetted. The lesion should then be
allowed to heal by secondary intention.
. Fistulectomy. Deeper fistulae should be treated
by coring out the epithelialized tract to its origin.
The fistula may recur.

Seton procedure. Complex fistulae or fistulae that
traverse the sphincter can be treated by looping a
heavy suture through the entire tract under tension.
The suture should be tightened weekly until it
"cuts" gradually to the surface. The tract will heal
gradually behind the suture.

Colorectal Cancer

Charles Theuer, MD

Colorectal cancer is the second most common solid
malignancy in adults and the second leading cause of
cancer death in the US.

I. Clinical evaluation of colorectal cancer

A. Flexible sigmoidoscopy is indicated for screening
of asymptomatic, healthy adults over age 50. All
adults with anemia or guaiac positive stools should
be evaluated for colorectal cancer; older adults
(>40) should be evaluated even if other sources of
bleeding have been found. Hemorrhoids and
cancer can coexist.

B. Flexible sigmoidoscopy plus air contrast barium
enema is adequate to evaluate the colon when the
source of bleeding is thought to be benign
anorectal disease. Total colonoscopy should be
performed for any adult with gross or occult rectal
bleeding and no apparent anorectal source.

C. Left-sided or rectal lesions are characterized by
blood streaked stools, change in caliber or
consistency of stools, obstipation, alternating
diarrhea and constipation, and tenesmus.

D. Right-sided lesions are characterized by a triad of
iron deficiency anemia, right lower quadrant mass,
and weakness. Cancers occasionally present as a
large bowel obstruction, perforation or abscess.

II. Laboratory evaluation

A. Complete blood count with indices will often reveal
a hypochromic, microcytic anemia. Liver function
tests may sometimes be elevated in metastatic
disease.

B. Carcinoembryonic antigen (CEA) may be
elevated in colorectal cancer, but it is a nonspecific
test which may also be elevated in other
malignancies, inflammatory bowel disease,
cigarette smokers, and some normal persons. CEA
is valuable in monitoring the response to treatment
and as a marker for recurrence or metastases,
requiring adjuvant therapy. It should be measured
prior to resection of the tumor and at intervals
postoperatively.

C. Colorectal cancer is detected by colonoscopy with
biopsies. Barium enema may complement
colonoscopy since BE shows the exact anatomic
location of the tumor. A chest X-ray should be done
to search for metastases to the lungs. A CT scan
should be done in cases where liver function test
are elevated.

III. Management of colorectal carcinoma

A. Surgical resection is indicated for colorectal
adenocarcinoma, regardless of stage. Resection of
the primary lesion prevents obstruction or
perforation.

B. Extremely advanced rectal lesions, which are not
resectable, may be candidates for palliative
radiation and a diverting colostomy.

C. The extent of resection is determined by the
relationship of the lesion to the lymphatic drainage
and blood supply of the colon.

1. Cecum or right colon. Right hemicolectomy.

2. Hepatic flexure. Extended right hemicolectomy.

3. Mid-transverse colon: Transverse colectomy
or extended left or right hemicolectomy.

4. Splenic flexure or left colon. Left
hemicolectomy.

5. Sigmoid colon. Sigmoid colectomy.

6. Upper or middle rectum. Low anterior
rectosigmoid resection with primary
anastomosis.

7. Lower rectum. Abdominoperineal resection
with permanent, end-colostomy or local
excision.

D. Preoperative bowel preparation

1. Mechanical cleansing of the lumen, followed by
decontamination with nonabsorbable oral
antibiotics decreases the chance of infectious
complications and allows for primary

anastomosis. Fully obstructed patients cannot
be prepped and must have a temporary
colostomy.

2. Polyethylene glycol solution (CoLyte or
GoLYTELY) is usually administered as 4 liters
over 4 hours on the day before surgery. Oral
phospho-soda (given as two 11/2 ounce doses
in 8 ounces of water) can be substituted for
polyethylene glycol in patients with normal renal
function. The Nichols-Condon prep consists of
1 g neomycin sulfate and 1 g erythromycin base
PO at 2:00, 3:00 and 1 1 :00 pm the day before
operation. Cefotetan is given 1-2 gm IV 30
minutes before operation.

3. Patients with middle and lower rectal tumors
should be staged with endoanal ultrasound.
Tumors that invade through the muscularis
propria (T3) or involve lymph nodes (N1) should
be offered neoadjuvant therapy with radiation
therapy and 5-fluorouracil.

E. Adjuvant chemotherapy is recommended for
advanced colon lesions with the addition of pelvic
radiation for advanced rectal tumors. Adjuvant
therapy is reserved for locally advanced lesions
(B2) or those with metastases to regional lymph
nodes or distant organs (C1 , C2, D).

F. Pathologic staging of the tumor is done
postoperatively by histologic examination of the
surgical specimen.

IV. Staging of colorectal carcinoma

A. Astler-Coller modification of Dukes'
Classification

Stage A: Limited to mucosa and submucosa.
Nodes negative.
Stage B1: Extends into, but not through,

muscularis propria; nodes negative.
Stage B2: Extends through muscularis propria;
nodes negative.

Stage C1 : Same as B1 , except nodes positive.
Stage C2: Same as B2, except nodes positive.

V. Management of obstructing carcinomas of the left
colon

A. Correct fluid deficits and electrolyte abnormalities.
Nasogastric suction is useful, but it is not adequate
to decompress the acutely obstructed colon.

B. The Hartmann procedure is indicated for distal
descending and sigmoid colon lesions. This
procedure consists of resection of the obstructing
cancer and formation of an end-colostomy and
blind rectal pouch. The colostomy can be taken
down and anastomosed to the rectal pouch at a
later date.

C. Primary resection with temporary end-colostomy
and mucous fistula should be done for lesions of
the transverse and proximal descending colon.
This procedure consists of resection of the
obstructing cancer and creation of a functioning
end-colostomy and a defunctionalized distal limb
with separate stomas. The colostomy can be taken
down and continuity restored at a later date.

D. An emergency decompressive loop colostomy can
be considered for acutely ill patients. After four to
six weeks, a hemicolectomy can be completed. A
primary anastomosis may be done in selected
patients with a prepared bowel.

VI. Management of obstructing carcinomas of the
ascending colon. Correct fluid deficits, electrolyte
abnormalities, and initiate nasogastric suction. A right
hemicolectomy with primary anastomosis of the
terminal ileum to the transverse colon can be
performed on most patients. A temporary ileostomy is
rarely needed.

References: See page 112.

Mesenteric Ischemia

Mesenteric ischemia is classified as acute mesenteric
ischemia (AMI) and chronic mesenteric ischemia (CMI).
AMI is subdivided into occlusive and nonocclusive
mesenteric ischemia. Occlusive mesenteric ischemia
results from either thrombotic or embolic arterial or
venous occlusion.

Approximately 80% of cases of AMI are occlusive in
etiology, with arterial emboli or thromboses in 65% of
cases and venousthrombosis in 15%. Arterial occlusions
result from emboli in 75% of patients and in situ
thrombosis cause the remaining 25%. Nonocclusive
mesenteric ischemia is caused by low perfusion states
and is responsible for 20% of AMI.

I. Clinical evaluation

A. Mesenteric arterial embolism

1. The median age of patients presenting with
mesenteric arterial embolism is 70 years. The

overwhelming majority of emboli lodge in the
superior mesenteric artery (SMA). Emboli
originating in the left atrium or ventricle are the
most common cause of SMA embolism.

2. Risk factors include advanced age, coronary
artery disease, cardiac valvular disease, history
of dysrhythmias, atrial fibrillation, post-
myocardial infarction mural thrombi, history of
thromboembolic events, aortic surgery,
aortography, coronary angiography, and aortic
dissection. A previous history of peripheral
emboli is present in 20%.

3. The disorder usually presents as sudden onset
of severe poorly localized periumbilical pain,
associated with nausea, vomiting, and frequent
bowel movements. Pain is usually out of propor-
tion to the physical findings and may be the only
presenting symptom.

4. The abdomen may be soft with only mild
tenderness. Absent bowel sounds, abdominal
distension or guarding are indicative of severe
disease.

5. Blood in the rectum is present in 16% of
patients, and occult blood is present in 25% of
patients. Peritoneal signs develop when the
ischemic process becomes transmural.

B. Mesenteric arterial thrombosis

1. Thrombosis usually occurs in the area of
atherosclerotic narrowing in the proximal SMA.
The proximal jejunum through the distal
transverse colon becomes ischemic.

2. SMA thrombosis usually occurs in patients with
chronic, severe, visceral atherosclerosis. A
history of abdominal pain after meals is present
in 20-50% of patients. Patients are often elderly,
with coronary artery disease, severe peripheral
vascular disease, or hypertension.

3. SMA thrombosis presents with gradual onset of
abdominal pain and distension. A history of
postprandial abdominal pain and weight loss is
present in half of cases. Pain is usually out of
proportion to the physical findings, and nausea
and vomiting are common.

4. Signs of peripheral vascular disease, such as
carotid, femoral or abdominal bruits, or
decreased peripheral pulses are frequent.
Abdominal distension, absent bowel sounds,
guarding, rebound and localized tenderness,
and rigidity indicate advanced bowel necrosis.

II. Diagnostic evaluation of acute mesenteric
ischemia

A. Leukocyte count is elevated in most cases of
mesenteric ischemia. In patients with SMA emboli,
42% have a metabolic acidosis. The serum
amylase is elevated in half of patients.

B. Plain radiography. Abdominal and chest x-rays
help to exclude the presence of free air or bowel
obstruction. In rare instances, plain films of the
abdomen reveal signs of ischemic bowel such as
pneumatosis intestinalis, portal venous gas, or a
thickened bowel wall with thumbprinting. However,
plain films will be normal in the majority of cases.

C. Angiography isthe gold standard for the diagnosis
of AMI and is also used for therapeutic infusion of
the vasodilator, papaverine. After obtaining plain
abdominal films to rule out the presence of free air
or obstruction, angiography must be obtained,
especially in those patients in whom there is a
strong clinical suspicion for AMI.

III. Emergency management

A. Stabilization and initial management

1. Patients with significant hypotension require
rapid fluid resuscitation, and vasopressors may
be used.

2. If hemoglobin is low, blood should be given.
Patients who appear acutely ill should receive
parenteral antibiotics to cover for gram-negative
enteric bacteria as well as anaerobes after
blood cultures are drawn.

B. Papaverine

1. Intraarterial infusion of papaverine into the
superior mesenteric artery will increase
mesenteric perfusion by relieving mesenteric
vasoconstriction.

2. Papaverine is started at angiography and
continued postoperatively if laparotomy is
performed. The dosing is 60 mg IV bolus,
followed by a 30-60 mg/h continuous infusion at
a concentration of 1 mg/mL. Papaverine
improves survival by 20-50%.

C. Acute mesenteric infarction with embolism

1. Once embolism is confirmed at angiography,
papaverine infusion is started, then laparotomy
should be performed to evaluate bowel viability.
Surgical intervention may involve arteriotomy

with embolectomy and bowel resection if
nonviable necrotic bowel is found. Postoperative
anticoagulation is recommended for all patients.
2. Patients without peritoneal signs with minor
emboli, who achieve pain relief with vasodilator
infusion, may be managed nonoperatively with
repeated angiograms.
D. Acute mesenteric infarction with thrombosis

1. Acute mesenteric ischemia secondary to
thrombosis is treated initially with a papaverine
infusion started at angiography. Patients without
peritoneal signs with minor thrombi may be
treated with papaverine only.

2. Patients with major thrombi with good collateral
vasculature, without peritoneal signs, may be
observed in the hospital without a papaverine
infusion. Patients with peritoneal signs and
documented thrombosis require laparotomy.

References: See page 112.

Intestinal Obstruction

I. Clinical evaluation

A. Intestinal obstruction is characterized by nausea,
vomiting, cramps, and obstipation. Suspected
intestinal obstruction requires immediate surgical
consultation.

B. Small-bowel obstruction. Auscultation may reveal
high-pitched rushes or tinkles that coincide with
episodes of cramping. Pain usually is epigastric or
periumbilical.

1. Proximal obstruction. Frequent non-bilious
vomiting is prominent if the obstruction is
proximal to the ampulla of Vater. Colicky pain
occurs at frequent intervals (2-5 minutes).
Obstipation may not occur until late, and
distention is minimal or absent.

2. Distal obstruction. Vomiting is bilious and less
frequent. The vomiting may be feculent if the
obstruction has been long-standing. Colicky pain
occurs at intervals of 10 minutes or more, and it
is less intense. A dull ache may persist between
cramps. Distention increases gradually.

C. Colonic obstruction

1 . Colonic obstruction is caused by colon cancer in
60-70% of cases, and diverticulitis and volvulus
account for 30%. Obstruction is more common
in the left colon than the right.

2. Milder attacks of pain often occur in the weeks
preceding the acute episode. Colic is perceived
in the lower abdomen or suprapubically, and
obstipation and distention are characteristic.
Nausea is common, and vomiting may occur.

3. Tenderness is usually mild in uncomplicated
colonic obstruction. Rectal exam or
sigmoidoscopy may detect an obstructing lesion.

D. Colonic pseudo-obstruction (Ogilvie's
syndrome) may occur in the elderly, bedridden or
institutionalized individual, often after recent
surgery.

E. Strangulated obstruction is characterized by
constant pain, fever, tachycardia, peritoneal signs,
a tender abdominal mass, and leukocytosis.

F. Laboratory evaluation of intestinal obstruction

1. Hypokalemic alkalosis is the most common
metabolic abnormality resulting from vomiting
and fluid loss. Elevated BUN and creatinine
suggests significant hypovolemia.
Hypochloremic acidosis with increased anion
gap may occur with strangulated obstruction.

2. Leukocyte count frequently is normal in
uncomplicated obstruction; however,
leukocytosis suggests strangulation.

3. Serum amylase may be elevated with bowel
infarction.

G. Radiography

1. Plain films

a. Small-bowel obstruction. Plain radiographs
may demonstrate multiple air-fluid levels
with dilated loops of small intestine, but no
colonic gas. Proximal jejunal obstruction may
not cause dilatation. Distal obstruction is
characterized by a ladder pattern of dilated
loops of bowel.

b. Colonic obstruction. Obstructive lesions
usually are located in the left colon and
rectum and cause distention of the proximal
colon. Dilated colon has a peripheral location
within the abdomen, and haustral markings
are present and valvulae conniventes are
absent.

2. Contrast studies

a. Barium contrast enema. In colonic
obstruction, a single-column contrast study

with a water-soluble contrast enema should
be performed. Contrast enema is
contraindicated in obstruction from acute
diverticulitis or in the presence of toxic
megacolon,
b. Upper Gl series. In acute small bowel
obstruction, plain films are usually sufficient.
An upper Gl series may be useful in partial
small bowel obstruction.
H. Endoscopy

1 . Upper endoscopy is the best test in obstruction
of the gastric outlet or duodenum.

2. Colonoscopy can confirm the diagnosis of
colon obstruction by cancer. Non-strangulated
volvulus can often be reduced endoscopically,
and elective resection can be completed at a
later time.

References: See page 112.

Acute Pancreatitis

Blanding U. Jones, MD and Russell A. Williams, MD

The incidence of acute pancreatitis ranges from 54 to
238 episodes per 1 million per year. Patients with mild
pancreatitis respond well to conservative therapy, but
those with severe pancreatitis may have a progressively
downhill course to respiratory failure, sepsis, and death
(less than 10%).

I. Etiology

A. Alcohol-induced pancreatitis. Consumption of
large quantities of alcohol may cause acute
pancreatitis.

B. Cholelithiasis. Common bile duct or pancreatic
duct obstruction by a stone may cause acute
pancreatitis. (90% of all cases of pancreatitis occur
secondary to alcohol consumption or cholelithiasis).

C. Idiopathic pancreatitis. The cause of pancreatitis
cannot be determined in 10 percent of patients.

D. Hypertriglyceridemia. Elevation of serum
triglycerides (>l,000mg/dL) has been linked with
acute pancreatitis.

E. Pancreatic duct disruption. In younger patients,
a malformation of the pancreatic ducts (eg,
pancreatic divisum) with subsequent obstruction is
often the cause of pancreatitis. In older patients
without an apparent underlying etiology, cancerous
lesions of the ampulla of Vater, pancreas or
duodenum must be ruled out as possible causes of
obstructive pancreatitis.

F. Iatrogenic pancreatitis. Radiocontrast studies of
the hepatobiliary system (eg, cholangiogram,
ERCP) can cause acute pancreatitis in 2-3% of
patients undergoing studies.

G. Trauma. Blunt or penetrating trauma of any kind to
the peri-pancreatic or peri-hepatic regions may
induce acute pancreatitis. Extensive surgical
manipulation can also induce pancreatitis during
laparotomy.

Causes of Acute Pancreatitis

Alcoholism

Infections

Cholelithiasis

Microlithiasis

Drugs

Pancreas divisum

Hypertriglyceridemia

Trauma

Idiopathic causes

Medications Associated with Acute Pancreatitis

Asparaginase (Elspar)

Mercaptopurine

Azathioprine (Imuran)

(Purinethol)

Didanosine (Videx)

Pentamidine

Estrogens

Sulfonamides

Ethacrynic acid

Tetracyclines

(Edecrin)

Thiazide diuretics

Furosemide (Lasix)

Valproic acid

(Depakote)

Pathophysiology. Acute pancreatitis results when an

initiating event causes the extrusion of zymogen

granules, from pancreatic acinar cells, into the

interstitium of the pancreas. Zymogen particles cause

the activation of trypsinogen into trypsin. Trypsin

causes auto-digestion of pancreatic tissues.

. Clinical presentation

A. Signs and symptoms. Pancreatitis usually

presents with mid-epigastric pain that radiates to

the back, associated with nausea and vomiting.

The pain is sudden in onset, progressively

increases in intensity, and becomes constant. The

severity of pain often causes the patient to move
continuously in search of a more comfortable
position.
B. Physical examination

1. Patients with acute pancreatitis often appear
very ill. Findings that suggest severe
pancreatitis include hypotension and
tachypnea with decreased basilar breath
sounds. Flank ecchymoses (Grey Tuner's
Sign) or periumbilical ecchymoses (Cullen's
sign) may be indicative of hemorrhagic
pancreatitis.

2. Abdominal distension and tenderness in the
epigastrium are common. Fever and
tachycardia are often present. Guarding,
rebound tenderness, and hypoactive or absent
bowel sounds indicate peritoneal irritation.
Deep palpation of abdominal organs should be
avoided in the setting of suspected
pancreatitis.

IV. Laboratory testing

A. Leukocytosis. An elevated WBC with a left shift
and elevated hematocrit (indicating
hemoconcentration) and hyperglycemia are
common. Pre-renal azotemia may result from
dehydration. Hypoalbuminemia, hyper-
triglyceridemia, hypocalcemia, hyperbilirubinemia,
and mild elevations of transaminases and alkaline
phosphatase are common.

B. Elevated amylase. An elevated amylase level
often confirms the clinical diagnosis of
pancreatitis.

C. Elevated lipase. Lipase measurements are more
specific for pancreatitis than amylase levels, but
less sensitive. Hyperlipasemia may also occur in
patients with renal failure, perforated ulcer
disease, bowel infarction and bowel obstruction.

D. Abdominal Radiographs may reveal non-specific
findings of pancreatitis, such as "sentinel loops"
(dilated loops of small bowel in the vicinity of the
pancreas), ileus and, pancreatic calcifications.

E. Ultrasonography demonstrates the entire
pancreas in only 20 percent of patients with acute
pancreatitis. Its greatest utility is in evaluation of
patients with possible gallstone disease.

F. Helical high resolution computed tomography
is the imaging modality of choice in acute
pancreatitis. CT findings will be normal in 14-29%
of patients with mild pancreatitis. Pancreatic
necrosis, pseudocysts and abscesses are readily
detected by CT.

Selected Conditions Other Than Pancreatitis

Associated with Amylase Elevation

Carcinoma of the

Acute alcoholism

pancreas

Diabetic ketoacidosis

Common bile duct

Lung cancer

obstruction

Ovarian neoplasm

Post-ERCP

Renal failure

Mesenteric infarction

Ruptured ectopic pregnancy

Pancreatic trauma

Salivary gland infection

Perforated vise us

Macroamylasemia

Renal failure

Prognosis. Ranson's criteria is used to determine
prognosis in acute pancreatitis. Patients with two or
fewer risk factors have a mortality rate of less than 1
percent, those with three or four risk-factors a
mortality rate of 16 percent, five or six risk factors, a
mortality rate of 40 percent, and seven or eight risk
factors, a mortality rate approaching 100 percent.

Ranson's Criteria for Acute Pancreatitis

At admission

During initial 48 hours

1 . Age >55 years

2. WBC>16,000/mm 3

3. Blood glucose >200
mg/dL

4. Serum LDH >350
IU/L

5. AST >250 U/L

1 . Hematocrit drop >1 0%

2. BUN rise >5 mg/dL

3. Arterial p0 2 <60 mm Hg

4. Base deficit >4 mEq/L

5. Serum calcium <8.0 mg/dL

6. Estimated fluid
sequestration >6 L

VI. Treatment of pancreatitis

A. Expectant management. Most cases of acute
pancreatitis will improve within three to seven
days. Management consists of prevention of
complications of severe pancreatitis.

B. NPO and bowel rest. Patients should take
nothing by mouth. Total parenteral nutrition should
be instituted for those patients fasting for more
than five days. A nasogastric tube is warranted if
vomiting or ileus.

C. IV fluid resuscitation. Vigorous intravenous
hydration is necessary. A decrease in urine output
to less than 30 mL per hour is an indication of
inadequate fluid replacement.

D. Pain control. Morphine is discouraged because it
may cause Oddi's sphincter spasm, which may
exacerbate the pancreatitis. Meperidine
(Demerol), 25-100 mg IV/IM q4-6h, is favored.
Ketorolac (Toradol), 60 mg IM/IV, then 15-30 mg
IM/IV q6h, is also used.

E. Antibiotics. Routine use of antibiotics is not
recommended in most cases of acute pancreatitis.
In cases of infectious pancreatitis, treatment with
cefoxitin (1-2 g IV q6h), cefotetan (1-2 g IV q12h),
imipenem (1 .0 gm IV q6h), or ampicillin/sulbactam
(1 .5-3.0 g IV q6h) may be appropriate.

F. Alcohol withdrawal prophylaxis. Alcoholics may
require alcohol withdrawal prophylaxis with
lorazepam (Ativan) 1-2mg IM/IV q4-6h as needed
x 3 days, thiamine 100mg IM/IV qd x 3 days, folic
acid 1 mg IM/IV qd x 3 days, multivitamin qd.

G. Octreotide. Somatostatin is also a potent inhibitor
of pancreatic exocrine secretion. Octreotide is a
somatostatin analogue, which has been effective
in reducing mortality from bile-induced
pancreatitis. Clinical trials, however, have failed to
document a significant reduction in mortality

H. Blood sugar monitoring and insulin
administration. Serum glucose levels should be
monitored.
VII. Complications

A. Chronic pancreatitis

B. Severe hemorrhagic pancreatitis

C. Pancreatic pseudocysts

D. Infectious pancreatitis with development of sepsis
(occurs in up to 5% of all patients with
pancreatitis)

E. Portal vein thrombosis
References: See page 112.

Acute Cholecystitis

Russell A. Williams, MD

Acute cholecystitis is a bacterial inflammation of the
gallbladder which may cause severe peritonitis.
Gallstones are present in the gallbladder in about 95% of
cases. The incidence of acute calculous cholecystitis is
higher in females, with a female-to-male ratio of 3:1 up to
the age of 50 and a ratio of 1 .5:1 thereafter.

I. Pathophysiology. Patients who have symptoms
from gallstones have an elective cholecystectomy to
avoid acute cholecystitis and its complications. Acute
calculous cholecystitis is caused by obstruction of the
cystic duct by a stone. Positive bacterial cultures of
bile or gallbladder wall are found in 50% to 75% of
cases.

II. Clinical evaluation

A. Persistent pain in the area of the gallbladder is
present in almost every case. Frequently, the pain
develops after ingestion of a meal. The pain is
usually in the right upper quadrant, the
epigastrium, or both.

B. The pain often radiates toward the tip of the
scapula. Pain in the right shoulder is present when
the diaphragm is irritated by the inflammation.

C. Nausea and vomiting occur in 60% to 70% of
patients.

III. Physical examination

A. Fever is present in about 80% of patients. The
most common and reliable finding on physical
examination is tenderness in the right upper
quadrant, the epigastrium, or both. About half of
all patients have muscle rigidity in the right upper
quadrant, and about one fourth have rebound
tenderness.

B. Murphy's sign, consisting of inspiratory arrest
during deep palpation of the right upper quadrant,
is not a consistent finding but is almost
pathognomonic when present. A mass in the
region of the gallbladder is palpable in about 40%.

IV. Laboratory evaluation and imaging studies

A. White blood cell count is elevated in 85% of
cases. One half have elevation of the serum
bilirubin, and the serum amylase is increased in
one third.

B. Radionuclide scan (HIDA scan). The specific
test for acute cholecystitis is the HIDA scan.
Normally, the scan outlines the liver and the
extrahepatic biliary tract, including the gallbladder,
and shows the nuclide flowing into the upper small
intestine. In acute cholecystitis, the gallbladder is
not seen on the scan. Radionuclide has a
sensitivity of almost 100% and a specificity of
95%.

C. Ultrasound. Calculi within the gallbladder can be
accurately detected by ultrasonography, but this
test is not specificfor acute calculous cholecystitis.
A thickened gallbladder wall and pericholecystic
fluid are sometimes present.

V. Differential diagnosis. Acute appendicitis,
perforated or penetrating duodenal ulcer, acute or
perforated gastric ulcer, and acute pancreatitis. In
approximately 15% of cases of acute cholecystitis,
the serum amylase is elevated, suggesting the
possibility of acute pancreatitis.

VI. Treatment

A. Patients suspected of having acute cholecystitis
should be hospitalized. Intravenous crystalloids
should be given to restore intravascular volume.
Preoperative management should include
administration of an antibiotic that is effective
against gram-positive and -negative aerobes and
anaerobes. Those present most frequently are
Escherichia coli, Klebsiella species, Streptococcus
faecalis, Clostridium welchii, Proteus species,
Enterobacter species, and anaerobic
Streptococcus species.

B. A second-generation cephalosporin is
recommended for most cases of acute
cholecystitis and reservation of the triple drug
combination for patients who are seriously ill with
sepsis. Antibiotic therapy should be initiated as
soon as the diagnosis is made and should be
continued for 24 hours postoperatively, unless
peritonitis is severe, in which case it should
continue for 7 days.

1. Ampicillin 1-3.0 gm IVq6h OR

2. Ampicillin-sulbactam (Unasyn) 1 .5-3.0 gm IV
q6h AND

3. Gentamicin, 1 .5-2 mg/kg, then 2-5 mg/kg/d IV.

4. Cefoxitin (Mefoxin) 1-2 gm IV q6-8h.

5. Ticarcillin/clavulanate (Timentin) 3.1 g IV q4-
6h.

6. Piperacillin/tazobactam (Zosyn) 4.5 gm IV q6h.

7. Meperidine (Demerol) 50-100 mg IV/IM q4-6h
prn pain.

C. The definitive treatment of acute cholecystitis is
early laparoscopic cholecystectomy. Operative
cholangiography is routinely performed unless the
extent of inflammation makes it unsafe.

Laparoscopic Cholecystectomy
Procedure

I. Advantages of laparoscopic surgery: Usually less
postoperative pain, reduced recovery time; several
small puncture wounds instead of a large surgical
incision, and early return to work.

II. Contraindications to laparoscopic
cholecystectomy: Adhesions, extreme gallbladder
scarring, severe acute inflammation, and bleeding.

III. Technique

A. Preoperative antibiotic therapy with cefoxitin
(Mefoxin) 1-2 gm IV q6h is usually used routinely.
The procedure is performed with the patient under
general or epidural anesthesia.

B. The stomach is decompressed with a nasogastric
tube to facilitate exposure. With the patient in the
supine position, a 2-cm incision is made superior
or inferior to the umbilicus. Using S-shaped
retractors, the fascia is identified and grasped with
a small Kocher or Allis clamp. The fascia is
elevated and incised to allow for easy admission
of a finger to confirm entrance into the abdominal
cavity and sweep away any adhesions. A U-stitch
is placed using an absorbable suture. The Hasson
cannula is inserted and secured with the suture
used for the U-stitch.

C. After setting the insufflator to an insufflation
pressure of 12 mm Hg, C0 2 is instilled at a low
flow (1 L/min) into the abdominal cavity through
the Hasson cannula. Approximately 1 L C0 2 is
instilled at a low flow rate, and then the flow rate is
adjusted to the maximum (20 L/min). The
endoscope is inserted, and the abdominal and
pelvic cavities are inspected.

D. The patient is placed in reverse Trendelenburg
position to allow the colon and omentum to fall

inferiorly. After the pelvis and upper abdomen are
visually inspected, a 10-mm cannula is inserted
two thirds of the way between the umbilicus and
the xiphisternum just to the right of the midline. A
5-mm cannula is inserted 3 cm inferior to the
costal margin in the midclavicular line, and a
second 5-mm cannula is inserted 4 cm inferior to
the costal margin in the midaxillary line. All three
cannulas are inserted using a trocar under direct
endoscopic vision. The umbilical cannula is used
for the endoscope and C02 inflow, and the
epigastric port is used for dissection. Through the
most lateral right subcostal cannula, a grasper
retracts the dome of the gallbladder over the liver
toward the right diaphragm. Through the other
subcostal cannula, a grasper retracts the neck of
the gallbladder laterally and anteriorly.

E. Adhesions are dissected off of the gallbladder, and
dissection is begun at the neck of the gallbladder
and proceeds along the cystic duct. After the cystic
duct and artery have been identified by removal of
the peritoneum overlying these structures, a
titanium clip is placed at the junction of the neck
and cystic duct. A cholangiogram is performed by
partially transecting the cystic duct using scissors.
The cholangiocatheter is inserted into the
cholecystodochotomy, and a cholangiogram is
performed using 30% Renografin.

F. If the cholangiogram is normal, the catheter is
removed and the cystic duct is secured just inferior
to the ductotomy with two titanium clips and
divided. The cystic artery is clipped and divided.
The infundibulum and neck of the gallbladder are
rotated medially or laterally, and the peritoneal
reflection onto the gallbladder is incised using the
hook cautery. The gallbladder is dissected from its
bed, and before the last attachments at the dome
are divided, the gallbladder bed is irrigated and
inspected for bleeding and bile leaks. The stumps
of the cystic duct and artery are inspected for
bleeding and bile leaks.

G. When hemostasis is attained, the remaining
attachments between the gallbladder and the liver
are divided and the gallbladder is positioned just
superior to the liver. The laparoscope and CO,
insufflation tubing are transferred to the epigastric
cannula, and the extraction sack is passed under
direct visualization through the umbilical cannula.
The sack is opened, and the gallbladder placed in
the bag and extracted.

H. The umbilical incision is closed under direct
visualization by tying the U-stitch. The subcostal
cannulas are removed under direct visualization.
The epigastric cannula is positioned over the liver
away from the omentum, CO, insufflation stopped,
and residual CO, allowed to escape from the
abdomen through the cannula. The cannula is
removed, and the incisions are closed with a
subcuticular stitch and sterile strips. Dressings are
placed overthe incisions, and the nasogastric tube
and Foley catheter are removed. The patient may
be discharged after observation. Most patients can
be discharged within a few hours.

Open Cholecystectomy Procedure

A. After induction of anesthesia place a nasogastric
tube to decompress the stomach. The most
commonly used incision is Kocher's right
subcostal. Place incision 4 cm below and parallel
to the costal margin, and extend it from the midline
to the anterior axillary line. Open the anterior
rectus sheath with a knife in the line of the incision.
Divide the rectus muscle with cautery, and open
the peritoneum between forceps.

B. Systematically explore the peritoneal cavity and
note the appearance of the hiatus, stomach,
duodenum, liver, pancreas, intestines, and
kidneys. Palpate the gallbladder from the ampulla
towards the fundus, then palpate the common
duct, noting any dilation or foreign bodies.
Carefully palpate the colon for neoplasms.

C. Grasp the gallbladder with a Rochester-Pean
clamp near the fundus. Hold forceps in one hand,
and introduce the right hand over the right lobe of
the liver, permitting the liver to descend. Divide
any adhesions to the omentum, colon or
duodenum, and place a pack over these
structures. Retract the structures inferiorly with a
broad-bladed Deaver's retractor.

D. Inspect the anatomy of the biliary tree by carefully
dividing the peritoneum covering the anterior
aspect of the cystic duct, and continue dissecting
into the anterior layer of the lesser omentum

overlying the common bile duct. Bluntly dissect
with a dissector (Kitner), exposing Charcot's
triangle bounded by the cystic duct, common bile
duct and inferior border of the liver. The cystic
artery should be seen in this triangle. Carefully
observe the arrangement of the duct system and
arterial supply. Do not divide any structure until the
anatomy has been identified, including the cystic
duct and common bile duct.
Pass a ligature around the cystic duct with a right-
angle clamp, and make a loose knot near the
common duct. Partially divide the cystic duct below
the infundibulum, and place a small polyethylene
catheter attached to a syringe filled with saline into
the cystic duct for 1-2 cm. Tighten the ligature
holding the catheter in position.
Attach a second syringe containing contrast
material to the catheter, and remove all
instruments. Place a sterile sheet, and slowly
inject 10-15 cc of diluted dye into the common
duct. An operative cholangiogram should be
performed to detect stones and evaluate the duct
system.

Palpate the lower end of common bile duct,
pancreas, and the foramen of Winslow. Palpate
the ampulla, checking for stones or tumor. Hold
the forceps on the gallbladder in the left hand, and
clear the cystic artery of soft tissue with a pledget
held in forceps. Follow the artery to the
gallbladder, and clamp it with a right angle clamp.
Divide and ligate the artery close to the edge of
the gallbladder, using clips or 000 silk.
Reaffirm the junction of the cystic duct with the
common bile, then completely divide the exposed
cystic duct, leaving a stump of 5 mm.
Incise the peritoneum anteriorly over the
gallbladder with a scalpel. Elevate the peritoneum
from the gallbladder, and separate the gallbladder
gently with sharp and blunt dissection. Tissue
strands containing vessels should be cauterized
before division.

Inspect the gallbladder bed for bleeding and
cauterize and/or ligate any bleeding areas. Control
any persistent oozing from the bed with a small
pack of hemostatic gauze.
Irrigate the site with saline. If there is excessive
fluid present, place a soft rubber Penrose drain or
closed suction drain in the area of the dissection,
and bring it out through a separate stab wound in
the right upper quadrant. Inspect the operative
field, including the ligatures on the arteries and the
cystic duct. Approximate the peritoneum with
continuous nonabsorbable suture.
Irrigate the wound with saline and approximate the
rectus fascia and fascia of the oblique muscles
with interrupted, nonabsorbable sutures. Irrigate
the subcutaneous space with saline, and close the
skin with staples, or absorbable subcuticular
sutures.

Choledocholithiasis

Choledocholithiasis results when gallstones pass from
the gallbladder through the cystic duct into the common
duct.

I. Clinical evaluation

A. Patients with choledocholithiasis generally present
with jaundice . The patient may have pain or
symptoms from associated biliary colic or acute
cholecystitis.

B. Physical examination. Icterus is typical unless
there is associated acute cholecystitis.
Ultrasonography can demonstrate gallstones in the
gallbladder and in the common bile duct in 20-50%
of patients with choledocholithiasis.

C. The diagnosis depends on demonstrating enlarged
common bile and intrahepatic ducts associated with
abnormal liver function tests.

D. Alkaline phosphatase and bilirubin are usually
elevated.

E. Ultrasound may reveal a dilated common bile duct,
and stones may be seen. Frequently, gallstones in
the lower common bile duct cannot be
demonstrated by ultrasonography because of
overlying bowel gas.

F. Endoscopic retrograde cholangiopan-
creatography (ERCP) or percutaneous trans-
hepatic cholangiography (PTC) are often used to
confirm the diagnosis. Theses tests can opacify the
biliary tree and demonstrate intraductal stones.

II. Management of choledocholithiasis

A. All jaundiced patients and those known to have
many, large, or intrahepatic stones should have

preoperative ERCP to rule out malignancy and

retrieve the stones.

Preoperative ERCP with sphincterotomy should be

performed in all patients who are at high risk of

common bile duct stones or in whom common bile

duct stones have been demonstrated.

Laparoscopic cholecystectomy may be completed

later.

If ERCP is unsuccessful at clearing the common

bile duct, the patient may require a laparoscopic or

open cholecystectomy.

Disorders of the Breast

John A. Butler, MD

Breast Cancer Screening and
Diagnosis

Breast cancer is the second most commonly diagnosed
cancer among women, after skin cancer. Approximately
182,800 new cases of invasive breast cancer are
diagnosed in the United States per year. The incidence
of breast cancer increases with age. White women are
more likely to develop breast cancer than black women.
The incidence of breast cancer in white women is about
113 cases per 100,000 women and in black women, 100
cases per 100,000.

I. Risk Factors

Risk Factors for Breast Cancer

Age greater than 50 years

Age greater than 30 at

Prior history of breast

first birth

cancer

Obesity

Family history

High socioeconomic

Early menarche, before

status

age 12

Atypical hyperplasia on

Late menopause, after

biopsy

age 50

Ionizing radiation

Nulliparity

exposure

A. Family history is highly significant in a first-degree
relative (ie, mother, sister, daughter), especially if
the cancer has been diagnosed premenopausally.
Women who have premenopausal first-degree
relatives with breast cancer have a three- to
fourfold increased risk of breast cancer. Having
several second-degree relatives with breast cancer
may further increase the risk of breast cancer. Most
women with breast cancer have no identifiable risk
factors.

B. Approximately 8 percent of all cases of breast
cancer are hereditary. About one-half of these
cases are attributed to mutations in the BRCA1 and
BRCA2 genes. Hereditary breast cancer commonly
occurs in premenopausal women. Screening tests
are available that detect BRCA mutations.

II. Diagnosis and evaluation

A. Clinical evaluation of a breast mass should
assess duration of the lesion, associated pain,
relationship to the menstrual cycle or exogenous
hormone use, and change in size since discovery.
The presence of nipple discharge and its character
(bloody or tea-colored, unilateral or bilateral,
spontaneous or expressed) should be assessed.

B. Menstrual history. The date of last menstrual
period, age of menarche, age of menopause or
surgical removal of the ovaries, previous
pregnancies should be determined.

C. History of previous breast biopsies, cyst
aspiration, dates and results of previous
mammograms should be determined.

D. Family history should document breast cancer in
relatives and the age at which family members
were diagnosed.

III. Physical examination

A. The breasts should be inspected for asymmetry,
deformity, skin retraction, erythema, peau d'orange
(breast edema), and nipple retraction,
discoloration, or inversion.

B. Palpation

1 . The breasts should be palpated while the patient
is sitting and then supine with the ipsilateral arm
extended. The entire breast should be palpated
systematically. The mass should be evaluated
for size, shape, texture, tenderness, fixation to
skin or chest wall.

2. A mass that is suspicious for breast cancer is
usually solitary, discrete and hard. In some
instances, it is fixed to the skin or the muscle. A
suspicious mass is usually unilateral and
nontender. Sometimes, an area of thickening
may represent cancer. Breast cancer is rarely
bilateral. The nipples should be expressed for
discharge.

3. The axillae should be palpated for adenopathy,
with an assessment of size of the lymph nodes,
number, and fixation.

IV. Mammography. Screening mammograms are
recommended every year for asymptomatic women
40 years and older. Unfortunately, only 60 percent of
cancers are diagnosed at a local stage.

Screening for Breast Cancer in Women

Age

American Cancer Society
guidelines

20 to 39 years

Clinical breast examination every

three years

Monthly self-examination of breasts

Age 40 years
and older

Annual mammogram

Annual clinical breast examination

Monthly self-examination of breasts

V. Methods of breast biopsy

A. Palpable masses. Fine-needle aspiration biopsy
(FNAB) has a sensitivity ranging from 90-98%.
Nondiagnostic aspirates require surgical biopsy.

1. The skin is prepped with alcohol and the lesion
is immobilized with the nonoperating hand. A 10
mL syringe, with a 14 gauge needle, is
introduced in to the central portion of the mass
at a 90° angle. When the needle enters the
mass, suction is applied by retracting the
plunger, and the needle is advanced. The
needle is directed into different areas of the
mass while maintaining suction on the syringe.

2. Suction is slowly released before the needle is
withdrawn from the mass. The contents of the
needle are placed onto glass slides for
pathologic examination.

3. Excisional biopsy is done when needle biopsies
are negative but the mass is clinically suspected
of malignancy.

B. Stereotactic core needle biopsy. Using a
computer-driven stereotactic unit, the lesion is
localized in three dimensions, and an automated
biopsy needle obtains samples. The sensitivity and
specificity of this technique are 95-100% and 94-
98%, respectively.

C. Nonpalpable lesions

1. Needle localized biopsy

a. Under mammographic guidance, a needle
and hookwire are placed into the breast
parenchyma adjacent to the lesion. The
patient is taken to the operating room along
with mammograms for an excisional breast
biopsy.

b. The skin and underlying tissues are infiltrated
with 1% lidocaine with epinephrine. For
lesions located within 5 cm of the nipple, a
periareolar incision may be used or use a
curved incision located over the mass and
parallel to the areola. Incise the skin and
subcutaneous fat, then palpate the lesion and
excise the mass.

c. After removal of the specimen, a specimen x-
ray is performed to confirm that the lesion
has been removed. The specimen can then
be sent fresh for pathologic analysis.

d. Close the subcutaneous tissues with a 4-0
chromic catgut suture, and close the skin with
4-0 subcuticular suture.

D. Ultrasonography. Screening is useful to
differentiate between solid and cystic breast
masses when a palpable mass is not well seen on
a mammogram. Ultrasonography is especially
helpful in young women with dense breast tissue
when a palpable mass is not visualized on a
mammogram. Ultrasonography is not used for
routine screening because microcalcifications are
not visualized and the yield of carcinomas is
negligible.

References: See page 112.

Breast Cysts

I. Clinical evaluation

A. A breast cyst is palpable as a smooth, mobile, well-
defined mass. If the cyst is tense, the texture may
be very firm, resembling a cancer. Aspiration will
determine whether the lesion is solid or cystic.
Breast cyst fluid may vary from straw-colored to
dark green. Cytology is not routinely necessary.
The cyst should be aspirated completely.

B. If a mass remains after drainage or if the fluid is
bloody, excisional biopsy is indicated. If no pal-
pable mass is felt after drainage, the patient should
be reexamined in 3-4 weeks to determine whether
the cyst recurs. Recurrent cysts can be re-
aspirated. Repeated recurrence of the cyst requires
an open biopsy to exclude intracystic tumor.

C. Nonpalpable cysts. If the cyst wall is seen clearly

seen on ultrasound and there is no interior debris
or intracystic tumor, these simple cysts do not need
to be aspirated. Any irregularity of the cyst wall or
debris within the cyst requires a needle localized
biopsy.

Fibroadenomas

I. Clinical evaluation

A. Fibroadenomasfrequently present in young women
as firm, smooth, lobulated masses that are highly
mobile. They have a benign appearance on
mammography and are solid by ultrasound.

B. A tissue diagnosis can be obtained by fine needle
aspiration biopsy or excisional biopsy.

II. Management of fibroadenomas

A. Fibroadenomas may be followed conservatively
after the diagnosis has been made. If the mass
grows, it should be excised.

B. Large fibroadenomas (>2.5 cm) should usually be
excised. Often fibroadenomas will grow in the
presence of hormonal stimulation, such as
pregnancy.

References: See page 112.

Breast Cancer

The initial management of the breast cancer patient
consists of assigning a clinical stage based on
examination. The stage may be altered once the final
pathology of the tumor has been determined. Staging of
breast cancer is based on the TNM staging system.

I. Preoperative staging in stage I and II breast
cancer. Preoperative workup should include a CBC,
SMA18, and chest x-ray. If elevated alkaline
phosphatase or hypercalcemia is present, a bone
scan should be completed. Abnormal liver function
tests should be investigated with a CT scan of the
liver.

American Joint Committee on Cancer TNM

staging for breast cancer

Stage

Description

Tumor

TX

Primary tumor not assessable

TO

No evidence of primary tumor

Tis

Carcinoma in situ

T1

Tumor <2 cm in greatest dimension

T1a

Tumor <0.5 cm in greatest dimension

T1b

Tumor >0.5 cm but not > 1 cm

T1c

Tumor >1 cm but not >2 cm

T2

Tumor >2 cm but <5 cm in greatest

T3

dimension

T4

Tumor >5 cm in greatest dimension
Tumor of any size with direct extension into

T4a

the chest wall or skin

Extension to chest wall (ribs, intercostal

T4b

muscles, or serratus anterior)

T4c

Peau d'orange, ulceration, or satellite skin

T4d

nodules

T4a plus b

Inflammatory breast cancer

Regional lym

)h nodes

NX

Regional lymph nodes not assessable

NO

No regional lymph node involvement

N1

Metastasis to movable ipsilaterai axillary

N2

lymph nodes

N3

Metastases to ipsilaterai axillary lymph

nodes fixed to one another or to other

structures

Metastases to ipsilaterai internal mammary

lymph nodes

Distant metas

tases

MX

Non-accessible presence of distant

MO

metastases

M1

No distant metastases

Existent distant metastases (including

ipsilaterai supraclavicular nodes)

American Joint Committee on Cancer
classification for breast cancer based on TNM
criteria

Stage

Tumor

Nodes

Metastase
s

Tis

NO

MO

1

T1

NO

MO

MA

TO, 1
T2

N1
NO

MO
MO

MB

T2
T3

N1
NO

MO
MO

IMA

TO, 1, 2
T3

N2
N1,2

MO
MO

1MB

T4
AnyT

Any N
N3

MO
MO

IV

AnyT

Any N

M1

II. Surgical options for stage I and II breast cancer

A. Breast conservation therapy (BCT) has been
shown to result in survival and local recurrence
rates equivalent to modified radical mastectomy;
therefore, breast conservation is the preferred
therapy for stage I and II breast cancer. The
technique includes lumpectomy, axillary lymph
node dissection, and breast irradiation.

1. Contraindications to BCT

a. Contraindications to radiotherapy (ie, prior
breast irradiation, ongoing pregnancy)

b. Steroid-dependent collagen vascular disease

c. Tumor-breast ratio that would result in an
unacceptable cosmetic result (eg, a large
tumor in a small breast)

d. Diffuse, malignant microcalcifications on
mammography

e. Tumor greater than 5 cm in diameter

2. Lumpectomy technique. Incisions should be
curvilinear and parallel with the nipple. A gross
margin of 1 cm should be removed. The
lumpectomy specimen is given immediately to
the pathologist for inking and for an assessment
of the gross margins. Subcutaneous tissue is
closed, and the skin is approximated with a
subcuticular suture.

3. Follow-up following BCT consists of a physical
examination every 3-4 months for the first 3
years, every 6 months for the next 2-3 years,
then yearly. A SMA18 and CBC are done at
each visit and a chest x-ray is done yearly.

4. A posttreatment mammography of the treated
side is done 6 months after the completion of
radiotherapy, then every 6 months for the first 2
years, followed by annual mammograms. Yearly
mammography should be performed on the
opposite breast.

B. Modified radical mastectomy consists of a total
mastectomy and an axillary node dissection. In
staging axillary lymphadenectomy, levels I and II
are removed routinely. Reconstruction of the breast
should be offered to all patients undergoing
mastectomy. Physical examination schedule and
blood work are the same as for lumpectomy. The
chest wall should be examined for of recurrence.
Mammography of the opposite breast should con-
tinue yearly.

III. Locally advanced breast cancer (LABC) consists of
T3 NO (stage MB), MIA, and 1MB breast cancer. All
LABC patients should undergo staging with CBC,
SMA18, bone scan, and CT scan of chest and
abdomen.

A. Noninflammatory LABC. Multimodality therapy
consists of neoadjuvant chemotherapy (ie, given
before surgery), modified radical mastectomy,
radiotherapy to the chest wall, axilla and
supraclavicular nodes, and further chemotherapy.

B. Inflammatory LABC (T4d). Inflammatory breast
cancer is characterized by erythema of the skin,
skin edema, warmth, tenderness, and an under-
lying tumor mass. Treatment requires aggressive
multi-modality therapy.

C. Follow-up. Patients should be followed closely
because they are at higher risk of local and distant
recurrence.

IV.Ductal carcinoma in situ (DCIS) consist of Tis, stage
lesions. These lesions consists of malignant ductal

cells that have not penetrated the basement
membrane. DCIS is a precursor of invasive ductal
cancer.

A. Physical examination is usually normal with
DCIS. The most common presentation is
suspicious microcalcifications on mammography.
DCIS can cause a nipple discharge or a palpable
mass.

B. Surgical therapy

1. BCT. Lumpectomy and adjuvant radiotherapy
are an alternative to mastectomy in well-
localized DCIS when negative microscopic
margins can be obtained.

2. Total mastectomy, including removal of the
nipple areolar complex and breast tissue,
results in survival rates of 98-99%. An axillary
dissection is not done routinely because the
chance of nodal involvement is only 1-2%.

References: See page 112.

Urologic Disorders

C. Garo Gholdoian, MD
David A. Chamberlin, MD

Prostate Cancer

The average age at diagnosis of prostate cancer is 73
years. The prevalence of prostate cancer is 30% in men
over the age of 50. One in six men will be diagnosed with
prostate cancer during their lifetimes. Prostate cancer is
the most common cancer in men except for skin cancer.

I. Clinical evaluation

A. Prostate cancer is usually asymptomatic at
presentation, and it is usually detected by
abnormalities on rectal examination or a high
serum prostate specific antigen (PSA)
concentration.

B. Prostate cancer can cause urinary urgency,
nocturia, frequency, and hesitancy; these
symptoms are more likely to be caused benign
prostatic hypertrophy (BPH) than cancer. The new
onset of erectile dysfunction raises the suspicion of
prostate cancer.

C. Serum PSA elevation. A total serum PSA
concentration >4.0 ng/mL is considered abnormal,
and is suspicious for prostate cancer. An elevated
serum PSA between 4 to 10 ng/mL has a positive
predictive value (PPV) of 21 percent, and a PSA
above 10 ng/mL has a positive predictive value of
64 percent. Causes of an elevated PSA include
benign prostatic hyperplasia, prostate cancer,
prostatitis, and perineal trauma.

D. Abnormal prostate examination. The PPV of an
abnormal digital rectal examination for prostate
cancer is 5 to 30 percent. All men with induration,
asymmetry, or palpable nodularity of the prostate
gland require further diagnostic studies to rule out
prostate cancer. A serum PSA should be obtained
prior to biopsy.

II. Screening for prostate cancer

A. Age is the most important risk factor for prostate
cancer. Prostate cancer rarely occurs before the
age of 45, but the incidence rises rapidly thereafter.
Prostate cancer is more common in black men.

B. Recommendations for screening. The American
Cancer Society recommends that serum prostate
specific antigen testing and digital rectal
examination should be offered annually to men 50
years of age and older who have a life expectancy
of 10 years. Screening should begin at age 45 in
patients at high-risk for prostate cancer (eg, African
Americans and men with two or more first-degree
relatives with prostate cancer). PSA testing is also
recommended for men who ask their clinicians to
make the decision about screening on their behalf.
The American Urological Association also supports
this policy.

C. If the serum PSA concentration is abnormal
(>4.0 ng/mL), the test should be repeated in four
weeks for confirmation. The most common
explanation for an elevated serum PSA value is
BPH. A man who has a high serum PSA
concentration should be treated with an antibiotic
(trimethoprim-sulfamethoxazole ([Bactrim] 1 DS
tablet bid for 3 weeks) because prostatitis is a
common cause of a high PSA. The PSA
concentration should be repeated in 4 weeks. A
return of the PSA to normal is expected if prostatitis
was solely responsible.

D. Prostate biopsy is the gold standard for prostate
cancer diagnosis. Transrectal biopsy is a simple
office technique that requires no analgesia. In a
standard ultrasound-guided biopsy, a specimen is
removed with a biopsy gun from any suspicious
areas (eg, by rectal examination or biopsy) followed
by six to ten tissue cores from the base, midzone,
and apical areas of the right and left lobes of the
gland (sextant biopsies).

III. Diagnostic and staging evaluation of prostate
cancer

A. The tumor-node-metastasis (TNM) system is the
most popular method of staging prostate cancer.
Men are usually assigned a clinical stage, or "c"
stage, and a pathological stage, or "p" stage. The
"c" stage is determined by the digital rectal
examination, while the "p" stage is determined after
a pathologist has evaluated a radical prostatectomy
specimen.

IV. Staging of prostate cancer

Staging of Prostate Cancer by 2002 AJCC

Staging System

Clinical tumor (cT)

Substage

stage

Stage cT1

T1a

Tumor incidental

Clinically inapparent

histologic finding in

tumor neither

five percent or less of

palpable nor visible

tissue resected

by imaging

T1b

Tumor incidental
histologic finding in
more than five percent
of tissue resected

T1c

Tumor identified by
needle biopsy (eg,
because of elevated
PSA)

Stage cT2

T2a

Tumor involves one-

Tumor confined

half of one lobe or less

within the prostate

T2b

Tumor involves more
than one-half of one
lobe but not both
lobes

T2c

Tumor involving both
lobes

Stage cT3

T3a

Extracapsular
extension (Unilateral
or bilateral)

T3b

Tumor invades the
seminal vesicle(s)

Stage cT4

Tumor is fixed or invades adjacent structures other than

seminal vesicles: bladder neck,

external sphincter,

rectum, levator muscles, and/o

pelvic wall.

Stage Grouping for Prostate Cancer, 2002 AJCC
Criteria

Stage I

T1a

NO

M0

G1"

Stage II

T1a

NO

M0

G2, 3-4

NO

M0

AnyG

NO

M0

AnyG

NO

M0

AnyG

NO

M0

AnyG

Stage
III

T3

NO

M0

AnyG

Stage
IV

T4

NO

M0

AnyG

AnyT

N1

M0

AnyG

AnyT

Any N

M1

AnyG

"Grade: tumor grade is assessed as follows:

Grade 1: Well differentiated (slight anaplasia), Gleason

score 2-4

Grade 2: Moderately differentiated (moderate anaplasia)

Gleason score 5-6

Grade 3-4: Poorly differentiated/undifferentiated (marked

anaplasia) Gleason score 7-10

Tumor histology (Gleason score). Analysis of
the tumor histology provides an index of prognosis
and may guide local therapy. Gleason score of
one represents the most well-differentiated
appearance, and Gleason score ten represents
the most poorly differentiated.
Clinical staging

1. Serum PSA. This value is not used for staging,
but may help to predict the local extent of
disease in men with prostate cancer. There is
a higher likelihood of finding organ-confined
disease when the serum PSA concentration is
less than 4.0 ng/mL. A serum PSA
concentration of 4.1 to 10.0 ng/mL increases
the likelihood of finding an organ-confined
tumor larger than 0.5 mL, but also increases
the odds of finding extracapsular extension by
5.1-fold. A serum PSA concentration higher
than 10.0 ng/mL increases the likelihood of
finding extraprostatic extension by 24 to 50-
fold.

2. Radionuclide bone scan. A positive
radionuclide bone scan indicates extraprostatic
spread and eliminates the potential for curative
surgery. Bone scan need not be performed in
a patient with clinical stage T1 or T2 cancer on
physical examination, a Gleason score of six or
less, and a serum PSA value less than 10

ng/mL

3. CT scan should be considered in men who are
going to be treated with external beam
radiation therapy, and in men who have a PSA
>10 to 15 ng/mL or a Gleason score greater
than six. These men have an increased
likelihood of pelvic lymph node metastasis.

4. Endorectal coil magnetic resonance
imaging (MRI) of the prostate gland utilizing an
endorectal probe can determine the likelihood
of either seminal vesicle involvement or
extracapsular extension in patients who are
thought to have clinically localized prostate
cancer. The likelihood of cure with either
radiation therapy or radical prostatectomy is
low in these locally advanced patients, and
surgery is usually not recommended.

V. Treatment for early prostate cancer (organ-
confined)

A. The three standard therapies for men with early
stage (organ-confined) prostate cancer are radical
prostatectomy (RP), radiotherapy (RT), and
watchful waiting. Hormone therapy is reserved for
patients with locally advanced or metastatic
prostate cancer.

B. Radical prostatectomy

1. RP involves excising the entire prostate from
the urethra and bladder, which are then
reconnected. This treatment offers the best
chance of long-term survival. The retropubic
approach to RP permits pelvic lymph node
sampling prior to prostate removal to confirm
the presence or absence of metastases. The
prostate is removed if the lymph nodes are free
of disease.

2. Fifteen-year progression-free survival rates
have been reported to be 80 to 85 percent for
men with organ-confined disease.

3. Complications

a. Incontinence. About 1.6 percent report no
urinary control, 7 percent report frequent
leakage, and 42 percent report occasional
leakage.

b. Impotence. The potency rate after surgery is
100 percent in men in their 40s, 55 percent
for men in their 50s, 43 percent for men in
their 60s, and percent for men in their 70s.

4. Perineal prostatectomy can be considered for
men with lower grade and low volume tumors,
such as those with Gleason score <6 and a
serum PSA less than 10 ng/mL. The likelihood
of extraprostatic disease is less than 5 percent
in such patients, making pelvic lymph node
dissection unnecessary.

C. Radiation therapy

1. Radiation therapy (RT) does not require
hospitalization and normal activity can usually
be maintained during the course of treatment.
Cure rates with RT appear to be comparable to
those with RP for clinically localized disease for
the first five years. Late recurrences following
RT ten years or more after treatment occur
more frequently than with RP.

D. Watchful waiting

1 . Watchful waiting describes patients who forego
treatment. Such patients are followed with
serum PSA measurements and digital rectal
examination every three months for the first
year, and then less frequently. Definitive or
palliative therapy is initiated if a significant
change in the serum PSA concentration or
DRE occurs.

2. Men with early stage disease (TO to T2, NX,
MO) were followed for ten years, and only 9
percent died of prostate cancer. The survival
rate of this "watched" group was similar to the
survival rate of the treated group.

E. Recommendations

1 . Early stage (organ-confined) prostate cancer is
a curable disease in the majority of men.
Surgery and radiation therapy offer equivalent
survival outcomes for the first ten years after
therapy; beyond that time, there is a higher risk
of recurrence with radiation. Younger men
should undergo surgery because of the
potential for late recurrence with radiation
therapy. Older men may prefer radiation
therapy.

2. Watchful waiting is not a good option for men
with high-risk tumors (eg, Gleason score 7 or
higher) unlessthey have significant comorbidity
that suggests a markedly reduced life
expectancy. The ideal candidate for watchful
waiting is over the age of 70 to 75 with a life
expectancy of 10 to 15 years or less who has a

low grade tumor (eg, Gleason score 2 to 4).
F. Endocrine therapy of advanced prostate
carcinoma. Treatment of stage IV prostate cancer
involves surgical or medical castration. Total
blockade with leuprolide (Lupron) plus flutamide
(Eulexin) is slightly better than leuprolide alone.
Orchiectomy is an outpatient procedure that is the
safest and least expensive option. The incidence
of impotence with orchiectomy is no different than
with medical castration therapies.
References: See page 112.

Renal Colic

Approximately 5% of the U.S. population will pass a
urinary tract stone during their lifetime.

I. Pathophysiology

A. Calcium-containing stones are the most common
(70%).

B. Magnesium-ammonium-phosphate stones, also
known as struvite stones, are almost always
associated with urinary tract infection with urea-
splitting bacteria, such as Proteus mirabilis.

C. Uric acid stones are less common and are
radiolucent, making diagnosis by plain films alone
difficult.

D. Cystine stones are rare and associated with
cystinuria, a rare autosomal recessive hereditary
disorder.

II. Clinical evaluation

A. Renal colic is characterized as severe colicky pain
that is intermittent and usually in the flank or lower
abdomen. Patients usually cannot find a
"comfortable position," and the pain often radiates
to the testes or groin. A history of previous stones,
poor fluid intake, urinary tract infections, or
hematuria is common.

B. Obstruction located at the ureteropelvic junction
causes pure flank pain, while upper ureteral ob-
struction causes flank pain that radiates to the
groin. Midureteral stones cause lower abdominal
pain and may mimic appendicitis or diverticulitis,
but without localized point tenderness or guarding.
Lower ureteral stones may cause irritative voiding
symptoms and scrotal or labial pain.

C. Patients with nephrolithiasis generally complain of
nausea and vomiting. They commonly have gross
or microscopic hematuria, fever, and an increased
white blood cell count may. Prior episodes of renal
colic or a family history of renal stones is often
reported.

D. Physical examination

1. Generally the patient is agitated, diaphoretic,
and unable to find a comfortable position.

2. Hypertension and tachycardia are common.

3. Costovertebral angle tenderness is the classic
physical finding; however, minimal abdominal
tenderness without guarding, rebound or rigidity
may be present. Right or left lower quadrant
tenderness or an enlarged kidney may
sometimes be noted.

III. Differential diagnosis. Appendicitis, salpingitis,
diverticulitis, pyelonephritis, ovarian torsion, prostatitis,
ectopic pregnancy, bowel obstruction, carcinoma.

IV. Laboratory evaluation

A. A urinalysis with microscopic, serum electrolytes,
BUN, creatinine, complete blood count, and urine
culture should be obtained. An elevated white
blood cell count may be noted. A significant
number of white cells in the urine also suggests
infection.

B. A plain abdominal film may demonstrate a
calcification along the course of the urinary tract.
Ninety percent of all calculi are radiopaque.
Calcifications are frequently obscured by overlying
bowel gas.

C. Intravenous pyelogram. IVP is the gold standard
for the diagnosis of urolithiasis, and it allows rapid
assessment of the degree of obstruction, location
of the stone and any renal function impairment.
Acute ureteral obstruction may appear as a dense
nephrogram with a delay in excretion of contrast.

D. Ultrasound may be useful in patients with renal
failure or an intravenous contrast allergy.

V. Management of renal calculi

A. Most renal calculi will pass spontaneously, and
only expectant management with hydration and
analgesia is necessary. Obstruction associated
with fever indicates urinary tract infection, and it
requires prompt drainage with either a ureteral
stent or percutaneous nephrostomy.

B. Indications for admission

1. High fever, uncontrollable pain

2. Intractable nausea and vomiting with an inability
to tolerate oral fluids

3. Solitary kidney

C. Inpatient management

1 . Vigorous intravenous hydration and intravenous
antibiotics are important when infection is
suspected. Parenteral narcotics are often
necessary.

2. Ketorolac (Toradol), 60 mg IM/IV, then 15-30
mg IM/IV q6h, is effective and provides a good
alternative to narcotics.

3. Strain all urine in an attempt to retrieve
spontaneously passed stones for X-ray crystal-
lographic analysis.

4. Stones measuring 5 to 10 mm have a
decreased likelihood of passage, and early
elective intervention should be considered

5. Extracorporeal shock-wave lithotripsy (ESWL)
is the most common procedure for small renal
or ureteral stones. Eighty percent of patients
become stone-free after one treatment.

6. Ureteroscopy with laser, ultrasound or
electrohydraulic lithotripsy may be used as well.
Open surgical stone removal is rarely
necessary.

D. Outpatient management

1. Most patients with renal colic do not require
admission. The majority of stones measuring
less than 4 mm will pass spontaneously (90-
95%), and 80% of these will pass within 4
weeks.

2. Patients should increase intake of oral fluids,
take narcotic pain medication, and strain all
urine. Plain abdominal films may be used to
assess movement of the stone.

E. Follow-up care

1. After the stone has passed, a metabolic
evaluation is important because 70% of patients
will have repeat stones if not diagnosed.

2. Evaluation may include chemistry screening,
calcium, uric acid, phosphorous, urine cystine
(nitroprusside test), 24 hour urine collection for
uric acid, calcium, creatinine.

References: See page 112.

Urologic Emergencies

I. Acute urinary retention

A. Acute urinary retention is characterized by a
sudden inability to void. It often presents with
suprapubic pain and severe urgency. There is
usually a history of preexisting obstructive voiding
symptoms related to bladder outlet obstruction or
poor detrusor function.

B. Benign prostatic hyperplasia is the most
common cause of acute urinary retention in men
over the age of 50.

1. Patients present with progressively worsening
voiding difficulties, resulting in bladder
overdistention and subsequent urinary
retention.

2. Prostate size on digital rectal examination has
no bearing on the degree of outlet obstruction
because minimal enlargement of the prostate
can cause significant obstruction.

C. Prostate cancer accounts for 25% of patients with
acute urinary retention. Ten percent of patients
with prostate cancer initially present with bladder
outlet obstruction.

D. Additional causes of acute urinary retention
include urethral strictures, bladder neck
contractures, bladder stones, and acute bacterial
prostatitis. Acute urinary retention may be caused
by prolonged obstruction, diabetes mellitus,
neurologic disorders (spinal cord injury, herniated
vertebral disk), and medications.

E. Urinary retention after surgery sometimes
temporarily develops in elderly men. Preexisting
bladder dysfunction or outlet obstruction is usually
present.

F. Anticholinergic medications (antihistamines,
antidiarrheals, antispasmodics, tricyclic
antidepressants) can suppress bladder function.
Sympathomimetic drugs (decongestants and diet
pills) that cause contraction of the bladder neck
can precipitate an increase in outlet resistance.

G. Complications of acute urinary retention include
postobstructive diuresis, bladder mucosal
hemorrhage, hypotension, sepsis, renal failure,
and autonomic bladder hyporeflexia

H. Clinical evaluation of acute urinary retention
1 . Retention is characterized by an inability to void
and suprapubic discomfort. A progressive
history of difficulty voiding and irritative voiding

symptoms, such as frequency, nocturia or
urgency is often noted.

2. Some patients are incontinent as a result of
extreme overdistention of the bladder. A past
history of gonorrhea, trauma, underlying dis-
eases, or medications should be sought.

3. Palpate for a distended bladder and assess size
and consistency of the prostate. Tenderness of
the prostate on rectal examination suggests
acute prostatitis; a diffusely hard or nodular
prostate suggests carcinoma.

4. The penis should be examined to rule out
phimosis, paraphimosis, or meatal stenosis. A
neurologic exam should include anal sphincter
reflex and perineal sensation.

5. Laboratory evaluation. Serum electrolytes,
blood urea nitrogen (BUN), creatinine,
urinalysis, and urine culture.

I. Management of acute urinary retention

1. The entire bladder contents should be drained
with a Foley catheter. Adequate volume
replacement is necessary to prevent
hypotension.

2. Lubrication with 2% lidocaine jelly (injected
directly into the urethra with a syringe) will
facilitate insertion of a urethral catheter.
Medium-sized catheters (#18 to #22 French)
should be used because they tend to be stiffer
and easier to insert than smaller ones.

3. In patients with large prostates, Coude'
catheters (which have a curved tip) may be
helpful. The curve of the Coude' catheter should
be directed superiorly. Other methods of
drainage include urethral sounds, filiforms with
followers, and percutaneous suprapubic tubes.

4. Admission to the hospital is not required for
most patients with acute urinary retention
unless infection or renal failure are present.
Most patients can be managed with a Foley
catheter and discharged home with oral
antibiotics and a leg urine bag.

. Testicular torsion

A. Testicular torsion is an emergency. Delay in
treatment may result in testicular loss. A four- to
six-hour delay may impair normal testicular
function. Torsion can occur at any age; however, it
is most common in adolescents, peaking at the
age of 15 to 16 years.

B. Testicular torsion presents with sudden onset of
pain and swelling in one testicle, occasionally
associated with minor trauma. Nausea, vomiting,
and lower abdominal or flank pain are common. A
history of previous similar episodes with
spontaneous resolution is common.

C. A urinalysis is essential in differentiating testicular
torsion from epididymitis; however, a negative
urinalysis does not rule out epididymitis.

D. Differential diagnosis of testicular torsion

1 . Epididymitis due to Neisseria gonorrhoeae and
Chlamydia trachomatis is much more common
than torsion in adult men.

2. Torsion of an appendix testis or appendix
epididymis may mimic testicular torsion . Torsion
of the appendix testis may manifest as a tender,
pea-sized nodule at the upper pole of the
testicle with a small blue-black dot seen through
the scrotal skin (the blue dot sign). Management
is conservative; however, if there is diagnostic
uncertainty, surgical exploration is required.

3. Other less common conditions that may present
similarly to torsion include acute hemorrhage
into a testicular neoplasm, orchitis, testicular
abscess, incarcerated hernia, and testicular
rupture.

E. Physical examination

1. Testicular torsion usually presents with severe
unilateral testicular pain with an acute onset.
The pain is associated with an extremely tender
testicle with a transverse lie or an anterior
epididymis that lies high in the scrotum.

2. With testicular torsion, the testis is usually high
in the scrotum (Brunzel's sign). The presence of
a cremasteric reflex almost always rules out
testicular torsion.

3. Relief of pain by elevation of the affected testis
(Prehn's sign) suggests epididymitis. A negative
Prehn's sign suggests testicular torsion.

F. Diagnostic imaging. Diagnostic testing should not
delay surgical exploration in acute torsion. If the
diagnosis is unclear, diagnostic tests may be
useful. Color Doppler ultrasound is the most
valuable diagnostic study, with nearly a 100%
sensitivity and specificity.

G. Management of testicular torsion

1. Immediate detorsion is imperative for all cases

of testicular torsion. Testicular salvage rates
decrease to 50% at 10 hours and to 10-20% at
24 hours.

2. Manual detorsion can be attempted as an ur-
gent measure by rotating the testicle medially
about its pedicle. Surgical orchiopexy is still
required.

3. If an infarcted testicle is noted during surgical
exploration, it should be removed. If the testicle
is viable, both testicles should be fixed in the
scrotum with nonabsorbable sutures.

III. Priapism

A. Priapism is defined as a prolonged penile erection.
Most cases of priapism in adults are idiopathic. In
children the most common causes are sickle cell
anemia, hematologic neoplasms (leukemia), and
trauma.

B. Evaluation of priapism

1 . Patients usually complain of a persistent, painful
erection. They may have fever and voiding
difficulties.

2. Physical examination should include a
neurologic evaluation and perineal inspection
for neoplasms. Examination of the penis usually
reveals a flaccid glans despite a rigid corpora
cavernosa. Hematologic studies should be
performed to rule out sickle cell anemia and
leukemia.

C. Treatment of priapism

1. Early treatment reduces the risk of long-term
impotence, which may occur in 50%. Discomfort
can be reduced with parenteral narcotic
analgesics and sedation. Detumescence may
be achieved using cold compresses, ice packs,
warm- or cold-water enemas, and prostate
massage.

2. If these treatments are unsuccessful, the static
blood may be aspirated from the corpora using
a large bore needle. Followed by irrigation of
the corpora with saline containing a
vasoconstricting agent (phenylephrine,
epinephrine, or metaraminol).

3. If this process fails to achieve detumescence, a
shunt may be created between the affected
corpora cavernosa and unaffected corpus
spongiosum with a Tru-Cut biopsy needle.
When priapism is secondary to sickle cell
anemia, therapy also includes hydration,
oxygen, and blood transfusion.

References: See page 112.

Vascular and Orthopedic
Surgery

Peripheral Arterial Occlusive
Disease

Peripheral arterial occlusive disease affects about 18
percent of persons over 70 years of age. The disease
presents with intermittent claudication with pain in the
calf, thigh or buttock, which is elicited by exertion and
relieved with a few minutes of rest. In most cases, the
underlying etiology is atherosclerotic disease of the
arteries.

I. Pathophysiology

A. The incidence of claudication rises sharply between
ages 50 and 75 years, particularly in persons with
coronary artery disease. This condition affects at
least 10% of persons over 70 years of age and 2%
of those 37-69 years of age.

B. Risk factors. Cigarette smoking is the most
important risk factor for PAOD. Seventy to 90% of
patients with arterial insufficiency are smokers.
Other risk factors include hyperlipidemia, diabetes
mellitus, and hypertension.

C. After five years, 4% of patients with claudication
lose a limb and 16% have worsening claudication
or limb-threatening ischemia. The five-year
mortality rate for patients with claudication is 29%;
60% of deaths result from coronary artery disease,
15% from cerebrovascular disease, and the
remainder result from nonatherosclerotic causes.

II. Clinical evaluation of claudication
A. Claudication

1. The key clinical features of claudication are
reproducibility of muscular pain in the thigh or
calf aftera given level of activity and cessation of
pain after a period of rest.

2. Patients should be asked about the intensity of
claudication, its location, and the distance they
have to walk before it begins. The degree of
functional impairment should be assessed.

3. Aortoiliac disease is manifest by discomfort in
the buttock and/or thigh and may result in
impotence and reduced femoral pulses.
Leriche's syndrome occurs when impotence is
associated with bilateral hip or thigh
claudication.

4. Iliofemoral occlusive disease is characterized
by thigh and calf claudication. Pulses are
diminished from the groin to the foot.

5. Femoropopliteal disease usually causes calf
pain. Patients have normal groin pulses but
diminished pulses distally.

6. Tibial vessel occlusive disease may lead to
foot claudication, rest pain, non-healing wounds,
and gangrene.

7. Rest pain consists of severe pain in the distal
portion of foot due to ischemic neuritis. The pain
is deep and unremitting, and it is exacerbated by
elevation of the foot and is relieved by dangling
the foot over the side of the bed.

III. Physical examination

A. Evaluation of the peripheral pulses should
include the femoral, popliteal, posterior tibial, and
dorsalis pedis arteries. Pallor on elevation of the
extremity and rubor when the limb is dependent is
common.

B. Other signs of chronic arterial insufficiency include
brittle nails, scaling skin, hair loss on the foot and
lower leg, cold feet, cyanosis, and muscle atrophy.
The feet should be inspected for skin breakdown or
ulceration.

C. Bruits may be auscultated distal to the arterial
obstruction. Abdominal examination for a "pulsatile
mass" should be performed because of the
association between abdominal aortic aneurysm
and peripheral arterial disease.

D. Ankle-brachial index is an effective screening tool.
The ankle-brachial index is calculated by dividing
the ankle pressure by the brachial systolic
pressure.

1 . The normal ABI is above 1 .0, since the pressure
is higher in the ankle than in the arm.

2. An ABI below 0.9 has a 95 percent sensitivity for
detecting angiogram-positive peripheral vascular
disease.

3. An ABI of 0.40 to 0.90 suggests a degree of
arterial obstruction often associated with
claudication.

4. An ABI below0.4 represents advanced ischemia

5. In patients with an abnormal ankle-brachial
index, testing with segmental arterial pressures
and a pulse volume recording before and after
exercising to the point of absolute claudication
are indicated.

Ankle-Brachial Index Interpretation

Normal

>1

Abnormal

<0.95

Intermittent
claudication

0.4-0.9

Severe
disease/ischemia

less than 0.4

E. Segmental arterial pressures. The proximal lower
extremity pressures should be equal to or greater
than the upper extremity pressures, and the drop in
Doppler pressure between segments no greater
than 20 mm Hg. These studies help predict the
location and severity of the disease.

F. Arteriography or magnetic resonance
angiography is required to delineate the extent of
the disease when intervention is anticipated.

IV. Management

A. Risk factor modification

1. The goals of risk factor modification in patients
with PAOD are the same as those in patients
with coronary artery disease. Hypertension
should be controlled. Beta-blockers do not
usually worsen claudication.

2. Lipid abnormalities must be treated. The
target LDL cholesterol level is less than 100 mg
per dL in patients with symptomatic vascular
disease.

3. Tobacco is directly toxic to the vascular
endothelium and worsens atherosclerosis. All
patients must abstain from tobacco use.

B. Antiplatelet agents

1. Aspirin should be considered for use in any
patient with coronary artery disease,
cerebrovascular disease or PAOD.

2. Clopidogrel (Plavix), 75 mg qd, or ticlopidine
(Ticlid), 250 mg bid with meals, should be
considered in patients who are intolerant of
aspirin therapy. Clopidogrel and ticlopidine are
platelet inhibitors; however, clopidogrel has a
lower risk of neutropenia.

C. Exercise. Walking improves the symptoms of
claudication. Patients should walk at least three
times per week for at least 30 minutes at each
session. Near-maximal claudication pain (absolute
claudication distance) should be the resting point,
and the patient should follow the program for at
least six months.

D. Medication

1. Cilostazol (Pletal), 100 mg bid, is a
phosphodiesterase inhibitor that suppresses
platelet aggregation and acts as a direct arterial
vasodilator. Cilostazol results in a 35 percent
increase in the distance before claudication and
a 41 percent increase in absolute claudication
distance.

2. Pentoxifylline (Trental), 400 mg tid with meals,
provides small improvements in the initial
claudication distance and absolute claudication
distance.

E. Operative and endovascular procedures

1. Most patients with claudication respond to
conservative therapy. Surgery is reserved for
patients with rest pain or tissue loss. Patients
who have intermittent calf claudication alone are
not surgical candidates unless the claudication
severely limits their lifestyle or occupational
functioning.

2. Patients with rest pain, tissue loss as a result of
gangrene, or non-healing ulcers with an ABI less
than 0.6 are surgical candidates.

3. Percutaneous transluminal angioplasty hasa
greater than 90% success rate in the treatment
of short-segment aortoiliac occlusive disease,
and these results may be improved with the
placement of an intra-arterial stent. However,
five-year patency rates are only 40-60%.

4. Surgical bypass therapy is an effective
treatment for claudication; however, it is
associated with 5% morbidity and mortality rates.
Aortobifemoral grafting has a 90% 5-year
patency rate. Aortoiliac, femoral-femoral
crossover, and reversed and in-situ saphenous

vein bypass grafting from the common femoral to

the popliteal artery have 60-70% 5-year patency

rates. A synthetic polytetrafluoroethylene graft

(PTFE) is indicated for above knee

femoral-popliteal bypass, and it has a 50% 5-

year patency rate.

5. Axillofemoral bypass is useful for high risk,

elderly patients who are unable to tolerate an

aortic procedure.

Management of the acutely threatened limb. An

acutely occluded artery can cause limb loss within

hours. The patient will complain of sudden onset of

severe unrelenting rest pain. Atrial fibrillation often

may cause acute embolic arterial occlusion. These

patients require emergency surgical evaluation and

immediate heparinization.

Abdominal Aortic Aneurysms

S.E. Wilson, MD

Abdominal aortic aneurysms (AAAs) are the most
common type of arterial aneurysm. Approximately 5% of
people older than 60 years develop an abdominal aortic
aneurysm, and the male-female ratio is 3:1. Other risk
factors include smoking, hypertension, and a family
history of an aneurysm. Abdominal aortic aneurysms are
caused atherosclerosis in 90% of patients; 5% of
aneurysms are inflammatory.

I. Clinical evaluation

A. Abdominal aortic aneurysms are usually
asymptomatic. Aneurysm expansion or rupture
may cause severe back, flank, or abdominal pain
and shock. Distal embolization, thrombosis, and
duodenal or ureteral compression can produce
symptoms.

B. Physical examination. Almost all AAAs greater
than 5 cm are palpable as a pulsatile mass at or
above the umbilicus. Abdominal aortic aneurysms
range from 3 to 15 cm in diameter.

II. Laboratory evaluation. Complete blood count,
electrolytes and creatinine, blood urea nitrogen,
coagulation studies, blood type and cross-matching,
and urinalysis should be obtained.

III. Radiologic evaluation

A. Abdominal cross-table lateral films allow for
estimation of aneurysm diameter.

B. Ultrasonography and computed tomographic
(CT) scanning demonstrate AAAs with an
accuracy of 95% and 100%, respectively.

IV. Elective management of abdominal aortic
aneurysms

A. Small aneurysms can be followed using ultrasound
or CT scan every 6 months.

B. Indications for repair include symptomatic
aneurysms of any size, aneurysms exceeding 5.0
cm, those increasing in diameter by more than 0.5
cm per year, and saccular aneurysms.

C. Preoperative management includes optimizing
cardiopulmonary function and placement of a
pulmonary artery catheter or a central venous line.
An arterial line permits continuous BP and blood
gas monitoring. Two peripheral venous catheters
should be placed.

D. Operative management. The aneurysm is
approached through a midline abdominal incision
and exposed by incising the retroperitoneum.

E. The duodenum and left renal vein are dissected off
the aorta. After heparinization, the aorta is cross-
clamped first distal and then proximal to the
aneurysm. Aortotomy is then made and extended
longitudinally to the aneurysm "neck," where the
aorta is either transected or cut in a T fashion. The
aneurysm is opened, thrombus is removed, and
bleeding lumbar arteries are suture ligated. Using
a tube or bifurcation graft, the proximal
anastomosis is performed to nonaneurysmal aorta.
The distal anastomosis is completed at the aortic
bifurcation (tube graft) or at the iliac or femoral
arteries (bifurcation graft).

F. Endovascular treatment of AAA uses a catheter
to place a stent-graft. Early results suggest an 83%
success rate and less than 6% mortality.

References: See page 112.

Orthopedic Fractures and
Dislocations

Harry Skinner, MD
Michelle Schultz, MD

I. Clinical evaluation of the injured limb

A. Physical examination of the injured limb. 1)

Inspection, 2) Palpation, and 3) Movement.
Examine the bone for instability and examine the
soft tissue for associated injury. Document
neurologic and vascular status.

B. Clinical features of fractures

1 .Pain and tenderness. All fractures cause pain in

the neurologically intact limb.
2. Loss of function. Pain and loss of structural

integrity of the limb cause loss of function.
3. Deformity. Change in length, angulation, rotation

and displacement.
4. Attitude. The position of the fractured limb is

sometimes diagnostic. The patient with a

fractured clavicle usually supports the limb and

rotates his head to the affected side.
5.Abnormal mobility and crepitus: These signs

should not be sought deliberately because pain

and injury may result.

C. Clinical features of dislocations

1 .A dislocation occurs when the articular surfaces
of a joint are no longer in contact. Subluxation
(partial dislocation) is a less severe condition that
occurs when the orientation of the surfaces is
altered but they remain in contact.

2.Pain and tenderness. Severe pain may be
completely relieved when the joint is relocated.

3. Loss of motion. Both active and passive motion
are limited in dislocations.

4. Loss of normal joint contour. In the anteriorly
dislocated shoulder, the deltoid is flattened and
the greater tuberosity of the humerus is no longer
lateral to the acromion.

5. Attitude. The patient carefully holds the anteriorly
dislocated shoulder in abduction and external
rotation.

6. Neurologic injury. The incidence of neurologic
injuries is much higherwith dislocations than with
fractures. Shoulder dislocations are often
associated with axillary nerve injury. Posterior
dislocations of the hip can result in sciatic nerve
contusion. Careful examination for neurologic
status is indicated before any intervention.

II. Clinical description of fractures

A. Anatomic location
I.What bone is fractured?

2. Where on the bone is the fractured?

a. Metaphyseal - at the flare of the bone.

b. Diaphyseal - fracture through the diaphysis
(proximal, middle, or distal third of shaft).

c. Epiphyseal - fracture at the end of the bone.
3.Salter classification of fractures (children):

a. Type I. Fracture through physis, between the
epiphysis and metaphysis.

b. Type II. Fracture through physis, involving the
metaphysis.

c. Type III. Fracture through physis, involving the
epiphysis.

d. Type IV. Fracture through physis, involving the
metaphysis and epiphysis.

e. Type V. Crush injury to physis, between the
epiphysis and metaphysis.

B. Bony deformity: Describe any change in bone
length, angulation, rotation, or displacement.

C. Direction of the fracture line. Describe the
radiographic direction of the fracture.

1 .Transverse - perpendicular to the long axis of the

bone
2. Oblique -fracture is at an angle to the bone.
3. Spiral - occurring secondary to torsional stress.

D. Comminution: Fracture with more than two
fragments.

E. Open vs. Closed: In an open fracture the bone
protrudes through the skin.

F. Greenstick Fracture: one cortex is broken while
the other remains intact

III. Radiological evaluation of fractures. A minimum of
two views at right angles to each other should be
obtained. Visualize the joint above and below the
injury and check for soft tissue swelling. Views of the
uninjured extremity are often useful for comparison in
children.
IV. Management of fractures
A. Fracture reduction

I.The fracture must be restored to a normal

anatomical position
2. Muscle spasm should be relieved with traction,

analgesics, and muscle relaxants.
3. Bones must be in apposition, properly aligned in

linear and rotatory directions, and set to proper

length.
4. Fractures should must be held in place with a

splint or cast.

B. Indications for operative treatment

1 .Failure of closed methods to reduce or maintain

reduction of the fracture.
2. Displaced intraarticular fractures, where the

fragments are sufficiently large to allow internal

fixation.
3. Multiple injuries - in a multiple trauma patient,

operative treatment can allow early mobilization.

Early mobilization can sometimes avoid the

morbidity and mortality associated with prolonged

recumbency.

C. Upper extremity fractures and dislocations

1. Distal radius fracture is often associated with
fracture of the ulnar styloid. Treatment consists of
closed reduction, casting and elevation of the
extremity until swelling subsides. After reduction,
check alignment with an x-ray, and rule out
median nerve injury.

2.Forearm shaft fracture: In adults, radius and
ulna shaft fractures require open reduction and
internal fixation.

3. Humerus fracture: X-ray the entire bone and
check for radial nerve injury (wrist drop).
Humerus fractures are usually treated with a
collar and cuff sling or coaptation splint

4. Clavicle fractures. Subclavian artery and
brachial plexus injury may occur. The fracture
should be splinted with a figure of eight bandage
or sling. Clavicle fracture rarely requires surgery.

5.Anterior shoulder dislocation occurs when the
humeral head has been forced anterior to the
glenoid. It is usually caused by extension force
applied to abducted arm. The patient presents
with the arm in slight abduction, and he cannot
bring his elbow to the side. There is a slightly
depressed deltoid prominence and arm motion
causes pain. Axillary nerve injury may occur,
causing a sensory deficit over the deltoid.
Treatment consists of reduction with gentle
traction.

6.Posterior shoulder dislocation occurs when the
humeral head has been forced posterior to the
glenoid. Dislocation may occur secondary to
seizures or electrocution. The arm is held in
adduction with internal rotation. Treatment
consists of reduction with gentle traction.

D. Lower extremity fractures and dislocations

1. Femoral neck fractures: Osteoporotic bone
predisposes to this intracapsular fracture. Internal
fixation or endoprosthesis (artificial hip) are
required.

2. Intertrochanteric fractures usually occur in the
elderly after a fall. The fracture is located outside
the joint capsule. Treatment consists of internal
fixation.

3.Femoral shaft fracture: Early intramedullary
nailing is recommended in adults. This fracture is
rarely associated with a fat embolism syndrome.

4.Patella fracture: If the bone is nondisplaced, it
can be treated in a cast. If it is displaced more
than 2 mm, it should be treated with internal
fixation. Quadriceps function should be checked.

5.Tibial shaft fracture can be treated closed or
with internal fixation.

6.Ankle fracture: Evaluate the stability of the ankle
fracture by examining the joint space between the
talus and tibial plafond. Unstable injuries require
internal fixation.

E. Knee injuries

LKnee ligament testing

a. Varus/valgus femur stress test. The
examiner stabilizes the femur, and pressure is
exerted outward or inward at the ankle; a tear
of the collateral ligament is indicated by
excess mobility.

b. Anterior drawer test. Pull tibia anteriorly with
the knee flexed 90 degrees to test for tear of
anterior cruciate ligament.

c. Posterior drawer test. Push tibia posteriorly
with the knee flexed 90 degrees to test for tear
of the posterior cruciate ligament.

2. The most common ligamentous injuries are
tearing of the medial collateral ligament by a blow
from the lateral side of the knee, and tear of the
anterior cruciate ligament by twisting on a planted
foot. Brace immobilization is usually sufficient for
medial collateral ligament tears.

3. Dislocation of the knee often results in multiple
ligament injury. Popliteal artery trauma should be

excluded. Immobilization of the knee, followed by
ligament reconstruction should be completed.

Ankle Sprains

A sprain is the most common ankle injury. Injury may
range from minor ligamentous damage to complete tear
or avulsion. Sprain occurs when stress is applied while
the ankle is in an unstable position, causing the
ligaments to overstretch. Stresses usually occur during
running or walking over uneven surfaces.

I. Clinical evaluation

A. Ligaments of the lateral ankle consist of the anterior
talofibular ligament, calcaneofibular ligament, and
posterior talofibular ligament.

B. Sprains may be classified as first-degree, involving
stretching of ligamentous fibers, second-degree,
involving a tear of some portion of the ligament with
associated pain and swelling, and third-degree,
implying complete ligamentous separation.

C. An inversion injury is the most common type of
sprain, causing damage to the lateral ligaments.

II. Physical examination

A. The examiner's fingertips should be used to check
the anterior capsule and medial and lateral
ligaments.

B. Anterior draw sign suggests significant injury. The
sign is elicited by grasping the distal tibia in one
hand and the calcaneus and heel in the other and
sliding the entire foot forward. This is done both
with the ankle in neutral position and with 30°" of
plantar flexion. With disruption of the anterior or
lateral ligaments, 4 mm or more of anterior shift will
occur.

C. Passive inversion of the ankle may produce pain.
Swelling occurs anterior to the lateral malleolus at
the onset; ecchymoses are common. The talus tilts
if the calcaneus is adducted.

III. Radiographic evaluation

A. X-rays are useful in cases of moderate to severe
injury, helping to identify any associated skeletal
injury in addition to assessing degree of
ligamentous damage.

B. A stress view is obtained (with local anesthesia, if
necessary) to check for talar tilt. A tilt of more than
15° is suggestive of lateral ligament injury; more
than 25°' of tilt is diagnostic.

IV. Management of ankle sprains

A. Grade I sprains are defined as stretch of the
ligaments without disruption. Grade I sprains should
be treated with rest, ice, compression with an
elastic bandage, elevation, and weight bearing as
tolerated.

B. Grade II sprains consist of partial tears of the ankle
ligaments. Grade II sprains should be treated with
rest, ice, compression with an elastic bandage, and
elevation. A splint can be applied for a few days,
followed by early range of motion.

C. Grade III sprains consist of a complete tear of the
ligaments. Treatment of grade III strains consists of
rest, ice, compression with an elastic bandage, and
elevation. A splint or cast can be applied for a short
period of time, followed by early range of motion.