Purulent inflammatory diseases of bones, joints and soft tissue

Purulent inflammatory diseases of bones, joints and soft tissue

1. Special features of diagnostics Special features of diagnostics
and management of purulent and management of purulent
inflammation in children.inflammation in children.

2. Plan:Plan:
1.Systemic Inflammatory Response Syndrome
(SIRS) ,Sepsis.
2.Acute hematogenous osteomyelitis.
3.Chronic osteomyelitis.
4.Neonatal phlegmon
5.Neonatal mastitis.
6.Lung abscess

3. Overview
The problem of management of suppurative
infections is one of the longest standing in the
history of pediatric surgery. Widespread use of
anti-bacterial madication and consequent
microbial resistance to these medications has
lead to changes in the type and characteristics of
infecting microbes. Important aspects of the
study of this problem includes early diagnosis
with etiopathogenetic treatment and prevention
of these infections in childhood.

4. Інфекція
Infection
Опіки,
панкреонекроз
Burnes,
pancreonecrosis
ss
Синдром системної
запальної відповіді
(ССЗВ)
Systemic inflammatory
Respound syndrome
(SIRS)
Масивна
крововтрата
Massive
bleeding
Травма
Trauma

5. SYSTEMIC INFLAMMATORY SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME (SIRS),RESPONSE SYNDROME (SIRS),
BACTERIAL SEPSISBACTERIAL SEPSIS
Sepsis can be simply defined as a spectrum
of clinical conditions caused by the
immune response of a patient to infection
that is characterized by systemic
inflammation and coagulation.
It includes the full range of response from
systemic inflammatory response (SIRS)
to organ dysfunction to multiple organ
failure and ultimately death

6. Factors contributing to the Factors contributing to the
increasing incidence of sepsisincreasing incidence of sepsis
chemotherapy and radiation therapy
corticosteroid and immunosuppressive therapies
diabetics, cancer patients, patients with major
organ failure, and with granulocyopenia.
Neonates are more likely to develop sepsis (ex.
group B Streptococcal infections).
surgical protheses, inhalation equipment, and
intravenous, umbilical and urinary catheters.

7. The following is the 1992 Consensus Conference's The following is the 1992 Consensus Conference's
definitions for diagnosis of SIRS to MODSdefinitions for diagnosis of SIRS to MODS
–Systemic Inflammatory Response Syndrome
(SIRS)
–Sepsis
–Severe Sepsis
–Septic Shock
–Multiple Organ Dysfunction Syndrome
(MODS)

8. Systemic Inflammatory Response Systemic Inflammatory Response
Syndrome (SIRS)Syndrome (SIRS)
heart rate > 90 beats/minute
temperature > 38°C or < 36°C
respiration > 20/min or PaCO2 < 32mm
Hg
leukocyte count > 12,000/mm3, <
4,000/mm3 or > 10% immature (band)
cells

9. SepsisSepsis
SIRS plus a documented infection site
(documented by positive culture for organisms
from that site).
Blood cultures do NOT need to be positive.
Bacteremia may be transient, as is seen
commonly after injury to a mucosal surface,
primary (without an identifiable focus of
infection), or more commonly secondary, to
an intravascular or extravascular focus of
infection

10. Severe SepsisSevere Sepsis
Sepsis associated with organ dysfunction,
hypoperfusion abnormalities, or
hypotension.
Hypoperfusion abnormalities include but
are not limited to:
–lactic acidosis,
–oliguria,
–or an acute alteration in mental status

11. Septic ShockSeptic Shock
hypotension despite fluid
resuscitation
plus hypoperfusion abnormalities

12. Multiple Organ Dysfunction Multiple Organ Dysfunction
Syndrome (MODS)Syndrome (MODS)
Presence of altered organ function in an
acutely ill patient such that
homeostasis cannot be maintained
without intervention

13. Microbial triggers of sepsisMicrobial triggers of sepsis
gram-negative bacteria: endotoxin, formyl
peptides, exotoxins, and proteases
gram-positive bacteria: exotoxins,
superantigens (toxic shock syndrome toxin
(TSST), streptococcal pyrogenic exotoxin
A (SpeA)), enterotoxins, hemolysins,
peptidoglycans, and lipotechoic acid
fungal cell wall material

14. Organ Dysfunctions associated with Organ Dysfunctions associated with
Severe Sepsis and Septic ShockSevere Sepsis and Septic Shock
Lungs: early fall in arterial PO2, Acute Respiratory
Distress Syndrome (ARDS): capillary-leakage into
alveoli; tachypnea, hyperpnea
Kidneys (acute renal failure): oliguria, anuria,
azotemia, proteinuria
Liver- elevated levels of serum bilirubin, alkaline
phosphatase, cholestatic jaundice
Digestive tract- nausea, vomiting, diarrhea and ileus
Heart- cardiac output is initially normal or
elevated,
Brain - confusion

16. Skin -Skin - ecthyma gangrenosum ecthyma gangrenosum

17. THERAPY: three THERAPY: three prioritiespriorities
1.Immediate Stabilization of the
Patient
2.The blood must be rapidly cleared
of microorganisms
3.The original focus of infection must
be treated

18. Immediate Stabilization of the Patient.Immediate Stabilization of the Patient.
The immediate concern for patients with severe sepsis is reversal
of life-threatening abnormalities (ABCs: airway, breathing,
circulation). Altered mental status or depressed level of
consciousness secondary to sepsis may require immediate protection
of the patient's airway. Intubation may also be necessary to deliver
higher oxygen concentrations. Mechanical ventilation may help
lower oxygen consumption by the respiratory muscles and increase
oxygen availibility for other tissues. Circulation may be
compromised and significant decreases in blood pressure may require
aggressive combined empiric therapy with fluids (with crystalloids or
colloids) and inotropes/vasopressors (dopamine, dobutamine,
phenylephrine, epinephrine, or norepinephrine). In severe sepsis
monitoring of the circulation may be necessary. Normal CVP (central
venous pressure) is 10-15 cm of 0.9% NaCl; normal PAW
(pulmonary arterial wedge pressure) is 14-18 mm Hg; maintain
adequate plasma volume with fluid infusion.

19. The blood must be rapidly cleared of The blood must be rapidly cleared of
microorganisms.microorganisms.
Certain antimicrobial agents may cause the patients to get
worse. It is believed that certain antimicobials cause more
LPS to be released cause more problems for the patient.
Antimicrobials that do NOT cause the patient to get worse
are: carbapenems, ceftriaxone, cefepime, glycopeptides,
aminoglycosides, and quinolones.
Prompt institution of empiric treatment with antimicrobials
is essential. The early institution of antimicrobials has been
shown to decrease the development of shock and to lower the
mortality rate. After the appropriate samples are obtained
from the patient a regimen of antimicrobials with broad
spectrum of activity is needed. This is because antimicrobial
therapy is almost always instituted before the organisms
causing the sepsis are identified.

20. The drugs used depends on the source of the The drugs used depends on the source of the
sepsis.sepsis.
•Community acquired pneumonia a 2 drug regimen is usually utilized.
Usually a third (ceftriaxone) or fourth (cefepime) generation cephalosporin
is given with an aminoglycoside.
•Nosocomial pneumonia: Cefipime or Imipenem-cilastatin and an
aminoglycoside.
•Abdominal infection: Imipenem-cilastatin or Pipercillin-tazobactam and
aminoglycoside.
•Nosocomial abdominal infection: Imipenem-cilastatin and aminoglycoside
or Pipercillin-tazobactam and Amphotericin B.
•Skin/soft tissue: Vancomycin and Imipenem-cilastatin or Piperacillin-
tazobactam
•Nosocomial skin/soft tissue: Vancomycin and Cefipime
•Urinary tract infection: Ciprofloxacin and aminoglycoside
•Nosocomial urinary tract infection: Vancomycin and Cefipime
•CNS infection: Vancomycin and third generation cephalosporin or
Meropenem
•Nosocomial CNS infection: Meropenem and Vancomycin

21. The original focus of infection must be The original focus of infection must be
treatedtreated..
Remove foreign bodies. Drain purulent
exudate, particularly for anaerobic infections.
Remove infected organs; debride or amputate
gangrenous tissues.

22. Acute hematogenous Acute hematogenous
osteomyelitisosteomyelitis
Acute hematogenous osteomyelitis(AHO)-bacterial
infections of bones with subsequent involving of the
surrounding soft-tissue
Antacedent infections -Immunological disbalance
-widesread by way of bloodstream -hematogenous
abscess in the marrow cavity
The most common pathogen culture is Staphyloccus
aureus
The male: female ratio is 3:2
The most common involving long tubular bones

23. Hematogenous osteomyelitisHematogenous osteomyelitis
Frequency. The
overall prevalence is
1 per 5,000 children.
 Neonatal prevalence
is approximately 1
per 1,000.
50 % are preschool-
aged children

25. Classification of AHO by clinical Classification of AHO by clinical
pictures:pictures:
Toxic (adynamic) type
Septico-pyemic type
Local

26. Pathogenetic stages of AHOPathogenetic stages of AHO
Bone marrow phlegmon
Periosteal abscess
Soft tissue phlegmone
Dermal fistula

27. Classification of AHO by
localization
•Epiphyseal
•Metaphyseal
•Diaphyseal
•Metadiaphyseal
•Pelvic
•Other localization

28. Bacterial causes of acute Bacterial causes of acute
hematogenous osteomyelitis: hematogenous osteomyelitis:
–Newborns (younger than 4 mo): S aureus,
Enterobacter species, and group A and B
Streptococcus species;
–Children (aged 4 mo to 4 y): S aureus, group A
Streptococcus species, Haemophilus influenzae, and
Enterobacter species;
–Children, adolescents (aged 4 y to adult): S aureus
(80%), group A Streptococcus species, H
influenzae, and Enterobacter species;
–Adult: S aureus and occasionally Enterobacter or
Streptococcus species

29. Bacterial causes Bacterial causes
of direct osteomyelitisof direct osteomyelitis
–Generally: S aureus, Enterobacter species,
and Pseudomonas species;
–Puncture wound through an athletic
shoe: S aureus and Pseudomonas species.

30. Clinical manifestationsClinical manifestations
(1(1
stst
phase) phase)
Acute hematogenous osteomyelitis is
often preceded by the signs and
symptoms of bacteremia:
fever,
inflammation,
malaise,
cephalgia,
myalgia,
anorexia

31. The 2The 2
ndnd
phase of the osteomyelitis is the phase of the osteomyelitis is the
clinical onset of clinical onset of involvement of boneinvolvement of bone::
restricted motion,
pseudoparalysis,
soft tissue around the inflamed bone
which is, hyperemic, warm,
edematous, tender,
bone tenderness

32. Findings at physical Findings at physical
examination examination
Fever (present in only 50% of neonates)
Edema
Warmth
Fluctuance
Tenderness to palpation
Reduction in the use of the extremity (eg,
reluctance to ambulate, if the lower extremity is
involved or pseudoparalysis of limb in
neonates)
Sinus tract drainage (usually a late finding or
one that occurs with chronic infection)

33. pseudoparalysispseudoparalysis

34. Lab StudiesLab Studies
The WBC count may be elevated, but it
frequently is normal. A leftward shift is
common with increased polymorphonuclear
leukocyte counts
The C-reactive protein level usually is
elevated and nonspecific
The erythrocyte sedimentation rate usually
is elevated (90%)

35. Imaging Studies:Imaging Studies:
RadiographRadiograph
X-ray evidence of acute osteomyelitis first is
suggested by overlying soft-tissue edema at 3-5
days after infection.
Bony changes are not evident for 10-14 days
and initially manifest as periosteal elevation
followed by cortical or medullary lucencies.
 Approximately 40-50% focal bone loss is
necessary to cause detectable lucency on plain
films.

36. Radiographic image depicting long-bone regions (left labels) and bony changes (right labels)
due to Staphylococcus aureus osteomyelitis occurring in the distal right humerus of a 12-
month-old infant.
Conrad D A Pediatrics in Review 2010;31:464-471
©2010 by American Academy of Pediatrics

37. osteomyelitis of osteomyelitis of
the tibiathe tibia
(X-ray)(X-ray)
periosteal
elevation
medullary
lucencies

38. The involucrum-subperiosteal new boneThe involucrum-subperiosteal new bone

40. Imaging StudiesImaging Studies ((osteomyelitis)osteomyelitis)
Magnetic resonance imaging (MRI) can be
extremely helpful in unclear situations.
Sensitivity ranges from 90-100%
An ultrasound examination can detect fluid
collections (e.g., an abscess) and surface
abnormalities of bone (e.g., periostitis)
Computed tomographic (CT) scanning can
reveal small areas of osteolysis in cortical
bone, small foci of gas and minute foreign
bodies

41. Magnetic resonance image (short T1 inversion recovery pulse sequence) depicting long-bone
regions (left femur) and extensive marrow edema and significant enhancement of the periosteum
and adjacent soft tissues (right femur) due to Staphylococcus aureus osteomyelitis occurring in
the distal right femur of a 26-month-old infant.
Conrad D A Pediatrics in Review 2010;31:464-471
©2010 by American Academy of Pediatrics

42. ProceduresProcedures
Needle aspiration: During this test, a needle
is used to remove a sample of fluid and cells
from the vertebral space or bony area. It is
then sent to the lab to be evaluated by allowing
the infectious agent to grow on media.
Biopsy: A biopsy (tissue sample) of the
infected bone may be taken and tested for
signs of an invading organism. This can be
accomplished by needle core often
accomplished under radiographic control
(fluoroscopy or CT scan).

43. The diagnosis of osteomyelitis The diagnosis of osteomyelitis
requires 2 of the 4 following requires 2 of the 4 following
criteriacriteria
1.Pus on aspiration
2.Positive bacterial culture from bone or
blood
3.Presence of classic signs and symptoms
of acute osteomyelitis
4.Radiographic changes typical of
osteomyelitis

44. Differential diagnosis Differential diagnosis
Rheumatic fever
Monoarthritic rheumatoid arthritis
Poliomyelitis
Septic arthritis
Bacterial cellulitis
In newborns and infants in whom
osteomyelitis may present as a
pseudoparalysis, also consider nervous system
disease, cerebral hemorrhage, trauma, scurvy,
and child abuse

45. Features of neonatal Features of neonatal
osteomyelitisosteomyelitis
–S. aureus, enteric gram-negative bacilli (eg,
Escherichia coli, Klebsiella species), and group
B streptococci are common pathogens.
–IV sites, scalp electrodes, and puncture
wounds are often predisposing factors.
–Diagnosis may be delayed because swelling and
erythema may not be evident at onset.
–Decreased movement (pseudoparalysis) of the
affected area may be the only symptom.

46. Features of neonatal osteomyelitisFeatures of neonatal osteomyelitis
As many as 50% of affected newborns may
have multiple bone involvement.
Associated arthritis also is common.
Unlike radiographic findings in older children,
plain radiographs of newborns often have a
lytic area at the time of diagnosis.
A significant number of patients develop
permanent sequelae due to involvement of the
adjacent joint and damage to the cartilaginous
growth plate

47. X-ray findings of neonatal acute X-ray findings of neonatal acute
hematogenous osteomyelitishematogenous osteomyelitis

48. TreatmentTreatment
Medications
Drainage
Splinting or cast
immobilization
Surgery
Alternative
treatment

50. Initial Antibiotic Regimens for Patients with OsteomyelitisInitial Antibiotic Regimens for Patients with Osteomyelitis
Organism Antibiotic(s) of first choice Alternative antibiotics
Staphylococcus aureus or
coagulasenegative (methicillin-
sensitive) Staphylococci
Nafcillin (Unipen), 2 g IV every 6 hours,
or clindamycin phosphate (Cleocin
Phosphate), 900 mg IV every 8 hours
First-generation cephalosporin or
vancomycin (Vancocin)
S. aureus or coagulase-negative
(methicillin-resistant) staphylococci
Vancomycin, 1 g IV every 12 hoursTeicoplanin (Targocid),* trimethoprim-
sulfamethoxazole (Bactrim, Septra) or
minocycline (Minocin) plus rifampin
(Rifadin)
Various streptococci (groups A and B
β-hemolytic organisms or penicillin-
sensitive Streptococcus pneumoniae)
Penicillin G, 4 million units IV every 6
hours
Clindamycin, erythromycin,
vancomycin or ceftriaxone (Rocephin)
Intermediate penicillin-resistant S.
pneumoniae
Cefotaxime (Claforan), 1 g IV every 6
hours, or ceftriaxone, 2 g IV once daily
Erythromycin or clindamycin
Penicillin-resistant S. pneumoniaeVancomycin, 1 g IV every 12 hoursLevofloxacin (Levaquin)
Enterococcus species Ampicillin, 1 g IV every 6 hours, or
vancomycin, 1 g IV every 12 hours
Ampicillin-sulbactam (Unasyn)
Enteric gram-negative rods Fluoroquinolone (e.g., ciprofloxacin
[Cipro], 750 mg orally every 12 hours)
Third-generation cephalosporin
Serratia species or Pseudomonas
aeruginosa
Ceftazidime (Fortaz), 2 g IV every 8 hours
(with an aminoglycoside given IV once
daily or in multiple doses for at least the
first 2 weeks)
Imipenem (Primaxin I.V.), piperacillin-
tazobactam (Zosyn) or cefepime
(Maxipime; given with an
aminoglycoside)
Anaerobes Clindamycin, 600 mg IV or orally every 6
hours
For gram-negative anaerobes:
amoxicillin-clavulanate (Augmentin) or
metronidazole (Flagyl)
Mixed aerobic and anaerobic
Organisms
Amoxicillin-clavulanate, 875 mg and 125
mg, respectively, orally every 12 hours
Imipenem

51. Splinting or cast Splinting or cast
immobilization immobilization
This may be necessary to immobilize the
affected bone and nearby joints in order to
avoid further trauma and to help the area
heal adequately and as quickly as possible.
Splinting and cast immobilization are
frequently done in children. However,
eventually early motion of joints after
initial control is important to prevent
stiffness and atrophy.

52. Treatment of neonatal AHO:ShadeTreatment of neonatal AHO:Shade’’s s
reduction traction reduction traction

53. Immobilization-wide diapering as a Immobilization-wide diapering as a
prophylactic management of prophylactic management of
acquired dislocation of the hipacquired dislocation of the hip

54. Surgical CareSurgical Care
Immediate bone aspiration
If signs and symptoms do not resolve within
48-72 hours of initiation of appropriate
antimicrobial treatment, consider repeat
bone aspiration to drain the pus
Joint aspiration
Most well-established bone infections are
managed through open surgical procedures
during which the destroyed bone is scraped
out

55. Alternative treatment of Alternative treatment of
OsteomyelitisOsteomyelitis
General recommendations for the
treatment of infections include increasing
vitamin supplements, such as vitamins A
and C.
Liquid garlic extract
Herbs such as echinacea (Echinacea spp.),
goldenseal (Hydrastis canadensis), Siberian
ginseng (Eleutherococcus senticosus), and
myrrh (Commiphora molmol)
Juice therapists recommend drinking
combinations of carrot, celery, beet, and
cantaloupe juices

56. ComplicationsComplications
Bone abscess
Sepsis
Fracture
Overlying soft-tissue cellulitis
Draining soft-tissue sinus tracts

57. Further complication of AHO:varus Further complication of AHO:varus
deformation and limb contractiondeformation and limb contraction

58. Symptomatology of the primary Symptomatology of the primary
subacute haematogenous subacute haematogenous
osteomyelitisosteomyelitis
insidious in onset,
looks a systemic reaction and mimics
various benign and malignant
condition
symptoms for 2 weeks or more,
negative blood cultures
positive findings on plain x-rays

59. CHRONIC OSTEOMYELITIS:CHRONIC OSTEOMYELITIS:
Clinical FeaturesClinical Features
With progressive osteonecrosis a large mass
of dead bone forms and detaches from
healthy bone as “sequestrum”
The living bone surrounding it is known as
“involucrum”
The sinus continues to discharge pus and
small pieces of dead bone

60. CHRONIC OSTEOMYELITISCHRONIC OSTEOMYELITIS
X-RayX-Ray

61. Treatment of Chronic Treatment of Chronic
Osteomyelitis:Osteomyelitis:
removal of all dead bone (may be
very extensive and require external
fixation and later grafting)
and long periods of antibiotic
therapy

62. Serious Complications of Chronic Serious Complications of Chronic
Osteomyelitis:Osteomyelitis:
Damage to epiphyseal plates results in
growth arrest and deformity
Chronic infection can lead to amyloid
disease
Skin margins can undergo malignant
change – Squamous Cell Carcinoma
(Marjolin's ulcer)
Risk of septic arthritis in nearby joints

63. Atypical forms of osteomyelitisAtypical forms of osteomyelitis
Brodie’s abscess
Albuminous osteomyelitis
Sclerosing osteomyelitis
“Antibiotic” osteomyelitis

64. Brodie's Brodie's
abscessesabscesses
radiolucent radiolucent
with with
adjacent adjacent
sclerosissclerosis

65. Neonatal phlegmonNeonatal phlegmon
Neonatal phlegmon-acute soft-tissue
infections in childhood. Types: simple, toxic
and septicopyemic.
Etiology: most common-Staphylococcus
epidermidis
Typical localizations: lumbar area, back,
anterior and lateral superficies of the thorax
Local symptoms: pain, local rise in
temperature, hyperemia, swelling.

66. Neonatal phlegmonNeonatal phlegmon

67. Neonatal phlegmonNeonatal phlegmon

68. Neonatal phlegmon-surgical Neonatal phlegmon-surgical
treatmenttreatment

69. Neonatal mastitisNeonatal mastitis
Neonatal mastitis is a local bacterial infection
during the first mounth (first weeks) of life
Causative organisms. Staphylococcal organisms
(S.epidermidis,S.aures)
The male:female ratio is 1:1
Physiological enlargement of mammalian glands
is a prepodisposatary factor for the development
of the disease
General symptoms
Local symptoms (tenderness, swelling,
hyperemia, local rise in temperature, fluctuation)

70. Neonatal mastitisNeonatal mastitis

71. Neonatal mastitis.Surgical Neonatal mastitis.Surgical
managementmanagement

72. Special features of conservative treatment of
neonates with acute suppurative infections
1. Anti-bacterial therapy.
2. Intensive infusive therapy of hemostatic dysbalance
(IV and IM administration of drugs)
3. Passive and active immunization
4. Symptomatic treatment
5. Desensitization and hormonal therapy
6. Administration of physiotherapeutic procedures
(compresses, warm baths, ultraviolet therapy)
7. Hyperbaric oxygen therapy.

73. Special features of surgical methods of
management of acute suppurative
infections in childhood
Operative aproach (wide excision of the infection site)
Drainage
Collection of pus for culture
Special features of surgical management of neonatal
phlegmon (multiple cuts in the zone of the lesion including
the border with healthy tissue and frequent dressing every 6 -
8 hours)
Special features of surgical management of neonatal mastitis
depending on clinical type
Peculiarities of placement and removal of sutures

74. Pneumothorax
General considerations
Air within the pleural space
Spontaneous pneumothorax is especially common in male teenagers,
caused for example by rupture of a small lung bubble without any lung
disease
Risk of recurrence is 16% after the first and 80% after the third
episode
Pneumothorax may be caused by trauma (lung injured by broken ribs),
a penetrating chest wall injury (sucking chest wound), injury to the
tracheobronchial tree, a severe asthma attack, pulmonary infections
with development of an air fistula, artificial ventilation, resuscitation,
or by a congenital cystic lung disease
Induced by a valve-like mechanism, tension pneumothorax is caused
by increasing accumulation of air within the pleural cavity leading to a
mediastinal shift which develops into a dangerous situation

75. Signs
-Mild dyspnea or no signs in cases of mild
spontaneous pneumothorax
-Chest pain and shortness of breath
-Varying degrees of respiratory distress
-Reduced or absent breath sounds on the side
of the pneumothorax
-In patients suffering from tension
pneumothorax (in addition to respiratory
insufficiency) hemodynamic deterioration (neck
vein distension in normovolemic patients) occurs

76. Preoperative work-up
-Chest X-ray (misinterpretation of medial
margin of the scapula with the lung surface)
-CT scan if necessary

77. Therapy
- Observation in cases of minimally closed stable pneumothorax. Supplemental
oxygen may be necessary
Chest tube insertion
If significant signs occur insert a chest tube [2nd or 3rd intercostal space in the
midclavicular line (classic technique) or in the midaxillary line at the level of the breast
nipples] to provide a water seal drainage (Bulau drainage)
• Make a small skin incision with the patient under general anesthetic
• Perforate the intercostal space slowly via the upper edge of the rib with the tip of
a clamp
• Remove the clamp and insert the chest tube (reinforced by a trocar) through the
prepared canal
• Remove the trocar and fix the tube with sutures (size: 3-0 to 1).
A second purse suture is placed to close the skin after the chest tube has been removed
• Connect the chest tube to the water-sealed drainage system (Bulau system)
• Induced by breathing movements, air bubbles should pass through the water-
sealed drainage system

78. Operation
- Surgical therapy should be considered under the following
conditions:
•If the air leak is persistent over a period of 1 week of water-
sealed drainage
•If the CT scan shows an underlying lung disease
•In the case of a second episode
•If full lung expansion is not possible
Surgical methods
•Closure of the air leak (suture or stapling with bleb resection) and/or
parietal pleurectomy (apical and anterolateral areas) via thoracotomy or
thoracoscopic surgery. Pulmonary blebs may be overlooked when using just
the thoracoscopic approach
•In cases of multiple recurrence, intrapleural instillation of tetracycline
(for pain control instill 2% lidocaine into the chest tube 30min beforehand) to
obliterate the pleural cavity (pleurodesis) may beindicated
Postoperative care
-Chest tubes may be removed if the lung is fully expanded and drainage
volumes decrease to below 20-50 ml within a 24-h period
-Start respiratory exercises and physiotherapy as soon as possible