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Postoperative complications 35
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Table5.2 The Two- Level Wells score forestimating theclinical probability ofa pulmonary embolism
Clinical Feature Points
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Tachycardia >100 bpm 1.5
Immobilization for > 3days or surgery in the previous 4weeks 1.5
History of DVT or PE 1.5
Haemoptysis 1
Cancer, either undergoing treatment or treated in the last 6months, or palliated 1
Management
• LMWH should be commenced immediately while
diagnosis is confirmed.
•
DOACs are an alternative treatment option in
ambulatory patients.
Mechanical compression stockings – once antico-
•
agulation has been started, patients should be
encouraged to mobilize and to wear mechanical
compression stockings, such as ThromboEmbolus Deterrent (TED) stockings.
Pulmonary embolism
This occurs when a clot, usually originating in a femoral vein or a pelvic vein (and occasionally in a calf
vein), detaches and travels to the heart to become
lodged in the pulmonary arterial tree.
Clinical features
Pulmonary emboli classically occur around the 10th
postoperative day but may occur sooner or later. The
clinical features of PE may vary from dyspnoea, or mild
pleuritic chest pain, to sudden death due to occlusion of
the pulmonary artery trunk. Minor symptoms include
pleuritic chest pain, dyspnoea and haemoptysis. Severe
dyspnoea may occur with cyanosis and shock, and larger
emboli may prompt acute right heart failure and death.
It is important to appreciate that pulmonary embolus
may occur without any preceding warning signs of
thrombosis in the leg. Indeed, once there are obvious
clinical features of deep vein thrombosis, detachment of
an organized and adherent clot from this limb is unlikely,
especially if anticoagulant therapy has been commenced
so that fresh clot formation is inhibited. The great
majority of fatal pulmonary emboli are unheralded.
On examination, the patient has tachypnoea, often
with a spike of fever. There is a tachycardia and a
raised jugular venous pressure (JVP) reflecting the
pulmonary hypertension. A pleural rub may be audible if the emboli are small and peripheral. Oxygen
saturations on ambulation are frequently reduced.
Risk prediction ofa pulmonary
embolus
Risk factors for PE, and their relative importance, are
illustrated by the two- level PE Wells score
in Table 5.2 and recommended by NICE. The Wells
score also permits triage of patients:
•
Score ≥4: PE likely- investigate with CT pulmo-
nary angiography (CTPA)
•
Score <4: PE unlikely- initial investigation with
- dimer
Special investigations
• Arterial blood gases may confirm hypoxaemia;
hypocapnia (low CO
ondary to tachypnoea.
• Chest radiograph is often normal initially, but
patchy shadowing of the affected segment may be
present. It is more useful in identifying alternative
causes such as pneumonia.
• - Dimer: A degradation product of fibrin present in
the blood of patients with intravascular thrombi. A
negative result effectively rules out thromboembolism in patients with a two-
• CT pulmonary angiography (CTPA) is the defini-
tive diagnostic test used when pulmonary emboli
are suspected and is particularly useful when pulmonary disease is present.
5
Philip Steven Wells, contemporary, Haematologist and
Professor of Medicine, University of Ottawa, Ontario
) may also be present sec-
2
level PE Wells score <4.
5
illustrated
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• Ventilation- perfusion (V/Q) scans can be considered
where it is preferable to minimize the radiation dose
exposure (such as pregnant patients).
•
Electrocardiogram (ECG) findings include rhythm
changes (e.g. atrial fibrillation, heart block) or features of right heart strain (ST segment depression
in leads V1 to V3, III and aVF, with right axis deviation), as the heart pumps against the obstructed
pulmonary arterial tree. The oft- mentioned ‘S1–
Q3–T3’ pattern (S wave in lead I, with a Q wave and
an inverted T wave in lead III) is seldom present.
Echocardiogram is most useful in patients with a
•
confirmed massive PE to detect signs of right heart
failure and pulmonary hypertension.
Treatment
1 Oxygen should be commenced if hypoxic.
2 LMWH at a therapeutic dose should be com-
menced immediately a PE is suspected pending
the formal diagnosis.
3
DOAC therapy is commenced once a PE is con-
firmed, assuming it is safe to do so, and the likelihood of bleeding complications is minimal. It is
continued for at least 3months.
Inferior vena cava (IVC) filters are designed to trap
4
fragmented thromboemboli from the deep leg veins
en route to the pulmonary circulation (while preserving blood flow in the IVC). They are indicated in
patients where anticoagulation is contraindicated
or where emboli recur in spite of anticoagulation.
5
Thrombolysis may be indicated in the first 48
hours after PE if there is evidence of haemodynamic compromise. Thrombolysis can either be
given into a peripheral vein (systemic thrombolysis) or directly into the pulmonary arteries via a
catheter (catheter- directed thrombolysis). Recent
surgery (within 14days) is a contraindication to
systemic thrombolysis due to risk of bleeding.
6 Surgical pulmonary embolectomy, with the patient
on cardiopulmonary bypass (Chapter13), is indicated in patients with massive pulmonary embolus who have a high risk of bleeding with
thrombolysis and of dying without treatment.
Management ofthe unwell
postoperative patient
Between 2% and 4% of postoperative patients will have
a severe complication. The evaluation of a critically
unwell patient is the same irrespective of the setting
and applies equally to a surgical patient. It is important to have a simple scheme to follow in each case.
The ABCDE approach discussed next follows guidance from Resuscitation Council UK. It occurs in two
phases, an initial rapid assessment followed by a more
detailed assessment.
Initial assessment
The initial rapid assessment determines whether
the patient looks unwell, whether they are able to
communicate or whether they are unresponsive
and require cardiopulmonary resuscitation.
Surgical drains should be inspected for evidence of
bleeding. Measurement of vital signs (pulse and
blood pressure) and pulse oximetry are important,
with ECG monitoring if available. Where possible
venous access through a peripheral cannula should
be obtained and can be combined with taking
bloods.
ABCDE assessment
Following the initial assessment, a systematic ABCDE
assessment takes place.
A: Airway
• Airway obstruction: Is the airway clear, or does it
require clearing/suctioning? The presence of stridor or wheeze imply partial airway obstruction.
If wheeze is present, nebulized salbutamol may
help.
• Airway maintenance: Physical manoeuvres such
as chin lift and jaw thrust lift the tongue from the
oropharynx and allow airflow. A number of
devices are available to maintain an airway:
– nasopharyngeal airway;
– oropharyngeal airway (e.g. a Guedel airway);
– supraglottic airway device (e.g. an I- Gel),
which sits over the laryngeal inlet.
• Endotracheal intubation: This may be required if
an airway cannot otherwise be maintained. In
extreme circumstances, a cricothyroid membrane
puncture may be necessary, or a formal tracheostomy if circumstance and time permit.
• Oxygen should be given at high concentration,
aiming for an oxygen saturation of >94% (88%–
92% if at risk of hypercapnic respiratory failure,
such as in some patients with chronic obstructive
pulmonary disease [COPD]).
B: Breathing
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During the assessment of breathing, it is important to
diagnose and treat conditions that are an immediate
threat to life, such as a tension pneumothorax and
massive haemothorax. In addition, nonditions such as acute asthma and pulmonary oedema
may need to be treated.
•
Signs of respiratory distress: the use of accessory
muscles of respiration, abdominal breathing and
sweating.
•
Respiratory rate and depth: shallow and/or rapid
breaths (>25 bpm) are adverse signs.
•
Chest wall: Is the chest deformed? Is the trachea
deviated? Is there paradoxical movement or
movement of only one hemithorax? Is surgical
emphysema present suggesting pneumothorax?
• Auscultation: may reveal features of pneumothorax or pneumonia.
Investigations include measurement of oxygen saturations and arterial blood gases help to establish the
extent of respiratory compromise and the effects of
treatment. A chest radiograph is important if chest
pathology is suspected. If fluid overload is suspected,
then diuretics or dialysis may be indicated, depending on renal function.
surgical con-
C: Circulation
Shock is discussed in Chapter8. Hypovolaemia is the
most likely cause of shock post operatively, but cardiac (e.g. myocardial infarction) and pulmonary (e.g.
tension pneumothorax, PE) causes are also common.
In assessing a surgical patient, the following should
be considered:
•
Peripheral skin colour: Pallor, cyanosis and mot-
tling of hands or fingers suggest hypoperfusion.
• Capillary refill time over 2 seconds suggests poor
perfusion but may also be present in the elderly or
a cold environment.
• Heart rate and pulse strength: Tachycardia and a
weak, thready pulse are common in shock.
• Blood pressure. In young patients, the blood pres-
sure may be maintained in spite of significant fluid
loss; the elderly tend not to be able to compensate
for haemodynamic insults.
• Auscultation of the heart may reveal a new mur-
mur or pericardial rub or heart sounds may be
inaudible in cardiac tamponade.
Postoperative complications 37
•
Urine output reflects end organ perfusion. Oliguria
(<30mL/h) suggests renal hypoperfusion.
The operative site and surgical drains, with par-
•
ticular reference to features of peritonitis after
abdominal surgery and blood in the drains. Note
that significant intrabdominal or intrathoracic
bleeding may occur with little or no blood appearing in the drains if the drains are blocked by clot.
An ECG and troponin levels should be checked to
rule out an acute coronary syndrome. If bleeding is
suspected, blood should be crossassessment should be made as to whether an immediate return to theatre or urgent imaging is
appropriate.
matched and an
D: Disability
Disability refers to the patient’s inability to follow
commands, usually as a result of loss of consciousness. It may be a consequence of hypoxia or impaired
perfusion of the brain, drugs (e.g. opiates, sedatives)
or metabolic disorders (e.g. hypoglycaemia)
•
Assess the level of consciousness using the Glasgow
Coma Scale (Chapter17).
•
Check the capillary blood glucose level and treat
hypoglycaemia (glucose <4mmol/L) with a glucose infusion (50mL of 10% glucose, repeated as
necessary).
• Seizures require initial treatment with benzodiaz-
epines.
Exclude drug causes, including:
•
– Opiates: small, pinpoint pupils, slow respira-
tion give naloxone (often requires repeated
doses)
– Benzodiazepine: give flumazenil
•
Exclude metabolic causes, such as hyponatraemia.
E: Exposure
Having gone through the aforementioned screening
process, it is important that a full examination exposing the whole body is undertaken to ensure nothing
has been missed.
At the end of the assessment, it should be clear
what immediate investigations are required, their
urgency, and where the patient is best nursed (ICU,
high dependency unit or ward). Repeated observation and reassessment are important adjuncts to
achieving the correct diagnosis.
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Postoperative
haemorrhage
Surgical bleeding may be divided into primary bleeding at the time of surgery; reactionary (or early) bleeding, which occurs within 24 hours of surgery; and
secondary (or delayed) bleeding, which has a peak
incidence between 7 and 10days. The consequences
of bleeding may be hypovolaemia presenting with
hypotension and tachycardia, or in closed spaces like
the cranium, it may present with pressure effects (loss
of consciousness).
or intraluminal bleeding which does not manifest
immediately. This may occur in spite of the placement of drains. In this setting, the diagnosis is suggested by a patient becoming tachycardic and
hypotensive, cold, sweaty and an appearance of pallor, all reflecting sympathetic nervous system stimulation shutting down the peripheral circulation.
Chapter8 discusses hypovolemic shock. It should be
remembered that the young tend to maintain their
blood pressure by peripheral vasoconstriction in
spite of significant haemorrhage, making the initial
diagnosis difficult without a high index of
suspicion.
Reactionary bleeding
Reactionary bleeding from the operative field may be
a consequence of several things, such as:
•
a blood vessel that was in spasm, or minimally
bleeding intraoperatively but that opens up with
restoration of normal blood pressure and patient
warming;
• a vessel from which a ligature or laparoscopic clip
has slipped;
•
unnoticed damage to an abdominal wall blood
vessel as a drain was placed while closing– commonly the inferior epigastric artery in abdominal
surgery, an intercostal artery in thoracic surgery;
a raw surgical bed following resection where hae-
•
mostasis is difficult;
•
an underlying bleeding disorder, or anticoagula-
tion, or in patients taking aspirin or clopidogrel.
Secondary haemorrhage
Secondary haemorrhage is usually a consequence of
infection in the operative field, possibly related to
leakage of enteric contents or pancreatic juice. It is
particularly common following resection of the head
of pancreas when an enzyme leak may often present
with catastrophic haemorrhage. It may also manifest
with intraluminal bleeding from the site of an intestinal anastomosis, or haemorrhage from an infected
vascular anastomosis.
Clinical features
Bleeding may be overt or concealed. Overt bleeding,
where there is visible blood loss, is readily appreciated. In concealed bleeding there may be intracavity
Management
Initial management follows the ABCDE principles outlined previously. Further management of postoperative
bleeding depends on the manner of its presentation.
Reactionary haemorrhage often requires an
•
immediate return to theatre, with little role for
imaging.
Secondary haemorrhage may also require urgent
•
re- exploration, but there is often a short period
where investigations may take place. In some
cases, radiological intervention, embolizing a
bleeding vessel identified on a prior CT scan, may
be the treatment of choice.
Postoperative fever
Postoperative fever may be defined as a temperature
over 38 °C on two consecutive postoperative days or a
single reading over 39 °C on any postoperative day.
While it may be a manifestation of the inflammatory
response to surgery, it may signify a serious postoperative complication.
There are many possible causes of pyrexia, which
can either be considered in terms of the timing postoperatively (Table 5.3) or by considering local and
general causes both infectious and non- infectious:
Local causes
•
Infectious: wound infection, anastomotic leak
• Non- infectious: post- surgical inflammatory response
General causes
Infectious: aspiration, pneumonia, urinary tract
•
infection
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Table5.3 Causes ofpostoperative fever according topostoperative day
Phase Postoperative day Causes
Immediate 0–1 Blood transfusion reaction
Acute 0–3 Basal atelectasis
3–5 Pneumonia or aspiration
5–10 Surgical site infection
Early 10–28 Intra-
Delayed >28 Viral infections
Anaesthetic reaction (such as malignant
hyperthermia)
Bacteraemia from instrumentation of infected
viscus
Gas gangrene of dirty wound
Urinary tract infection
Deep venous thrombosis
Surgical site infection
Early anastomotic leak
Pneumonia or aspiration
Line infection (e.g. central venous catheter)
Pulmonary Embolus
abdominal collection
Partially treated deep space infection
• Non- infectious: blood transfusion reaction,
anaesthetic reaction, drug reaction, DVT, PE,
basal atelectasis and thyroid crisis
Patients who are immunosuppressed have a
reduced inflammatory response and may lack fever
and have minimal physical signs in spite of serious
infection.
Assessment
A systemic approach is required in assessing the
patient:
1
The ABCDE approach to evaluate severity
2 The operation notes should be reviewed, looking
in particular for any anastomoses or gastrointestinal (GI) tract sutures placed to repair bowel and
any other operative concerns that may result in
postoperative problems.
3
Examine systems, in turn, and in particular:
a Inspect the wound: superficial wound infection
or haematoma
b Inspect venous cannula sites: thrombophlebitis
is common when a cannula has remained in
situ for a few days or when irritant infusions
have passed through it
Examine the chest clinically, considering pul-
c
monary collapse, infection, infarction and subphrenic abscess
d
Examine the legs: deep vein thrombosis
e Rectal examination: pelvic abscess
f Urine culture: urinary infection
g
Stool culture: for C. difficile toxin to exclude
enterocolitis
Consider the possibility of drug sensitivity
h
Following this, investigations should be initiated
according to the most likely diagnosis or diagnoses.
These may include:
•
Cultures of blood, lines, urine, sputum and stool
(where appropriate)
Chest radiograph
•
• Duplex of the deep veins if DVT is suspected
• Contrast- enhanced CT scan if intra- abdominal
cause is suspected
• C TPA for suspected pulmonary embolus
In patients who are very unwell, it may be necessary to commence antibiotics before the initial assessment has been completed, in which case it is
important to ensure that relevant cultures have been
taken. The antibiotic most likely to treat the probable
infective cause should be selected.
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Postoperative respiratory
problems
Respiratory problems are common after surgery,
being particularly common following open upper
abdominal surgery. Causes can be divided into those
presenting with shortness of breath and those where
respiration is suppressed.
Aetiology
A useful classification of causes by system is:
1
Respiratory
a Atelectasis
b Pneumonia, often secondary to aspiration
c
Pneumothorax, e.g. from central line placement
d Exacerbation of underlying COPD or asthma
2 Cardiovascular
a Left ventricular failure due to fluid overload
b
Myocardial infarction
c PE
3 General
a Metabolic acidosis, with compensatory hyper-
ventilation giving the impression of
breathlessness
b
Anaemia
4 Suppressed respiration
a Neuromuscular blockade, due to incomplete
anaesthetic reversal postoperatively
b
Opiates causing respiratory depression, espe-
cially in the presence of renal failure
Sleep apnoea
c
ABCDE assessment and management should be
undertaken. Oxygen should be administered, and the
underlying cause investigated, which usually requires
arterial blood gases, chest radiograph and 12-
lead ECG.
Pulmonary collapse
andinfection
Some degree of pulmonary collapse, also called atelectasis, occurs after almost every abdominal or transthoracic procedure within the first 48 hours of surgery.
Mucus is retained in the bronchial tree, blocking the
smaller bronchi; the alveolar air is then absorbed, with
collapse of the supplied lung segments (usually the
basal lobes). The collapsed segment or entire lung continues to be perfused and acts as a shunt, which
reduces oxygenation. The lung segment may become
secondarily infected by inhaled or aspirated organisms, and, rarely, abscess formation may occur.
Aetiology
Preoperative factors
• chronic obstructive airway disease;
•
smoking;
• asthma (which increases the amount of bronchial
secretion);
chest wall disease, such as ankylosing spondylitis,
•
which restricts ventilation and makes coughing
difficult;
•
poor mobility;
• obesity.
Operative factors
• anaesthetic drugs, such as atropine, which
increases the viscosity of secretions;
•
surgery in the upper abdomen or thorax;
• long operative time;
• excessive fluid replacement (goal- directed
replacement – the gold standard using cardiac
output monitoring).
Opiates, renal failure,
andrespiratory depression
Opiates are partially eliminated through the kidneys,
therefore clearance is impaired by renal failure.
Naloxone will reverse the effects of the opiates but
may require repeated doses because the half- life of
naloxone (60–90 minutes) is much shorter than that
of most opiates. An infusion of naloxone is usually
required in patients with renal failure if a delayed respiratory arrest is to be avoided.
Postoperative factors
• insufficient analgesia to permit full inspiration
opening all alveoli and expectoration;
• abdominal distension causing diaphragmatic
splinting.
Clinical features
The patient is dyspnoeic with a rapid pulse and
elevated temperature. There may be cyanosis. The
Postoperative complications 41
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patient attempts to cough, but this is painful and,
unless encouraged, may fail to expectorate. The sputum is at first frothy and clear but may become purulent later, diagnostic of secondary infection. The chest
movements are diminished, particularly on the
affected side; there may be basal dullness with
reduced air entry and coarse crackles.
The haemoglobin oxygen saturation on pulse oximetry may fall, and chest radiograph may reveal an opacity
of the involved segment(s) (usually basal or midzone),
together with mediastinal shift to the affected side if a
significant portion of one lung is affected.
Treatment
Preoperatively
Breathing exercises are given, and smoking is discouraged. Any prior chest infection is treated, and
surgery delayed, if possible, until the chest is
optimized.
Operatively
The surgical approach associated with the least respiratory compromise should be considered where
appropriate; laparoscopic surgery is preferable to
open surgery. Epidural or spinal anaesthesia is used
where possible and continued postoperatively.
Intercostal nerve blocks may be used for thoracic or
upper abdominal surgery and continued postoperatively. Transversus abdominus plane (TAP) anaesthetic blocks or catheters may be placed alongside
abdominal wounds to minimize immediate postoperative pain.
Postoperatively
The patient is encouraged to take deep breaths and
cough while supporting any abdominal wound with
their hands. Chest physiotherapy, saline/salbutamol
nebulizers and incentive spirometry are initiated.
Incentive spirometry encourages patients to take
slow, deep breaths and uses devices that provide visual cues to the patients to confirm that the desired
flow or volume has been achieved.
In the event of development of shortness of breath
or low oxygen saturations, a full ABCDE assessment
should take place to resuscitate the patient and confirm the diagnosis of chest infection with chest radiograph. Sputum cultures are sent, and antibiotic
treatment begun.
It is important to recognize adverse clinical features
that suggest that increased levels of respiratory support
may be required, ranging from increased inspired oxygen to nonairways pressure [CPAP]) to intubation and ventilation
on an intensive care unit. Recognizing these can allow
prescores have developed to aid nurses and doctors in recognizing such patients, such as the National Early
Warning Score (NEWS) 2 used in the UK. Features suggesting respiratory support may be required include:
use of accessory muscles, intercostal recession;
•
respiratory rate >25 bpm, which may be followed
•
respiratory rate <8 bpm;
•
•
decreasing vital capacity (shallow breathing);
• tachycardia and sweating (reflecting sympathetic
agitation and restlessness;
•
•
sitting up, unwilling to lie flat;
• hypoxaemia, with pO
HbO
•
• hypercapnia;
• impaired level of consciousness.
invasive ventilation (e.g. continuous positive
emptive treatment. A number of early warning
by exhaustion and respiratory failure;
activity);
< 11kPa when the FiO2 is
40%, or <8kPa on air;
saturations ≤90%;
2
2
Postoperative ileus
This is discussed in Chapter30.
Abdominal wound
dehiscence
Wound dehiscence is an uncommon complication of
surgery, being more common after emergency than
elective surgery. It may be divided into superficial and
full-
thickness dehiscence:
•
Superficial dehiscence is a failure of the skin clo-
sure such that subcutaneous tissue and even rectus sheath become exposed.
•
Full- thickness dehiscence occurs when all layers of
the wound fail such that some of the abdominal
contents (usually small bowel) prolapse out. This
is often termed a ‘burst abdomen’, a term that
reflects the shock of patient and staff alike when
they encounter bowel in the bed.
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Risk factors
Predisposing factors can be divided into preoperative,
operative and postoperative as follows:
Preoperative
Malnutrition (common with some cancers and emergency conditions), diabetes, COPD, obesity, smoking,
liver and renal failure, steroids and mTOR inhibitors
(everolimus and sirolimus). Previous radiotherapy
may compromise the vascularity of a wound, rendering it more prone to break down.
Operative
Emergency surgery, intra- abdominal sepsis, long
operations (increased incidence of wound infection),
early reoperations where the fascia becomes friable,
poor suture choice (insufficient strength or rapidly
absorbed) and poor operative technique. Midline
incisions are more likely to dehiscence than paramedian or grid iron appendix incisions.
One recommended technique for abdominal closure uses a continuous suture that is four times the
length of the wound, with individual ‘bites’ placed
1 cm apart (Jenkins’ rule
proposed even smaller bites of 5 mm. The key is to
place the suture into healthy fascia without tension
either laterally or longitudinally to avoid a ‘cheese
wire’ effect cutting through the fascia.
6
). Some researchers have
Postoperative
Excessive coughing (such as with COPD or chest infection), abdominal distension due to prolonged ileus or
obstruction, wound infection, wound haematoma and
delayed introduction of nutrition. Prolonged periods in
intensive care have also been cited as a cause.
nal cavity after operation and which seeps through
the wound breakdown.
The wound may open slightly, at which point loose
suture material and the smooth pink surface of small
bowel may be seen in its depths, or a more extensive
dehiscence may occur, especially after coughing or
straining, with intestine and omentum prolapsing
through.
Management
Depends on the clinical presentation. In both types of
dehiscence, wound swabs are taken to determine the
nature of any infecting organism.
Superficial dehiscence should be explored to con-
•
firm the integrity of the deep fascia and then managed expectantly with wound dressings or negative
pressure dressings.
Full- thickness dehiscence is a shocking and psy-
•
chologically disturbing occurrence for the patient
who will need strong reassurance. The bowel is
covered with a sterile dressing soaked in saline,
and the patient returned to theatre. The abdomen
is explored, and wound edges debrided. If there is
no distension, the wound is closed primarily once
again. In the presence of distension such that the
wound edges will not oppose, the abdomen may
be left open as a laparostomy or a vacuumwound closure device with mesh- mediated fascial
traction may be considered. This technique
involves suturing a polypropylene mesh across the
wound to bridge the gap in the fascial closure. The
mesh is gradually tightened over several days
under general anaesthetic to draw the muscles
together and aid delayed closure.
Following closure of superficial or fulldehiscence, there is a high incidence of subsequent
incisional hernia.
assisted
thickness
Clinical features
Signs usually develop approximately 10 days after
surgery. Overt wound infection may precede dehiscence, but often, there is a small defect in the skin
where pink fluid discharges. This represents the
blood- stained serous effusion, which is always present during the first week or two within the abdomi-
6
Terence PN Jenkins, Surgeon, St Luke’s Hospital and Royal
Surrey County Hospital, Guildford.
Anastomotic leak
An anastomosis is a join between two luminal structures, such as bowel, bile duct, pancreatic duct, ureter
or blood vessel. It may be hand sewn or stapled, the
latter being most common in bowel anastomoses. An
anastomotic leak results in luminal contents passing
through the suture or staple line into the extra- luminal
space.
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Risk factors
There are several factors that increase the risk of an
anastomotic leak. A classification for an anastomotic
leak following a bowel anastomosis is given below,
although many of the factors apply to anastomoses of
other luminal structures:
•
Preoperative: Medication (such as corticoster-
oids), smoking, diabetes, obesity, malnutrition,
intra-
abdominal sepsis, liver disease and cirrhosis, neoadjuvant chemotherapy or radiotherapy
for cancer
Operative: emergency surgery, long intra- operative
•
time, peritoneal contamination (pus or faeces),
site of anastomosis (e.g. in the rectum, oesophagus
or pancreas), poor blood supply to the cut ends of
bowel, and distal obstruction. Operative technique
is important, to avoid poor blood supply, tension
across the anastomosis, malignancy at the anastomosis (i.e. inadequate resection) and incorrect orientation (e.g. a twist of the bowel)
• Postoperative: hypotension, inotropic support
(vasoconstriction reducing blood supply to the
anastomosis) and respiratory failure
Clinical features
Anastomotic leaks are important to recognize early.
The consequences of a leak depend on the luminal
contents. In the case of a vascular anastomosis, it is
associated with haemorrhage, which is usually brisk
with arterial anastomoses. Bile and urine cause a sterile chemical peritonitis. In contrast, a pancreatic duct
leak causes release of digestive enzymes, which may
result in necrosis of neighbouring tissues, causing
bowel perforation or haemorrhage. A leak from a
bowel anastomosis causes peritoneal soiling and sepsis. The remainder of this section considers bowel
anastomotic leaks, but similar principles apply to
other anastomoses.
Early diagnosis and treatment are important. Delay
leads to prolonged contamination of the abdomen or
chest by the luminal contents, leading to the develop-
organ
failure and death.
Leaks from a bowel anastomosis classically present
with abdominal pain combined with high fever, a leucocytosis and raised CRP. It can present without localizing abdominal signs, or with cardiovascular instability,
atrial fibrillation or even myocardial infarction. For this
reason, it should be considered whenever a patient’s
recovery is not progressing as normal. On examination,
patients may be pyrexial and tachycardic and may have
signs of peritonism. There may be faeculant material in
the wound or drains.
Early postoperatively, a leak will drain freely into
the peritoneal cavity. Later, by day 10, the anastomosis tends to be walled off by inflammatory tissue and
surrounding bowel and omentum so the leak may be
‘contained’.
Special investigations
• CT scan will demonstrate free gas and fluid in the
peritoneal cavity. Oral contrast such as gastrografin will be seen to leak outside of the bowel
lumen.
• Endoscopy, usually under anaesthetic, to directly
inspect an oesophago- gastric or rectal anastomosis will reveal a defect.
Management
The definitive management varies depending on the
site of the leak, its extent, the amount of contamination and the physiological status of the patient. It also
depends on whether the anastomosis was in a defunctioned segment of bowel, that is, one for which a
proximal stoma was fashioned to divert the faecal
stream to permit healing.
Contained leaks
Contained leaks are generally managed by drainage.
This usually involves a radiologically placed drain
into the infected cavity. It is particularly effective
where the faecal stream has been diverted by a proximal stoma during the initial surgery. An alternative
for oesophago- gastric and low rectal anastomotic
leaks is to pass an endoluminal vacuum therapy
device such as the Endolumen into the cavity. This is a sponge through which
negative pressure is applied, which prompts granulation tissue and healing. The sponge needs changing
every 2 to 3days, usually under general anaesthetic.
SPONGE® via the bowel
Uncontained (‘free’) leaks
Surgery is required for an uncontained leak, to wash
out the infected material. This may be performed laparoscopically if the original surgery was minimally
44 Postoperative complications
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invasive but is more commonly performed via an
open laparotomy approach. The anastomosis usually
requires resection with formation of a proximal end
stoma. Repair of an anastomosis is seldom successful
because of local sepsis, poor vascularity and suboptimal condition of the patient.
Whether a contained or uncontained leak, optimizing the patient’s nutrition is important and parenteral
nutrition is usually required.
Postoperative fistula
A fistula is as an abnormal connection between two
epithelial surfaces; an enterocutaneous fistula is a
communication between the bowel and the skin.
Most enterocutaneous fistulae are a consequence of
anastomotic leaks or inadvertent injury to the bowel
during surgery or following trauma. Spontaneous
enterocutaneous fistulae may occur from Crohn’s disease, malignancy, diverticulitis or radiotherapy.
Similar factors are responsible for postoperative
fistulas and anastomotic leaks. An alternative classification is to consider them in terms of general factors
and local factors.
General factors include uraemia, anaemia, jaundice, protein deficiency or cachexia from malignant
disease.
Local factors include factors affecting anastomotic
healing (e.g. blood supply and tension), local sepsis
before or during surgery, a distal obstruction or the
presence of local malignancy or chronic inflammation such as Crohn’s disease.
Clinical features
Diagnosis of a fistula is usually obvious, with bowel
contents or bile leaking from the wound or drain site,
usually between 10 and 14days post- surgery. If the
diagnosis is in doubt, the fluid can be tested for bilirubin to diagnose a biliary leak and creatinine for a urinary tract leak, while the fluid from a pancreatic or
small bowel leak is rich in amylase. Water- soluble contrast or methylene blue can be given by mouth and the
fistula imaged or observed for the presence of dye.
The patient is typically pyrexial with localized
abdominal pain. The enzyme- rich fluid of the upper
alimentary tract and of a pancreatic fistula produces
rapid excoriation of the surrounding skin. This is less
marked in a faecal fistula, as the contents of the colon
are relatively poor in proteolytic enzymes.
Classication
Fistulas are usually classified by the volume of output
and the area of the GI tract involved in the fistula.
•
Output: High output (>500 mL over 24 hours),
moderate output (between 200 and 500mL over
24 hours) and low output (<200mL over 24 hours).
Site of origin of fistula: oesophageal, gastroduode-
•
nal, small bowel, large bowel. A fistula occurring
from bowel exposed in an open wound is termed
an enteroatmospheric fistula.
Treatment
The management has four aims, which can be considered to form the acronym SNAP:
1
Skin and Sepsis control
a Local control to protect the skin around the fis-
tula: The edges of the wound are covered by
Stomahesive® (which adheres even to moist
surfaces) or aluminium paste or silicone barrier cream. It may be possible to collect the
effluent by means of a stoma appliance and
thus reduce skin soiling. If the mouth of the
fistula is large, continuous suction may be
necessary.
Antibiotics and radiological drainage of puru-
b
lent collections: Repeated drainage may be
necessary.
2
Nutritional support: In a high alimentary fistula,
gastric and pancreatic secretions, which are stimulated when feeding enterally, are lost through the
fistula. Instead, the patient is kept ‘nil by mouth’
and parenteral nutrition commenced (Chapter3).
A low fistula, occurring in the distal alimentary
tract, may be managed with an elemental diet
given by mouth. This is rapidly absorbed in the
upper intestine and is thus not lost through the fistula. Regular monitoring of nutritional state is
important.
3 Anatomical delineation of the fistula: A CT scan
with water- soluble contrast either by mouth or via
the fistula tract will identify the site of leakage,
assess the likelihood of spontaneous closure and
facilitate planning of any future intervention.
4 Procedure for definitive control: Whether closure of
the fistula tract is required depends on the likelihood
of spontaneous closure. Good nutritional support,
eradication of sepsis, no distal obstruction, low fistula output and small bowel fistulas are associated
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