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114
Manipal Manual of Surgery
Tuberculous lymphadenitis presents as a gradually
increasing painless swelling of one or more lymph nodes and lasts from a few weeks to a few months. Multiple sites may be involved.
Systemic symptoms such as chills, fever, weight loss,
fatigue, and night sweats are common, especially in those with extensive disease. Seen in about 40% of patients.
In tuberculosis, interleukin-1(IL-1) and interleukin-6
(IL-6) are released, resulting in high-grade fever. However, this effect is somewhat counteracted by cortisol levels (which are also increased), resulting in low-grade fever.
Stages of Tuberculous (TB) Lymphadenitis
1. Stage of L
ymphadenitis (Fig. 22.5)
Common in young adults between 20 and 30 years
of age.
Upper anterior deep cervical nodes are enlarged.
Nontender, discrete, mobile, firm lymph nodes are
palpable.
2. Stage of Periadenitis/Stage of Matting (Fig. 22.6)
Results due to capsular involvement
Nodes move together—matting
Firm, nontender
Matting is pathognomonic of tuberculosis
Other rare causes of matting are chronic lympha-
denitis and anaplastic variety of lymphoma.
3. Stage of Cold Abscess (Figs 22.7–22.11)
It occurs due to caseating necrosis of the lymph nodes, which results in a fluctuant swelling in the neck. Clinical features of a cold abscess in the neck are:
No local rise of temperature, tenderness, or redness
Fig. 22.7: Cold abscess in the midline above suprasternal
notch—another common site
Fig. 22.5: TB lymphadenitis—discrete nodes
Section II General Surgery
Fig. 22.6: TB lymphadenitis—matted nodes Fig. 22.9: Cold abscess in the second intercostal space
Fig. 22.8: TB lymphadenitis—cold abscess
Acute Infections, Sinuses, Fistula and Surgical Site Infections
Fig. 22.10: Cold abscess of the right sternoclavicular joint
115
Fig. 22.12A and B: Nondependent aspiration
4. Stage of Collar Stud Abscess (Figs 22.13 and 22.14)
It results when a cold abscess deep to the deep fascia ruptures through the deep fascia and forms another swelling, which is fluctuant, in the subcutaneous plane. Cross fluctuation test may be positive. It is treated like a cold abscess.
Fig. 22.11: Cold abscess in the paravertebral region secondary
to tuberculosis of spine
Soft, cystic, fluctuant, transillumination—negative
swelling.
It becomes less prominent on sternocleidomastoid
contraction test, indicating that it is deep to the deep fascia.
Multiple, matted, mobile lymph nodes are characteristic of tuberculosis.
Differential Diagnosis
Branchial cyst may be confused for cold abscess in the anterior triangle. Cold abscess is of a shorter duration and may present with
other lymph nodes in the neck. Branchial cyst, being a congenital swelling, is of a longer duration.
Treatment of Cold Abscess (Figs 22.12A and B)
Nondependent aspiration using a wide bore needle
to avoid a persistent sinus.
A wide bore needle is preferred because the caseous
material is thick.
Incision and drainage should not be done as it causes
persistent tuberculous sinus.
Antituberculous treatment is administered.
Fig. 22.13: Collar stud abscess
Fig. 22.14: Collar stud abscess
5. Stage of Sinus (Fig. 22.15)
A sinus is a blind tract leading from the surface down
into the tissues.
It occurs when a collar stud abscess ruptures through
the skin.
In India, tubercular sinus is the most common sinus
in the neck.
Section II General Surgery
116
Fig. 22.15: Multiple tubercular sinuses in the neck and in front
of the ear
Manipal Manual of Surgery
It is common in young females. There may be
multiple sinuses.
Tubercular sinuses have a wide opening.
The sinus resembles an ulcer with an undermined
edge.
There is no induration.
Surrounding skin is hyperpigmented and sometimes
bluish in colour.
A group of lymph nodes is usually palpable under-
neath the sinus.
Tuberculosis of Intrathoracic Nodes
Occurs is about 25% of all TB lymphadenitis cases.
Pressure on the bronchus gives rise to atelectasis and
lung infection.
Pressure on the oesophagus causes dysphagia and
oesophagotracheal fistula (Fig. 22.16).
Retroperitoneal nodes may give rise to chylous ascites
and chyluria.
HIV infection and lymph node TB (Key Box 22.4).
Section II General Surgery
Fig. 22.16: Large mediastinal lymph nodes
Key Box 22.4
HIV Infection and Lymph Node Tuberculosis
It is more common than lymphoma and sarcomaPatients are male and olderMultiple sites are more commonly affectedDisseminated disease (virulent) may be seenNodes can be tenderWeight loss is more common
TB-IRIS: Tuberculosis associated Immune Reconstitution Inflammatory Syndrome. This is seen in patients with tubercular lymphadenitis on retroviral therapy. It manifests as deterioration of a treated infection or as a new presentation of a previously subclinical infection. Thus, lymph nodes may persist or may become bigger.
• It occurs due to an antigenic response caused by the bactericidal action of antitubercular drugs.
• It needs only reassurance and anti-inflammatory drugs.
• A short course of steroids may be needed if pressure symptoms are present.
• However, if lymph nodes do not respond and are increasing, a biopsy should be done to rule out lymphoma.
Investigations
TB lymphadenitis is most commonly diagnosed by histopathology. Other investigations used for diagnosis are acid-fast bacilli (AFB) smear or Ziehl-Neelsen (ZN) staining and culture of lymph node material.
Collection of sample/material for examination
may
be done by either:
1. Fine needle aspiration, or
2. Excisional lymph node biopsy.
1. Fine needle aspiration (FNA): It is considered as the
first line of evaluation of suspected tuberculous lymphadenopathy. FNA had good sensitivity and specificity (77% and 93%, respectively). Materials obtained should be tested for:
AFB smear microscopy (ZN staining or fluore-
a.
scence microscopy)
b. Mycobacterial culture with drug susceptibility testing
c. Cytology
d. Nucleic acid amplification testing (Xpert MTB/RIF)
and line probe assays.
2. Excisional biopsy: This allows for a larger sample to
be collected and has a higher diagnostic yield than FNA. Because a sinus tract may form if an incisional biopsy is performed, excisional biopsy is preferred. Materials obtained should be tested for:
AFB smear microscopy (ZN staining or fluore-
a.
scence microscopy)
Acute Infections, Sinuses, Fistula and Surgical Site Infections
117
b. Mycobacterial culture with drug susceptibility
testing
c. Histology: TB may be confirmed if epithelioid cell
granulomas and caseation are seen. The chance of diagnosing TB is increased if multinucleated cells are present. In patients living with HIV, these typical granulomas are usually not found, as T cells (which are essential for their formation) are affected.
d. Nucleic acid amplification testing (Xpert MTB/RIF)
and line probe assays.
Histopathology findings of caseating granulo-
mas, Langhans giant cells and foreign body giant cells are suggestive of TB.
Nucleic acid amplification testing (NAAT)—CB-
NAAT (cartridge-based NAAT)/Xpert MTB/RIF helps in both the tion of rifampicin resistance. NAAT identifies the complex nucleic acid of Mycobacterium tuber- culosis but cannot assess the viability of the bacteria. It cannot be used for monitoring the response to the treatment as it identifies the complex nucleic acid of dead Mycobacterium tuberculosis bacilli as well.
Line probe assays are molecular tests which
make use of PCR to evaluate drug susceptibility to isoniazid, rifampicin, aminoglycosides, and fluoroquinolones.
Mycobacterial culture is the gold standard for
diagnosis. It also helps in performing drug susceptibility testing (DST) on MTB complex growth, which may be used for decision making by the treating physician/surgeon.
Tuberculin skin test (Mantoux test) is a delayed
type hypersensitivity reaction to antigens of Mycobacterium tuberculosis. The reagent used is protein purified derivative (PPD) which is injected intradermally. The induration is measured between 48 and 72 hours. An induration >10 mm is considered to be reactive and is suggestive of M. tuberculosis infection. However, it does not indicate active disease. A 5–9 mm induration is an intermediate response and may be attributed to BCG vaccination, M. tuberculosis, or atypical mycobacterial infections. An induration <4 mm is considered negative.
Interferon-gamma release assays (IGRAs) may
be used in place of Mantoux test for diagnosing TB infection.
Imaging:
Chest X-ray should be done in all patients
a.
suspected with lymph node tuberculosis, as
diagnosis of TB and in detec-
lungs are the portal of entry for bacilli. It may show features suggestive of active pulmonary tuberculosis or apical fibrosis suggesting previous exposure to tuberculosis. Positive chest radiograph abnormalities are more commonly seen in patients living with HIV.
b. HRCT scan of the thorax or abdomen may be
done if mediastinal or abdominal lymphadeno­pathy is suspected.
c. Ultrasound scanning of the suspected
anatomical site may be done to confirm the lymph node swelling, abscess and also helps in guided FNA.
d. EBUS (endobronchial ultrasound) helps in
localising the mediastinal lymph node and in guiding transbronchial needle aspiration (FNA) of mediastinal lymph nodes (media­stinoscopy or CT-guided FNA/biopsy are preferred if mediastinal lymph nodes are not accessible through EBUS).
Definitions of Diagnosis (INDEX TB Guidelines)
Bacteriologically Confirmed LNTB Cases
Lymph Node TB)
(
A patient with symptoms and signs of LNTB who has at least one of the following:
Positive microscopy for AFB on examination of
lymph node fluid or tissue
Positive culture of Mycobacterium tuberculosis from
lymph node fluid or tissue
Positive validated PCR-based test (such as Xpert
MTB/RIF)
Clinically Diagnosed LNTB Case
A presumptive LNTB patient who undergoes diagnostic testing and has all of the following:
Negative microscopy, negative culture, and negative
PCR-based tests
No other diagnosis to explain the clinical features
Strongly suggestive evidence of LNTB by radio-
logical findings, histopathological findings, or clinical course
TREATMENT
Antitubercular drugs are the cornerstone of treatment for LNTB.
Isoniazid (H), rifampicin (R), pyrazinamide (Z),
ethambutol (E) and streptomycin (S) are the 1st line antitubercular drugs and are very important in treating drug-sensitive tuberculosis.
Section II General Surgery
118
Manipal Manual of Surgery
Regimen
IP (intensive phase) of 2 months of HRZE followed by CP (continuation phase) of 4 months of HRE in new cases (patients without a history of previous exposure to ATT).
TREATMENT OF DRUG-RESISTANT CASES
MDR-resistance to Rifampicin and Isoniazid
IP (intensive phase): 6–9 months of kanamycin,
levofloxacin, pyrazinamide (Z), ethambutol (E), cycloserine, and ethionamide.
CP (continuation phase): 18 months of levofloxacin,
ethambutol (E), cycloserine, and ethionamide.
If sensitive to isoniazid and resistant to rifampicin,
isoniazid can be added to the above regimen in both phases.
If resistant to isoniazid and sensitive to rifampicin
(isoniazid monoresistance), treat with:
IP: 3–6 months of kanamycin, levofloxacin,
rifampicin (R), pyrazinamide (Z), ethambutol (E).
– CP: 6 months of levofloxacin, rifampicin (R),
pyrazinamide (Z), ethambutol (E).
– Individual monoresistance should be treated
according to drug sensitivity testing results.
HIV CO-INFECTION
In India, the most common opportunistic infection related to HIV is tuberculosis. Patients with latent tuberculosis are more prone to develop tuberculosis in their lifetime, if they become infected with HIV. Extra­pulmonary tuberculosis is more common in patients living with HIV (PLHIV) than in non-HIV infected patients. HIV has been accepted by WHO as a defining criteria for clinical stage 4 disease diagnosis. Tuber­culous lymphadenopathy often suggests disseminated tuberculosis in PLHIV. In PLHIV, lymph node enlarge­ment is usually symmetrical and multiple. Significant mycobacterial load is often reported in PLHIV. Chest X-ray findings of pulmonary tuberculosis are a common association with tuberculous lymphadenitis in PLHIV. Response to treatment with antitubercular treatment is similar to HIV negative patients; however, recurrence and death are higher in PLHIV.
Incidence of Different Lymph Node Sites Involved
The cervical group of lymph nodes is the most common group of lymph nodes involved (63.3%), followed by the mediastinal lymph nodes (26.7%) and the axillary lymph nodes (8.3%).
Cervical and mediastinal lymph nodes together
constitute around 70% of the cases of TBLN. Axillary,
Section II General Surgery
mesenteric, hepatic, periportal, and inguinal lymph nodes constitute the rest. In descending order, the incidence of involvement of lymph nodes are cervical (64.9%), axillary (27%), and mediastinal (8%) nodes.
TBLN may involve single or multiple sites. When all TB lymphadenopathies are analysed, the incidence is as follows: Only cervical nodes (63.6%), cervical + axillary + inguinal nodes (15.1%), only hilar nodes (6%), only inguinal nodes (3%), axillary + inguinal nodes (3%) and axillary + abdominal + hilar lymph nodes (3%).
Role of Surgery in Tuberculous Lymphadenitis
Biopsy: Lymph node biopsy, wedge biopsy from the
edge of the sinus.
Aspiration: Non-dependent aspiration of cold
abscess and pus should be sent for AFB staining,
Ziehl-Neelsen (ZN) staining.
Excision of lymph nodes if they persist in spite of
antitubercular treatment.
Excision of sinus wall along with the tract.
OTHER SPECIAL TYPES OF PYOGENIC INFECTIONS
BOIL (Key Boxes 22.5 and 22.6)
This is also called a furuncle. It is a hair follicle infec-
tion caused by Staphylococcus aureus or a secondary
infection of a sebaceous cyst.
It starts with a painful indurated swelling with
surrounding oedema. After about 1–2 days, softening
occurs in the centre and a pustule develops which
bursts spontaneously and discharges pus. Necrosis
of subcutaneous tissues produces a greenish slough.
Skin overlying the boil also undergoes necrosis.
Hence, boil is included under acute infective
gangrene.
Key Box 22.5
Precipitating Factors Common Locations
Scratching Face and back of the neckDiabetes AxillaPoor immunity Gluteal region
Key Box 22.6
Facts about a Boil
Dangerous boil : On the skin of faceTender boil : External auditorySweet boil : Diabetic patientsBoil likes : Oily skinBlind boil or dull boil : Subsides without suppuration
Acute Infections, Sinuses, Fistula and Surgical Site Infections
119
Furuncle of the external auditory meatus is a very
painful condition because of the rich nerve supply of the skin. Pain is also due to the dense adherence of the skin to the perichondrium (there is no sub­cutaneous tissue).
Treatment of Boil
Incision and drainage with excision of slough. Antibiotic cloxacillin is given. Diabetes, if present, is treated.
Complications of Boil
Necrosis of the skin.
Pyaemic abscess and septicaemia.
Cavernous sinus thrombosis due to a boil on the face
or a stye on the eyelid.
CARBUNCLE (Figs 22.17A and B)
Name is derived from Latin: Carbunculus, a small
coal.
This is an infective gangrene of the subcutaneous
tissue caused by Staphylococcus aureus (Key Box
It commonly occurs in diabetic patients
22.7). Patients with poor immunity or those undergoing radiotherapy may also develop carbuncle.
Sites: Nape of the neck is the most common site,
followed by the back and shoulder region. The skin of these sites is coarse and has poor vascularity.
Carbuncle can also occur in kidney.
Pathology
The initial lesion is similar to a boil in the form of a hair follicle infection with perifolliculitis. Since the majority of patients are diabetic, infection takes a virulent course and results in subcutaneous fat
necrosis, giving rise to
multiple abscesses. These abscesses are intercommunicat-
ing and open to the exterior by multiple sieve-like openings. This appearance is described as cribriform
appearance which is pathognomonic of a carbuncle.
Clinical Features
Typically, the patient is a diabetic.
Severe pain and swelling in the nape of the neck.
Constitutional symptoms, such as fever with chills
and rigors, are severe.
Surface is red and angry-looking like red hot coal.
Surrounding area is indurated.
Later, skin over the centre of carbuncle softens and
peripheral satellite vesicles appear, which rupture and discharge pus,
giving rise to a cribriform appea-
rance (Fig. 22.17A).
The end result is the development of a large crateri-
form ulcer with central slough.
Complications
1. Worsening of diabetic status, resulting in diabetic ketoacidosis.
. Extensive necrosis of the skin overlying the carbuncle.
2
Hence, it is included under acute infective gangrene.
3. Septicaemia, toxaemia.
Fig. 22.17A and B: (A) Carbuncle of the back of neck—
common site, sieve-like appearance, (B) after excision of the carbuncle—wound heals within 2 to 3 weeks. Some cases require split skin grafting
Key Box 22.7
Staphylococcal Infections of Surgical Importance
Boil ParotitisCarbuncle OsteomyelitisBreast abscess
Treatment (Key Box 22.8)
Key Box 22.8
Summary of Carbuncle
Caused by CocciAbscesses CommunicatingRed hot like CoalAppearance Cribriform, Crateriform ulcerGangrene Cutaneous (subcutaneous)Drug of choice CloxacillinDiabetes ControlIncision Cruciate Observe 8 Cs
Treatment of carbuncle is excision.
Control diabetes, preferably with injectable insulin.
Appropriate parenteral antibiotics are given till
complete resolution occurs. Most strains of Staphylo- coccus aureus are sensitive to cloxacillin, flucloxacillin,
Section II General Surgery
120
Fig. 22.18: Carbuncle with central slough. A cruciate incision
should be given followed by excision
Manipal Manual of Surgery
When it occurs over the face, it involves the pinna
because erysipelas is basically a cuticular lymph-
angitis. This is described as Milian’s ear sign positive, which is used to differentiate cellulitis of
the face from facial erysipelas. In cellulitis of face, the pinna does not get involved because of the close adherence of the skin and cartilage.
Complications
1. Toxaemia and septicaemia
. Gangrene of the skin and subcutaneous tissue
2
3. Lymphoedema of face and eyelids due to lymphatic obstruction and fibrosis
erythromycin, and some cephalosporins. However,
methicillin-resistant Staphylococcus aureus (MRSA)
bacteria are resistant to these drugs. They are sensi­tive only to the expensive drug vancomycin, which has to be given intravenously.
Improve general health of the patient.
If the carbuncle does not show any softening or shows
evidence of healing, it is not incised
and may be left open to the exterior. Alternatively, saline dressings may be applied to reduce oedema. Complete resolu­tion may take place within 10–15 days.
Surgery is required when there is pus (Fig. 22.18). A
cruciate incision is preferred because of the multiple abscesses and extensive subcutaneous necrosis. Edges of the skin flap are excised, the pus is drained, loculi are broken down, slough is excised, and the cavity is irrigated with antiseptic agents. Like pyogenic abscess, wound heals with granulation tissue from the depth.
ERYSIPELAS
It is an acute inflammation of the skin and sub-
cutaneous tissue associated with severe lymphangitis. The causative organism is Streptococcus pyogenes. The precipitating factors are malnourishment, chronic diseases, etc. Thus, children and old people are commonly affected.
Infection sets in after a small scratch or abrasion and
spreads very rapidly, resulting in toxaemia. Sites: Face, eyelids, scrotum, and in infants, the umbilicus.
Clinical Features
Rose-pink rash with a raised edge (on palpation) and
a button hole consistency.
Vesicles appear later and rarely become pustular.
Oedema of the eyelids or scrotum, depending on the
site.
Features of toxaemia
Section II General Surgery
Treatment
Injection crystalline penicillin 10 lakh units 6th hourly IM/IV for 5–10 days.
CHRONIC ABSCESS
It occurs when the initial infective process or cause is not fully identified and properly treated.
Sites
Foot, hand, thigh, etc.
Causes
. Foreign bodies: These are the most common causes
1
chronic abscess. There is a typical history of a
of a recurrent swelling discharging pus. Wooden pieces impacted in the thigh or in the foot are common. Infection of the synthetic mesh used in hernial repair is another example.
2. Dead tissue: As it occurs in diabetic patients.
3. Pilonidal sinus: This condition gives rise to recurrent
abscesses. There is a typical history of pain and a swelling that ruptures and is followed by sponta­neous recovery. However, the sinus persists.
4. Chronic disease: Tuberculosis is one of the causes.
All features of cold abscess may be present but in an unusual location.
A 40-year-old female presented with swelling of the left thigh of 8 months duration. There were no signs of inflammation. FNAC was inconclusive. During surgery, a localised abscess with a thick wall and fleshy tissue was removed. The final report was tubercular abscess.
There was no evidence of tuberculosis anywhere in the body. Tuberculosis may present in different forms, as seen in this case. Detailed investigations were unable to reveal any evidence of pulmonary tuberculosis.
Acute Infections, Sinuses, Fistula and Surgical Site Infections
NECROTISING FASCIITIS
It is a spreading, destructive, invasive infection of the skin and soft tissues, which includes the deep fascia, but relatively spares muscle.
Risk factors are given in Key Box 22.9.
Key Box 22.9
Necrotising Fasciitis—Risk Factors
Diabetes mellitus, malnutritionObesity, corticosteroidsImmune deficiency
Common Sites
It is common in the lower extremities. Other sites are the genitalia, groin, and lower abdomen. In these places, it is comparable or similar to gangrene and is called Meleney’s gangrene.
121
Types and Microorganisms
Type I necrotising fasciitis : Polymicrobial: It is due
to a synergistic combination of anaerobes and coli­forms or nongroup A streptococci— Very often, there is no history of injury when it occurs in the lower limbs.
Type II necrotising fasciitis (Key Box 22.10): Mono-
microbial: It is due to group A β-haemolytic streptococci. This has been referred to as flesh eating disease.
Type III necrotising fasciitis: Gas gangrene due to
clostridium (Chapter 3).
Type IV necrotising fasciitis (others): Fungal
(candida) and vibrio species-marine organisms.
Pathogenesis:
Numerous cytokines, such as IL-1, IL-6, and TNF-α, are
released due to inflammation caused by M proteins, which are produced by Streptococci.
Streptococci also produce exotoxins, which destroy
neutrophils. This results in the growth of bacteria, which in turn destroy the tissues.
Clinical Features
Sudden pain in the affected area with gross swelling
of the limbs (Figs 22.19–22.21).
Key Box 22.10
Specific Features of Type II Necrotising Fasciitis
Caused by Streptococcus pyogenesOccur in young healthy peopleMinor abrasions, laceration may be a precipitating factorSevere systemic illness with multiorgan failure—
streptococcal toxic shock syndrome
Fig. 22.19: Type II necrotising
fasciitis in a healthy man. In spite of debridement and intensive care, he died of multiorgan failure
Fig. 22.21: Observe the skin changes in necrotising fasciitis
Fig. 22.20: This patient presen-
ted with features of cellulitis with renal failure. There were no preci­pitating factors. After debride­ment, recovery was complete
The part is swollen, red, erythematous, and
oedematous with skip lesions of skin necrosis and ulceration.
Skin changes: Bronze hue, brawny induration, blebs,
or crepitus are other important features. Very soon, skin patches and a dusky blue colour, followed by blebs and bullae appear.
Thrombosis of the nutrient artery results in
gangrene. Interestingly, muscles are spared.
High degree fever, jaundice, and renal failure may
occur soon in untreated cases.
Section II General Surgery
122
Manipal Manual of Surgery
Diagnosis
Early diagnosis may be made by a scoring system
proposed by Wong et al., which considers white cell count, CRP (C-reactive protein), haemoglobin, sodium, creatinine, and glucose levels. This system is called the Laboratory Risk Indicator of Necrotising
Fasciitis—LRINEC.
Full thickness biopsy taken at bedside may give the
full diagnosis. Watery pus (dishwater liquid) is also characteristic.
A high index of suspicion is required to diagnose
necrotising fasciitis. When in doubt, one can do exploratory fasciotomy. Lack of resistance between normally adherent fascia to blunt dissection is diagnostic of necrotising fasciitis.
The finger test is a bedside procedure done under
local anaesthesia. A 2-cm incision is made and deepened to the deep fascia, at which level gentle probing with the index finger is applied. The presence of dishwater liquid and a lack of resistance are characteristic of necrotising fasciitis.
Treatment
Early, aggressive management with supportive and surgical treatment.
Supportive treatment includes hospitalisation,
adequate hydration, treatment of hypotension and broad-spectrum antibiotics.
First and second generation cephalosporins are used
to treat Staphylococcus aureus. However, in cases of resistant cases due to MRSA (methicillin resistant
Staphylococcus aureus) vancomycin with carbapenem may be urgently required. Surgery should be performed
as early as possible. Severe pain, colour changes in the skin, and drowsiness are indicators of sepsis. In such cases, do not wait for all reports and perform debridement on an emergency basis. This involves wide excision and generous debridement, followed by skin grafting after a few days or weeks. Debride­ment may have to be repeated till healthy tissue is encountered. Do not hesitate to amputate if the patient’s life is in danger, because in a few patients, that is the only life-saving measure.
Type II cases (streptococcal): High dose penicillins
with clindamycin is the treatment of choice.
Clindamycin has a special effect as it is a potent suppressor of bacterial toxin synthesis.
Intravenous immunoglobulin (IVIG) has recently
been described as a reasonable and desirable option
Section II General Surgery
for neutralizing streptococcal toxins.
ACUTE PYOMYOSITIS
Definition
Pyomyositis refers to a localised area of suppuration within striated muscle. It occurs after trauma (Key Box 22.11).
Key Box 22.11
Pathogenesis of Acute Pyomyositis
Trauma
(Striated muscles are rich in iron)
Release of iron
Profuse growth of bacteria
Intramuscular abscess
Spreading infection
Septicaemia
Clinical Features
Classically, the quadriceps, gluteus, and shoulder and
upper arm muscles are affected. Pain over the part, oedema, fever, and jaundice are common. Tenderness, induration, and muscle spasms
are characteristic.
Renal failure follows soon.
Investigations
Sonographic-guided aspiration of pus followed by
culture
CT and MRI are ideal to determine the spread of the
infection.
Creatine kinase may go up to 50,000–2,00,000 units/L
during the acute phase because of rhabdomyolysis.
Treatment
Early diagnosis and early aggressive treatment
Antibiotics
Exploration—for diagnosis and treatment
Wide excision of muscles and compartmental excision
until viable tissues become visible (Figs 22.22 and 22.23).
Summary—Key Box 22.12.
NOSOCOMIAL INFECTIONS
An acquired infection from the hospital is known as
a nosocomial infection.
Infection may occur from the patient’s own
organisms (self-infection) or from external organisms.
Acute Infections, Sinuses, Fistula and Surgical Site Infections
Fig. 22.22: Extensive pyomyositis affecting muscles of the back
123
associated with systemic inflammatory response syndrome (SIRS), it is called sepsis, and if it is associated with organ failure and requires inotropes, it is called severe sepsis. More details are given under septic shock (page 65).
When to Suspect SSIs?
A postoperative patient with elevated temperature,
tachycardia, tachypnoea, and an elevated white blood cell (WBC) count.
The wound shows signs of inflammation such as
rubor, colour, dolor, and tumour (swelling). These are the part of SIRS (systemic inflammatory response syndrome).
Wound is tender with discharge.
Microorganisms are identified in blood, pus, or urine.
SIRS may be caused by variety of diseases, such as
pancreatitis, polytrauma, malignancies, transfusion reactions, as well as infection.
SIRS caused by an infection is known as sepsis. SIRS
is mediated by the production of proinflammatory mediators, such as lipopolysaccharides (endotoxin) derived from gram-negative organisms and peptido­glycans from gram-positive organisms.
Fig. 22.23: Healing after 2 weeks
Key Box 22.12
Pyomyositis
TraumaTransient bacteraemiaTropical countriesThigh muscles are affectedTender intramuscular abscessTenderness, temperature, toxicityTotal renal failure—rhabdomyolysisTreatment—early aggressive exploration and excision
Observe 8 Ts
Surgical site infections (SSIs) are the third most
frequently reported nosocomial infection, after pneumonia and catheter-related infections (including urinary tract infection).
SURGICAL SITE INFECTIONS (SSIs)
Definition
SSIs refer to infections of the tissues, organs, or spaces that have been exposed during invasive surgical procedures. They may be superficial, such as redness of a postoperative wound or a swollen local part. When
PIRO Classification Scheme
Predisposition: Advancing age or immunosuppression that may affect survival.
Insult (infection): It depends on the infecting organism or location of the disease.
Response: It refers to the development of SIRS, shock, elevated C-reactive protein, etc.
Organ dysfunction: Failure or dysfunction of organ
(s).
Clinical Features
Superficial SSI: The wound is tender, erythematous,
and oedematous.
Deep incisional SSI: Tenderness extends, and
crepitus, vesicles, and/or bullae may be present.
Intra-cavitary SSI: This depends on the system
involved. A classical example is paralytic ileus continuing in abdominal infections.
Common Sources of Infections
Major surgical site infections present with systemic manifestations, whereas minor surgical site infections present with suture site discharge only.
In surgical wards, discharging wounds, infected
urine, faeces, and sputum are sources of nosocomial infections.
Section II General Surgery