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Surgical Complications Surgical Wound Complications
Complications of Thermal Regulation
Pulmonary Complications
Cardiac Complications
Renal and Urinary Tract Complications
Gastrointestinal Complications
Hepatobiliary Complications
Neurologic Complications
Ear, Nose, and Throat Complications
Surgical complications remain a frustrating and difficult
aspect of the operative treatment of patients. Regardless of
how technically gifted and capable surgeons are, all will
have to deal with complications that occur after operative
procedures. The cost of surgical complications in the
United States runs into millions of dollars; in addition,
such complications are associated with lost work
productivity, disruption of family life, and stress to
employers and society in general.
Frequently, the functional results of the operation are
compromised by complications; in some cases the patient
never recovers to the preoperative level of function. The
most significant and difficult part of complications is the
suffering borne by a patient who enters the hospital
anticipating an uneventful operation but is left suffering
and compromised by the complication.
Complications can occur for a variety of reasons. A surgeon
can perform a technically sound operation in a patient who
is severely compromised by the disease process and still
have a complication. Similarly, a surgeon who is sloppy or
careless or hurries through an operation can make technical
errors that account for the operative complications. Finally,
the patient can be healthy nutritionally, have an operation
performed meticulously, and yet suffer a complication
because of the nature of the disease. The possibility of
postoperative complications remains part of every surgeon's
mental preparation for a difficult operation.
Surgeons can do much to avoid complications by careful
preoperative screening. When the surgeon sees the
surgical candidate for the first time, a host of questions
come to mind, such as the nutritional status of the patient
and the health of the heart and lungs. The surgeon will
make a decision regarding performing the appropriate
operation for the known disease. Similarly, the timing of
the operation is often an important issue. Some operations
can be performed in a purely elective fashion, whereas
others must be done in an urgent fashion.
Occasionally, the surgeon will require that the patient lose
weight before the operation to enhance the likelihood of a
successful outcome. At times a wise surgeon will request
preoperative consultation from a cardiologist or
pulmonary specialist to make certain that the patient will
be able to tolerate the stress of a particular procedure.
Once the operation has begun, the surgeon can do much to
influence the postoperative outcome. Surgeons must
handle tissues gently, dissect meticulously, and honor
tissue planes. Performing the technical portions of the
operation carefully will lower the risk for a significant
complication. At all costs, surgeons must avoid the
temptation to rush, cut corners, or accept marginal
technical results. Similarly, the judicious use of antibiotics
and other preoperative medications can influence the
outcome. For a seriously ill patient, adequate resuscitation
may be necessary to optimize the patient before giving a
general anesthetic.
Once the operation is completed, compulsive
postoperative surveillance is mandatory. Thorough and
careful rounding on patients on a regular basis
postoperatively gives the operating surgeon an opportunity
to be vigilant and seek postoperative complications at an
early stage when they can be most effectively addressed.
During this process the surgeon will carefully check all
wounds, evaluate intake and output, check temperature
profiles, ascertain what the patient's activity levels have
been, evaluate nutritional status, and check pain levels.
Over years of experience, the clinician can begin to assess
the aforementioned parameters and detect deviations from
the normal postoperative course. Expeditious response to a
complication makes the difference between a brief,
inconvenient complication and a devastating, disabling
one. In summary, a wise surgeon will deal with
complications quickly, thoroughly, and appropriately.
Surgical wound complications
Seroma
Hematoma
Acute Wound Failure (Dehiscence)
Surgical Site Infection (Wound Infection)
Chronic Wounds
SeromaEtiology
A seroma is a collection of liquefied fat, serum, and
lymphatic fluid under the incision. The fluid is usually
clear, yellow, and somewhat viscous and is found in the
subcutaneous (SC) layer of the skin. Seromas represent
the most benign complication after an operative procedure
and are particularly likely to occur when large skin flaps
are developed in the course of the operation, as is often
seen with mastectomy, axillary dissection, groin
dissection, and large ventral hernias.
SeromaPresentation and Management
A seroma is usually manifested as a localized and well-
circumscribed swelling, pressure or discomfort, and
occasional drainage of clear liquid from the immature
surgical wound.
Prevention of seroma formation may be achieved by
placing suction drains under the skin flaps or in potential
dead space created by lymphadenectomy. Premature
removal of drains frequently results in large seromas that
require aspiration under sterile conditions, followed by
placement of a pressure dressing.
SeromaA seroma that reaccumulates after at least two aspirations
is evacuated by opening the incision and packing the
wound with saline-moistened gauze to allow healing by
secondary intention. In the presence of synthetic mesh, the
best option is open drainage in the operating room with
the incision closed to avoid exposure and infection of the
mesh; closed suction drains are generally placed. An
infected seroma is also treated by open drainage. The
presence of synthetic mesh in these cases will prevent the
wound from healing.
Seroma
Management of the mesh depends on the severity and
extent of infection. In the absence of severe sepsis and
spreading cellulitis and the presence of localized infection,
the mesh can be left in situ and removed at a later date
when the acute infectious process has resolved. Otherwise,
the mesh must be removed and the wound managed with
open wound care.
Hematoma
Etiology
A hematoma is an abnormal collection of blood, usually in
the SC layer of a recent incision or in a potential space in
the abdominal cavity after extirpation of an organ, for
example, splenic fossa hematoma after splenectomy or
pelvic hematoma after proctectomy. Hematomas are more
worrisome than seromas because of the potential for
secondary infection. Hematoma formation is related to
inadequate hemostasis, depletion of clotting factors, and
the presence of coagulopathy.
Hematoma
A host of disease processes can contribute to
coagulopathy, including myeloproliferative disorders, liver
disease, renal failure, sepsis, clotting factor deficiencies,
and medications. Medications most commonly associated
with coagulopathy are antiplatelet drugs, such as aspirin,
clopidogrel bisulfate (Plavix), ticlopidine hydrochloride
(Ticlid), eptifibatide (Integrilin), and abciximab (ReoPro),
and anticoagulants, such as ultrafractionated heparin, low-
molecular-weight heparin (LMWH: enoxaparin
[Lovenox], dalteparin sodium [Fragmin], tinzaparin
[Innohep]), and warfarin sodium.
Hematoma
Presentation and Management
The clinical manifestations of a hematoma vary with its
size and location. A hematoma may appear as an
expanding, unsightly swelling or pain in the area of a
surgical incision, or both. In the neck a large hematoma
may cause compromise of the airway; in the
retroperitoneum it may cause paralytic ileus, anemia, and
ongoing bleeding because of local consumptive
coagulopathy; and in the extremity and abdominal cavity
it may result in compartment syndrome.
On physical examination, a hematoma appears as a
localized soft swelling with purplish/blue discoloration of
the overlying skin. The swelling varies from small to large
and may be tender to palpation or associated with drainage
of dark red fluid out of the fresh wound.
Hematoma formation is prevented preoperatively by
correcting any clotting abnormalities and discontinuing
medications that alter coagulation. Antiplatelet
medications and anticoagulants are given to patients
undergoing surgery for a variety of reasons: after
implantation of a coronary stent, for the treatment of
coronary artery disease (CAD) and stroke, after
implantation of a mechanical mitral valve, and in the
presence of atrial fibrillation, venous thromboembolism,
and hypercoagulable states. These medications must be
discontinued before surgery.
One must balance the risk of significant bleeding due to
uncorrected medication-induced coagulopathy and the risk
of thrombosis after discontinuation of therapy. In patients
at high risk for thrombosis who are scheduled to undergo
an elective major surgical procedure, warfarin must be
discontinued 3 days before surgery to allow the
international normalized ratio (INR) to be less than 1.5.
Then they are given heparin intravenously (IV) or an
equivalent dose SC.
Those receiving standard heparin can have the medication
discontinued 2 to 3 hours before surgery and those
receiving LMWH (variable half-life), 12 to 15 hours
before surgery. Anticoagulants are then resumed 24 to 48
hours after surgery. Patients taking clopidogrel must have
the medication withheld 5 to 6 days before surgery;
otherwise, the surgery must be delayed. During surgery,
adequate hemostasis must be achieved with ligature,
electrocautery, fibrin glue, or topical bovine thrombin
before closure. Closed suction drainage systems are placed
in large potential spaces and removed postoperatively
when output is not bloody and scant.
Evaluation of a patient with a hematoma, especially one
that is large and expanding, includes assessment of
preexisting risk factors and coagulation parameters
(prothrombin time, partial thromboplastin time, INR,
platelet count). A small hematoma does not require any
intervention and will eventually resorb. Most
retroperitoneal hematomas can be managed by expectant
waiting after correction of the associated coagulopathy.
A large or expanding hematoma in the neck is managed in
similar fashion and best evacuated in the operating room
urgently after securing the airway if there is any
respiratory compromise. Similarly, hematomas detected
soon after surgery, especially those developing under skin
flaps, are best evacuated in the operating room.
Acute Wound Failure (Dehiscence)
Etiology
Acute wound failure (wound dehiscence or a burst
abdomen) refers to postoperative separation of the
abdominal musculoaponeurotic layers. It is among the
most dreaded complications faced by surgeons and of
greatest concern because of the risk of evisceration, the
need for immediate intervention, and the possibility of
repeat dehiscence, surgical wound infection, and
incisional hernia formation.
Acute Wound Failure (Dehiscence)
Acute wound failure occurs in approximately 1% to 3% of
patients who undergo an abdominal operation. Dehiscence
most often develops 7 to 10 days postoperatively but may
occur anytime after surgery from 1 to more than 20 days.
A multitude of factors may contribute to wound
dehiscence. Acute wound failure is often related to
technical errors in placing sutures too close to the edge,
too far apart, or under too much tension. A deep wound
infection is one of the most common causes of localized
wound separation.
Acute Wound Failure (Dehiscence)
Increased intra-abdominal pressure and factors that
adversely affect wound healing are often cited as
contributing to the complication. In healthy patients, the
rate of wound failure is similar whether closure is
accomplished with a continuous or interrupted technique.
In high-risk patients, however, continuous closure is
worrisome because suture breakage in one place weakens
the entire closure.
Presentation and Management
Acute wound failure may occur without warning and
evisceration makes the diagnosis obvious. Sudden,
dramatic drainage of a relatively large volume of a clear,
salmon-colored fluid precedes dehiscence in a fourth of
patients. Probing the wound with a sterile, cotton-tipped
applicator or gloved finger may detect the dehiscence.
Prevention of acute wound failure is largely a function of
careful attention to technical detail during fascial closure.
For very high-risk patients, interrupted closure is often the
wisest choice. Alternative methods of closure must be
selected when primary closure is not possible without
undue tension. Although retention sutures were used
extensively in the past, their use is less common today,
with some surgeons opting to use a synthetic prosthesis or
tissue graft.
Once dehiscence is diagnosed, treatment depends on the
extent of fascial separation and the presence of
evisceration or significant intra-abdominal contamination
(intestinal leak, peritonitis). A small dehiscence in the
proximal aspect of an upper midline incision 10 to 12 days
postoperatively can be managed conservatively by
packing the wound with saline-moistened gauze and using
an abdominal binder. In the event of evisceration, the
eviscerated intestines must be covered with a sterile,
saline-moistened towel and preparations made to return to
the operating room after a very short period of fluid
resuscitation.
Once in the operating room, thorough exploration of the
abdominal cavity is performed to rule out the presence
of a septic focus or an anastomotic leak that may have
predisposed to the dehiscence. Treatment of the infection
is of critical importance before attempting closure.
Management of the incision is a function of the
condition of the fascia. When technical mistakes are
made and the fascia is strong and intact, primary closure
is warranted. If the fascia is infected or necrotic,
débridement is performed.
If after débridement the edges of the fascia cannot be
approximated without undue tension, consideration needs
to be given to closing the wound with absorbable mesh or
the recently developed biologic prostheses (decellularized
porcine submucosa and dermis and human cadaveric
dermis). Attempts to close the fascia under tension
guarantee a repeat dehiscence and possible intra-
abdominal hypertension. Definitive surgical repair to
restore the integrity of the abdominal wall will eventually
be required if absorbable mesh is used but not if a biologic
prosthesis is used.
Absorbable mesh and biologic prostheses protect from
evisceration, maintain the abdominal domain, and provide
a barrier to prevent bowel desiccation, bacterial invasion,
and nonadherent, potentially permanent closure.
Autologous skin grafts are used to reconstitute the
epithelial barrier, and flaps (local/regional or free) are
used to reconstruct the abdominal wall.
For short-term management of a dehisced wound, a
wound vacuum system can be used that consists of open-
cell foam placed on the tissue, semiocclusive drape to
cover the foam and skin of the patient, and suction
apparatus. The wound vacuum system provides immediate
coverage of the abdominal wound and acts as a dressing
that minimizes heat loss and does not require suturing to
the fascia.
By using negative pressure, the device removes interstitial
fluid and thus lessens bowel edema, decreases wound size,
reduces bacterial colonization, increases local blood
perfusion, and induces the healing response. Successful
closure of the fascia can be achieved in 85% of cases of
abdominal wound dehiscence. The technique, however,
may be associated with evisceration, intestinal
fistulization, and hernia formation.
Surgical Site Infection (Wound
Infection)Etiology
Surgical site infections continue to be a significant
problem for surgeons in the modern era. Despite
significant improvements in antibiotics, better anesthesia,
superior instruments, earlier diagnosis of surgical
problems, and improved techniques for postoperative
vigilance, wound infections continue to occur.
Surgical Site Infection (Wound
Infection)
Although some may view the problem as a merely
cosmetic one, that view represents a very shallow
understanding of this problem, which causes significant
patient suffering, morbidity and even mortality, and a
financial burden to the health care system. Currently, in
the United States wound infections account for almost
40% of hospital-acquired infections among surgical
patients.
The surgical wound encompasses the area of the body,
both internally and externally, that involves the entire
operative site. Wounds are thus categorized into three
general groups:
1. Superficial, including the skin and SC tissue
2. Deep, including the fascia and muscle
3. Organ space, including the internal organs of the body if
the operation includes that area
Surgical site infection is caused by bacterial
contamination of the surgical site, which can occur in a
variety of ways: violation of integrity of the wall of a
hollow viscus, skin flora, and a break in the surgical sterile
technique that allows exogenous contamination from the
surgical team, the equipment, or the surrounding
environment. The pathogens associated with a surgical site
infection reflect the area that provided the inoculum for
the infection to develop.
Staphylococcus aureus and coagulase-negative
Staphylococcus remain the most common bacteria
colonized from wounds. However, at locations where high
volumes of gastrointestinal (GI) operations are performed,
the predominant bacteria will include Enterobacter
species and Escherichia coli. In most studies, group D
Enterococcus continues to be a common pathogen isolated
from surgical site infections. Surgical wounds are
classified into clean, clean-contaminated, contaminated,
and dirty according to the relative risk for development of
a surgical site infection .
Presentation and Management
Surgical site infections most commonly occur 5 to 6 days
postoperatively but may develop sooner or later than that.
About 80% to 90% of all postoperative infections occur
within 30 days after the operative procedure. With the
increased utilization of outpatient surgery and decreased
length of stay in hospitals, 30% to 40% of all wound
infections have been shown to occur after hospital
discharge. Nevertheless, although less than 10% of
surgical patients are hospitalized for 6 days or less, 70%
of postdischarge infections occur in that group.
Superficial and deep surgical site infections are
accompanied by erythema, tenderness, edema, and
occasionally drainage. The wound is often soft or
fluctuant at the site of infection, which is a departure from
the firmness of the healing ridge present elsewhere in the
wound. The patient may have leukocytosis and a low-
grade fever.
According to the Joint Commission on Accreditation of
Healthcare Organizations, a surgical wound is considered
infected if it meets the following criteria:
1. Grossly purulent material drains from the wound
2. The wound spontaneously opens and drains purulent
fluid
3. The wound drains fluid that is culture positive or
Gram stain positive for bacteria
4. The surgeon notes erythema or drainage and opens
the wound after deeming it to be infected
Treatment of surgical site infection starts with the
implementation of preventive measures before and during
surgery. Patients who are heavy smokers are encouraged
to stop smoking around the time of the operation. Obese
patients must be encouraged to lose weight if the
procedure is elective and there is time to achieve
significant weight loss. Tight control of glucose levels,
especially in diabetics, will lower the risk for wound
infection. Similarly, patients who are taking high doses of
corticosteroids will have lower infection rates if they are
weaned off corticosteroids or are at least taking a lower
dose.
The night before surgery, patients are encouraged to take a
shower or bath in which an antibiotic soap may be used.
Patients undergoing major intra-abdominal surgery are
administered bowel preparation in the form of lavage
solutions or strong cathartics, followed by oral,
nonabsorbable antibiotics, particularly for surgery on the
colon and small bowel. Such preparation lowers the
patient's risk for infection from that of a contaminated
case (25%) to a clean-contaminated case (5%).
Preoperative antibiotics for prophylaxis are given
selectively. For dirty or contaminated wounds, the use of
antibiotics is for therapeutic intentions rather than for
prophylaxis. For clean cases, prophylaxis is controversial.
However, a small but significant benefit may be achieved
with the prophylactic administration of a first-generation
cephalosporin for certain types of clean surgery (e.g.,
mastectomy and herniorrhaphy). For clean-contaminated
procedures, administration of preoperative antibiotics is
indicated.
The appropriate preoperative antibiotic is a function of the
most likely inoculum based on the area being operated on.
For example, when a prosthesis may be placed in a clean
wound, preoperative antibiotics would include something
to protect against S. aureus and Streptococcus species.
A first-generation cephalosporin, such as cefazolin, would
be appropriate in this setting. For patients undergoing
upper GI tract surgery, complex biliary tract operations, or
elective colonic resection, administration of a second-
generation cephalosporin such as cefoxitin or a penicillin
derivative with a β-lactamase inhibitor is more suitable.
The surgeon will give a preoperative dose, appropriate
intraoperative doses approximately 4 hours apart, and two
postoperative doses appropriately spaced.
Timing of administration of prophylactic antibiotics is
critical. To be most effective, the antibiotic is administered
IV within 30 minutes before the incision so that
therapeutic tissue levels are present when the wound is
created and exposed to bacterial contamination. Most
often, a period of anesthesia induction, preparation, and
draping takes place that is adequate to allow tissue levels
to build up to therapeutic levels before the incision is
made.
Of equal importance is making certain that the
prophylactic antibiotic is not administered for extended
periods postoperatively. To do so in the prophylactic
setting is to invite the development of drug-resistant
organisms, as well as serious complications such as
Clostridium difficile colitis.
At the time of surgery the operating surgeon plays a major
role in reducing or minimizing the presence of
postoperative wound infections. The surgeon must be
attentive to personal hygiene (hand scrubbing) and that of
the entire team. In addition, the surgeon must make certain
that the patient undergoes a thorough skin preparation
with appropriate antiseptic solutions and is draped in a
sterile careful fashion.
During the operation, steps that have a positive impact on
outcome are followed:
1. Careful handling of tissues
2. Meticulous dissection, hemostasis, and débridement of
devitalized tissue
3. Compulsive control of all intraluminal contents
4. Preservation of blood supply of the operated organs
5. Elimination of any foreign body from the wound
6. Maintenance of strict asepsis by the operating team (no
holes in gloves, avoidance of the use of contaminated
instruments, avoidance of environmental contamination
such as debris falling from overhead)
7. Thorough drainage and irrigation of any pockets of
purulence in the wound with warm saline
8. Ensuring that the patient is kept in a euthermic state,
well monitored, and fluid resuscitated
9. At the end of the case, a judgment with regard to closing
the skin or packing the wound
The use of drains remains somewhat controversial in
preventing postoperative wound infections. In general,
there is virtually no indication for drains in this setting.
However, placing closed suction drains in very deep, large
wounds and wounds with large wound flaps to prevent the
development of a seroma or hematoma is a worthwhile
practice.
Once a surgical site infection is suspected or diagnosed,
management depends on the depth of the infection. For
both superficial and deep surgical site infections, skin
staples are removed over the area of the infection, and a
cotton-tipped applicator may be easily passed into the
wound with efflux of purulent material and pus. The
wound is gently explored with the cotton-tipped applicator
or a finger to determine whether the fascia or muscle
tissue is involved.
If the fascia is intact, débridement of any nonviable tissue
is performed, and the wound is irrigated with normal
saline solution and packed to its base with saline-
moistened gauze to allow healing of the wound from the
base anteriorly and prevent premature skin closure. If
widespread cellulitis is noted, administration of IV
antibiotics must be considered.
However, if the fascia has separated or purulent material
appears to be coming from deep to the fascia, there is
obvious concern about dehiscence or an intra-abdominal
abscess that may require drainage or possibly a
reoperation.
Wound cultures are controversial. If the wound is small,
superficial, and not associated with cellulitis or tissue
necrosis, culture may not be necessary. However, if fascial
dehiscence and a more complex infection are present,
material is sent for culture. A deep surgical site infection
associated with grayish, dishwater-colored fluid, as well
as frank necrosis of the fascial layer, raises suspicion for
the presence of a necrotizing type of infection.
The presence of crepitus in any surgical wound or gram-
positive rods (or both) suggests the possibility of infection
with Clostridia perfringens. Rapid and expeditious
surgical débridement is indicated in these settings.
Most postoperative infections are treated with healing by
secondary intention (allowing the wound to heal from the
base anteriorly, with epithelialization being the final
event). In some cases when there is a question about the
amount of contamination, delayed primary closure may be
considered. In this setting, close observation of the wound
for 5 days may be followed by closure of the skin if the
wound looks clean and the patient is otherwise doing well.
Recently, wound vacuum systems have been used in large,
deep, or moist wounds with generally successful
outcomes. Their advantage is a decrease in the nursing
time previously required for dressing changes, as well as
less pain for the patient.
Chronic Wounds
Etiology
A chronic wound is a wound that has not healed completely
within 30 to 90 days of the operative procedure. These
wounds are commonly found in patients taking high doses
of corticosteroids, cancer patients treated with
immunosuppressants, patients who are undergoing
chemotherapy, patients who have had radiation therapy,
malnourished patients, morbidly obese patients with huge
wounds, or those in whom wound dehiscence occurred and
there is a large granulating base. Nonhealing perineal
wounds can occur in patients with previous radiation
therapy, Crohn's disease, acquired immunodeficiency
syndrome (AIDS), or cancer.
Presentation and Management
Chronic wounds may be large and are usually covered
with shaggy granulation tissue, exuberant granulation
tissue, or areas of purulent fibrinous exudation.
Meticulous wound care, débridement, and the use of a
fenestrated skin graft, rotation flaps, or a wound vacuum
device may accelerate healing of these chronic wounds.
Quantitative wound cultures may be helpful in selecting
more targeted antibiotic therapy. Reducing corticosteroid
doses, improving nutritional status, and the use of
epidermal growth factor preparations may help heal some
types of chronic wounds.
Preventing large chronic wounds is often difficult, but in
situations in which one can, avoiding an operation in an
irradiated field, encouraging obese patients to lose weight
or improve their nutritional status before surgery, and
having patients cease smoking may all contribute to
prevention of a chronic wound infection.
Complications of Thermal
Regulation
Hypothermia
Malignant Hyperthermia
Postoperative Fever
Cardiac complications
Chest pain
Taking a careful pain history should help differentiate
between the causes of chest discomfort listed in the box
below.
Cardiac complicationsCauses of postoperative chest pain
Dull, central ache
Myocardial ischaemia (usually brought on by exertion)
Gastric distension
Central pain radiating through to back
Thoracic aneurysm or dissection
Peptic ulcer disease, oesophagitis, rarely pancreatitis
Cardiac complicationsPain on movement
Musculoskeletal pain
Chest drains
Pleuritic pain
Chest infection
Pneumothorax
Haemothorax, pleural effusion, empyema
Chest drain in situ
Pulmonary embolism
Diagnosis
Take a careful history and examine the patient.
A CXR will demonstrate most lung pathology.
12-lead ECG should help exclude myocardial ischaemia.
Recent WCC and CRP help identify sepsis.
Review previous medical history for peptic ulcer disease
and the drug chart for NSAID use.
Myocardial ischaemiaPatients, particularly in vascular surgery, may have pre-
existing ischaemic heart disease. Surgery can precipitate
ischaemia through:
stress response to major surgery (endogenous
catecholamine release triggered by anxiety, pain);
fluid overload postoperatively;
profound hypotension;
failing to restart anti-anginal medication postoperatively.
Myocardial ischaemiaDiagnosis
Take a history, particularly of chest discomfort brought on
by exertion and relieved by GTN. Check that the patient is
back on any regular cardiac medication. The
physiotherapists may report bradycardia on exercising. A
12-lead ECG will confirm the presence of myocardial
ischaemia. Cardiac enzymes (CKMB and troponin I and T)
may be slightly raised postoperatively, but serial
measurements showing a continued rise would suggest
ongoing myocardial damage.
Management
Sit patient up; give high flow O2.
Ensure the patient is on aspirin 75mg od PO and LMWH,
e.g. 40mg enoxaparin (Clexane) SC.
Give GTN sublingually.
Re-start preoperative anti-anginal medication.
Discuss urgently with a cardiologist.
Perioperative myocardial infarction
Perioperative MI may be difficult to diagnose because the
patient may be unable to give a good history, or to
distinguish between chest and upper abdominal pain.
The presentation is similar to that of myocardial
ischaemia, but the duration is longer (>20min), and may
be associated with haemodynamic instability, nausea,
vomiting, confusion, and distress.
The patient will be cold, clammy, and may be hypoxic.
Perioperative myocardial infarction
Diagnostic criteria for myocardial infarction
In the setting of symptoms suggestive of acute coronary
syndrome:
ECG shows ST segment elevation: ST segment elevation
MI (STEMI)
no ST elevation, but elevated CKMB and troponin
positive. Non Q wave or non ST segment elevation Ml
(NSTEMI)
Management
Attach an ECG monitor, and a sats probe, and get a 12-
lead ECG.
Make sure the defibrillator trolley is close at hand.
Give high flow O2.
Get IV access.
Give morphine 5mg IV and metoclopramide 10mg IV.
Give aspirin 300mg PO/PR and GTN 0.5mg SL.
Contact cardiologists urgently.
Key revision points-physiology of
coronary blood flow
Myocardial cells extract up to 70% of O2 from blood
Coronary blood flow occurs during diastole
Tachycardia reduces diastolic interval and increases O2
demand, which may reveal occult ischaemia
Coronary vasodilatation is mediated by adenosine, K+,
hypoxia, and the N2O pathway.
Respiratory complications
These are common after surgery as a result
of the effect of general anaesthetic,
postoperative pain, and immobility.
Respiratory failureDefinitions of respiratory failure
Hypoxia: PaO2 < 10.5kPa
Hypercapnia: PaCO2 > 6.5kPa. Hypocapnia: PaCO2 <
3.5kPa
Type I respiratory failure: PaO2 < 8.0kPa on air.
Type II respiratory failure: PaO2 < 8kPa and PaCO2 >
6.0kPa
Basic assessment and management
Sit the patient up and give high flow O2 through a tight
fitting mask.
Assess the airway: is chest expansion asymmetrical?
Auscultate the chest. Listen for bilateral breath sounds,
poor air entry, wheeze, bronchial breathing, crepitations.
Assess circulation and treat shock, which causes
hypoxaemia .
Treat bronchospasm with nebulized salbutamol 5mg.
Get a CXR. Look for consolidation, oedema, effusions,
and pneumothoraces.
Chest infectionDiagnosis
Cough with purulent sputum.
Pyrexia.
Bronchial breath sounds and reduced air entry on
auscultation.
Leucocyte neutrophilia, raised CRP.
Consolidation on CXR.
Culture of sputum may yield sensitivities of causative
organisms.
In the dyspnoeic, hypoxic patient perform arterial blood
gases to guide immediate management.
Chest infectionPrevention
There is no good evidence that prophylactic physiotherapy
helps to prevent chest infection after surgery. The single
most important intervention is to prevent patients with
active chest infections undergoing surgery. Any elective
patient with a current cough (dry or productive),
temperature, clinical signs of chest infection, neutrophilia,
or suspicious CXR should be deferred for a fortnight and
then reassessed. Other risk factors include active smokers
or those who have stopped smoking within the last 6 weeks;
patients with COPD, obesity; patients requiring prolonged
ventilation postoperatively; and patients who aspirate.
Chest infectionManagement
Physiotherapy helps the patient with a cough to
expectorate sputum, and prevent mucus plugging.
Effective analgesia is important to allow patients to cough.
Definitive treatment is antibiotics: ciprofloxacin 250mg
PO provides good Gram -ve and +ve cover until organism
sensitivities are known.
Chest infectionManagement
Suspected aspiration pneumonia should be treated with IV
cefuroxime 1g tds and IV metronidazole 500mg tds.
If the patient requires oxygen (PaO2 < 8.0kPa on room
air), humidifying it reduces the risk of mucus plugs, and
makes secretions easier to shift.
CPAP can be used to improve basal collapse.
The hypoxic, tachypnoeic, tiring patient on respiratory
support should be reviewed urgently by the critical care
team.
Exacerbation of COPD
The incidence of moderate to severe COPD in surgical
patients is 5%.
Most studies show that moderate COPD is not associated
with an increase in postoperative complications, mortality,
or length of stay.
Severe COPD and preoperative steroid use are associated
with increased morbidity and mortality after surgery.
Ensure that all patients on preoperative β-agonist inhalers
are routinely prescribed regular postoperative nebulizers
(saline 5mL prn, salbutamol 2.5-5mg qds prn, and
becotide 500mcg qds prn).
Exacerbation of COPD
In hypoxic patients with COPD give maximal O2 by CPAP
and titrate against PaCO2 and PO2: do not restrict oxygen
empirically.
Key revision points-monitoring/measuring lung function
Pulse oximetry estimates the percentage of saturated
haemoglobin present in capillary blood by the change in
wavelength ratios of absorbed red light. It is inaccurate in
CO poisoning, cold peripheries, low flow states, and
tachydysrhythmias.
Exacerbation of COPD
PaO2 can be approximately estimated from the SaO2
95%, > 12kPa
85%, ~ 10kPa
75%, < 6kPa
Capnography works on similar principles: different gases
(e.g. CO2) absorb different amounts of infrared light
Renal complications
Renal dysfunction
Creatinine: >126µmol/L in males; >102µmol/L in
females
Urea: >7.0mmol/L
Creatinine clearance: <90mL/min
Aetiology of renal failure
Preoperative risk factors.
Age > 75y; creatinine > 150µmol/L; LV dysfunction,
hypertension, diabetes, peripheral vascular disease,
hypoperfusion as a result of diuretic therapy and
vasodilators, sepsis, congestive cardiac failure, intrinsic
renal damage caused by NSAIDs, contrast,
aminoglycosides, diuretics, endocarditis, obstructive
uropathy.
Intraoperative risk factors. Cardiac surgery, aortic surgery.
Aetiology of renal failure
Postoperative risk factors.
Pre-renal: shock, e.g. hypovolaemic, septic, cardiogenic
Renal: sepsis, hypoxia, drugs (NSAIDs, gentamicin,
vancomycin, teicoplanin), haemoglobinuria, myoglobinuria.
Post-renal: obstructive uropathy, obstructed Foley catheter,
prostatic hypertrophy.
Preventing renal failure There are a number of measures that reduce the risk of renal
dysfunction.
Preoperatively, ensure adequate hydration particularly before
undergoing procedures involving contrast.
Identify and eliminate nephrotoxic medications where possible,
particularly NSAIDs and ACE-inhibitors.
Consider whether the patient would benefit from HDU preop.
Avoid intraoperative hypotension.
Postoperatively maintaining satisfactory cardiac output and
optimizing intravascular volume are the most important factors
in avoiding renal dysfunction.
Management of renal failure
The management of established oliguric renal failure.
The aim is firstly to avoid the potentially lethal
complications of renal failure (hyperkalaemia, acidosis,
pulmonary and cerebral oedema, severe uraemia, and drug
toxicity) and secondly to avoid exacerbating the renal
insult.
Investigation of the underlying causes of renal failure is
also important.
Aim for higher BP (stop antihypertensives; optimize fluid
balance) except in established anuria.
Treat hypoxia aggressively.
Aim for daily fluid balance of even to negative 500mL to
avoid pulmonary oedema in anuric patients.
Monitor electrolytes daily, and potassium and acid-base
balance every few hours. Avoid potassium supplements
and medication that increases potassium levels (ACE-
inhibitors).
Avoid nephrotoxic drugs (aminoglycosides, NSAIDs,
ACE inhibitors) and monitor serum levels of drugs
dependent on renal excretion (digoxin, antibiotics such as
vancomycin and gentamicin).
Essential amino acid diets are recommended for patients
who are able to eat. Patients on dialysis require high
protein content (1.5g/kg/day) as dialysis results in
negative nitrogen balance.
Enteral and parenteral feeds can be similarly adjusted.
Renal ultrasound, renal angiography may be indicated.
Hyperkalaemia
Hyperkalaemia (K+ > 5.0) is seen in the setting of renal
failure, tissue necrosis, and potassium sparing diuretics
and supplements. Acute hyperkalemia (K+ > 6.0) can
cause life-threatening ventricular arrhythmias. ECG
changes that herald myocardial dysfunction are flattened P
waves, wide QRS complexes, tenting of T waves, and, in
peri-arrest, a sine wave.
Treat the patient with ECG changes as an emergency.
Treat the underlying cause.
Give 50mL of 50% dextrose containing 15 units of
Actrapid as an IV infusion over 10-20min, repeating as
necessary, monitoring blood sugars after each infusion. If
inadequate response:
Give 10mL calcium gluconate 10% IV over 2min; repeat.
Calcium resonium enema binds K and removes it from the
body.
Dialysis should be urgently considered in patients with
refractory hyperkalemia despite these measures,
irrespective of renal function.
Hypokalaemia
Hypokalaemia (K+ < 3.0) is common. It predisposes
patients to dysrhythmias. It is normally related to diuretic
therapy, insulin sliding scales, diarrhoea and vomiting,
steroids, and poor nutrition. Acute severe hypokalaemia
(K+ < 2.5) may result in life-threatening arrhythmias. It
can be recognized by small or inverted T waves, depressed
ST segments, prolonged PR interval, and U waves on the
ECG.
Educate the patient about which foods are rich in
potassium (bananas, prunes, apricots, tomatoes, orange
juice) and ensure availability.
Change frusemide to co-amilofruse 5/40 or 2.5/20 which
contains frusemide (either 40mg or 20mg) and amiloride
(5mg or 2.5mg).
Add oral potassium supplements up to 160mmol daily (1
tablet of Sando K+ contains 20 mmol of K+, 1 tablet of
Slow K+, which is better tolerated by most patients,
contains 12.5mmol KCL).
If a central line is in place give 20mmol KCL in 50-
100mL of 5% dextrose over 20min to 1h.
If it is necessary to use a peripheral line place a maximum
of 40mmol of potassium in 1L 5% dextrose running at a
maximum of 125mL/h.
Monitor K+ daily, and avoid discharging the patient home
on a combination of potassium supplements and
potassium sparing.
Urinary complications
OliguriaTerminology
Oliguria = urine output < 0.5mL/kg/h
Anuria = no measurable urine output
Urine ouput is an indicator of glomerular filtration rate,
which is an indicator of renal plasma flow and renal
perfusion. Hence urine output is an indirect measure of
renal (and hence systemic) blood flow as well as renal
function. Patients with normal renal function usually
maintain a urine output of at least 0.5mL/kg/h.
Management of oliguria
Check that the Foley catheter is not the problem
The urine catheter may be obstructed, bypassing, or
malpositioned. Is the bed wet? Flush with 60mL
saline—can you draw this amount back without
difficulty? If not, or if the urine is bypassing the catheter,
or if the bladder is palpable, change the catheter.
Optimize cardiac function
Patients who were markedly hypertensive preoperatively may
require high blood pressures to maintain a satisfactory urine
output.
Is the patient overfilled or underfilled ?
Make sure the patient is adequately filled by giving careful fluid
challenges to achieve CVP of 14-16mmHg, or raise the JVP
moderately .
But not too filled. If the CVP rises to > 16mmHg and stays up
with a fluid challenge, or if the BP falls, the patient may be
overfilled and need diuretics.
Invasive monitoring. If the patient does not rapidly respond to
basic measures, they need CVP line insertion and monitoring.
Loop diuretics
Frusemide will not prevent acute tubular necrosis but it
does have a useful role in offloading fluid from the over-
filled patient. It converts oliguric renal failure to polyuric
renal failure.
If the patient is adequately filled and mean arterial
pressures are satisfactory give a loop diuretic: 20mg of
frusemide IV. If there is no response, give a further 40mg
frusemide IV.
If the urine produced in response to diuretic challenges is
concentrated, the patient is probably inadequately filled.
Important problems associated with oliguria of any cause
Pulmonary and cerebral oedema.
Congestive cardiac failure .
Hyperkalaemia.
Acidosis.
Drug toxicity.
Further assessment and management
Haemodialysis is indicated in the oliguric patient to avoid
pulmonary oedema indicated by deteriorating blood gases
despite increasing respiratory support, hyperkalaemia, and
acidosis. It is not indicated purely for rising serum
creatinine and urea in the first instance.
Acute urinary retention
Common postoperatively, especially in elderly males, after
abdominopelvic or groin surgery and after
anticholinergics.
Clinical features
Suprapubic discomfort, inability to initiate micturition, or
dribbling.
History of prostatic disease or symptoms preoperatively.
Percussable bladder on examination.
Management
Conservative. Improve analgesia, treat constipation,
mobilize, warm bath to encourage micturition, restart
preoperative tamsulosin.
Insert urethral catheter if conservative measures fail and
patient in great discomfort, or renal dysfunction is
suspected.
Urinary tract infection
Common in females, and patients catheterized for
prolonged periods.
Clinical features
Dysuria, frequency, dribbling, offensive smell, pyrexia.
Dipstick urine to confirm (dipstick should test nitrites and
leucocytes).
Send specimen for microbiology to identify organism and
sensitivities.
Management
Remove catheters as soon as possible
Encourage drinking or increase fluid infusion if safe to
increase urine flow.
Treat empirically with trimethoprim 400mg bd until
sensitivities known.
Gastrointestinal complicationsParalytic ileus
This is the cessation of GI tract motility.
Causes
Prolonged surgery and handling of the bowel.
Peritonitis and abdominal trauma.
Electrolyte disturbances (most can affect GI function!!).
Anticholinergics or opiates.
Prolonged hypotension or hypoxia.
Immobilization.
Paralytic ileus
Clinical features
Nausea and vomiting and hiccoughs.
Abdominal distension, tympanic or dull on percussion.
Absent bowel sounds.
Air/fluid-filled loops of small and/or large bowel on AXR.
Prognosis
Intestinal ileus usually settles with appropriate treatment
Paralytic ileus
Treatment
Pass a nasogastric tube to empty the stomach of fluid and
gas if the patient is nauseated or vomiting. Small volumes
of tolerated oral intake may help mild ileus to resolve.
Ensure adequate hydration by IV infusion
Maintain the electrolyte balance.
Reduce opiate analgesia, and encourage the patient to
mobilize.
After 5-7 days, look for other causes and consider
nutritional status.
Postoperative mechanical small bowel obstruction
It is important to distinguish between mechanical
obstruction and ileus since management is different.
Causes
Early adhesions (usually self-limiting).
Internal, external, parastomal, or wound herniation.
Intraabdominal sepsis (usually slightly later presentation).
Postoperative mechanical small bowel obstruction
Clinical features
Nausea and vomiting.
Colicky abdominal pain.
Abdominal distension, tympanic on percussion.
Examine hernial orifices and stoma if any for incarcerated
hernias.
High-pitched bowel sounds.
Dilated loops of small bowel (relative paucity of gas in
colon).
Postoperative mechanical small bowel obstruction
Treatment
As for paralytic ileus with strict bowel rest.
Consider CT scan to define level of the obstruction.
Prognosis
Surgery is rarely indicated (for suspected herniation or
complications or, very occasionally, adhesional
obstruction that fails to resolve).
Nausea and vomiting
This affects up to 75% of patients. It predisposes to
increased bleeding, incisional hernias, aspiration
pneumonia, absorption of oral medication, poor nutrition,
and K+. Causes include:
prolonged surgery; anaesthetic agents, e.g. etomidate,
ketamine, N2O, opioids; spinal anaesthesia; gastric
dilatation from CPAP;
postoperative ileus; bowel obstruction; constipation;
gastric reflux; peptic ulceration or bleeding; medications
including many antibiotics, NSAIDs, opiates, statins;
pancreatitis; sepsis; and hyponatraemia.
Classification of antiemeticsCombining two different types of antiemetic increases
efficiency.
Antidopaminergic agents
Good against opioid nausea and vomiting, sedative,
extrapyramidal side-effects
E.g. prochlorperazine 12.5mg IM, metaclopramide 10mg
IV/IM/PO tds.
Antihistamines
Sedation, tachycardias, hypotension with IV injection
E.g. cyclizine 50mg IM/IV/PO tds
Classification of antiemeticsCombining two different types of antiemetic increases
efficiency.
Anticholinergics
Active against emetic effect opioids, sedation, confusion,
dry mouth
E.g. hyoscine (scopolamine) 0.3-0.6mg IM
Antiserotonergics
Lowest side-effect profile of all antiemetics
Ondansetron 1-8mg PO/IV/IM tds, granisetron 1mg
PO/IV tds
Constipation
Failure to pass stool is common. Caused by lack of privacy,
immobility, pain from wounds or anal fissures, dehydration,
poor nutrition, dietary fibre, opiates, iron supplements, and
spinal anaesthesia. Treat with:
Bulking agents, e.g. Fybogel 1 sachet PO bd.
Stool softeners, e.g. sodium docusate 30-60mg od PO.
Osmotic agents, e.g. lactulose 5-10mL bd.
Stimulants, e.g. senna 1 tablet bd PO, bisacodyl 5-20mg
nocte PO.
Diarrhoea
Common causes in postoperative patients:
resolving ileus or obstruction
related to underlying disease or surgery (e.g. ileal pouch
or Crohn's
antibiotic-related diarrhoea (send for M, C, & S);
Clostridium difficile diarrhoea (send stool for C. difficile
toxin)
pseudomembranous colitis
Neurological complicationsConfusion
Confusion is common postoperatively. It is often obvious,
with a disoriented, uncooperative, or hallucinating patient.
Frequently it is more subtle, consisting of inactivity,
quietness, slowed thinking, and labile mood, and it is only
spotted by relatives or nursing staff. Actively assess
whether the patient is oriented in time, person, and place.
Perform a quick mini-mental state examination if you are
still unsure.
Confusion
Common causes of confusion
Medication (particularly benzodiazepines, opiates,
anticonvulsants)
Stroke
Hypoxia, hypercapnia
Shock
Sepsis
Alcohol withdrawal
Metabolic disturbances ( glucose, Na+, pH; ↑ Ca2+, Cr,
urea, bilirubin)
Post-ictal
Preoperative dementia
Management
If the patient's behaviour poses a physical danger to
themself or others, it may be necessary to sedate as first-
line management. Haloperidol 2.5mg may be given up to a
total of 10mg in 24h PO, IM, or IV, but, if the patient
remains disturbed, 2.5-5mg of midazolam should be given
IV and the patient placed under close observation.
Beware of sedating the hypoxic or hypotensive patient as
this may trigger a cardiorespiratory arrest: confusion is a
common symptom of shock and profound hypoxia.
Reassess the drug chart: stop opiates and benzodiazepines.
Correct abnormalities, e.g. glucose, Na.
Management
Alcohol withdrawal is diagnosed from a history of
chronically high alcohol consumption often with raised Îł-
GT, combined with psychomotor agitation
postoperatively. It can be treated with either diazepam 5-
10mg tds PO/PR, haloperidol 2.5-5mg tds PO/IM/IV, or
allowing the patient alcohol 1 unit orally.
Perform a neurological examination to look for focal
neurological deficit and consider head CT to exclude
stroke.
Reassure patient and relatives: confusion is common,
almost always reversible.
Neurological complications
Stroke
Stroke is most common in vascular and cardiac surgical
patients (2%), but elderly patients undergoing other major
surgery are at risk.
Risk factors for stroke
Increasing age (> 80y risk of CVA 5-10%).
Diabetes.
Previous history of stroke or TIA (increases risk
threefold).
Carotid artery atherosclerosis.
Perioperative hypotension.
Left-sided mural thrombus.
Mechanical heart valve.
Postoperative AF.
Aetiology
Embolic: carotid stenosis/atheroma, thrombus from AF.
Haemorrhagic: postoperative warfarinization.
Cerebral hypoperfusion: profound hypotension, raised
ICP.
Hypoxia.
Clinical features
Any deficit resolving within 24h is called a transient
ischaemic attack (TIA). Clinical features of perioperative
stroke include:
failure to regain conciousness once sedation has been
weaned;
hemiplegia (middle cerebral artery or total carotid artery
occlusion);
initial areflexia becoming hyperreflexia and rigidity after a
few days;
Clinical features
aphasia, dysarthria, ataxia (gait or truncal), inadequate gag
reflex;
visual deficits, unilateral neglect, confusion, seizures;
persistent, marked hypertension;
Hypercapnia.
Diagnosis
The aim is to establish a definitive diagnosis, establish a
cause to guide appropriate secondary prevention, and
establish a baseline of function to help plan long-term
rehabilitation or withdrawal of therapy.
Carry out a full neurological examination (cognitive
function, cranial nerves, and tone, power, reflexes, and
sensation in all four limbs).
Modern contrast head CT will show infarcts within 2h
(older scanners may not pick up lesions until they are 2-3
days old. You must distinguish between haemorrhagic and
ischaemic CVAs (1 in 10 are haemorrhagic). MRI is
necessary to image brainstem lesions.
Initial management
Assess the airway, breathing, and circulation .
If the patient is unable to maintain their airway insert a
Guedel airway, bag and mask, ventilate with high flow O2,
and call an anaesthetist.
Monitor BP, but do not attempt to correct high pressures
as these are critical for adequate cerebral perfusion.
Monitor oxygen saturations.
Secure IV access and give colloid if indicated.
Initial management
If the patient is able to maintain their own airway and is
not haemodynamically compromised explain what has
happened and reassure them.
Perform a full neurological examination.
Put the patient NBM if there is no gag reflex.
Send blood cultures if there is any history of endocarditis,
pyrexia.
Request a CT head and consider a transthoracic echo.
Hepatobiliary complicationsBile Duct Injuries
Etiology
The most dreaded complication of gallbladder surgery is
injury to the extrahepatic bile duct system.
Cholecystectomy accounts for the great majority of
postoperative biliary injuries and strictures. The rate of
major bile duct injury after laparoscopic cholecystectomy
ranges from 0.4% to 0.7%, as opposed to 0.2% after open
cholecystectomy.
Hepatobiliary complicationsBile Duct Injuries
Etiology
Bile leak may be due to a bile duct injury, cystic duct
stump leak, divided accessory duct, or injury to the
intestine. Acute cholecystitis, a foreshortened cystic duct,
anomalies of the biliary tree, hemorrhage from injury to
the cystic or hepatic artery, dissection with thermal
instruments in the triangle of Calot, and failure to clearly
define the anatomy in the triangle of Calot are among the
most important factors associated with a higher frequency
of duct injury after laparoscopic cholecystectomy.
Hepatobiliary complicationsBile Duct Injuries
Etiology
The most common injury sustained during the
laparoscopic procedure is complete transection at or below
the hepatic duct bifurcation. Other less complex injuries
include occlusion of the duct with a clip, thermal injury,
avulsion of the cystic duct, and partial laceration.
Bile Duct Injuries
Presentation and Diagnosis
Most bile duct injuries are not identified at the time of
surgery. Early in the postoperative period patients may
have manifestations related to a bile leak or later have
signs of a bile duct stricture. Bile leaking from a lacerated,
divided duct may accumulate in the subhepatic space and
form a biloma or seep into the peritoneal cavity and result
in bile ascites. Patients in this situation have right upper
quadrant pain, fever, nausea, abdominal distention, and
malaise. The bile, on the other hand, may drain through an
intraoperatively placed drain and be manifested as a bile
leak.
Bile Duct Injuries
Presentation and Diagnosis
In this setting patients may have leukocytosis and slightly
elevated bilirubin. Patients with a clipped bile duct do not
usually have symptoms but do have elevated liver
enzymes. Bile duct strictures are usually accompanied by
cholangitis, pain, fever, chills, and jaundice.
Bile Duct Injuries
Presentation and Diagnosis
Diagnosis of bile duct injury requires the use of nuclear
medicine imaging to demonstrate the presence of a leak or
obstruction, a CT scan to identify bile collections or
ascites, and ERCP to accurately define the type and level
of injury. Percutaneous transhepatic cholangiography is
indicated in cases of complete transection to define the
proximal anatomy and site of injury. Magnetic resonance
cholangiopancreatography is becoming the test of choice
to diagnose late strictures and define the bile duct
anatomy.
Bile Duct Injuries
Treatment
Prevention of bile duct injury starts with proper surgical
technique and adequate identification of the anatomy. The
anatomic variability associated with severe inflammation
creates a low threshold for converting a laparoscopic to an
open cholecystectomy. During laparoscopic
cholecystectomy, the infundibulum of the gallbladder
must be retracted laterally and inferiorly to expose the
triangle and widen the cystic–common bile duct angle.
Dissection of the cystic duct and artery must commence
close to the infundibulum of the gallbladder.
Bile Duct Injuries
Treatment
The cystic duct and artery are divided once the anatomy is
clearly delineated. Excessive traction on the gallbladder
must be avoided because it will result in tenting of the
common duct. If there is bleeding in the area of the cystic
duct, blind clipping and cautery must be avoided, and
adequate exposure must be achieved even if placement of
another port is required. If there is an unexpected bile
leak, unusual anatomy, or a second bile duct identified or
when technical difficulties and excessive bleeding are
encountered, intraoperative cholangiography helps
identify the anatomy and any injuries. Early conversion to
an open procedure must also be considered.
Bile Duct Injuries
Treatment
Once a leak is diagnosed intraoperatively, immediate
repair must be performed. The procedure is converted to
an open one and the extent of duct injury is assessed. An
accessory duct can be ligated, partial transection of the
common duct is repaired over a T-tube, a divided duct or
nearly circumferential transection of the common duct is
repaired with an end-to-end anastomosis over a T-tube,
and a high injury is repaired with a Roux-en-Y biliary-
enteric anastomosis. If repair of a high duct injury is
difficult, drains are placed in the subhepatic space and the
patient is referred to a tertiary center.
Bile Duct Injuries
Treatment
A leak or injury identified early in the postoperative
period is treated as follows: the biloma is drained
percutaneously, and a sphincterotomy is performed or a
stent is placed (or both) if ERCP demonstrates a leak or
partial narrowing. Surgical intervention is indicated in
patients with major obstruction of the bile duct, a major
injury, or suspicion of a bowel injury. After adequate
resuscitation, administration of antibiotics, and adequate
drainage, patients are watched for a few days to make
certain that they are not septic at the time of the operation.
Bile Duct Injuries
Treatment
If there is evidence of adequate control of the leak, the
surgeon may wait up to 5 to 7 days for inflammation in the
area to subside before undertaking operative repair.
Meticulous and careful dissection is required in this area
because there is usually loss of common bile duct
substance. After identifying the source of the bile
extravasation, dissection plus débridement of nonviable
common bile duct is prudent. Once it is ascertained that
there is tissue with good integrity, a Roux-en-Y limb can
be anastomosed to the common bile duct. Multiple drains
are left around the site of the repair.
Ear, Nose, and Throat
ComplicationsEpistaxis
Epistaxis may be associated with primary blood dyscrasias
such as leukemia and hemophilia, excessive
anticoagulation, and hypertension. Epistaxis is divided
into two general categories: anterior and posterior.
Anterior trauma is often caused by contusion or laceration
of the nasal septum or turbinates during insertion of an
NG or endotracheal tube.
Ear, Nose, and Throat
ComplicationsEpistaxis
Firm pressure applied between the thumb and index finger
to the nasal ala and held for 3 to 5 minutes is generally
successful in stopping most cases of anterior epistaxis.
Occasionally, packing with strip gauze for 10 to 15
minutes will aid in a particularly refractory case. If the
bleeding fails to stop, packing for an extended period with
petrolatum-covered strip gauze may be required. Removal
of the packing in 1 to 3 days is usually associated with
successful treatment of refractory epistaxis, along with
treatment of the underlying condition or reversal of
anticoagulation.
Ear, Nose, and Throat
ComplicationsEpistaxis
A more serious scenario is posterior nasal septal bleeding,
which on occasion can be life threatening. If all attempts
to stop anterior nasal septal bleeding are unsuccessful, one
may infer the probability of a posterior nasal hemorrhage,
which may necessitate placement of a posterior pack of
strip gauze covered in petrolatum ointment. For
particularly refractory cases, a Foley catheter with a 30-
mL balloon can be passed through the nasal passages, and
after the pack is placed, pressure can be applied to the
pack by pulling on the Foley catheter.
Ear, Nose, and Throat
ComplicationsEpistaxis
This type of epistaxis may require concomitant anterior
nasal packing to be successful. The packs on a difficult
hemorrhage such as this may need to be left in place for 2
to 3 days. For epistaxis that defies all attempts at
conservative management, ligation of the sphenopalatine
artery or the anterior ethmoidal artery may be required.
Ear, Nose, and Throat
ComplicationsAcute Hearing Loss
Abrupt loss of hearing in the postoperative period is an
uncommon event. An immediate physical examination is
performed to ascertain the degree of hearing loss.
Unilateral hearing loss is generally associated with
obstruction or edema related to an NG or feeding tube.
Bilateral hearing loss is more often neural in nature and is
usually associated with pharmacologic agents such as
aminoglycosides and diuretics.
Ear, Nose, and Throat
ComplicationsAcute Hearing Loss
Examination with an otoscope will often reveal the
presence of cerumen impaction or edema from a middle
ear infection. If the otologic examination is completely
normal, one needs to suspect neural injury related to the
agents just mentioned. These agents need to be
discontinued immediately and hearing monitored over the
ensuing 2 to 3 days to see whether recovery occurs. For
cerumen impaction, use of a delicate speculum under
direct vision is indicated. If the hearing loss is associated
with edema related to an NG tube, merely removing the
NG tube will result in resolution of the edema.
Ear, Nose, and Throat
ComplicationsNosocomial Sinusitis
Nosocomial sinusitis is a recently recognized
complication in the critically ill. Left untreated, sinusitis
may be complicated by brain abscess formation,
postorbital cellulitis, and nosocomial pneumonia. Patients
at high risk for sinusitis are those receiving ventilatory
support via a nasotracheal tube and those with nasal
colonization with gram-negative bacteria. Also at risk are
patients with facial trauma, those with an NG or feeding
tube, and patients who have received antibiotic therapy.
Ear, Nose, and Throat
ComplicationsNosocomial Sinusitis
The majority of nosocomial sinusitis occurs in the second
week of hospitalization, and the maxillary sinuses are the
most commonly affected. The classic signs encountered
with community-acquired sinusitis (i.e., facial pain,
malaise, fever, and purulent nasal discharge) may not be
present because the patient is usually unconscious and
intubated, has other sources of infection, and is receiving
analgesics and antipyretics. The diagnosis is often made
when a CT scan is performed to look for a source of fever
and the sinuses are included in the cuts.
Ear, Nose, and Throat
ComplicationsNosocomial Sinusitis
The CT scan generally shows thickened mucosa and the
presence of an air-fluid level or opacification of the sinus.
Once diagnosed or suspected, nasal tubes are removed,
decongestant is administered, and antibiotic therapy
targeting the two most common organisms, S. aureus and
Pseudomonas species, is given. Other organisms that play
a major role in nosocomial infections, such as methicillin-
resistant S. aureus, vancomycin-resistant Enterococcus,
and Acinetobacter species, are also included in the
coverage.
Ear, Nose, and Throat
ComplicationsNosocomial Sinusitis
With such treatment, clinical response occurs in 48 hours
and clinical and radiologic cure occurs in two thirds of
patients. Failure of medical therapy leads to surgical
drainage of the sinus involved. In rare cases, severe
intractable sinusitis may require a drainage procedure via
an operative technique.
Ear, Nose, and Throat
ComplicationsParotitis
Parotitis most commonly occurs in an elderly man with
poor oral hygiene and poor oral intake with an associated
decrease in saliva production. The pathophysiology
involves obstruction of the salivary ducts or an infection
in a diabetic or immunocompromised patient. The patient
is noted to have significant edema and focal tenderness
surrounding the parotid gland, which eventually
progresses to involve edema of the floor of the mouth. If
left undiagnosed and untreated, the parotitis can cause
life-threatening sepsis.
Ear, Nose, and Throat
ComplicationsParotitis
In the worst-case scenario, the infection can dissect into
the mediastinum and cause stridor from partial airway
obstruction. Patients with advanced parotitis will have
dysphagia and some respiratory occlusion. If the diagnosis
of parotitis is being entertained, the patient receives IV,
high-dose, broad-spectrum antibiotics with good coverage
of Staphylococcus (the most common agent cultivated
from this disease). In the presence of a fluctuant area,
incision plus drainage is indicated, with care taken to
avoid the facial nerve.
Ear, Nose, and Throat
ComplicationsParotitis
On rare occasion, advanced disease may even require
emergency tracheostomy. Most patients with parotitis will
have the condition arise 4 to 12 days after the initial
operation. Because of the rapid progression of this disease,
one must be aware of the diagnosis and, when present,
institute immediate therapy, including emergency surgery
on occasion for patients with an obvious fluctuant area.
Thank you for your attention!
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