surgical complications postoperative...surgical complications remain a frustrating and difficult...

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.


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 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.


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.


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 .


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.


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 Î˛-agonist inhalers

are routinely prescribed regular postoperative nebulizers

(saline 5mL prn, salbutamol 2.5-5mg qds prn, and

becotide 500mcg qds prn).


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.


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: >126Âµmol/L in males; >102Âµmol/L in

females

Urea: >7.0mmol/L

Creatinine clearance: <90mL/min

Aetiology of renal failure

Preoperative risk factors.

Age > 75y; creatinine > 150Âµmol/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

salineâ€”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).


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).


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; â†‘ 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.


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.


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


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


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.



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.



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.



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.


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.


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.


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.



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.



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.



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.


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.



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.



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!

surgical complications postoperative...surgical complications remain a frustrating and difficult...

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