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104
Key Box 21.2
Diabetes and Wound Healing Factors
Tissue hypoxia due to atherosclerosis
Thickened basement membrane →↓ tissue perfusion
Trauma—repetitive due to neuropathy
Tissue metabolism is increased—relative hypoxia
Total failure of defence mechanism
Observe 5 Ts
Key Box 21.3
Chemotherapeutic Drugs
Decrease mesenchymal cell proliferation
Reduce number of platelets
Reduce inflammatory cells
Reduce growth factors
Decrease wound breaking strength
Manipal Manual of Surgery
3. In diabetic patients, wound healing is delayed
because of several factors such as microangiopathy,
atherosclerosis, decreased phagocytic activity,
proliferation of bacteria due to high blood sugar, etc.
(Key Box 21.2). Also, a poor immune response is seen
in diabetic patients.
4. Jaundiced and uraemic patients have poor wound
healing because fibroblastic repair is delayed.
5. Cytotoxic drugs such as doxorubicin and malignancy
delay healing (Key Box 21.3).
6. Systemic infection/inflammation: Infection/
inflammation in some part of the body delays wound
healing.
7. Corticosteroids, if given early, may delay wound
healing because of their anti-inflammatory
properties. However, they do not interfere once
healing is established.
8. Malnutrition: This results in delayed wound healing
including intestinal anastomotic leakage and wound
dehiscence.
Collagen synthesis is reduced and collagenolysis is
increased. Antibiotics should be given immediately
or within 2 hours to prevent infection.
3. Haematoma precipitates infection.
4. Faulty technique of wound closure.
5. Tension while suturing.
6. Hypoxia: This may reduce the killing property of
macrophages and the production of fibroblasts. If
contamination occurs, the tissue oxygen level decreases.
• Collagen synthesis is affected in cases of hypoxia.
In anaemic patients, wound healing is delayed
because of decreased angiogenesis and decreased
collagen production.
• Smoking causes vasoconstriction and elevated
carbon monoxide levels.
7. Ionising radiation: It causes endothelial cell injury
with endarteritis and results in atrophy and fibrosis.
8. Foreign body prevents healing because it precipitates
infection.
COMPARTMENT SYNDROME
• Typically occurs in closed lower limb injuries.
• Following trauma, an inflammatory reaction results
in gross oedema of the region.
• These occur in tight, divided compartments in the
leg that contain nerves and vessels.
Albumin levels must be <2 g/dL to have an effect on wound
healing.
Local Factors
1. Poor blood supply: Wounds over the knee or shin
heal very slowly, but wounds on the face heal fast.
2. Local infection: Organisms eat away the suture
material, destroy granulation tissue, and cause slough
and purulent discharge. If the bacterial count exceeds
5
organisms/mg tissue or if any β-haemolytic
10
Section II • General Surgery
streptococci are present, the wound will not heal.
Definition
It is a serious condition characterised by increased
pressure in one of the compartments of the body (e.g.
lower limb in case of fracture leg), resulting in ischaemia
of the tissues. In the lower limb, vessels, nerves and
muscles are enclosed by tight unyielding fascia. This is
the reason why even small amount of blood within a
compartment can give rise to compartment syndrome.
Types
• Acute: Following trauma—especially fractures of
long bones of the lower limb
Wound, Keloid and Hypertrophic Scar
105
• Chronic: Due to repeated injury to the muscles of the
leg—may be induced by exercise.
Pathogenesis
Following trauma to the leg, damage to the blood vessels
results in ischaemia to the muscles, which in turn results
in an inflammatory reaction that leads to diffuse oedema
of the tissues. This is aggravated by bleeding within the
compartment, resulting in compartment syndrome.
Factors precipitating compartment syndrome include
crush injuries, plaster cast applications, tight compression bandages, anticoagulants, burns, etc.
Clinical Features
• Severe pain in the leg, disproportionate to the severity
of the trauma.
• Sensory disturbances due to nerve compression.
• Pain, pallor, pulselessness, paraesthesia (Fig. 21.8), and
paralysis are other features which may occur within
12 hours of the onset of compartment syndrome.
• Painful passive stretching of the limb is characteristic
of compartment syndrome.
Measurement of Compartmental Pressure
• It is measured by introducing a transducer catheter
within 5 cm of the injury zone.
• Compartment pressure >30 mmHg of the diastolic
blood pressure is suggestive of increased compartmental pressure and is an indication for urgent
fasciotomy.
Treatment
• The lower leg has four compartments: Anterior,
lateral, superficial posterior, and deep posterior. The
fasciotomy of the lower leg can be done with either a
single incision or two incisions (lateral and medial).
• The two-incision technique is more common. The
lateral incision (Fig. 21.9) is made longitudinally,
approximately 2 cm anterior to the fibular shaft. The
medial incision is made longitudinally, 1–2 cm
posterior to the subcutaneous posteromedial border
of the tibia.
• The incisions are made 8 cm long. After incising the
deep fascia, the muscles bulge out. The soleus muscle
must be detached from the tibia to decompress the
deep flexor compartment.
• The most important aim is to preserve the blood
supply by relieving the compression on the posterior
tibial and peroneal arteries.
Complications
• Infections
• Gangrene requiring amputation.
HYPERTROPHIC SCAR AND KELOID
• As the name suggests, there is hypertrophy of mature
fibroblasts (excessive collagen) in hypertrophic scars.
Blood vessels are minimal in this condition.
• However, in keloids, proliferation of immature
fibroblasts with immature blood vessels are found.
These two conditions represent variations in the
normal process of wound healing (Table 21.2).
• Keloids are very common in Africans and are least
common in Caucasians (Key Boxes 21.4 and 21.5).
• A keloid is not a true tumour, but has a marked
tendency for local recurrence after excision.
• Keloids take the shape of a butterfly over the sternum,
which is its most common site of occurrence. It is
extremely difficult to treat keloids over the sternum.
Key Box 21.4
Types of Scar
Atrophic
Hypertrophic
Keloid
Fig. 21.8: Paraesthesia between
first and second toes
Fig. 21.9: Fasciotomy
Key Box 21.5
Aetiology of Keloid
Key factors: Surgery, burns, vaccinations
Elevated levels of growth factor (more of type ‘B’ collagen)
Laceration or abrasion
Over the sternum (incision)
Inheritance and injection
Deep pigmented skin (Blacks)
Remember as KELOID
Section II • General Surgery
106
Manipal Manual of Surgery
Table 21.2 Comparison of hypertrophic scar and keloid (Figs 21.10 to 21.12)
Hypertrophic scar
General features
• It occurs from a prolonged inflammatory phase of wound
healing. It never gets worse after 6 months
• Itching is not usually present. If present, it is not severe
• Nontender
• Not vascular
• Does not extend beyond the boundary of the original incision
or wound. It rises above skin
Precipitating factors
• Scar crossing normal skin creases
• Over sternum, over joints
• Young persons
Natural history
• May become small
Complications
• Do not occur
Treatment
• It is often not necessary
• Stocking, armlets, gloves
• Elastic bandage may help
• Excision can be done
• Silicone application
• Topical retinoids
Keloid
• It continues to get worse even after 1 year and up to a few
years
• Severe itching is present
• Margin is tender
• Vascular, red, erythematous (immature blood vessels)
• Extends to normal tissues, has claw-like process. Hence the
name
• Black race
• Tuberculosis patients
• Incision over the sternum, ear lobe
• Equal in both sexes
• Hereditary and familial
• Vaccination sites, injection sites, incision sites, piercing sites
• Does not become small
• Ulceration, infection
• It is difficult. Injection of steroid preparation such as
triamcinolone acetate (Kanacort)
has been found to be extremely useful. It flattens the keloid.
Intrakeloidal excision and skin grafting are to be tried last.
Recurrence is common. Care should be taken not to extend
the incision onto the normal surrounding tissues.
• Silicone application
• Topical retinoids
Any form of excision has high
chance of recurrence
into the lesion (intralesional)
We once had a patient who had undergone wide
excision and grafting 6 times for a sternal keloid. The
jaw and sites of vaccination are other common sites
for keloids (Figs 21.10–21.12, Key Box 21.6).
Collagen bundles are virtually absent in keloids. It is extremely
difficult to treat a keloid.
Fig. 21.10: Recurrent keloid over the sternum. Excision attempted
Section II • General Surgery
three times
Fig. 21.11: Keloid over
vaccination site
Key Box 21.6
Fig. 21.12: Extensive keloid of
the ear (Courtesy: Dr BP Suresh,
Subbaiah Institute of Medical
Sciences Shivamogga)
Keloid Sites
High chances Least chances
Skin of ear lobe Eyelid
Presternal Genitalia
Deltoid Palm, sole
Upper back Across joint
Wound, Keloid and Hypertrophic Scar
107
What is a Contracture?
When a scar crosses joints or flexion creases, a tight ‘web’
may form which is referred to as a contracture (see
Chapter 32: Burns and Skin Grafting for more details).
MISCELLANEOUS
Healing of Specialised Tissues (Key Box 21.7)
Key Box 21.7
Healing of Specialised Tissues
Once Destroyed
Nerve cells of brain Cannot be replaced by proli-
and spinal cord feration of other nerve cells
Peripheral nerves Regenerative capacity is
present
Stomach and Healing is good after
intestines anastomosis, rarely leaks
Colon and Healing is precarious, chances
oesophagus of leakage are high
Wounds on the Healing is excellent due to
face good vascularity
Muscles Can heal completely or may
be replaced by fibrosis
Bone Rapid proliferation of osteo-
blasts
SURGICAL WOUNDS
Surgical wounds may be classified depending upon
their nature (Table 21.3, Figs 21.13–21.16).
Fig. 21.13: Excision of neck swelling—clean
Fig. 21.14: Cholecystectomy—clean contaminated
Table 21.3 Classification of surgical wounds
Wounds class
Clean
(Fig. 21.13)
Clean
contaminated
(Fig. 21.14)
Contaminated
(Fig. 21.15)
Dirty
(Fig. 21.16)
Definition
• Nontraumatic
• Elective surgery
• Gastrointestinal,
respiratory or genitourinary
tract not entered.
• Respiratory,
genitourinary or
gastrointestinal tracts entered
but minimal contamination
• Open, fresh, traumatic wounds
• Uncontrolled spillage from
an unprepared viscus
• Minor break in sterile tech-
nique
• Open, traumatic dirty
wounds
• Traumatic perforated viscus
• Pus in the operative field
Examples of typical
procedures
• Mastectomy
• Vascular procedures
• Gastrectomy
• Hysterectomy
• Cholecystectomy
• Ruptured appendix
• Resection of
unprepared bowel
• Resection of gangrene
Wound infection
2
<10
20
30–70
rate (%)
Usual organism
Staphylococcus
aureus
Related to viscus
entered
Depends on
underlying cause
Depends on
underlying cause
Section II • General Surgery
108
Manipal Manual of Surgery
Fig. 21.16: Peritonitis—dirtyFig. 21.15: Appendicular abscess—contaminated
1. Platelet aggregation occurs in which phase of wound
healing?
A. Inflammatory phase B. Proliferative phase
C.
Remodelling phase D. Scar formation phase
2. A chronic scar can change into:
A. Martorell’s ulcer B. Marjolin’s ulcer
C.
Meleney’s ulcer D. Malignant melanoma
3. The ideal solution for washing wounds is:
A. Saline B. Betadine
Hydrogen peroxide D. Eusol
C.
4. The following are true for wound healing except:
A. Vitamin C is necessary for the synthesis of collagen
B.
Diabetic patients have decreased phagocytic activity
C. Once healing is established, corticosteroids may
be given
D. Poor wound healing in jaundiced patients is due
to poor functioning of macrophages
5. The following are true for compartment syndrome
except:
A. It usually occurs in the lower limbs
B.
The most prone site is the posterior compartment
C. Paraesthesia between the 1st and 2nd toe may be
a feature
D. Compartment pressure >30 mmHg is an indication
for urgent fasciotomy
6. The following are true for keloid except:
A. It extends into normal skin
It continues to become worse even after several
B.
years
C. It does not give rise to itching
D. It often recurs after excision
7. The following are true for hypertrophic scar except:
A. It does not extend into normal skin
It does give rise to itching
B.
C. It becomes worse even after 2 years
D. It is more common in Africans
8. The following are true for keloid except:
A. Sternum is one of the common sites
Collagen bundles are present
B.
C. Intrakeloidal injections may be used to treat it
D. Deeply pigmented skin is more vulnerable for its
formation
Section II • General Surgery
1. A 2. B 3. A 4. D 5. B 6. C 7. C 8. B
Answers
22
Acute Infections, Sinuses, Fistula
and Surgical Site Infections
Cellulitis
Ludwig’s angina
Lymphangitis
Abscess
Cervical tuberculous lymphadenitis
Boil, carbuncle
Erysipelas
Chronic abscess
SU6.1: Define and describe the aetiology and patho-
genesis of surgical infections.
INTRODUCTION
Ever since surgery evolved as a speciality, infection and
haemorrhage have been two well-known enemies of
surgeons. Although many newer antibiotics have come
into existence, infection still dominates and is a major
cause of morbidity and mortality in patients with
‘benign disease.’ This is the sad outcome of disease
complications. Hence, it is important to effectively diagnose and treat infections as early as possible. Common
surgical infections and their details are given below.
CELLULITIS
Cellulitis is a spreading subcutaneous inflammation
caused by haemolytic Streptococci that produce hyaluro-
nidase and streptokinase. This leads to spreading of
inflammatory exudates in the subcutaneous and fascial
planes, resulting in a gross swelling of the affected part.
Cellulitis spreads quickly in areas of loose subcutaneous
tissue, such as the scrotum, or in areas of loose connective and interstitial tissue, such as the face and forearm.
Sources of Infection
• Injury—minor or major
• Graze/scratch/abrasion
• Snakebite, scorpion bite, etc.
Necrotising fasciitis
Acute pyomyositis
Surgical site infections, PIRO classification
Asepsis and antisepsis
Hepatitis B
Hepatitis C
Sinus and fistula
Precipitating Factors
• Diabetes
• Low resistance of an individual
Common Sites
• Lower limbs
• Face and neck
• Scrotum
Clinical Features (Fig. 22.1)
The affected part shows evidence of inflammation such
as redness, itching, and a diffuse swelling. Skin is
stretched and shiny. Pain, fever, and toxaemia follow
later. It is differentiated from an abscess by the features
mentioned in Key Box 22.1.
In untreated cases, suppuration, sloughing, and
gangrene may occur.
Treatment
• Bed rest with legs elevated to reduce oedema of legs.
Key Box 22.1
Cellulitis Abscess
No edge (diffuse swelling) Well-circumscribed,
has an edge
No limit Limit is present
No pus Pus is present
No fluctuation Fluctuation is positive
109
110
Fig. 22.1: Cellulitis of the foot with abscess
Manipal Manual of Surgery
• Glycerine MgSO4 dressing—reduces oedema of the
part by osmotic effect.
• Diabetes mellitus, if present, is treated with injection
insulin given subcutaneously.
• Appropriate antibiotics such as injection cephalo-
sporins have to be given.
• Amoxycillin clavulanate potassium 25–40 mg/kg/
day every 12 hours for 5–7 days depending on the
severity of the condition.
• Antisnake venom is given in cases of snakebite.
Complications
1. Cellulitis may turn into an abscess which needs to
be drained.
2. Necrotising fasciitis: Certain highly invasive strains
of Streptococcus pyogenes may cause extensive necrosis
of the skin and subcutaneous tissues, resulting in
necrotising fasciitis. This is treated by debridement
and skin grafting (see page 284) (Fig. 22.2).
3. Toxaemia and septicaemia: Streptococcal toxic shock
syndrome may result if exotoxins are produced by the
organisms.
4. Cellulitis may precipitate ketoacidosis in patients
with diabetes mellitus.
LUDWIG’S ANGINA
It refers to cellulitis of the submental and submandibular
regions combined with inflammatory oedema of the
mouth. Virulent streptococcal organisms are responsible
for infection surrounding the submandibular region.
Anaerobes also play a major role (Key Box 22.2).
Key Box 22.2
Precipitating Factors
Caries tooth
Cancer of the oral cavity
Calculi in the submandibular gland
Chemotherapy
Cachexia
Chronic disease—diabetes Observe 6 Cs
Clinical Features
• Elderly patients presenting with diffuse swelling in
the submandibular and submental regions (brawny
oedema).
• Oedema of the floor of the mouth, which pushes the
tongue upwards and results in difficulty swallowing.
• High grade fever with toxicity.
• Putrid halitosis is characteristic of this condition.
Treatment
• Rest and hospitalisation.
• Appropriate antibiotics.
• Intravenous fluids (to correct dehydration) and Ryle’s
tube feeding.
• If it does not respond to conservative treatment,
surgical intervention is recommended.
Fig. 22.2: Extensive cellulitis and necrotising fasciitis with gangrene
Section II • General Surgery
Surgery (Decompression)
Under general anaesthesia, a 5–6 cm curved incision is
made below the mandible in the submandibular region
over the most prominent part of the swelling. The
submandibular gland is mobilised, the mylohyoid
muscle is divided, and the pus is drained. Even if pus is
not found, the oedematous fluid comes out, which
greatly improves the condition of the patient. The
wound is closed with loose sutures after irrigating the
cavity with antiseptic agents, and a drainage tube is kept
in place.
Acute Infections, Sinuses, Fistula and Surgical Site Infections
111
Complications
1. Mediastinitis and septicaemia
. Swelling of the tissues in the floor of the mouth results
2
in elevation of the tongue, as the infection is contained
by the mylohyoid. This leads to upper airway obstruction and oedema of the glottis, resulting in stridor.
LYMPHANGITIS
• It is also a nonsuppurative, poorly localised infection
caused by streptococci, staphylococci, or clostridia.
• It presents as red painful streaks over the affected
lymphatics.
• Filarial infection is a common cause of lymphangitis
in coastal India (see page 216
).
• High grade fever, chills and rigors, and features of
systemic inflammatory response syndrome (SIRS) are
common.
• Tender, painful lymph nodes in the groin are
characteristic of lower limb lymphangitis.
Treatment
• Rest, elevation, MgSO
, local dressing, antibiotics,
4
anti-inflammatory drugs.
• Anti-filarial treatment in appropriate cases.
ABSCESS
An abscess is a localised collection of pus (dead, dying
neutrophils and proteinaceous exudate).
CLASSIFICATION
1
. Pyogenic abscess: It is the commonest form of an
abscess. It can be subcutaneous, deep, or can occur
within viscera such as the liver or kidney. In this
chapter, pyogenic abscess refers to soft tissue abscess.
2. Pyaemic abscess: Occurs due to circulation of
pyaemic emboli in the blood (pyaemia).
3. Cold abscess: Usually refers to tubercular abscess due
to involvement of either lymph nodes or spine.
PYOGENIC ABSCESS
It is usually produced by staphylococcal infections. The
organisms enter
the soft tissue through an external
wound (minor or major). It can also be due to cellulitis
or haematogenous spread from a distant focus such as
tonsillitis or caries tooth.
Pathophysiology
• Following injury, there is inflammation of the part
brought about by the organism such as Staphylococcus.
Pathological events are summarised in Fig. 22.3.
• The end-result is the production of pus composed of
dead leukocytes, bacteria, and necrotic tissue. The
area around the abscess is encircled by fibrin products
and it is infiltrated with leukocytes and bacteria. It is
called a pyogenic membrane.
Symptoms
The patient feels ill and complains of throbbing pain at
the site, which occurs due to pressure of the pus on the
nerve endings. Fever, with or without chills and rigors,
may be present.
Signs
. Calor–heat: The affected part is warmer due to local
1
rise of temperature.
2. Rubor–redness: It is due to inflammation resulting
in hyperaemia.
3. Dolor–pain: An abscess is extremely tender.
4. Tumour–swelling: It consists of pus. It is tensely
cystic with surrounding brawny oedema.
Fig. 22.3: Pathological events during inflammation
Section II • General Surgery
112
Manipal Manual of Surgery
5. Loss of function: The function of the part is impaired,
due to pain.
6. Fluctuation: It may be elicited. However, in a deep-
seated abscess (e.g. breast abscess), it may be negative.
• Untreated abscess tends to point spontaneously
along the area of least resistance to the nearest
epithelial surface, e.g. skin, gut, oral cavity.
• However, deep-seated abscess such as breast
abscess may cause much tissue destruction before
pointing.
Treatment
Incision and drainage (I&D) under general anaesthesia.
General anaesthesia is preferred because in the presence
of infection, local anaesthesia may not act and it would
be difficult to break all the loculi of an abscess without
causing pain.
Procedure
• A stab incision is made over the most prominent
(pointing) part of the abscess. The pus which comes
out is collected and sent for culture and sensitivity.
A sinus forceps or a finger is introduced within the
abscess cavity and all the loculi are broken down.
Fresh oozing of the pus is an indication that the
procedure is complete. The abscess cavity is irrigated
with saline or
a mild antiseptic agent like iodine
solution.
• The cavity, if large, may need to be packed with roller
gauze dipped in iodine solution, which is removed
1–2 days later. Roller gauze packing prevents
premature closure of the skin, thereby facilitating
healing from the depth of the cavity through granulation tissue formation. With appropriate antibiotics and
proper dressings, the wound heals within 5–
7 days.
• Antibiotic of choice is cloxacillin for staphylococcal
abscess. Dosage: 500 mg 6th hourly for 5–7 days.
• Modified Hilton’s method for I&D. This method is
followed if the abscess is situated in the vicinity of
important anatomical structures like vessels or nerves
(Table 22.1). The skin and superficial fascia are incised
(instead of a stab incision), and the abscess is opened
by sinus forceps to avoid damage to vital structures.
Table 22.1 Relationship of nerves or vessels with an
abscess
Site Anatomical structure
Axilla → Axillary vessels
Neck → Subclavian vessels and brachial plexus
Parotid region → Facial nerve
Midpalmar space → Median nerve
Differential Diagnosis
1. Ruptured aneurysm may present as a subcutaneous
abscess with pain, redness, local rise of temperature,
and sometimes even leukocytosis. Ruptured vertebral
artery aneurysm in the posterior triangle and popliteal artery aneurysm in the popliteal fossa have been
incised, mistaking them for an abscess (Table 22.2).
Caution: When in doubt, aspirate with a wide bore
needle before incising an abscess.
Before incising an abscess/swelling, look for Temperature and
Tenderness, Auscultate and Aspirate.
“Remember as TATA”
2. Soft tissue sarcoma in the thigh may be confused for
a deep-seated abscess. However, throbbing pain, high
grade fever with chills and rigors, and short duration
of the swelling clinches the diagnosis of an abscess.
Antibioma
It is an antibiotic-induced swelling (oma). Once an
abscess is formed, antibiotics seldom effect a cure but
the partially sterilise the pus. Antibiotics also produce
fibrosis, resulting in thickening of the abscess wall.
Clinically, this may result in a hard lump.
Common sites of antibioma are the breast, thigh, and
ischiorectal fossa. Antibioma in the breast may mimic
carcinoma of the breast.
PYAEMIC ABSCESS
This is due to pus-producing organisms in the circulation (pyaemia). It is the systemic effect of sepsis. It
commonly occurs in diabetics and in patients receiving
Table 22.2
Table 22.2 Differences between acute abscess and ruptured aneurysm
Acute abscess Ruptured aneurysm
No previous history of the swelling Previous history of the swelling will be present
Throbbing pain is characteristic Throbbing pain is usually absent
High grade fever with chills and rigors is present Low grade fever is present
Extremely tender Tender
Section II • General Surgery
Acute Infections, Sinuses, Fistula and Surgical Site Infections
113
chemotherapy and/or radiotherapy. Pyaemic abscess
is characterised by the following features:
• They are multiple
• They are deep-seated
• There is minimal tenderness
• There is no local rise of temperature
Hence, it is called nonreactive abscess to differentiate
it from pyogenic abscess. This is treated by multiple
incisions over the abscess site and drainage (like a
pyogenic abscess) with antibiotic cover.
Leptospirosis is a zoonosis caused by infected urine of cattle,
dogs or rats. It causes severe myalgia/myositis of thigh
muscles and thus can be confused for pyaemic abscesses.
High grade fever is also a feature. When in doubt ask for
ultrasound. Severe form of leptospirosis is called as Weil’s
disease. It can cause multiorgan failure and death.
COLD ABSCESS
• Even though this is a chronic abscess due to a chronic
disease (tuberculosis), for the completeness of the
chapter on abscess and for the convenience of
reading, it is discussed here.
• Cold abscess refers to an abscess that has no signs of
inflammation. Usually, it is due to tuberculosis, e.g.
following tubercular lymphadenitis or due to tuberculosis of spine. However, other chronic diseases like
leprosy, actinomycosis, and Madura foot also produce
abscesses that are ‘cold’ in nature (Key Box 22.3). In
this chapter, cold abscess due to cervical tubercular
lymphadenitis is discussed.
• The disease may be caused by Mycobacterium tuber-
culosis, atypical mycobacteria, or Mycobacterium bovis.
Aetiopathogenesis
• In 80% of the cases, mycobacteria pass through tonsillar
crypts and affect the tonsillar node or jugulodigastric
group of nodes in the anterior triangle of the neck.
• In 20% of the cases, lymph nodes in the posterior
triangle are affected due to adenoid involvement.
• Rarely, infection can spread from tuberculosis of the
apex of
the lung. Organisms directly penetrate
Sibson’s fascia (suprapleural membrane) and may
cause enlargement of supraclavicular node.
• Other lymph nodes in the neck, such as the preauri-
cular and submandibular nodes,
may also be affected.
• Tuberculous bacilli survive within macrophages, and
release a toxin called tuberculosis necrotising toxin
(TNT), which causes host cell death.
• In general, the incidences of lymphadenopathy at
various sites are shown in Fig. 22.4.
Pathological Types
• Caseating type: Most common type seen in young
adults.
• Hyperplastic type: Lymph nodes show marked
degree of lymphoid hyperplasia. Least caseation is
seen in patients with good body resistance.
• Atrophic type: Seen in elderly patients. Lymphoid
tissue undergoes degeneration. Glands are small
with early caseation.
A few lymph nodes may show
scattered calcifications.
Key Box 22.3
Cold Abscess—Causes
Tuberculosis (main cause)
Actinomycosis
Leprosy
Madura foot
CERVICAL TUBERCULOUS LYMPHADENITIS
• It is the most common form of extrapulmonary
tuberculosis.
• Tuberculous infections of the cervical lymph nodes—
often termed scrofula and king’s evil—are typically
caused by tuberculous mycobacteria, but may also
be caused by non-tuberculous mycobacteria.
• It is seen in endemic areas and in immunocompro-
mised individuals.
• Lymph node tuberculosis constitutes 20–40% of extra-
pulmonary tuberculosis. It is more common in children and women, and in Asians and Pacific islanders.
Clinical Features
• Common in the age group of 11–30 years.
• HIV-immunocompromised disease is a strong risk
factor for developing tuberculous infections.
Fig. 22.4: Incidence of lymph node tuberculosis
Section II • General Surgery