Surgical Site Infections Notes

Acute Infections Sinuses Fistula And Surgical Site Infection

Define and describe the aetiology and pathogenesis of surgical infections.

The aetiology and pathogenesis 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.’

Read And Learn More: General Surgery Notes

• 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.

 

Ludwigs 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.

Ludwigs Angina Precipitating Factors

• Caries tooth
• Cancer of the oral cavity
• Calculi in the submandibular gland
• Chemotherapy
• Cachexia
• Chronic disease—diabetes Observe 6 Cs

Ludwigs Angina 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.

Ludwigs Angina 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.

Ludwigs Angina 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.

Ludwigs Angina Complications

1. Mediastinitis and septicaemia
2. Swelling of the tissues in the floor of the mouth results 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.
• High-grade fever, chills and rigours, and features of systemic inflammatory response syndrome (SIRS) are common.
• Tender, painful lymph nodes in the groin are characteristic of lower limb lymphangitis.

Lymphangitis Treatment

• Rest, elevation, MgSO4, local dressing, antibiotics, and anti-inflammatory drugs.
• Anti-filarial treatment in appropriate cases.

Abscess

An abscess is a localised collection of pus (dead, dying neutrophils and proteinaceous exudate).

Abscess 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 the involvement of either lymph nodes or the spine.

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 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 in temperature

Hence, it is called a nonreactive abscess to differentiate it from a 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 an ultrasound. A severe form of leptospirosis is called 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, for example., following tubercular lymphadenitis or due to tuberculosis of the spine.
• However, other chronic diseases like leprosy, actinomycosis, and Madura’s foot also produce abscesses that are ‘cold’ in nature. In this chapter, cold abscess due to cervical tubercular lymphadenitis is discussed.

Cold Abscess—Causes

• Tuberculosis (main cause)
• Actinomycosis
• Leprosy
• Madura’s foot

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 radiological findings, histopathological findings, or clinical course

Clinically Diagnosed LNTB Case 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.

Clinically Diagnosed LNTB Case 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), and ethambutol (E).
  • CP: 6 months of levofloxacin, rifampicin (R), pyrazinamide (Z), and 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 the WHO as the 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.

HIV Coinfection 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, mesenteric, hepatic, periportal, and inguinal lymph nodes constitute the rest.
• In descending order, the incidence of involvement of lymph nodes is 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%), and 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%).

HIV CoInfection 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 and 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

• This is also called a furuncle. It is a hair follicle infection 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. The skin overlying the boil also undergoes necrosis. Hence, the boil is included under acute infective gangrene.
• 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 the 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.

 

Erysipelas

• It is an acute inflammation of the skin and subcutaneous 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.

Erysipelas Clinical Features

• Rose-pink rash with a raised edge (on palpation) and a buttonhole consistency.
• Vesicles appear later and rarely become pustular.
• Oedema of the eyelids or scrotum, depending on the site.
• Features of toxaemia
• When it occurs over the face, it involves the pinna because the erysipelas is basically a cuticular lymphangitis. This is described as Milian’s ear sign positive, which is used to differentiate cellulitis of the face from facial erysipelas.
• In cellulitis of the face, the pinna does not get involved because of the close adherence of the skin and cartilage.

Erysipelas Complications

1. Toxaemia and septicaemia
2. Gangrene of the skin and subcutaneous tissue
3. Lymphoedema of the face and eyelids due to lymphatic obstruction and fibrosis

Erysipelas 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.

Chronic Abscess Sites

Foot, hand, thigh, etc.

Chronic Abscess Causes

1. Foreign bodies: These are the most common causes of a chronic abscess. There is a typical history of 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 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 a cold abscess may be present but in an unusual location.

Chronic Abscess Clinical Notes

• 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 a 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.

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

Necrotising Fasciitis—Risk Factors

• Diabetes mellitus, malnutrition
• Obesity, corticosteroids
• Immune deficiency

Necrotising Fasciitis 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.

Necrotising Fasciitis Types and Microorganisms

• Type 1 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 2 necrotising fasciitis : Monomicrobial: It is due to group A β-haemolytic streptococci. This has been referred to as a flesh-eating disease.
  • Specific Features of Type 2 Necrotising Fasciitis
    • Caused by Streptococcus pyogenes
    • Occur in young healthy people
    • Minor abrasions, lacerations may be a precipitating factor
    • Severe systemic illness with multiorgan failure streptococcal toxic shock syndrome
• Type 3 necrotising fasciitis: Gas gangrene due to clostridium.
• Type 4 necrotising fasciitis (others): Fungal (candida) and vibrio species-marine organisms.

Necrotising Fasciitis 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.

Necrotising Fasciitis Clinical Features

Sudden pain in the affected area with gross swelling of the limbs.

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.

Necrotising Fasciitis 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.

Diagnosis 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 2 cases (streptococcal): High-dose penicillins with clindamycin are 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 for neutralizing streptococcal toxins.

Acute Pyomyositis

Acute Pyomyositis Definition

Pyomyositis refers to a localised area of suppuration within the striated muscle. It occurs after trauma.

Pathogenesis of acute pyomyositis

Acute Pyomyositis 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.

Acute Pyomyositis 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.

Acute Pyomyositis 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.

Summary Pyomyositis

• Trauma
• Transient bacteraemia
• Tropical countries
• Thigh muscles are affected
• Tender intramuscular abscess
• Tenderness, temperature, toxicity
• Total renal failure—rhabdomyolysis
• Treatment—early aggressive exploration and excision
• Observe 8 Ts

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.
• Surgical site infections (SSIs) are the third most frequently reported nosocomial infection, after pneumonia and catheter-related infections (including urinary tract infections).

Surgical Site Infections (Ssis)

Surgical Site Infections 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 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.

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, dolour, and tumour (swelling). These are part of SIRS (systemic inflammatory response syndrome).
• The wound is tender with discharge.
• Microorganisms are identified in blood, pus, or urine.
• SIRS may be caused by a 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.

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).

PIRO Classification Scheme 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.

PIRO Classification Scheme Organisms

Staphylococcus aureus remains the most common SSI pathogen, followed by coagulase-negative staphylococci, enterococci and Escherichia coli. Risk factors for the development of SSIs are presented.

Risk Factors for the Development of Surgical Site Infections

• Patient-related (Remember as PATIENT)
  • Peripheral vascular disease and smoking
  • Anaemia
  • Trauma
  • Immunosuppression including diabetes
  • Elderly (old age)
  • Nutritional: Malnutrition
  • Too much obesity
• Local features (Remember as LOCAL)
  • Long (prolonged) surgical procedure
  • Oxygenation is poor (hypoxia)
  • Contamination of instruments and skin (poor skin preparation)
  • Antibiotic prophylaxis is inadequate
  • Local tissue necrosis and low temperature (hypothermia)

Principles of Treatment of Established Surgical Site Infections

• Antibiotics: Empirical broad-spectrum antibiotics that cover all likely organisms must be started, and later switched to the appropriate antibiotic(s) as per the culture-sensitivity report.
• Care of the wound: Wound dressings
• Exploration of wound or peritoneal cavity, removal of the source of sepsis, draining abscess cavity.

What is the decisive period? It takes about 4 hours after surgery for the mobilisation of inflammatory, humoral, and cellular defences. This is the time when invading bacteria get established. Hence, prophylactic antibiotics should be given during this period.

PIRO Classification Scheme Preventing Sources of SSIs

Surgical site infections may be largely prevented or reduced by an approach called the surgical care bundle approach. A bundle refers to a structured process of care that improves patient outcomes. Surgeons may develop their own surgical care bundle for SSIs. This approach may be summarised by 6 Ss.

1. Standardised antibiotic prophylaxis: Antibiotics should be administered ideally 1 hour before the skin incision. It should be repeated every 3 hours if the surgery is prolonged.

2. Skin is prepared by iodophors (povidone iodine 10%) or chlorhexidine gluconate 4% in alcohol. Povidone iodine is safe, fast-acting, and has broad-spectrum (with some sporicidal) activity. Preoperative hair removal (clipping) should be done immediately before any operation.

3. Sterile dressings and proper wound care help protect the incision.

4. Safe operating room: Environmental cleaning and disinfection of the operating room (OR), maintenance of the ventilation system (the bacterial threshold limit for an empty OR is 35 CFU/m³), and minimizing the OR traffic with continuous monitoring.

• SSI may be prevented by maintaining positive pressure in the operating rooms, mechanical ventilation, air conditioning providing filtered air, maintaining temperature, etc.
• The surgeon and team should scrub for at least 3–5 minutes with 4% chlorhexidine gluconate. However, chlorhexidine alcohol-based ‘fast rub’ is more popular now.
• OT attire and drapes: Scrub suits, caps, masks, double gloves, and dedicated footwear are used as barriers. The life of a sterile glove is 3 hours. It should be changed if the surgery lasts > 3 hours.

5. Showers and decolonization with chlorhexidine gluconate 4% during the hospital stay.

6. Screening for colonization of the surgical site.

PIRO Classification Scheme Bacterial factors

Thus, good surgical technique, gentle tissue handling, perfect haemostasis, removal of dead tissues, and appropriate use of sutures, drains, and antibiotics play a major role in preventing SSI.

A summary of the prevention of SSIs is given.

 

PIRO Classification Scheme Prevention of Hospital Infection

• Avoid unnecessary antibiotics to prevent the development of resistant organisms
• Autoclaving and sterilisation should be done optimally
• Proper ventilation of the wards
• Proper scrubbing before any procedure
• Proper disposal of urine, faeces, sputum
• Use of disinfectants
• Antibiotic prophylaxis

Antimicrobial Prophylaxis Operation Likely pathogens

• Breast – S. aureus, coagulase-negative, staphylococci
• Appendicectomy – Gram-negative bacilli, anaerobes
• Biliary tract – Gram-negative bacilli, anaerobes
• Upper GI – Gram-negative bacilli, streptococci, oropharyngeal anaerobes (peptostreptococci)
• Cefazolin is generally accepted as the antimicrobial agent of choice for clean-contaminated operations.
• Dose: 1–2 g/adult dose.
• Timing: No more than 30 minutes before skin is incised.

Prophylactic regimens

• Vascular: 3 doses of flucloxacillin with or without gentamicin, vancomycin.
• Oesophagogastric: 1 dose of 2nd generation cephalosporin and metronidazole.
• Biliary: One dose of 2nd generation of cephalosporin.
• Small bowel: 1 dose of 2nd generation of cephalosporin with metronidazole.
• Appendix or colorectal: 1 dose of 2nd generation of cephalosporin with metronidazole.

Points in SSI

• SSI within 24 hours is caused by clostridia and streptococci
• SSI after 48 hours (5 days) is caused by gram-negative and other bacteria.
• Nasal carriers of Staph. aureus have ↑ risk of SSI.
• Prevention of SSI is by aseptic and antiseptic techniques in OT as introduced by Lister, the use of prophylactic antibiotics and the patient’s own ability to prevent infection.
• Skin is to be prepared by germicidal antibiotics such as tincture of iodine, povidone iodine or chlorhexidine.
• The first dose of prophylactic antibiotics is given intravenously at the induction of anaesthesia.
• Monofilament sutures are better to decrease the SSI.

Asepsis And Antisepsis

Strictly speaking, they are equivalent and there is not much of a difference between them.

• Asepsis refers to precautions taken before any surgical procedure to prevent the development of infection. Some examples are: wearing gloves, cleaning the patient’s abdomen with iodine and spirit, sterilisation of instruments, and autoclaving.
• Antisepsis: It is defined as the practice of using antiseptics to eliminate disease-causing microorganisms. All surgical procedures today are performed only after taking aseptic precautions.
  • Dressing of an already contaminated wound using carbolic acid, and iodine.
  • Broad-spectrum antibiotics are used in the presence of infection.
  • Wearing a mask and cap in the operation theatre.

Transmissible Viral Infections Hepatitis B

It is a viral infection caused by hepatitis B virus (HBV). It injures the liver. It can result in both acute and chronic disease. It is a major global health problem. Chronic disease results in death from cirrhosis and hepatocellular carcinoma.

• Method of transmission: Contact with blood or other body fluids, including sexual intercourse with an infected partner, injections-drug use that involves sharing needles, and syringes. It can also occur with needle sticks or exposure to sharp instruments. It can also occur from tattooing, or piercing.
• Hepatitis B can be prevented by vaccines that are safe, available and effective.
• Symptoms: There can be febrile illness. It may last from a few days to several weeks. Jaundice, yellow urine, weakness, nausea, and vomiting are other features. Abdominal pain is due to an enlarged liver. A few patients with acute hepatitis can develop acute liver failure, which can lead to death.
• Diagnosis: It is done by detection of the hepatitis B surface antigen HBsAg.
• Methods of prevention: Prophylaxis by taking a vaccine. In the hospitals, all blood donations should be tested for hepatitis B virus infections. Thus to avoid accidental transmission to people who receive blood products.
• This can happen more so in patients who require massive blood transfusions, urgent transfusions and multiple transfusions such as in haemophilia cases, etc.
• All healthcare workers should not only wear double gloves but to avoid accidental pricks during the suturing of tissues, or splashing of fluids during dental extractions etc.
• Treatment: Acute illness requires treatment with paracetamol if fever is present. Otherwise, no specific drugs are used. Tenofovir or entecavir—are the drugs to suppress the hepatitis B virus.

Hepatitis C

Hepatitis C is caused by hepatitis C virus which belongs to RNA virus. There are many forms of hepatitis C—the most common being type 1.

• The incubation period is an average of 45 days—however, it can be anywhere between 2 weeks and 12 weeks.
• Method of transmission: Almost similar in the lines of hepatitis B infections such as body fluids, injection drugs and needles, etc. Transmission does not occur via breast milk, kissing or coughing, sneezing, touching, etc.
• Initial presentation after exposure to the virus is an acute illness that lasts for the first 6 months and can be in the form of fever, clay stools, high-coloured urine, loss of appetite, etc.
• Some of these cases may be completely free by 6 months of time. However, in the majority of patients, the viral infection progresses to chronic hepatitis stage.
• Complications: Cirrhosis and liver cancer: Both these can occur in hepatitis B infections also but in cases of hepatitis C virus infections, these complications can occur early. Very advanced patients can have multiple organ involvement resulting in renal failure, cerebral dysfunction ascites, etc. Intractable itching is also a feature.
• Diagnosis is established by demonstrating AntiHepatitis C Virus (HCV) antibodies. Like many other viral infections, they are demonstrated after about 12 weeks.
• Treatment: No specific treatment or drugs for this condition but symptomatic treatment is given. A few drugs have been used—they are interferon and ribavirin.
• Prophylaxis: There is a vaccine for hepatitis C. The best way is to use universal precautions such as using double gloves, avoiding prick injuries, avoiding needle sharing, avoiding direct exposure to blood and blood products and practising safe sex.