Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_639_Библиотеки_им_академика_М_И_Перельмана.pdf
22 Part I Introduction
4 weeks) has an increased risk of VTE.
106
Preventive measures
include external pneumatic leg compression, early mobilization after surgery, and anticoagulation. Compression devices
are contraindicated in patients with severe peripheral vascular
disease, venous stasis, or risk of tissue necrosis. Inferior vena
cava (IVC) lters are indicated in patients who cannot take
anticoagulation or who have failed anticoagulation therapy.
Patients with a history of VTE benet from IVC lter placement in the short term, but IVC lter placement is accompanied by an increased incidence of deep venous throm-
107
bosis over the long term.
Systemic anticoagulation is the
preferred long-term option. LMWH and UFH are equally
eective for prevention of pulmonary embolism in patients
107
with deep venous thrombosis.
Recent VTE, atrial brillation, and mechanical heart valves are common indications for
warfarin treatment.
Clinically, UFH activity is measured by PTT and the therapeutic goal is usually 2.0–2.5 times normal. LMWH is a relatively stronger inhibitor of factor Xa and does not have the
same eect on the PTT. e anticoagulant eect of LMWH
is measured by factor Xa activity. Protamine can reverse the
eects of heparin, but may cause allergic reactions and induce
hypercoagulability, and should be used cautiously. FFP will
not reverse heparin, and can actually increase heparin activity
because it contains antithrombin III. Direct thrombin inhibitors can also prolong the PTT. Direct thrombin inhibitors are
not reversible with protamine and may require large amounts
of FFP for reversal.
Heparin can be used for the prevention and treatment of
VTE. Surgical patients over age 40 or those at increased risk for
VTE should receive 5,000 U SC every 8–12 hours, depending on their weight. High-risk patients with a history of VTE,
cancer, morbid obesity, or those having orthopedic procedures
should either receive SC heparin with a goal of high range of
normal or LMWH. In the event of acute VTE intravenous
heparin should be started promptly with a therapeutic goal
of PTT 1.5–2.0 times normal. Oral anticoagulation should
be started within 24 hours and continued for 3–6 months.
106
Heparin-induced thrombocytopenia (HIT) is a potentially
lethal complication of heparin therapy. HIT is caused by an
IgG mediated hypersensitivity reaction between the heparin moiety and platelet factor 4 (PF4). Patients with previous heparin exposure, such as orthopedic and cardiac surgical
patients, are at greatest risk. e incidence of HIT is 0.5–5.0%
in patients receiving UFH. HIT occurs with UFH or low
molecular weight heparin; the risk is highest with UFH.
Platelet counts usually drop 40–50% from baseline.
rombosis can be venous or arterial leading to deep vein
thrombosis, extremity ischemia, and mesenteric ischemia of
stroke. Digital ischemia and skin necrosis can also be seen.
HIT remains a clinical syndrome which can be diagnosed by
a decrease in platelet count <405 of baseline in 4–14 days of
heparin administration once other causes of thrombocytopenia have been ruled out. e diagnosis can be supported by
the ELISA assay for antiplatelet antibodies.
Because HIT can be life-threatening, heparin should be
stopped as soon as HIT is suspected, and treatment with an
alternative anticoagulant, such as the thrombin inhibitor
bivalrudin, should be started immediately. Platelets should
return to baseline after therapy is initiated. If thrombosis is
present, patients should be anticoagulated for 6 months with
Coumadin. Coumadin should not be started until platelet
counts have recovered.
Warfarin inhibits synthesis of vitamin K–dependent clotting factors (II, VII, IX, X, and proteins C and S). Poor diet,
prolonged antibiotic use, and fat malabsorption can also
cause vitamin K deciency and cause abnormal coagulation.
Liver disease can lead to multiple coagulation abnormalities
including factor deciencies, vitamin K deciency, brinolysis, and elevated levels of brin degradation products. All
patients with known or suspected liver disease should be
tested for coagulopathy. Vitamin K can be administered
subcutaneously or intravenously in decient patients. e
initiation of warfarin therapy is associated with a transient
thrombotic state because plasma concentrations of protein C
fall approximately 24 hours before concentrations of other
clotting factors.
Heparin is the drug of choice for VTE during pregnancy
because it does not cross the placenta. Adverse eects of heparin therapy may include hemorrhage, thrombocytopenia, and
osteoporosis. HIT is an immune disorder seen in patients
with prior exposure to heparin, which may cause thrombosis. Treatment includes cessation of heparin and utilization
of alternative anticoagulants such as lepirudin, danaparoid,
or argatroban. ese should be given until platelet counts
recover.
For patients on long-term anticoagulation therapy, the
INR should be 1.5 or lower before elective surgery. After warfarin is discontinued, it takes about 4 days for an INR in the
range of 2.0–3.0 to spontaneously reach 1.5, and about 3
days for the INR to reach 2.0 after it is restarted. If therapy
is withheld preoperatively, most patients will have a window
of 2–4 days when they are not anticoagulated and at risk for
venous thrombosis. is risk is compounded by the increased
108,109
risk of thromboembolism associated with surgery.
It
has been estimated that surgery increases the risk of VTE by
110
100-fold in patients with recurrent disease.
Without anticoagulation, there is a 50% chance of recurrence within the
3 months after the rst episode of venous thrombosis. Warfarin therapy reduces the risk to 10% after 1 month and 5%
after 3 months. It is not advisable to interrupt anticoagulation within 1 month after an event of VTE, and if possible,
surgery should be deferred until the patient has completed
110
3 months of therapy.
Chronic anticoagulation lowers the
risk of thromboembolism in patients with atrial brillation
and mechanical heart valves by 66% and 75%, respectively.
110
Patients with prior embolic episodes are at increased risk
for recurrence. Six percent of episodes of VTE and 20% of
110
arterial thromboembolism may be fatal,
and a signicant
percentage cause disability. Alternatively, the risk of death
111
after postoperative hemorrhage is less than 1%,
so the judicious use of postoperative anticoagulation can be relatively
protective. Preoperative heparinization is not required during the second and third months of warfarin treatment for
Chapter 2 Preoperative and Postoperative Management 23
deep vein thrombosis (DVT) because the risk is su ciently
low. Such patients have increased VTE risk after surgery and
should receive postoperative anticoagulation. Patients who
are at risk for recurrent DVT, and are within 2 weeks of the
rst episode, or who cannot tolerate anticoagulation are can-
107
didates for an IVC lter.
Elective surgery should be deferred for the rst month after
arterial embolism because of the high risk of recurrence during
this period. If necessary, patients should receive perioperative
heparin while oral anticoagulation is held. Patients on longterm anticoagulation to prevent arterial thromboembolism do
not need perioperative heparin because the risk of bleeding
outweighs the risk of arterial embolism during this period.
Heparin should be titrated to a goal PTT of 1.5–2.0 times
normal and given as a continuous intravenous infusion. It
should be stopped 6 hours prior to a procedure, and can be
restarted 12 hours after surgery if there was no evidence of
bleeding at the end of the case. Heparin can be restarted with-
110,
111
out a bolus at the anticipated maintenance infusion rate.
INFECTIOUS COMPLICATIONS
Infectious complications can be most unwelcome and dif cult to control after major abdominal surgery, yet they
are surprisingly frequent despite all modern prophylactic
measures. Reported surgical wound infection rates in elective operations vary from 2% for inguinal hernia repair
113
to 26% for colectomy,
114
surgery.
Surgical site infections (SSIs) increase overall mor-
and are even higher for emergency
tality and morbidity, and increase hospital length of stay and
overall costs. erefore prevention and treatment of infectious complications should be included in surgical decision
making for all abdominal procedures.
Prevention of SSIs begins with preoperative evaluation
and identi cation of patients at high risk for SSI. Patient factors implicated in risk of SSI include age, diabetes mellitus,
smoking, steroid use, malnutrition, obesity, active distant
infection, prolonged hospital stay, and nasal colonization
115–118
with Staphylococcus aureus .
Standard basic surgical rules should be followed with
every patient. ese were codi ed as formal guidelines by
the Centers for Disease Control and Prevention (CDC) in
119
and include recommendations for skin preparation
1999
with alcohol or iodophor, surgical barriers such as drapes and
gowns, careful hand scrubbing, and appropriate selection of
prophylactic antibiotics. Preoperative hair removal and antiseptic shower have not been shown to decrease SSI rates, and
shaving and clipping of hair can increase SSIs. e CDC recommendations are summarized in Table 2-7 . (See Table 2-3
for extended recommendations.)
Antibiotic prophylaxis may be indicated for patients at high
risk, or in contaminated surgical procedures, but antibiotics
should not be used indiscriminately. Overuse of antibiotics is
associated with emergence of multidrug-resistant bacteria and
increased rates of hospital-acquired infections. Selection of
patients for antimicrobial prophylaxis requires strati cation of
112
TABLE 2-7: CDC CATEGORY 1
RECOMMENDATIONS FOR REDUCTION OF
SURGICAL SITE INFECTIONS
ese are strongly recommended based on best clinical evidence:
Identify and treat distant infections prior to surgery
Do not remove hair routinely; if hair must be removed, use electric
clippers immediately prior to surgery
Control hyperglycemia in the perioperative period
Cease tobacco smoking 30 days prior to surgery
Antiseptic shower the night prior to surgery
Antiseptic skin preparation
Surgery team should practice hand scrubs
Administer appropriate antimicrobial prophylaxis
Surgical barriers (gown, gloves, hat, mask)
Do not close contaminated skin incisions
patient risk factors as discussed above and procedure-speci c
risk factors. e degree of contamination in the surgical site
has long been recognized as an independent risk factor for
120
leading to the wound classi cation system ( Table 2-8 )
SSI,
in use since 1983.
Patients undergoing class I (clean) procedures have a very
low infection rate and generally do not bene t from prophylactic antibiotics, unless there is some suspicion at the start
of the procedure that some contamination may occur, such
as unplanned enterotomy in a patient with many previous
abdominal procedures. In addition, many surgeons prefer
to use antibiotic prophylaxis in class I procedures when a
prosthesis is implanted; examples include hernia repair and
vascular bypass. In this setting, the risk of SSI is low, but
the morbidity and mortality of an infected prosthesis are
great, and prophylaxis may decrease the risk. To date, large
prospective trials have not shown bene t of antibiotic pro-
121,
122
phylaxis in preventing prosthetic infections,
trials have suggested a decrease in site infection without
TABLE 2-8: SURGICAL WOUND
CLASSIFICATION
Class I. Clean
Uninfected wounds without contamination
Class II. Clean/contaminated
Uninfected wounds in procedures where the respiratory,
gastrointestinal, or genitourinary tracts are entered in a controlled
fashion without gross spillage
Class III. Contaminated
An operation with major breaks in sterile technique, gross spillage,
or incisions into in amed but not suppurating infections; fresh
accidental wounds
Class IV. Dirty/infected
Wounds with necrotic or devitalized infected tissue
but smaller
24 Part I Introduction
change in implant infection rate.
123,124
erefore, there is no
strict guideline for the use of systemic antibiotics for implant
surgery, and the surgeon must tailor the use of antibiotics to
the individual patient’s risk.
Patients with class II (clean/contaminated) surgical
wounds do benet from systemic antibiotic prophylaxis.
e most studied example of this class of wound is elective
colon resection. Most current guidelines recommend systemic broad-spectrum antibiotic coverage using a secondgeneration cephalosporin plus metronidazole if the parenteral
route is used, and neomycin plus metronidazole or erythromycin base (both as nonabsorbable antibiotics), if the oral
125
route is used.
Published evidence supports administration
of antibiotics preoperatively in order to achieve maximum
therapeutic levels at the time of incision, and repeat dosing to
maintain therapeutic levels during a long procedure. ere is
no documented study showing benet to additional doses of
antibiotics after the procedure is over and the skin is closed,
and prolonged use of prophylactic antibiotics contributes to
emergence of resistant bacteria.
126,127
Patients with class III (contaminated) wounds are a mixed
population. Some of these wounds are the result of inadvertent
entry into a contaminated eld, some result from traumatic
injury, and some are planned operations for débridement of
infected tissue. In the latter case, antibiotic therapy is indicated for specic therapy rather than prophylaxis. In the case
of penetrating traumatic injury to the colon, there is strong
evidence to support single-dose antibiotic prophylaxis at the
time of laparotomy, similar to elective colon resection.
128,129
Surgical judgment must be individualized in these cases as to
whether the risk of skin closure can be justied due to the high
rate of wound infection despite antibiotic prophylaxis.
Patients with class IV (dirty) wounds are generally undergoing débridement of already infected and necrotic tissue, and
should be receiving antibiotic therapy targeted to the relevant
organisms. Skin wound closure is generally not advised in
these patients.
e wound classication system does not take into account
patient risk factors or site-specic risk factors. Various physiologic scoring systems including the Acute Physiology Score
and the Acute Physiology, Age, and Chronic Health Evaluation
index have been used to predict perioperative infection risk
with some success. In an eort to provide more accurate risk
stratication, the CDC’s National Nosocomial Infection Surveillance project has developed a risk index that accounts for
patient risk factors such as malnutrition and chronic medical
conditions, and operative factors including duration and site
130
of procedure.
Enlightened risk assessment of perioperative
infections should be included in the discussion for informed
surgical consent.
NUTRITIONAL EVALUATION
e importance of proper nutritional assessment and management cannot be overstressed. In surgical patients, malnutrition increases risk for major morbidity,
131,132
including wound
infection, sepsis, pneumonia, delayed wound healing, and
anastomotic complications. Careful preoperative clinical assessment can identify those patients at increased nutritional risk.
e assessment should include a thorough history and physical
examination with attention paid to usual weight, recent weight
loss, changes in eating and bowel habits, changes in abdominal girth, loss of muscle bulk, and the presence of diseases that
carry a risk of malnutrition such as COPD, diabetes mellitus,
inammatory bowel disease, and psychiatric conditions such as
bulimia and anorexia nervosa. e history and physical examination should identify those patients with nutritional risk; that
risk can be stratied by calculation of the Nutritional Risk
Index (NRI). e NRI is a simple calculation (15.19 × serum
albumin (g/dL)+ 41.7 × present weight/usual weight), which
has been shown in prospective studies to correlate with increased
rates of mortality and complications from major abdominal sur-
133,134
gery.
NRI less than 83 indicates a signicantly increased
rate of mortality and complications, especially wound dehiscence and infection. Severely malnourished patients have been
shown to benet from preoperative nutritional support.
Malnutrition can be classied into protein deciency
(kwashiorkor), calorie deciency (marasmus), or mixed protein calorie deciency. In order to complete the nutritional
assessment and to guide nutritional support, it is useful to
classify the patient’s specic nutritional state (Table 2-9).
Malnutrition states are much more common than is generally
acknowledged, with 30–55% of hospital inpatients meeting
criteria for one of the diagnoses.
Some interval of decient nutritional intake is expected
137
after an abdominal operation. In uncomplicated cases, this is
usually the result of postoperative adynamic ileus and resolves
promptly, in less than 7 days. Traditional surgical management includes provision of dextrose-containing intravenous
uids. e goal of this therapy is not to provide sucient
calories for complete nutritional support, but simply to
provide enough carbohydrate to prevent breakdown of lean
body mass. Certain organs, including the heart and brain,
have an obligate requirement for carbohydrate as a primary
energy source, and do not store energy in the form of fat or
glycogen. If intake is insucient to meet this requirement,
the body breaks down hepatic glycogen to provide glucose
to the circulation, and ultimately the brain and heart. Once
hepatic glycogen stores have been depleted (after about 1 day
of no intake), lean muscle mass is converted to glucose via
gluconeogenesis to produce carbohydrate. Provision of only
100 g of exogenous glucose per day is sucient to prevent
breakdown of lean muscle mass in otherwise healthy subjects.
In already malnourished patients, or in patients who do
not return to normal bowel function promptly, nutritional
support is indicated. As in the preoperative setting, a thorough evaluation of the patient’s nutritional status is necessary, as is the identication of the cause of bowel dysfunction. In the postoperative setting, there are many potential
causes of bowel dysfunction (Table 2-10), and nutritional
support should be individualized for each patient’s needs.
Some patients may respond to enteral support and some may
require parenteral support. Whenever available, the enteral
135,136
Chapter 2 Preoperative and Postoperative Management 25
TABLE 2-9: ASSESSMENT OF NUTRITIONAL
STATUS
Protein De ciency Criteria
Albumin <2.2 g/dL
Total lymphocyte count 800/mm
Weight maintained
Peripheral edema
Inadequate protein intake (<50% of goal for 3 days or <75% for 7
days)
Four criteria out of these ve establish the diagnosis of protein
de ciency
Calorie De ciency Criteria
Weight loss: 5% over 1 month or 7.5% over 3 months or 10% over
6 months
Underweight: less then 94% ideal body weight (IBW)
Clinically measurable muscle wasting
Serum protein maintained
Inadequate calorie intake (50% for 3 days or <75% for 7 days)
ree criteria out of these ve establish diagnosis of calorie
de ciency
Mixed Protein Calorie Malnutrition Criteria
Mild Moderate Severe
Weight loss 5–9% 10–15% 10–15% over 6
Underweight 94–85% 84–70% <70% ideal
Albumin 2.8–3.4 g/dL2.1–2.7 g/dL <2.1 g/dL
Total
lymphocytes
Transferrin 199–150
1499–1200/
3
mm
mg/dL
3
or less
months
weight
1199–800/mm3<800/mm
149–100 mg/dL <100 mg/dL
Muscle wasting
De cient intake
(at least 3 days)
3
route is the preferred route of support, as it has been shown
138
to cause less morbidity and mortality.
Enteral nutritional support is e ective in patients that have
functional small bowel; examples include esophageal or gastric
resection, patients with postoperative delirium or dysphagia,
and patients who have gastroparesis. In the short term, if the
dysfunction is expected to respond to treatment, nasogastric
tubes can be used e ectively to deliver full support. Patients
that need long-term enteral support are best served with gastrostomy or jejunostomy tubes, which may be placed operatively or percutaneously. With good preoperative nutritional
assessment and sound surgical judgment, these patients’ needs
for long-term postoperative support can often be anticipated,
and long-term feeding access can be included in the operative
plan. Enteral support may not be suitable for some patients;
examples include early postoperative bowel obstruction,
stula, or intestinal insu ciency (short-gut syndrome). In such
patients, parenteral support is indicated, and should be initiated without delay, and futile attempts to use the enteral route
should be avoided.
To establish the diagnoses of mild or moderate protein
calorie malnutrition, two of the ve criteria shown must be
met; to establish the diagnosis of severe protein calorie malnutrition, three of the seven criteria must be met.
Irrespective of the route of support, every patient on nutritional support should have his or her nutritional needs assessed
and provided. e assessment begins with the calorie requirement. ere are several formulas and nomograms that estimate
basal energy expenditure, taking into account height, weight,
139
age, gender, stress factors, and activity factors.
All of these
methods are estimations, and may underfeed or overfeed certain subgroups, especially the obese. e method in most common clinical use bases basal energy expenditure on adjusted
body weight (ABW). Using this method, ABW is de ned as the
patient’s ideal body weight (IBW) plus the di erence between
actual body weight (BW) and the IBW divided by two:
ABW = IBW + 0.5(BW – IBW)
e baseline caloric requirement for weight maintenance
based on ABW is 25 kcal/kg/d. is target may be adjusted
upward in patients with extreme metabolic demands, as is the
case in burns or head injury.
126
Furthermore, the ABW can be
used to establish the protein requirement. In unstressed normal subjects, the minimum daily protein requirement is 0.8 g
protein/kg/d. In postoperative patients with healing wounds,
this target is adjusted to 1.0–1.5 g/kg/d, and in severely ill
patients to 2.0 g/kg/d. e highest requirements are seen in
severe burn and bone marrow transplant patients.
Essential nutritional components must be provided, again
irrespective of the route of support. ese include water- and
lipid-soluble vitamins, trace elements such as zinc and selenium, essential fatty acids such as linoleic and linolenic acids,
and the eight essential amino acids. ese trace elements are
provided in abundance in all enteral feeds, and are part of the
standard additives in parenteral formula.
Once nutritional support has been initiated, the patient’s
response to support must be followed closely, especially in
parenteral support and in patients with preexisting metabolic conditions such as diabetes. Blood glucose should be
TABLE 2-10: POSTOPERATIVE CAUSES OF
DEFICIENT NUTRITIONAL INTAKE
Ileus
Bowel obstruction
Colitis (ischemic, infectious)
Fistula
Dysphagia
Gastric dysmotility
Intestinal insu ciency (short-gut syndrome)
26 Part I Introduction
monitored regularly during the rst few days of support.
Recent evidence has linked hyperglycemia in the postoperative setting, especially in critically ill patients, with increased
140,141
risk of death and infection.
In addition, electrolyte
abnormalities (especially those of potassium, magnesium,
and phosphate) are often seen in the early period of nutritional support, and should be corrected.
It is also important to follow the markers of nutrition
repletion to ensure that the calories and protein provided
(based on the initial estimate) are sucient, and the patient
is not mobilizing lean body mass due to inadequate support.
Serum markers such as prealbumin, retinol binding protein,
and transferrin can be useful in this regard. ey are serum
proteins with short (2–7 days) turnover times that reect the
139
body’s ability to synthesize new protein.
Unfortunately, the
serum concentrations of these proteins are also aected by acute
disease states and renal and hepatic failure, and can be dicult
to interpret in postoperative patients. Nitrogen balance can
also be used to monitor nutritional support and reects the
ability to synthesize new protein. Nitrogen balance is calculated by subtracting nitrogen excretion from nitrogen intake.
Nitrogen intake is calculated from the protein intake, where
each gram of protein divided by 6.25 is equal to the number
of grams of nitrogen. Nitrogen excretion has two components:
urinary urea nitrogen (UUN) and insensible loss. UUN can
be measured in a 24-hour urine collection; insensible loss is
generally accepted to be 4 g/d, unless there is another source
of loss, such as abdominal drainage of proteinaceous ascites,
enterocutaneous stula, or nephrotic syndrome. us, in most
cases, nitrogen balance can be simplied to:
Nitrogen balance = protein intake/6.25 – 24 hour UUN
– 4g (insensible loss)
A patient that takes in more nitrogen than he or she
excretes in the urine and feces is in positive nitrogen balance
and is synthesizing new protein. On the other hand, a patient
that is excreting more nitrogen than he or she is receiving
in nutritional support is in negative nitrogen balance, and is
therefore losing lean body mass, becoming more malnourished. ese patients should be reevaluated for nutritional
needs and for sources of nutritional depletion, such as uncontrolled diabetes mellitus, sepsis, and organ failure.
By itself, uncontrolled diabetes mellitus can be viewed as
a perioperative nutritional complication, as it results in nutritional depletion, interferes with delivery of parenteral and
enteral nutrition, and is associated with increased infectious
morbidity.
140,141
REFERENCES
1. Bauer M, Böhrer H, Aichele G, et al. Measuring patient satisfaction with
anaesthesia: perioperative questionnaire versus standardised face-to-face
interview. Acta Anaesthesiol Scand. 2001;45:65–72.
2. Ballantyne JC, Carr DB, Chalmers TC, et al. Postoperative patient-
controlled analgesia: meta-analyses of initial randomized control trials.
J Clin Anesth. 1993;5:182–193.
3. Nitschke LF, Schlösser CT, Berg RL, et al. Does patient-controlled
analgesia achieve better control of pain and fewer adverse eects than
intramuscular analgesia? A prospective randomized trial. Arch Surg.
1996;131:417–423.
4. Kenady DE, Wilson JF, Schwartz RW, et al. A randomized comparison
of patient-controlled versus standard analgesic requirements in patients
undergoing cholecystectomy. Surg Gynecol Obstet. 1992;174:216–220.
5. de Leon-Casasola OA, Karabella D, Lema MJ. Bowel function recovery
after radical hysterectomies: thoracic epidural bupivacaine-morphine
versus intravenous patient-controlled analgesia with morphine: a pilot
study. J Clin Anesth. 1996;8:87–92.
6. Block BM, Liu SS, Rowlingson AJ, et al. Ecacy of postoperative
epidural analgesia: a meta-analysis. JAMA. 2003;290:2455–2463.
7. Wang LP, Hauerberg J, Schmidt JF. Incidence of spinal epidural abscess
after epidural analgesia: a national 1-year survey. Anesthesiology.
1999;91:1928–1936.
8. Boylan, JF, Katz J, Kavanagh BP, et al. Epidural bupivacaine-morphine
analgesia versus patient-controlled analgesia following abdominal aortic
surgery: analgesic, respiratory, and myocardial eects. Anesthesiology.
1998;89:585–593.
9. Bois S, Couture P, Boudreault D, et al. Epidural analgesia and
intravenous patient-controlled analgesia result in similar rates of
postoperative myocardial ischemia after aortic surgery. Anesth Analg.
1997;85:1233–1239.
10. Wu CL, Naqibuddin M, Fleisher LA. Measurement of patient satisfaction as an outcome of regional anesthesia and analgesia: a systematic
review. Reg Anesth Pain Med. 2001;26:196–208.
11. Werawatganon T, Charuluxanun S. Patient controlled intravenous
opioid analgesia versus continuous epidural analgesia for pain after intraabdominal surgery. Cochrane Database Syst Rev. 2005;(1):CD004088.
12. Hendolin H, Lahtinen J, Lansimies E, et al. e eect of thoracic
epidural analgesia on respiratory function after cholecystectomy. Acta
Anaesthesiol Scand. 1987;31:645–651.
13. Cuschieri RJ, Morran CG, Howie JC, McArdle CS. Postoperative pain
and pulmonary complications: comparison of three analgesic regimens.
Br J Surg. 1985;72:495–498.
14. Scheinin B, Asantila R, Orko R. e eect of bupivacaine and morphine
on pain and bowel function after colonic surgery. Acta Anaesthesiol
Scand. 1987;31:161–164.
15. Bredtmann RD, Herden HN, Teichmann W, et al. Epidural analgesia
in colonic surgery: results of a randomized prospective study. Br J Surg.
1990;77:638–642.
16. Horattas MC, Evans S, Sloan-Stakle KD, et al. Does pre- operative
rofecoxib (Vioxx) decrease postoperative pain with laparoscopic
cholecystectomy? Am J Surg. 2004;188:271–276.
17. Bikhazi GB, Snabes MC, Bajwa ZH, et al. A clinical trial demonstrates
the analgesic activity of intravenous parecoxib sodium compared with
ketorolac or morphine after gynecologic surgery with laparotomy. Am J
Obstet Gynecol. 2004;191:1183–1191.
18. Lau H, Wong C, Goh LC, et al. Prospective randomized trial of preemptive analgesics following ambulatory inguinal hernia repair:
intravenous ketorolac versus diclofenac suppository. ANZ J Surg.
2002;72:704–707.
19. Mixter CG 3rd, Meeker LD, Gavin TJ. Preemptive pain control in
patients having laparoscopic hernia repair: a comparison of ketorolac and
ibuprofen. Arch Surg. 1998;133:432–437.
20. Morton NS, O’Brien K. Analgesic ecacy of paracetamol and diclofenac
in children receiving PCA morphine. Br J Anaesth. 1999;82:715–717.
21. Litaker D, Locala J, Franco K, et al. Preoperative risk factors for
postoperative delirium. Gen Hosp Psychiatry. 2001;23:84–89.
22. Moller JT, Cluitmans P, Rasmussen LS, et al. Long-term postoperative cognitive dysfunction in the elderly ISPOCD1 study. ISPOCD
investigators. International Study of Post-Operative Cognitive Dysfunction. Lancet. 1998;351:857–861.
23. Inouye SK, Charpentier PA. Precipitating factors for delirium in
hospitalized elderly persons. Predictive model and interrelationship with
baseline vulnerability. JAMA. 1996;275:852–857.
24. Mann C, Pouzeratte Y, Boccara G, et al. Comparison of intravenous or
epidural patient-controlled analgesia in the elderly after major abdominal
surgery. Anesthesiology. 2000;92:433–441.
25. Skrobik YK, Bergeron N, Dumont M, Gottfried SB. Olanzapine vs
haloperidol: treating delirium in a critical care setting. Intensive Care
Med. 2004;30:444–449.
Chapter 2 Preoperative and Postoperative Management 27
26. Mangano DT, Goldman L. Preoperative assessment of patients with known
or suspected coronary disease. N Engl J Med. 1995;333:1750–1756.
27. Eagle KA, Brundage BH, Chaitman BR, et al. Guidelines for perioperative
cardiovascular evaluation for noncardiac surgery: Report of the ACC/AHA
Task Force on Practice Guidelines. J Am Coll Cardiol. 1996;27:910–948.
28. Park KW. Preoperative cardiology consultation. Anesthesiology. 2003;
98:754–762.
29. Liu LI, Wiener-Kronish JP. Preoperative cardiac evaluation of women for
noncardiac surgery. Cardiol Clin. 1998;16:59–66.
30. Shackleford DP, Homan MK, Kramer PR Jr, et al. Evaluation of preoperative cardiac risk index values in patients undergoing vaginal surgery.
Am J Obstet Gynecol. 1995;173:80–84.
31. Mangano DT, Hollenberg M, Fegert G, et al. Perioperative myocardial
ischemia in patients undergoing non-cardiac surgery—I: Incidence and
severity during the 4 day perioperative period. e study of perioperative ischemia (SPI) research group. J Am Coll Cardiol. 1991;4:843–850.
32. ACC/AHA task force report: Special report: guidelines for perioperative cardiovascular evaluation for non-cardiac surgery. Circulation.
1996;93:1278–1317.
33. Mukherjee D, Eagle KA. Perioperative cardiac assessment for
noncardiac surgery, eight steps to the best possible outcome. Circulation.
2003;107:2771–2774.
34. Chui PT, Gin T, Oh TE. Anaesthesia for laparoscopic surgery. Anaesth
Intensive Care. 1993;21:163–171.
35. Madu EC. Transesophageal dobutamine stress echocardiography in the
evaluation of myocardial ischemia in morbidly obese subjects. Chest.
2000;117:657–661.
36. Dawood MM, Gupta DK, Southern J, et al. Pathology of fatal perioperative myocardial infarction: implications regarding pathophysiology and
prevention. Int J Cardiol. 1996;57:37–44.
37. Boersma E, Poldermans D, Bax JJ, et al. Predictors of cardiac events after
major vascular surgery: role of clinical characteristics, dobutamine echocardiography, and beta-blocker therapy. JAMA. 2001;285:1865–1873.
38. Gersh BJ, Braunwald E, Bonow RO. Chronic coronary artery disease.
In: Braunwald E, Zipes DP, Libby P, eds. Heart Disease. Philadelphia, PA:
WB Saunders; 2001:1272–1363.
39. McFalls EO, Ward HB, Moritz TE, et al. Coronary artery revascularization before elective major vascular surgery. N Engl J Med.
2004;352:2795–2804.
40. Posner KL, Van Norman GA, Chan V. Adverse cardiac outcomes after
noncardiac surgery in patients with prior percutaneous transluminal
coronary angioplasty. Anesth Analg. 1999;89:553–560.
41. Kaluza GL, Joseph J, Lee JR, et al. Catastrophic outcomes of noncardiac surgery soon after coronary stenting. J Am Coll Cardiol. 2000;35:
1288–1294.
42. Foster ED, Davis KB, Carpenter JA, et al. Risk of noncardiac operation
in patients with dened coronary disease: the Coronary Artery Surgery
Study (CASS) registry experience. Ann orac Surg. 1986;14:42–50.
43. Yusuf S, Zucker D, Peduzzi P, et al. Eect of coronary artery bypass graft
surgery on survival: overview of 10-year results from randomised trials
by the Coronary Artery Bypass Graft Surgery Trialists Collaboration.
Lancet. 1994;344:563–570.
44. Selzman CH, Miller SA, Zimmerman MA, Harkin AH. e case for
beta-adrenergic blockade as prophylaxis against perioperative cardiovascular morbidity and mortality. Arch Surg. 2001;136:286–290.
45. Lee RT, Grodinsky AJ, Frank EH, et al. Structure dependent dynamic
mechanical behavior of brous caps from human atherosclerotic plaques.
Circulation. 1991;83:1764–1770.
46. Rabbani R, Topol EJ. Strategies to achieve coronary arterial plaque
stabilization. Cardiovasc Res. 1999;4:402–417.
47. Mangano DT, Layug EL, Wallace A, et al; Multicenter Study of
Perioperative Ischemia Research Group. Eect of atenolol on mortality
and cardiovascular morbidity after noncardiac surgery. N Engl J Med.
1996;335:1713–1720.
48. Poldermans D, Boersma E, Bax JJ, et al; Dutch Echocardiographic
Cardiac Risk Evaluation Applying Stress Echocardiography Study
Group. e eect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. N Engl
J Med. 1999;341:1789–1794.
49. Lindenauer PK, Pekow P, Wang K, et al. Perioperative beta-blocker
therapy and mortality after major noncardiac surgery. N Engl J Med.
2005;353:349–361.
50. Brady AR, Gibbs JS, Greenhalgh RM, et al. Perioperative beta-blockade
(POBBLE) for patients undergoing infrarenal vascular surgery: results of a
randomized double-blind controlled trial. J Vasc Surg. 2005;41:602–609.
51. Yang H, Raymer K, Butler R, et al. e eects of perioperative betablockade: results of the Metoprolol after Vascular Surgery (MaVS) study,
a randomized controlled trial. Am Heart J. 2006;152:983–990.
52. Juul AB, Wetterslev J, Gluud C, at al. Eect of perioperative beta
blockade in patients with diabetes undergoing major non-cardiac
surgery: randomised placebo controlled, blinded multicentre trial. BMJ.
2006;332:1482.
53. Devereaux PJ, Yang H, Yusuf S, et al. Eects of extended-release
metoprolol succinate in patients undergoing non-cardiac surgery (POISE
trial): a randomised controlled trial. Lancet. 2008;371:1839–1847.
54. Devereaux PJ, Beattie WS, Choi PT, et al. How strong is the evidence
for the use of perioperative beta blockers in non-cardiac surgery?
Systematic review and meta-analysis of randomised controlled trials.
BMJ. 2005;331:313–321.
55. Detsky AS, Abrams HB, McLaughlin JR, et al. Predicting cardiac complications in patients undergoing non-cardiac surgery. J Gen Intern Med.
1986;1:211–219.
56. O’Kelly B, Browner WS, Massie B, et al. Ventricular arrhythmias in
patients undergoing noncardiac surgery: e Study of Perioperative
Ischemia Research group. JAMA. 1992;268:217–221.
57. Mahla E, Rotman B, Rehak P, et al. Perioperative ventricular dysrhythmias
in patients with structural heart disease undergoing noncardiac surgery.
Anesth Analg. 1998;86:16–21.
58. Eagle KA, Berger PB, Calkins H, et al. ACC/AHA guideline update for
perioperative cardiac evaluation for noncardiac surgery—executive summary: a report of the American College of Cardiology/American Heart
Association Task Force on Practice guidelines (Committee to Update the
1996 Guidelines on Perioperative Cardiac Evaluation for Noncardiac
Surgery). J Am Coll Cardiol. 2002;39:542–553.
59. Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial
endocarditis: recommendations by the American Heart Association.
JAMA. 1997;227:1794–1801.
60. Steckelberg JM, Wilson WR. Risk factors for infective endocarditis.
Infect Dis Clin North Am. 1993;7:9–19.
61. Boudoulais H, Wooley CF. Mitral valve prolapse. In: Emmanouilides
GC, Riemenschneider TA, Allen HD, Gutgesell HP, eds. Moss and
Adams Heart Disease in Infants, Children and Adolescents including the
Fetus and Young Adult. 5th ed. Baltimore, MD: Williams & Wilkins;
1995:1063–1086.
62. Carabello BA. Mitral valve disease. Curr Probl Cardiol. 1993;7:423–478.
63. Devereux RB, Hawkins I, Kramer-Fox R, et al. Complications of mitral
valve prolapse. Disproportionate occurrence in men and older patients.
Am J Med. 1986;81:751–758.
64. MacMahon SW, Roberts JK, Kramer-Fox R, et al. Mitral valve prolapse
and infective endocarditis. Am Heart J. 1987;113:1291–1298.
65. Devereux RB, Kramer-Fox R, Kligeld P. Mitral valve prolapse: causes,
manifestations, and management. Ann Intern Med. 1989;111:305–317.
66. Marks AR, Choong CY, Sanllipo AJ, et al. Identication of high-risk
and low-risk subgroups of patients with mitral-valve prolapse. N Engl J
Med. 1989;320:1031–1036.
67. Nishimura RA, McGoon MD, Shub C, et al. Echocardiographically
documented mitral-valve prolapse. Long-term follow up of 237 patients.
N Engl J Med. 1985;313:1305–1309.
68. Cheitlin MD, Alpert JS, Armstong WF, et al. ACC/AHA guidelines
for the clinical application of echocardiography: a report of the American College of Cardiology/ American Heart Association Task Force
Guidelines (Committee on Clinical Application of Echocardiography).
Circulation. 1997;95:1686–1744.
69. Durak DT. Prevention of infective endocarditis. N Engl J Med. 1995;
332:38–44.
70. Douketis, JD, Berger, PB, Dunn, AS, et al. e perioperative management of antithrombotic therapy: American College of Chest Physicians Evidence-based Clinical Practice Guidelines (8th Edition). Chest.
2008;133:299S–339S.
71. Lawrence VA, Dhanda R, Hilsenbeck SG, Page CP. Risk of pulmonary complications after elective abdominal surgery. Chest. 1996;110:
744–750.
72. Becquemin JP, Piquet J, Becquemin MH, et al. Pulmonary function after
transverse or midline incision in patients with obstructive pulmonary
disease. Intensive Care Med. 1985;11:247–251.
28 Part I Introduction
73. Celli BR, Rodriguez KS, Snider GL. A controlled trial of intermittent
positive pressure breathing, incentive spirometry, and deep breathing exercises in preventing pulmonary complications after abdominal surgery.
Am Rev Respir Dis. 1984;130:12–15.
74. Tarhan S, Mott EA, Sessler AD, et al. Risk of anesthesia and surgery
in patients with chronic bronchitis and chronic obstructive pulmonary
disease. Surgery. 1973;74:720–726.
75. Gerson MC, Hurst JM, Hertzberg VS, et al. Prediction of cardiac and
pulmonary complications related to elective abdominal and noncardiac
thoracic surgery in geriatric patients. Am J Med. 1990;88:101–107.
76. Williams-Russo P, Charlson ME, Mackenzie CR, et al. Predicting postoperative pulmonary complications. Is it a real problem? Arch Intern
Med. 1992;152:1209–1213.
77. Warner MA, Oord KP, Warner MA, et al. Role of pre-operative
cessation of smoking and other factors in postoperative pulmonary complications: a blinded prospective study of coronary artery bypass patients.
Mayo Clin Proc. 1989;64:609–616.
78. Pien LC, Grammer LC, Patterson R. Minimal complications in a surgical
population with severe asthma receiving prophylactic corticosteroids.
J Allergy Clin Immunol. 1988;82:696–700.
79. Kabalin CS, Yarnld PR, Grammer LC. Low complication rate of
corticosteroid-treated asthmatics undergoing surgical procedures. Arch
Intern Med. 1995;155:1379–1384.
80. Flancbaum L, Choban PS. Surgical implications of obesity. Annu Rev
Med. 1998;49:215–234.
81. Shepherd JW. Hypertension, cardiac arrhythmias, myocardial infarction
and stroke in relation to obstructive sleep apnea. Clin Chest Med.
1992;13:459–479.
82. Brooks-Brunn JA. Postoperative atelectasis and pneumonia. Heart Lung.
1995;24:94–115.
83. Zinner MJ, Zuidema GD, Smith PA, et al. e prevention of upper
gastrointestinal tract bleeding in patients in an intensive care unit. Surg
Gynecol Obstet. 1981;153:215–220.
84. Kaplan EB, Sheiner LB, Boeckmann AJ, et al. e usefulness of preoperative laboratory screening. JAMA. 1985;253:3576–3581.
85. Ifudu O. Care of patients undergoing hemodialysis. N Engl J Med.
1998;339:1054–1062.
86. Cochrane Injuries Group Albumin Reviewers. Human albumin
administration in critically ill patients: systematic review of randomized
controlled trials. BMJ. 1998;317:235.
87. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced
nephropathy with sodium bicarbonate. A randomized controlled trial.
JAMA. 2004;291:2328–2334.
88. Tepel M, van der Giet M, Schwarzfeld C, et al. Prevention of
radiographic- contrast-agent-induced reductions in renal function by
acetylcysteine. N Engl J Med. 2000;343:180–184.
89. Brienza N, Giglio MT, Marucci M, et al. Does perioperative hemodynamic optimization protect renal function in surgical patients? A
meta-analytic study. Crit Care Med. 2009;37:2079–2090.
90. Lobo DN, Bostock KA, Neal KR, et al. Eect of salt and water balance
on recovery of gastrointestinal function after elective colonic resection: a
randomised controlled trial. Lancet. 2002;359:1812–1818.
91. van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy
in the critically ill patients. N Engl J Med. 2001;345:1359–1367.
92. Marik PE, Preiser J. Toward understanding tight glycemic control in the
ICU: a systematic review and metaanalysis. Chest. 2010;137:544–551.
93. Krinsley JS. Association between hyperglycemia and increased hospital
mortality in a heterogeneous population of critically ill patients. Mayo
Clin Proc. 2003;78:1471–1478.
94. NICE-SUGAR Study Investigators. Intensive versus conventional glucose
control in critically ill patients. N Engl J Med. 2009;360:1283–1297.
95. Egi M, Bellomo R, Stachowski E, et al. Variability of blood glucose concentration and short-term mortality in critically ill patients.
Anesthesiol. 2006;105:244–252.
96. Suchman AL, Mushlin AI. How well does the activated partial thromboplastin time predict postoperative hemorrhage? JAMA. 1986;
256:750–753.
97. Houry S, Georgeac C, Hay JM, et al; e French Associations for
Surgical Research. A prospective multi-center evaluation of preoperative
hemostatic screening tests. Am J Surg. 1995;170:19–23.
98. Burns ER, Lawrence C. Bleeding time. A guide to its diagnostic and
clinical utility. Arch Pathol Lab Med. 1989;113:1219–1224.
99. Peterson P, Hayes TE, Arkin CF, et al. e preoperative bleeding time lacks
clinical benet: College of American Pathologists and American Society
of Clinical Pathologists’ position article. Arch Surg. 1998;133:134–139.
100. Gewirtz AS, Miller ML, Keys TF. e clinical usefulness of the preoperative bleeding time. Arch Pathol Lab Med. 1996;120:353–356.
101. Robbins JA, Rose SD. Partial thromboplastin time as screening test. Ann
Intern Med. 1979;90:796–797.
102. Eisenberg JM, Goldfarb S. Clinical usefulness of measuring prothrombin time as a routine admission test. Clin Chem. 1976;22:1644–1647.
103. Robbins JA, Mushlin AI. Preoperative evaluation of the healthy patient.
Med Clin North Am. 1979;63:1145–1156.
104. Kaluza GL, Joseph J, Lee JR, et al. Catastrophic outcomes of noncardiac surgery soon after coronary stenting. J Am Coll Cardiol. 2000;35:
1288–1294.
105. American Society of Anesthesiologists Task Force on Blood Component
erapy. Practice guidelines for blood component therapy: a report by
the American Society of Anesthesiologists Task Force on Blood Component erapy. Anesthesiology. 1996;84:732–747.
106. Ginsburg SJ. Management of venous thromboembolism. N Engl J Med.
1996;335:1816–1828.
107. Decousus H, Leizorovicz A, Parent F, et al. Prevention du Risque
d’Embolie Pulmonaire par Interruption Cave Study Group. A clinical
trial of vena caval lters in the prevention of pulmonary embolism
in patients with proximal deep-vein thrombosis. N Engl J Med.
1998;338:409–415.
108. Flanc C, Kakkar VV, Clarke MB. e detection of venous thrombosis
of the legs using 125 I-labelled brinogen. Br J Surg. 1968;55:742–747.
109. Carter CJ. e pathophysiology of venous thrombosis. Prog Cardiovasc
Dis. 1994;36:439–446.
110. Kearon C, Hirsch J. Management of anticoagulation before and after
elective surgery. N Engl J Med. 1997;336:1506–1512.
111. Hirsch J, Rasche R, Warkentin TE, et al. Heparin: mechanism of action,
pharmacokinetics, dosing considerations, monitoring, ecacy, and
safety. Chest. 1995;108(Suppl):258S–275S.
112. Sanchez-Manuel FJ, Seco-Gil JL. Antibiotic prophylaxis for hernia
repair. Cochrane Database Syst Rev. 2004;(4):CD003769.
113. Smith RL, Bohl JK, McElearney ST, et al. Wound infection after elective
colorectal resection. Ann Surg. 2004;239:599–605.
114. O’Neill PA, Kirton OC, Dresner LS, et al. Analysis of 162 colon
injuries in patients with penetrating abdominal trauma: concomitant stomach injury results in a higher rate of infection. J Trauma.
2004;56:304–312.
115. Christou NV, Nohr CW, Meakins JL. Assessing operative site infection
in surgical patients. Arch Surg. 1987;122:165–169.
116. Perl TM, Cullen JJ, Wenzel RP, et al. Mupirocin and the Risk of
Staphylococcus aureus Study Team. Intranasal mupirocin to prevent postoperative Staphylococcus aureus infections. N Engl J Med.
2002;346:1871–1877.
117. Gil-Egea MJ, Pi-Sunyer MT, Verdaguer A, et al. Surgical wound
infections: a prospective study of 4,486 clean wounds. Infect Control.
1987;8:277–280.
118. Forse RA, Karam B, MacLean LD, Christou NV. Antibiotic prophylaxis
for surgery in morbidly obese patients. Surgery. 1989;106:750–756.
119. Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis WR. Guidelines
for prevention of surgical site infection. Infect Control Hosp Epidemiol.
1999;20:247–278.
120. Polk HC Jr, Simpson CJ, Simmons BP, Alexander JW. Guidelines for
prevention of surgical wound infection. Arch Surg. 1983;118:1213–1217.
121. Perez AR, Roxas MF, Hilvano SS. A randomized, double-blind, placebocontrolled trial to determine eectiveness of antibiotic prophylaxis for
tension-free mesh herniorrhaphy. J Am Coll Surg. 2005;200:393–397.
122. Darouiche RO. Antimicrobial approaches for preventing infections
associated with surgical implants. Clin Infect Dis. 2003;36:1284–1289.
123. Yerdel MA, Akin EB, Dolalan S, et al. Eect of single-dose prophylactic
ampicillin and sulbactam on wound infection after tension-free inguinal
hernia repair with polypropylene mesh: the randomized, double-blind,
prospective trial. Ann Surg. 2001;233:26–33.
124. Bratzler DW, Houck PM. Antimicrobial prophylaxis for surgery: an
advisory statement from the National Surgical Infection Prevention
Project. Clin Infect Dis. 2004;38:1706–1715.
125. Hecker MT, Aron DC, Patel NP, et al. Unnecessary use of antimicrobials in hospitalized patients: current patterns of misuse with an
Chapter 2 Preoperative and Postoperative Management 29
emphasis on antianaerobic spectrum of activity. Arch Intern Med.
2003;163:972–978.
126. Eggiman P, Pittet D. Infection control in the ICU. Chest. 2001;120:
2059–2093.
127. Fullen WD, Hunt J, Altemeier WA. Prophylactic antibiotics in
penetrating wounds of the abdomen. J Trauma. 1972;12:282–289.
128. adepelli H, Gorbach SL, Broido PW, et al. Abdominal trauma,
anaerobes, and antibiotics. Surg Gynecol Obstet. 1973;137:270–276.
129. Dellinger EP. Antibiotic prophylaxis in trauma: penetrating abdominal
injuries and open fractures. Rev Infect Dis. 1991;13:S847–S857.
130. Gaynes RP, Culver DH, Horan TC, et al. Surgical site infection (SSI)
rates in the United States, 1992–1998: the National Nosocomial
Infections Surveillance System basic SSI risk index. Clin Infect Dis.
2001;33(Suppl 2):S69–S77.
131. Sungurtekin H, Sungurtekin U, Balci C, et al. e inuence of nutritional
status on complications after major intraabdominal surgery. J Am Coll
Nutr. 2004;23:227–232.
132. Rey-Ferro M, Castano R, Orozco O, et al. Nutritional and immunologic
evaluation of patients with gastric cancer before and after surgery. Nutrition.
1997;13:878–881.
133. Bozzetti F, Gavazzi C, Miceli R, et al. Perioperative total parenteral
nutrition in malnourished, gastrointestinal cancer patients: a randomized,
clinical trial. JPEN J Parenter Enteral Nutr. 2000;24:7–14.
134. e Veterans Aairs Total Parenteral Nutrition Cooperative Study
Group. Perioperative total parenteral nutrition in surgical patients.
N Engl J Med. 1991;325:525–532.
135. Reilly JJ Jr, Hull SF, Albert N, et al. Economic impact of malnutrition:
a model system for hospitalized patients. JPEN J Parenter Enteral Nutr.
1988;12:371–376.
136. Moore FA, Moore EE, Jones TN, et al. TEN versus TPN following
major abdominal trauma—reduced septic morbidity. J Trauma. 1989;29:
916–922.
137. Kudsk KA, Croce MA, Fabian TC, et al. Enteral versus parenteral feeding. Eects on septic morbidity after blunt and penetrating abdominal
trauma. Ann Surg. 1992;215:503–511.
138. Demling RH, Seigne P. Metabolic management of patients with severe
burns. World J Surg. 2000;24:673–680.
139. Haider M, Haider SQ. Assessment of protein-calorie malnutrition.
Clin Chem. 1984;30:1286–1299.
140. Pomposelli JJ, Baxter JK 3rd, Babineau TJ, et al. Early postoperative
glucose control predicts nosocomial infection rate in diabetic patients.
JPEN J Parenter Enteral Nutr. 1998;22:77–81.
141. Furnary AP, Zerr KJ, Grunkemeier GL, Starr A. Continuous intravenous
insulin infusion reduces the incidence of deep sternal wound infection
in diabetic patients after cardiac surgical procedures. Ann orac Surg.
1999;67:352–360.
This page intentionally left blank
ENDOSCOPY AND ENDOSCOPIC INTERVENTION
Jeffrey M. Marks • Jeffrey L. Ponsky
3
Over the past several decades, exible endoscopy has shifted
the management of numerous gastrointestinal diseases
from the surgeon to the endoscopist. What had started as
a diagnostic discipline has now become one of advanced
therapeutic potential. e concept of performing endoscopic
surgery has become a reality with the advancement of endoluminal therapies for neoplasia, gastroesophageal re ux, and
obesity. In addition, with the signi cant investigation into
natural ori ce translumenal endoscopic surgery (NOTES)
and the development of advanced endoscopic tools, the ability to perform intraperitoneal therapies without abdominal
scars continues to become more possible. is chapter will
address the indications and techniques for upper and lower
exible endoscopy as well as the recent advances in imaging
and interventional endoscopy.
THE FLEXIBLE ENDOSCOPE
Imaging
e exible endoscope was initially developed in 1957 as an
imaging device dependent on the delivery of light and transmission of the image along multiple bundles of chemically
treated glass bers. e beroptic bundle is 2–3 mm wide and
is composed of 20,000–40,000 individual ne glass bers,
each approximately 10 µm in diameter.
goes a series of internal re ections within each ber, which
are coated with low optical density glass to prevent escape
of light, as it is transmitted up the bundle. Due to formation of the bers and surrounding material, a characteristic
meshed image is seen in beroptic endoscopes, which inherently results in a lower resolution than that seen with rigid
lens systems. In addition, if the bers become cracked, the
image is not generated at this site of the bundle and multiple
black spots are seen.
When utilizing a beroptic endoscope, the endoscopist
views the image through the eyepiece at the instrument head,
1
e image under-
or alternatively, a video camera can be a xed to the eyepiece
to transmit the image to a video monitor. e progression
from beroptic scopes to the videoendoscopes, we use today,
has allowed for advancements in our ability to perform more
involved therapies, educate physicians and endoscopic assistants, and obtain static and dynamic recorded data images for
improved clinical management.
e majority of endoscopes in use today are videoscopic,
although in many parts of the world, beroptic systems are
still the standard. In these videoscopic systems, the visualized
image is created from re ections onto a charge coupled device
(CCD), which is a chip mounted at the end of the endoscope rather than via the beroptic bundles. e CCD chip
has thousands of pixels (light-sensitive points), which directly
increase image resolution.
2
Imaging Advances
ere have been many recent advances in endoscopic imaging
techniques. e purpose of most of these techniques is early
detection of dysplasia, which might elude standard endoscopic
visualization. Clinical use of new imaging is limited principally
to specialized centers, but future widespread application of an
imaging method for early dysplasia detection is a certainty.
CHROMOENDOSCOPY
e aim of chromoendoscopy is to detect subtle mucosal
abnormalities. Commonly used agents include Lugol’s solution, methylene blue, indigo carmine, and Congo red. A
2–3% solution of potassium iodide (Lugol’s solution) reacts
with glycogen in keratinized squamous epithelium. Normal
squamous epithelium stains a deep brown, but in ammation,
dysplasia, and carcinoma do not stain because of a lack of
glycogen. Lugol’s solution has been shown to be e ective in
detecting Barrett’s esophagus as well as screening for squamous cell carcinoma of the esophagus.
3
31