The draining surgical wound post total hip and knee arthroplasty: what are my options? A narrative review

Abstract

Total hip arthroplasty (THA) and total knee arthroplasty (TKA) are successful orthopaedic procedures with an ever-increasing demand annually worldwide, and persistent wound drainage (PWD) is a well-known complication following these procedures. Despite many definitions for PWD having been proposed, a validated description remains elusive. PWD is a risk factor for periprosthetic joint infection (PJI). PJI is a devastating complication of THA and TKA, and a leading cause of revision surgery with dramatic morbidity and mortality and a significant burden on health socioeconomics. Prevention of PJI has become an essential focus in THA and TKA. Understanding the pathophysiology, risk factors and subsequent management of PWD may aid in decreasing the rate of PJI. Risk factors of PWD can be divided into modifiable and non-modifiable patient risk factors, pharmacological and surgical risk factors. No gold standard treatment protocol to address PWD exists; however, non-operative options progressing to surgical interventions have been described. The aim of this study was to review the current literature regarding PWD and consolidate the risk factors and management strategies available.
Cite this article: EFORT Open Rev 2021;6:872-880. DOI: 10.1302/2058-5241.6.200054

Full text

EOR |   |  
DOI: 10.1302/2058-5241.6.200054
www.efortopenreviews.org
Total hip arthroplasty (THA) and total knee arthroplasty
(TKA) are successful orthopaedic procedures with an ever-
increasing demand annually worldwide, and persistent
wound drainage (PWD) is a well-known complication
following these procedures. Despite many definitions
for PWD having been proposed, a validated description
remains elusive.
PWD is a risk factor for periprosthetic joint infection (PJI).
PJI is a devastating complication of THA and TKA, and
a leading cause of revision surgery with dramatic mor-
bidity and mortality and a significant burden on health
socioeconomics.
Prevention of PJI has become an essential focus in THA and
TKA. Understanding the pathophysiology, risk factors and
subsequent management of PWD may aid in decreasing
the rate of PJI.
Risk factors of PWD can be divided into modifiable and
non-modifiable patient risk factors, pharmacological and
surgical risk factors. No gold standard treatment protocol
to address PWD exists; however, non-operative options
progressing to surgical interventions have been described.
The aim of this study was to review the current literature
regarding PWD and consolidate the risk factors and man-
agement strategies available.
Keywords: complications; periprosthetic joint infection;
persistent wound drainage; total joint arthroplasty
Cite this article: EFORT Open Rev 2021;6:872-880.
DOI: 10.1302/2058-5241.6.200054
Introduction
Primary total joint arthroplasty (TJA), including total hip
arthroplasty (THA) and total knee arthroplasty (TKA), are
highly successful, reproducible surgical procedures. The
demand for TJA is increasing globally, with projections
showing sustained increases beyond 2030.1,2 Associated
complications will subsequently increase in conjunction
with this demand.2 Persistent wound drainage (PWD) is
a post-operative wound complication following TJA. It is
reported to occur in between 0.2% to 21% of all cases of
primary TJA; however, there is lack of agreement on the
definition of PWD.3 PWD has been reported as a risk factor
for periprosthetic joint infection (PJI).4 Patel et al4 showed
that each extra day of PWD carried an additional 42% risk
of wound infection in TKA and 29% risk of wound infec-
tion in THA. The rate of PJI in wounds that persistently
drain post-operatively has been reported in various stud-
ies to range from 1.3% to up to 50%, with the wide range
possibly attributable to a lack of standardized definition of
persistent wound drainage used and the heterogenicity
and retrospective nature of available literature.4–6
PJIs are associated with significant morbidity and mor-
tality and place a heavy economic burden on healthcare
facilities and resources.3,7 PJI is the most common reason
for revision TKA and third most common cause of revision
THA. It is the most common reason for revision within two
years of TJA.6 A 3.58 times increased risk of death exists
after revision surgery for PJI and five-year mortality is
21%.8 Much focus is now devoted to the prevention of
PJI and the recognition and treatment of PWD should be
a logical step in preventing PJI. However, evidence-based
clinical guidelines for the diagnosis and treatment of PWD
in TJA are still lacking.
Pathophysiology
Surgical wound healing has been divided into different
phases needed to complete closure of the wound and
The draining surgical wound post total hip
and knee arthroplasty: what are my options?
A narrative review
Richard Peter Almeida
Lipalo Mokete
Nkhodiseni Sikhauli
Allan Roy Sekeitto
Jurek Pietrzak
6.20005EOR0010.1302/2058-5241.6.200054
review-article2021
Knee
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PERSISTENT WOUND DRAINAGE
restore the vital barrier to physical, chemical and bio-
logical pathogens.9 Wound healing starts with haemo-
stasis, inflammation, proliferation, maturation and ends
in remodelling, with any deviation within these phases
resulting in delayed or abnormal healing of a surgical
wound.9
Disturbance in wound healing may be physiologi-
cal and non-infectious, resulting in wound drainage for
a short duration. Surgical disruption of the superficial
capillaries may result in unimportant, transitory serous
or serosanguinous wound drainage post-operatively.10
This surgical disruption may result in drainage within
the first 72 hours, which is usually serosanguinous and
involves the superficial tissue layers.11 Drainage con-
tinuing after 72 hours may arise from fat necrosis sus-
tained during surgery, dissolving haematoma from poor
haemostasis, or fluid from a deep capsular defect, and
must be considered potentially infectious and demands
intervention.11
In PWD, the natural barrier of the skin is bypassed,
providing a retrograde pathway for pathogens to enter
the wound and ultimately contaminate the joint.1,12,13
The majority of wound drainage resolves spontaneously
with physiological healing.4 When normal healing does
not occur, PWD may forewarn of a developing, underly-
ing infectious process and should not be ignored.10,14–17
Whether delayed wound healing results in PWD or vice
versa, where exactly does the draining fluid originate
from within the wound and to what extent a retro-
grade pathway is made available for pathogens to enter
the joint are all difficult to clarify, yet remain important
considerations.3
Numerous definitions have been proposed for PWD, but
a single validated definition has yet to be fully adopted.3,10
It has been suggested that wound drainage from two to
nine days post-operatively is persistent. A wound is said
to be actively draining if an area of the wound dressing
of more than 2 × 2 cm is wet beyond 72 hours post-
operatively.3,11,18 Other definitions include drainage for
more than 48 hours soaking through the dressings; con-
tinued drainage beyond day four post-operatively; drain-
age beyond two days post-operatively for non-infected
cases and 5.5 days post-operatively for infected cases.10
The lack of consensus regarding the definition of PWD
was highlighted by an online survey of the Netherlands
Orthopaedic Association, which reported that 59.1% of
surgeons allowed three to seven days of PWD before start-
ing non-surgical management while 44.1% intervened
surgically only after 10 days of PWD after index TJA.19
According to the proceedings of international consensus
on orthopaedic infections, the suggested definition of per-
sistent wound drainage is ‘any continued fluid extrusion
from the operative site occurring beyond 72 hours from
index surgery’.10
Risk factors
The risk factors for PWD can be considered as patient-
specific, pharmacological and surgical.
Patient-specific risk factors
Patient factors associated with PWD include age, obesity,
malnutrition, diabetes, anaemia, inflammatory arthritis,
smoking, Staphylococcus aureus colonization, and malnu-
trition.2,6,11 Shahi et al6 retrospectively reviewed 4873 TJAs
and reported an incidence of PWD of 6.2% with a subse-
quent rate of PJI of 15.9%. Diabetes inferred a 21 times
greater risk of PWD. The possibility of PWD was increased
by 17.3 times in morbid obesity, 14.2 times in rheumatoid
arthritis, 4.3 times in chronic alcohol use and 2.8 times in
hypothyroidism.6
Obesity is a modifiable risk factor for complications
related to TJA, and an independent risk factor for PWD.2,6
This may be related to fat necrosis that occurs due to
larger surgical incisions as well as increased surgical
time.4,6 Therefore counselling patients about weight loss
is advisable pre-operatively.11
Malnutrition negatively affects the immune system and
wound healing. Reduced serum measurements of albu-
min < 35 g/L, total lymphocyte count of < 1500/mm3, or
transferrin level <2 g/L have been associated with wound
complications.11 Surgery is known to increase metabolic
demand, making borderline deficiencies pre-operatively
more significant, and therefore these deficits should be
restored.9 Protein malnutrition, identified with the surro-
gate measurement of albumin, is a significant risk factor
as there is increased protein turnover during the wound
healing process.9 Vitamin C, vitamin A, zinc and magne-
sium have been identified as key factors for wound heal-
ing, and supplementation of these has been suggested to
improve wound healing in deficient patients.9
Diabetes mellitus (DM) is a systemic disease, with mul-
tiple systems and mechanisms implicated in the patho-
genesis of poor wound healing. Hyperglycaemia as a
result of poorly controlled DM results in structural and
functional alteration of proteins and enzymes.9 The macro
and microvascular complications of DM also impair blood
flow and subsequent oxygen delivery at the tissue level.9
The altered proteins and enzymes, poor circulation as well
as the poor immune system associated with DM all affect
wound healing and contribute to increased risk of PWD.6,9
Thyroid hormone is associated with fibroblast prolifera-
tion needed in the process of wound healing, therefore,
suppression of thyroid hormone results in the disturbance
of collagen synthesis in wound healing.20 This is sup-
ported by Shahi et al,6 indicating hypothyroidism as a risk
factor for PWD.
Anaemia is a risk factor for PWD, but the exact relation-
ship between anaemia and PWD is poorly understood.
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874
However, it can be deduced that there would be a higher
rate of peri-operative allogenic blood transfusions in
anaemic patients. Blood transfusions have been shown
to be associated with increased superficial wound com-
plications possibly due to the associated immunomodu-
lation effect.2,21
Rheumatoid arthritis is associated with impaired
immune function and it has been suggested that both the
underlying disease process and the medications used in
the management are responsible for poor wound healing
and PWD.2,6 Steroids used in the management of inflam-
matory disorders lead to poor wound healing, due to the
anti-inflammatory effects, inhibition of epithelialization
and reduced collagen production.9
Smoking results in poor wound healing due to the
negative effects of nicotine, carbon monoxide and hydro-
gen cyanide.9 The effects of nicotine cause vasoconstric-
tion and local tissue hypoxia.9,11 Carbon monoxide binds
to haemoglobin and produces methaemoglobin, thereby
reducing the oxygen delivery of haemoglobin, and hydro-
gen cyanide inhibits oxidative metabolism.9 Due to these
effects, the cells needed during wound healing are dys-
functional at low oxygen levels, and collagen deposition
is reduced.9 Therefore cessation of smoking is advised,
and although uniform guidelines do not exist, cessation of
at least 4–8 weeks before and four weeks post-operatively
has been recommended.9,11
Bacterial colonization, particularly with Staphylococcus
aureus is a risk factor for surgical site infection.22 Bacteria
growth within a wound bed affects the various stages of
wound healing, and can alter haemostasis, needed in the
initial stage of wound healing.9 Whether PWD is a cause
or consequence of infection is debatable as it has been
suggested that wounds that are draining may be draining
because they already have some level of infection.23,24
HIV infection and the associated immunocompromised
state has been associated with post-operative wound com-
plications, and emphasis has been placed on pre-operative
optimization by improving cell cluster of differentiation
counts (CD4 > 200) and ensuring viral load suppression
to avoid those complications.25,26 Increased surgical site
complications including PWD have been reported with
hepatitis C infections.27,28 It has been hypothesized that
small vessel vasculitis together with liver, kidney, haema-
tological and immune system impairments affect wound
healing and wound infection.27
Chronic alcohol use has been identified as a risk factor
for PWD.6 Whether this is related to the reported associ-
ated risk factors of malnutrition or liver disease25 that can
result from chronic alcohol use needs further evaluation.
Chronic obstructive lung disease has been reported to
result in an increased risk of surgical site complications,29
with Gu et al30 reporting that patients with COPD are 2.9
times more likely to develop wound dehiscence. Whether
this is directly related to COPD, related comorbidities or
the association with current or previous smoking is yet
to be determined.
Pharmacological risk factors
The initial stage in wound healing starts with haemostasis,
therefore any disruption to this stage disrupts and pro-
longs wound healing.9 The use of anti-coagulation post-
operatively may disrupt haemostasis and potentially result
in PWD. Disrupted haemostasis may result in the forma-
tion of a haematoma, providing a rich medium for bac-
terial growth.22 Anti-coagulation therapies used include
warfarin, enoxaparin (low molecular weight heparin),
fondaparinux, rivaroxaban and aspirin to mitigate the
risk of venous thromboembolic events (VTE).4,31 Each of
the agents have different mechanisms of actions, dosages
and routes of administration, with negative and positive
attributes regarding their uses that need to be considered
in VTE prophylaxis. Peri-operative VTE can be catastrophic
but so too can deep and superficial wound complica-
tions, therefore risk stratification is needed to balance anti-
coagulation peri-operatively, and patients requiring thera-
peutic anti-coagulation need to be counselled about the
risk regarding wound complications and infection.32
When using the international normalized ratio (INR) to
monitor the response to warfarin, an INR of more than
1.5 is associated with increased risk of developing wound
complications.33 Shahi et al6 found that the rate of PWD
reduced from 6.3% to 3.1% when changing from the use
of warfarin to aspirin for post-operative VTE prophylaxis.
The time taken to a dry wound is longer in patients on
low molecular weight heparin (LMWH) than those on
aspirin and mechanical compression or warfarin.11 Jones
et al34 showed that the use of LMWH and the use of aspi-
rin resulted in a 4.92 and 3.64 times greater increase in
wound discharge respectively when compared to the use
of no pharmacological thromboprophylaxis. Lum et al31
proposed that prolonged wound drainage due to anti-
coagulation had a positive correlation with increased
length of stay (LOS) in hospital. This was supported by
Patel et al,4 therefore using LOS as a surrogate for wound
drainage assists in comparing anti-coagulation agents.31
In order of shortest to longest LOS, the use of aspirin was
2.6 days, warfarin was 3.7 days, Fondaparinux was 3.77
days, rivaroxaban was 4.1 days and enoxaparin was five
days.31 There have been numerous studies reporting the
effects of various anti-coagulation therapies, aiming to
identify the ideal therapy providing adequate prophylac-
tic effect against VTE while limiting post-operative surgical
site complications.35 Various guidelines have been pro-
posed, and although aspirin seems to be favoured for VTE
prophylaxis when considering possible wound complica-
tions, the debate continues for the most optimal prophy-
lactic regimen.35,36
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PERSISTENT WOUND DRAINAGE
Surgical risk factors
Surgical risk factors include previous surgery to the area,
surgical approach, pre-operative skin preparation, tour-
niquet use, total surgical time, blood loss, surgical and
anaesthetic technique.4,11,22
Previous surgery alters the native anatomy and blood
supply to the area, with risk of wound complications fol-
lowing subsequent surgeries. The presence of previous
skin incisions should be taken into consideration when
planning for future skin incisions.22 It has been advised
that around the knee joint, the most lateral vertical inci-
sion should be used and skin bridges between new and
old incisions of 2.5 cm to 5 cm should be avoided.11
Skin preparation prior to surgery is of paramount impor-
tance in prevention of infective complications. Currently
there is no evidence assessing the relationship between
skin preparation and PWD specifically. Many options have
been proposed, and the ideal agent is still under discus-
sion.2 Chlorhexidine-alcohol solution has been shown
to be more protective than povidone-iodine in reducing
infective complications in multiple studies.22,37 However
Carroll et al2 found skin preparation with chlorhexidine
and alcohol carried a five-fold increase in the risk of super-
ficial wound complications compared with iodine and
alcohol. The difference may be explained by the variation
in concentrations of the constituents of the skin prepara-
tion and may need further investigation.
Surgical techniques with meticulous handling and dissec-
tion of soft tissues, accurate closure of the relevant layers,
and adequate haemostasis prevent post-operative haema-
toma which can lead to PWD.22 The combination of electro-
cautery devices and pharmacological interventions, such as
intravenous and local application of tranexamic acid, have
been advocated in achieving haemostasis.11 Haemostasis
is also important in decreasing intra-operative blood loss
and the need for blood transfusion which is related to post-
operative wound complications.2
Surgical approach choice affects PWD. In THA, an
increased risk of PWD and superficial wound dehiscence
exists with the direct anterior approach (DAA).38–40 Both
the skin quality around the anterior hip and the location of
the surgical incision are contributory. The DAA surgical skin
incision may be in, or overlapping, the inguinal and waist
creases.39,40 This moist environment may precipitate the
incision being exposed to infectious organisms.39,40 Wound
healing may be inhibited by the shear forces generated by
hip movement forcibly separating the skin edges.38 Dia-
betic and obese patients are most at risk of post-operative
wound complications after DAA. In TKA, the subvastus sur-
gical approach has been shown to be protective of PWD.41
Wood et al42 reported that the time taken for wound
drainage to stop correlated strongly with the length of
the surgical incision. Woolson et al,43 however, reported
that the risk of wound complications associated with the
length of the wound was negligible provided it was less
than 10 cm.
Prolonged tourniquet time has been correlated with an
increase in superficial wound complications.2 This may
be attributable to local tissue hypoxia and inflammation
compromising post-operative wound healing, as well as
decreasing the local tissue concentration of prophylactic
antibiotics during surgery. In TKA, shorter tourniquet infla-
tion times and local infiltration of peri-articular anaesthe-
sia significantly decrease subsequent wound drainage.41
Inhibition of angiogenesis at the surgical incision edges
due to relative tissue hypoxia with tourniquet use inhibits
the migration of macrophages and fibroblasts necessary
for an adequate cellular response. Conversely, release of
a tourniquet after prolonged tourniquet use results in a
reactive hyperaemia, excessive bleeding and as much
as 10% increase in leg size, which places wound edges
under undue tensile forces.41,44 Local infiltration improves
pain and facilitates early mobilization which stimulates
and enhances soft tissue oxygenation.41,44
Duration of surgery in THA is positively correlated with
an increase in both minor and major complications within
30 days of surgery. Operating time in THA between 120
and 179 minutes and longer than 180 minutes increased
the risk of minor complications by 1.4 and 2.1 times.45
Although it has been documented that prolonged surgi-
cal time predisposes patients to wound complications,
we are not aware of any published studies that specifically
evaluate the relationship between PWD and surgical time.
Management
In general, management of PWD should include non-
surgical and surgical strategies. Jaberi et al14 reported
that PWD longer than 5–7 days was unlikely to respond
to non-surgical treatment. Importantly, successful surgi-
cal treatment of PWD was associated with expeditious
surgical intervention. Surgical debridement at five days
was more likely to result in no infective complications at
one year than delayed surgery after 10 days. Weiss et al13
reported that only a quarter of patients had positive cul-
tures when surgical debridement was carried out at 12
days post-operatively.
Prevention
Pre-operative, medical optimization is vital to allay the risk
of post-operative wound complications.11 Please refer to
Table 1 for optimization of risk factors in TJA.
Non-surgical management
Non-surgical management includes immobilization with
bed rest combined with braces and cessation of physical
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therapy, appropriate wound care, pressure bandages and
cessation of pharmacological VTE prophylaxis.3,11
Limiting motion at the surgical site, including provision-
ally halting physical therapy while monitoring wound
drainage for 24 to 48 hours, has been suggested.23 Con-
tinuous passive motion should be stopped. Reich and
Ezzet23 and Shahi et al6 suggested protocols whereby
physical therapy is temporarily put on hold and knee
immobilizers used.
The ideal dressing should protect the wound from infil-
tration of pathogens as well as be absorbent to deal with
excess exudate. Initial management of PWD may start
with absorbent dressings and pressure bandages.19 A
compressive dressing is all that may be needed for some
wounds.11 Pressure dressing together with other non-
operative measures were used successfully in managing
PWD by Shahi et al.6 The use of silver-impregnated dress-
ings has been proposed as their anti-microbial action has
shown some benefit.19
Negative pressure wound therapy (NPWT) has been
reported to decrease wound complications such as hae-
matoma, seroma, dehiscence and infection.66,67 NPWT
reduces local tissue oedema, prevents deformation of the
incision bed, stabilizes the wound environment, modu-
lates inflammation, promotes angiogenesis and expedites
the time to wound healing.66 Redfern et al68 reported a
45% reduction in post-operative haematoma and a 71%
decrease in surgical site infections with the use of prophy-
lactic NPWT. Wounds draining after the second or third
day may benefit from NPWT, with an expected dry wound
within 24 hours of application.11 Hansen et al12 found the
use of NPWT for PWD resulted in the resolution of PWD in
76% of the patients it was used for. Although NPWT has
been shown to be effective in managing PWD, prophylac-
tic use of NPWT for all wounds may be limited by addi-
tional costs, resource constraints and an increased risk of
severe blistering.66,69 NPWT has many reported benefits,
but there is no absolute indication for the use of NPWT,
Table 1. Summary of risk factors associated with wound complications in arthroplasty surgery
Risk parameters Suggestion
Pre-operative risk factors - modifiable
Obesity BMI > 40 Kg/m2Nutritional optimization 2,4,11,22,46,47
Hypoalbuminaemia Albumin < 35 g/L Nutritional optimization 3,11,22,48,49
Smoking 4–8 weeks cessation 11,47,50–52
Anaemia Hb < 13 g/Dl men
Hb < 12 g/Dl women
Identify cause of anaemia and provide
supplementation if needed
Avoid unnecessary peri-operative blood transfusions
2,3,11,21,53
Staphylococcus aureus colonization Nasal nare colonization Decolonization with nasal Mupirocin 22,54
Poor dentition Maintain favourable oral hygiene 55
Urinary tract infection Symptomatic urinary tract infections Treat symptomatic urinary tract infections 56,57
Pre-operative risk factors – non-modifiable
Inflammatory arthropathy Use of steroids and other
immunosuppressive agents
Reduce steroids and other immunosuppressive
agents
2,11,47,58
Diabetes mellitus HBA1C > 7–8% Medical optimization of treatment 3,11,22,47,59
COPD Pulmonary assessment and optimization 29,30
Chronic anti-coagulation therapy INR > 1.5 De-escalate pharmacological anti-coagulation
depending on initial indication. Mechanical
thromboprophylaxis with aspirin has least wound
complication risk
2–4,22,32–34,60
Hepatitis C Asymptomatic and symptomatic
chronic infection
Medical optimization and counselling 27,28
HIV < 200 CD4, viral load not suppressed Medical optimization of treatment 26
Previous surgery to area Adhere to correct surgical principles, adjust surgical
incision or approach
11,25
Intra-operative risk factors
Operating time Prolonged operating time > 180 min Optimize surgical time without compromising
technique
22,45,61,62
Surgical approach Higher risk with direct anterior
approach to hip in obese patients,
and with previous surgery
Tailor surgical approach to patient and patient’s risk
factors
11,39
Coagulation technique Poor haemostasis Meticulous haemostasis using surgical technique,
electrocautery and local/systemic haemostatic agents
11,63
Antibiotic administration Within 60 min of surgical time IV and local prophylactic antibiotic administration 22,64
Tourniquet time Prolonged tourniquet time more than
100 min
Reduce tourniquet time 2,41,44,65
Theatre etiquette Sterility control, laminar flow, reduced traffic, body
exhaust suits, temperature control
22
Skin preparation Iodine or chlorhexidine in 70% alcohol 2,22,37
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PERSISTENT WOUND DRAINAGE
and the use of NPWT should be directed by patient risk
factors and clinical condition.67,70
Pharmacological anti-coagulation therapy has previ-
ously been discussed under the heading of risk factors.
Anti-coagulation status needs to be reassessed with PWD,
balancing the risks versus benefits when prescribing VTE
prophylaxis, and short-term cessation should be con-
sidered depending on the agent prescribed and reason
for anti-coagulation.11,22,34 When pharmacological anti-
coagulation is temporarily discontinued then mechanical
VTE prophylaxis should be initiated or continued;11 how-
ever, the evidence does not currently support the sole use
of mechanical VTE prophylaxis in TJA.36 Reich and Ezzet23
suspended pharmacological anti-coagulation until the
wound was assessed to be stable, similar to the protocol
of Shahi et al.6 Although temporary discontinuation of
anti-coagulation therapy has been suggested, it is plau-
sible to say the effects on PWD will depend on the type
of anti-coagulation initially used, as each agent has differ-
ent mechanisms of action with varying half-lives, and this
needs further investigation (Fig. 1).
Antibiotic treatment has been described to treat PWD,
although there are fears that indolent infection may be
masked and subsequent laboratory investigations may
be compromised.23 A prospective observational study from
Geneva did not find a protective effect of pre-emptive anti-
biotic therapy regarding future surgical site infections in
the case of wound discharge or dehiscence.71 If antibiotic
therapy is chosen there should be a strong indication and
prior to administration of any antibiotics, aspiration of the
wound is suggested to confirm established infection and
direct the therapy.23 Culturing samples of wound drainage
pre-operatively is not indicated as the yield is habitually only
normal skin flora.23 The current consensus discourages the
indiscriminate use of antibiotics due to the lack of adequate
evidence and risk of increasing antibiotic resistance.3,24,72
Surgical site aspiration was used successfully by Reich
and Ezzet.23 The aspiration was diagnostic to rule out
infection as well as therapeutic in decompressing any
haematomas. If the aspiration was diagnostic for infection,
the non-surgical approach was abandoned and treatment
escalated to surgical debridement.23 Reich and Ezzet23 suc-
cessfully treated 24 of 25 patients with PWD using a stand-
ardized protocol utilizing surgical site aspiration together
with other mentioned non-surgical approaches including
closure of open areas of wounds, pausing anti-coagulation
therapy, limiting activity and selective prescription of anti-
microbial therapy. Limited experience with this treatment
strategy makes it difficult to recommend; however, Shahi
et al6 reported successfully managing 65% of patients with
PWD with similar approaches using local wound care,
pausing anti-coagulation, and reducing movement to
the surgical area. Therefore, a combination of these vari-
ous non-surgical interventions can be recommended with
further well-designed prospective studies needed to deter-
mine the best possible treatment protocol.
Surgical management
The 2013 International Consensus Meeting on muscu-
loskeletal infections15 strongly advised strict monitoring
of continued wound drainage persisting longer than 72
hours. Surgical management should be considered when
PWD continues for more than 5–7 days after initial surgery
despite non-surgical management.15,19 Early surgical explo-
ration and debridement within 5–7 days post-operatively
has been shown to resolve PWD in 76% of cases, and it has
been noted that delaying debridement may result in PJI.14
Surgical treatment for PWD is neither insignificant nor
minor surgery and may potentiate the risk of future mor-
bidity and PJI.11 If a wound has been deemed problematic
as described previously, a minimum of superficial explo-
ration with debridement and haematoma evacuation
should be performed.11
Joint aspiration is recommended prior to the skin inci-
sion of surgical debridement to exclude deep infection.11
Multiple intra-operative tissue samples during surgical
debridement should be obtained and cultured for up
to 14 days, and empiric antibiotic treatment adjusted
according to culture results.3,11,24 If the joint capsule
appears to be compromised intra-operatively, and deep
infection is suspected, surgical treatment can be escalated
to debridement, antibiotics and implant retention, com-
monly referred to as a DAIR procedure.1 As previously
suggested under the discussion of non-operative proto-
cols, once deep infection is confirmed the diagnosis and
management should shift to that of an acute peripros-
thetic joint infection. The objective of a DAIR procedure
is to reduce the infective microbial load around the pros-
thesis and wound, including breaking down biofilm.1,11
Surgical management involves open deep debridement
of the joint and thorough wound irrigation and wherever
possible modular bearings should be exchanged.3,11,22,24
The bearings are removed to provide better access to all
Fig. 1 An example of a surgical wound post total hip
arthroplasty complicated by persistent wound drainage as a
result of over anti-coagulation therapy
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prosthetic surfaces, and not exchanging the polyethylene
liners has been reported to increase the risk of failure.24,73
Antibiotic choice and duration of treatment post-
operatively is controversial and will depend on the suscep-
tibilities and virulence of pathogens isolated, route of
administration and the need for repeat procedures and
host factors.73 Empiric antibiotics are started after the pro-
cedure and de-escalated where appropriate as soon as
microbiology results are available.24 Discussion between
the orthopaedic surgeon, microbiologist and infectious dis-
ease specialist is suggested to determine the most optimal
treatment while still respecting antibiotic stewardship.73
Success of the DAIR procedure is defined as retention of
the implants without the need for subsequent DAIR pro-
cedures or long-term suppressive antibiotic therapy.74,75
Risk factors for an unsuccessful DAIR procedure include
raised inflammatory markers, infection with Staphylococ-
cus aureus, retention of polyethylene components, and
arthroscopic debridement.75 Longer duration of symp-
toms is also a predictor for failure, and therefore the sooner
the procedure is carried out the better the outcomes can
be expected.75 Studies have shown the risk of higher failure
rates of two-stage revisions if a DAIR procedure has failed,75
therefore once there is any wound complication suspected
following TJA every effort needs to be made to address the
identified problem in a timely and efficient manner.
Conclusion
The goal in managing PWD is to minimize the time to
achieve a dry, healed wound. Emphasis should be placed
on prevention of PWD by identifying and addressing previ-
ously discussed risk factors pre-operatively to optimize the
patient’s condition. Once PWD is identified there should
be no time delay in utilizing both non-surgical and surgical
treatment options to ultimately prevent the consequence
of PJI and the need for revision surgery. However, there
is still variation in clinical practice because of the lack of
consensus regarding the definition of PWD as well as the
lack of evidence-based guidelines in the management of
PWD. Future prospective and adequately powered studies
evaluating management protocols addressing all aspects
of PWD are needed.
ICMJE CONFLICT OF INTEREST STATEMENT
LM reports consultancy and lecture fees paid by Zimmerbiomet, and Consultancy
fees also from Advanced Orthopaedics, and Implantcast, for relevant nancial activi-
ties outside the submitted work.
All other authors declare no conicts of interest relevant to this work.
FUNDING STATEMENT
No benets in any form have been received or will be received from a commercial
party related directly or indirectly to the subject of this article.
SOCIAL MEDIA
http://linkedin.com/in/richard-almeida-a70987121
OPEN ACCESS
© 2021 The author(s)
This article is distributed under the terms of the Creative Commons Attribution-Non
Commercial 4.0 International (CC BY-NC 4.0) licence (https://creativecommons.org/
licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribu-
tion of the work without further permission provided the original work is attributed.
REFERENCES
. Löwik CAM, Wagenaar FC, van der Weegen W, et al; LEAK study group.
LEAK study: design of a nationwide randomised controlled trial to find the best way to treat
wound leakage after primary hip and knee arthroplasty. BMJ Open 2017;7:e018673.
. Carroll K, Dowsey M, Choong P, Peel T. Risk factors for superficial wound
complications in hip and knee arthroplasty. Clin Microbiol Infect 2014;20:130–135.
. Wagenaar FBM, Löwik CAM, Zahar A, Jutte PC, Gehrke T, Parvizi J.
Persistent wound drainage after total joint arthroplasty: a narrative review. J Arthroplasty
2019;34:175–182.
. Patel VP, Walsh M, Sehgal B, Preston C, DeWal H, Di Cesare PE. Factors
associated with prolonged wound drainage after primary total hip and knee arthroplasty.
J Bone Joint Surg [Am] 2007;89-A:33–38.
. Eveillard M, Mertl P, Canarelli B, et al. [Risk of deep infection in first-intention
total hip replacement: evaluation concerning a continuous series of 790 cases]. Presse Med
2001;30:1868–1875.
. Shahi A, Boe R, Bullock M, et al. The risk factors and an evidence-based protocol
for the management of persistent wound drainage after total hip and knee arthroplasty.
Arthroplast Today 2019;5:329–333.
. Carli AV, Negus JJ, Haddad FS. Periprosthetic femoral fractures and trying to
avoid them: what is the contribution of femoral component design to the increased risk of
periprosthetic femoral fracture? J Bone Joint Surg [Br] 2017;99-B:50–59.
. Natsuhara KM, Shelton TJ, Meehan JP, Lum ZC. Mortality during total hip
periprosthetic joint infection. J Arthroplasty 2019;34:S337–S342.
. Janis JE, Harrison B. Wound healing: part I. basic science. Plast Reconstr Surg
2016;138:9S–17S.
. Al-Houraibi RK, Aalirezaie A, Adib F, et al. General assembly, prevention,
wound management: proceedings of international consensus on orthopedic infections.
J Arthroplasty 2019;34:S157–S168.
. Scuderi GR. Avoiding postoperative wound complications in total joint arthroplasty.
J Arthroplasty 2018;33:3109–3112.
AUTHOR INFORMATION
Arthroplasty Unit, Division of Orthopaedic Surgery, Charlotte Maxeke
Johannesburg Academic Hospital, University of the Witwatersrand,
Johannesburg, South Africa.
Correspondence should be sent to: Dr. Richard Peter Almeida, Arthroplasty Unit,
Division of Orthopaedic Surgery, Charlotte Maxeke Johannesburg Academic
Hospital, University of the Witwatersrand, Johannesburg, South Africa.
Email: rich.almeida11@gmail.com
Downloaded from Bioscientifica.com at 11/25/2022 02:17:05PM
via free access

879
PERSISTENT WOUND DRAINAGE
. Hansen E, Durinka JB, Costanzo JA, Austin MS, Deirmengian GK. Negative
pressure wound therapy is associated with resolution of incisional drainage in most wounds
after hip arthroplasty. Clin Orthop Relat Res 2013;471:3230–3236.
. Weiss AP, Krackow KA. Persistent wound drainage after primary total knee
arthroplasty. J Arthroplasty 1993;8:285–289.
. Jaberi FM, Parvizi J, Haytmanek CT, Joshi A, Purtill J. Procrastination of
wound drainage and malnutrition affect the outcome of joint arthroplasty. Clin Orthop Relat
Res 2008;466:1368–1371.
. Parvizi J, Gehrke T, Chen AF. Proceedings of the international consensus on
periprosthetic joint infection. J Bone Joint Surg [Br] 2013;95-B:1450–1452.
. Zmistowski B, Karam JA, Durinka JB, Casper DS, Parvizi J. Periprosthetic
joint infection increases the risk of one-year mortality. J Bone Joint Surg [Am]. 2013;95-
A:2177-2184.
. Saleh K, Olson M, Resig S, et al. Predictors of wound infection in hip and knee
joint replacement: results from a 20 year surveillance program. J Orthop Res 2002;20:506–515.
. Ghanem E, Heppert V, Spangehl M, et al. Wound management. J Orthop Res
2014;32:S108–S119.
. Wagenaar F-C, Löwik CAM, Stevens M, et al. Managing persistent wound
leakage after total knee and hip arthroplasty: results of a nationwide survey among Dutch
orthopaedic surgeons. J Bone Jt Infect 2017;2:202–207.
. Ekmektzoglou KA, Zografos GC. A concomitant review of the effects of diabetes
mellitus and hypothyroidism in wound healing. World J Gastroenterol 2006;12:2721–2729.
. Weber EWG, Slappendel R, Prins MH, van der Schaaf DB, Durieux
ME, Strümper D. Perioperative blood transfusions and delayed wound healing after
hip replacement surgery: effects on duration of hospitalization. Anesth Analg 2005;100:
1416–1421.
. Illingworth KD, Mihalko WM, Parvizi J, Sculco T, McArthur B, El Bitar
Y, et al. How to minimize infection and thereby maximize patient outcomes in total joint
arthroplasty: a multicenter approach. J Bone Joint Surg [Am] 2013;95-A:1–13.
. Reich MS, Ezzet KA. A nonsurgical protocol for management of postarthroplasty
wound drainage. Arthroplast Today 2017;4:71–73.
. Barros LH, Barbosa TA, Esteves J, Abreu M, Soares D. Early debridement,
antibiotics and implant retention (DAIR) in patients with suspected acute infection after hip
or knee arthroplasty: safe, effective and without negative functional impact. J Bone Jt Infect
2019;4:300–305.
. Jones RE, Russell RD, Huo MH. Wound healing in total joint replacement. J Bone
Joint Surg [Br] 2013;95-B:144–147.
. Chang CH, Tsai SW, Chen CF, et al. Optimal timing for elective total hip
replacement in HIV-positive patients. Orthop Traumatol Surg Res 2018;104:671–674.
. Issa K, Boylan MR, Naziri Q, Perfetti DC, Maheshwari AV, Mont MA. The
impact of hepatitis C on short-term outcomes of total joint arthroplasty. J Bone Joint Surg
[Am] 2015;97-A:1952–1957.
. Pour AE, Matar WY, Jafari SM, Purtill JJ, Austin MS, Parvizi J. Total joint
arthroplasty in patients with hepatitis C. J Bone Joint Surg [Am] 2011;93-A:1448–1454.
. Yakubek GA, Curtis GL, Sodhi N, et al. Chronic obstructive pulmonary disease
is associated with short-term complications following total hip arthroplasty. J Arthroplasty
2018;33:1926–1929.
. Gu A, Wei C, Maybee CM, Sobrio SA, Abdel MP, Sculco PK. The impact of
chronic obstructive pulmonary disease on postoperative outcomes in patients undergoing
revision total knee arthroplasty. J Arthroplasty 2018;33:2956–2960.
. Lum ZC, Monzon RA, Bosque J, Coleman S, Pereira GC, Di Cesare PE.
Effects of fondaparinux on wound drainage after total hip and knee arthroplasty. J Orthop
2018;15:388–390.
. McDougall CJ, Gray HS, Simpson PM, Whitehouse SL, Crawford
RW, Donnelly WJ. Complications related to therapeutic anticoagulation in total hip
arthroplasty. J Arthroplasty 2013;28:187–192.
. Parvizi J, Ghanem E, Joshi A, Sharkey PF, Hozack WJ, Rothman RH.
Does ‘excessive’ anticoagulation predispose to periprosthetic infection? J Arthroplasty
2007;22:24–28.
. Jones CW, Spasojevic S, Goh G, Joseph Z, Wood DJ, Yates PJ. Wound
discharge after pharmacological thromboprophylaxis in lower limb arthroplasty.
J Arthroplasty 2018;33:224–229.
. Agaba P, Kildow BJ, Dhotar H, Seyler TM, Bolognesi M. Comparison of
postoperative complications after total hip arthroplasty among patients receiving aspirin,
enoxaparin, warfarin, and factor Xa inhibitors. J Orthop 2017;14:537–543.
. Pellegrini VD Jr. Prophylaxis against venous thromboembolism after total hip and
knee arthroplasty: a critical analysis review. JBJS Rev 2015;3:1–9.
. Ayoub F, Quirke M, Conroy R, Hill A. Chlorhexidine-alcohol versus povidone-
iodine for pre-operative skin preparation: a systematic review and meta-analysis. Int J Surg
Open [Internet] 2015;2015:41–46.
. Jahng KH, Bas MA, Rodriguez JA, Cooper HJ. Risk factors for wound complica-
tions after direct anterior approach hip arthroplasty. J Arthroplasty 2016;31:2583–2587.
. Watts CD, Houdek MT, Wagner ER, Sculco PK, Chalmers BP, Taunton
MJ. High risk of wound complications following direct anterior total hip arthroplasty in
obese patients. J Arthroplasty 2015;30:2296–2298.
. Purcell RL, Parks NL, Gargiulo JM, Hamilton WG. Severely obese patients
have a higher risk of infection after direct anterior approach total hip arthroplasty.
J Arthroplasty 2016;31:162–165.
. Butt U, Ahmad R, Aspros D, Bannister GC. Factors affecting wound ooze in
total knee replacement. Ann R Coll Surg Engl 2011;93:54–56.
. Wood JJ, Bevis PM, Bannister GC. Wound oozing after total hip arthroplasty.
Ann R Coll Surg Engl 2007;89:140–142.
. Woolson ST, Mow CS, Syquia JF, Lannin J, Schurman DJ. Comparison of
primary total hip replacements performed with a standard incision or a mini-incision. J Bone
Joint Surg [Am] 2004;86-A:1353–1358.
. Rama KRBS, Apsingi S, Poovali S, Jetti A. Timing of tourniquet release in knee
arthroplasty: meta-analysis of randomized, controlled trials. J Bone Joint Surg [Am] 2007;89-A:
699–705.
. Nowak LL, Schemitsch EH. Duration of surgery affects the risk of complications
following total hip arthroplasty. J Bone Joint Surg [Br] 2019;101-B:51–56.
. Shohat N, Fleischman A, Tarabichi M, Tan TL, Parvizi J. Weighing in on
body mass index and infection after total joint arthroplasty: is there evidence for a body mass
index threshold? Clin Orthop Relat Res 2018;476:1964–1969.
. Everhart JS, Andridge RR, Scharschmidt TJ, Mayerson JL, Glassman
AH, Lemeshow S. Development and validation of a preoperative surgical site infection
risk score for primary or revision knee and hip arthroplasty. J Bone Joint Surg [Am] 2016;98-
A:1522–1532.
. Bohl DD, Shen MR, Kayupov E, Della Valle CJ. Hypoalbuminemia
independently predicts surgical site infection, pneumonia, length of stay, and readmission
after total joint arthroplasty. J Arthroplasty 2016;31:15–21.
Downloaded from Bioscientifica.com at 11/25/2022 02:17:05PM
via free access

880
. Gu A, Malahias MA, Strigelli V, Nocon AA, Sculco TP, Sculco PK.
Preoperative malnutrition negatively correlates with postoperative wound complications
and infection after total joint arthroplasty: a systematic review and meta-analysis.
J Arthroplasty 2019;34:1013–1024.
. Debbi EM, Rajaee SS, Spitzer AI, Paiement GD. Smoking and total hip
arthroplasty: increased inpatient complications, costs, and length of stay. J Arthroplasty
2019;34:1736–1739.
. Duchman KR, Gao Y, Pugely AJ, Martin CT, Noiseux NO, Callaghan JJ. The
effect of smoking on short-term complications following total hip and knee arthroplasty.
J Bone Joint Surg [Am] 2015;97-A:1049–1058.
. Bedard NA, DeMik DE, Owens JM, Glass NA, DeBerg J, Callaghan JJ.
Tobacco use and risk of wound complications and periprosthetic joint infection: a systematic
review and meta-analysis of primary total joint arthroplasty procedures. J Arthroplasty
2019;34:385–396.e4.
. Kotzé A, Carter LA, Scally AJ. Effect of a patient blood management programme
on preoperative anaemia, transfusion rate, and outcome after primary hip or knee
arthroplasty: a quality improvement cycle. Br J Anaesth 2012;108:943–952.
. Sporer SM, Rogers T, Abella L. Methicillin-resistant and methicillin-sensitive
Staphylococcus aureus screening and decolonization to reduce surgical site infection in
elective total joint arthroplasty. J Arthroplasty 2016;31:144–147.
. Barrere S, Reina N, Peters OA, Rapp L, Vergnes JN, Maret D. Dental
assessment prior to orthopedic surgery: a systematic review. Orthop Traumatol Surg Res
2019;105:761–772.
. Ollivere BJ, Ellahee N, Logan K, Miller-Jones JCA, Allen PW. Asymptomatic
urinary tract colonisation predisposes to superficial wound infection in elective orthopaedic
surgery. Int Orthop 2009;33:847–850.
. Gou W, Chen J, Jia Y, Wang Y. Preoperative asymptomatic leucocyturia and
early prosthetic joint infections in patients undergoing joint arthroplasty. J Arthroplasty
2014;29:473–476.
. Somayaji R, Barnabe C, Martin L. Risk factors for infection following total joint
arthroplasty in rheumatoid arthritis. Open Rheumatol J 2013;7:119–124.
. Lopez LF, Reaven PD, Harman SM. Review: the relationship of hemoglobin A1c
to postoperative surgical risk with an emphasis on joint replacement surgery. J Diabetes
Complications 2017;31:1710–1718.
. Mortazavi SMJ, Hansen P, Zmistowski B, Kane PW, Restrepo C, Parvizi
J. Hematoma following primary total hip arthroplasty: a grave complication. J Arthroplasty
2013;28:498–503.
. Bohl DD, Ondeck NT, Darrith B, Hannon CP, Fillingham YA, Della Valle
CJ. Impact of operative time on adverse events following primary total joint arthroplasty.
J Arthroplasty 2018;33:2256–2262.e4.
. Pugely AJ, Martin CT, Gao Y, Schweizer ML, Callaghan JJ. The incidence of
and risk factors for 30-day surgical site infections following primary and revision total joint
arthroplasty. J Arthroplasty 2015;30:47–50.
. Remérand F, Cotten M, N’Guessan YF, et al. Tranexamic acid decreases risk
of haematomas but not pain after hip arthroplasty. Orthop Traumatol Surg Res 2013;99:
667–673.
. Chandrananth J, Rabinovich A, Karahalios A, Guy S, Tran P. Impact of
adherence to local antibiotic prophylaxis guidelines on infection outcome after total hip or
knee arthroplasty. J Hosp Infect 2016;93:423–427.
. Olivecrona C, Lapidus LJ, Benson L, Blomfeldt R. Tourniquet time affects
postoperative complications after knee arthroplasty. Int Orthop 2013;37:827–832.
. Manoharan V, Grant AL, Harris AC, Hazratwala K, Wilkinson MPR,
McEwen PJC. Closed incision negative pressure wound therapy vs conventional dry
dressings after primary knee arthroplasty: a randomized controlled study. J Arthroplasty
2016;31:2487–2494.
. Shiroky J, Lillie E, Muaddi H, Sevigny M, Choi WJ, Karanicolas PJ. The
impact of negative pressure wound therapy for closed surgical incisions on surgical site
infection: a systematic review and meta-analysis. Surgery 2020;167:1001–1009.
. Redfern RE, Cameron-Ruetz C, O’Drobinak SK, Chen JT, Beer KJ. Closed
incision negative pressure therapy effects on postoperative infection and surgical site
complication after total hip and knee arthroplasty. J Arthroplasty 2017;32:3333–3339.
. Howell RD, Hadley S, Strauss E, Pelham FR. Blister formation with negative
pressure dressings after total knee arthroplasty. Curr Orthop Pract 2011;22:176–179.
. Wang C, Zhang Y, Qu H. Negative pressure wound therapy for closed incisions in
orthopedic trauma surgery: a meta-analysis. J Orthop Surg Res 2019;14:427.
. Wuarin L, Abbas M, Harbarth S, et al. Changing perioperative prophylaxis
during antibiotic therapy and iterative debridement for orthopedic infections? PLoS One
2019;14:e0226674.
. Uçkay I, Agostinho A, Belaie W, et al. Noninfectious wound complications in
clean surgery: epidemiology, risk factors, and association with antibiotic use. World J Surg
2011;35:973–980.
. Qasim SN, Swann A, Ashford R. The DAIR (debridement, antibiotics and implant
retention) procedure for infected total knee replacement: a literature review. SICOT J 2017;3:2.
. Kim K, Zhu M, Cavadino A, Munro JT, Young SW. Failed debridement and
implant retention does not compromise the success of subsequent staged revision in
infected total knee arthroplasty. J Arthroplasty 2019;34:1214–1220.e1.
. Löwik CAM, Jutte PC, Tornero E, et al; Northern Infection Network Joint
Arthroplasty (NINJA). Predicting failure in early acute prosthetic joint infection treated
with debridement, antibiotics, and implant retention: external validation of the KLIC score.
J Arthroplasty 2018;33:2582–2587.
Downloaded from Bioscientifica.com at 11/25/2022 02:17:05PM
via free access