Prevention of Orthopaedic Infections — MCQs
In a surgical post-op ward, a patient developed wound infection. Subsequently 3 other patients developed similar infections in the ward. What is the most effective way of preventing the spread of infection?
Which organism causes prosthetic valve endocarditis within 60 days of surgery?
Which of the following is the drug of choice for preoperative antibiotic prophylaxis in a patient undergoing cardiac surgery?
When do we have to start antibiotics to prevent post-operative infection?
Preferred time for prophylactic antibiotic administration for surgery?
In postoperative intensive care unit, five patients developed postoperative wound infection on the same day. The best method to prevent cross infection occurring in other patients in the same ward is to:
The Henderson-Jones classification is used for:
All of the following factors affect osseointegration EXCEPT:
Osteosclerosis of bone occurs due to?
What is the usual site of tuberculous bursitis?
Prevention of Orthopaedic Infections Indian Medical PG Practice Questions and MCQs
Question 1: In a surgical post-op ward, a patient developed wound infection. Subsequently 3 other patients developed similar infections in the ward. What is the most effective way of preventing the spread of infection?
- A. Fumigation of the ward
- B. Wash OT instruments with 1% perchlorate
- C. Proper hand washing of all ward personnel (Correct Answer)
- D. Give IV antibiotics to all patients in the ward
Explanation: ***Proper hand washing of all ward personnel*** - **Hand hygiene** is the single most important and effective measure to prevent the spread of **healthcare-associated infections (HAIs)**, especially in a ward where multiple patients are affected. - It directly reduces the transmission of microorganisms from healthcare workers to patients and between patients. *Fumigation of the ward* - **Fumigation** is typically used for **terminal disinfection** or in situations involving highly resistant organisms or outbreaks, but it is not a routine or primary method for preventing day-to-day infection spread. - Its effectiveness is limited, and it can pose **health risks** to personnel and patients if not performed correctly, often requiring the ward to be vacated. *Wash OT instruments with 1% perchlorate* - This option focuses on the **sterilization of operating theater (OT) instruments**, which is crucial for surgical procedures but **irrelevant** to preventing the spread of wound infection within a general ward setting. - The problem describes a ward-based infection spread, not issues with surgical instrument sterility. *Give IV antibiotics to all patients in the ward* - **Prophylactic antibiotics** for all patients in a ward is generally **not recommended** as it can lead to **antibiotic resistance**, mask underlying infections, and cause adverse drug reactions. - Antibiotics should be prescribed judiciously based on specific indications and confirmed infections, not as a general preventive measure.
Question 2: Which organism causes prosthetic valve endocarditis within 60 days of surgery?
- A. Staphylococcus aureus
- B. Staphylococcus epidermidis (Correct Answer)
- C. Fungus
- D. Streptococcus viridans
Explanation: ***Staphylococcus epidermidis*** - This organism is the **most common cause of early prosthetic valve endocarditis (within 60 days of surgery)**, accounting for 30-40% of cases. - As a coagulase-negative Staphylococcus, *S. epidermidis* commonly colonizes the skin and can be introduced during the surgical procedure. - It produces **biofilms**, which allow it to adhere to prosthetic surfaces and resist antibiotic treatment. *Staphylococcus aureus* - *Staphylococcus aureus* is the **second most common cause of early prosthetic valve endocarditis** (20-25% of cases) and can cause both early and late infections. - It typically presents with a more **fulminant, aggressive course** compared to *S. epidermidis*. - While both staphylococcal species cause early PVE, *S. epidermidis* remains more frequent. *Fungus* - **Fungal endocarditis** on prosthetic valves (typically *Candida* species) accounts for 5-10% of early PVE cases. - More commonly seen in immunocompromised patients, those with prolonged antibiotic use, or after complicated cardiac surgery. - Its incidence is significantly lower than staphylococcal causes in the early post-operative period. *Streptococcus viridans* - *Streptococcus viridans* is the **most common cause of native valve endocarditis**, particularly in patients with pre-existing valvular heart disease. - It typically causes a **subacute presentation** and is more associated with **late prosthetic valve endocarditis** (>60 days post-surgery), not early PVE. - Rarely implicated in early prosthetic valve infections.
Question 3: Which of the following is the drug of choice for preoperative antibiotic prophylaxis in a patient undergoing cardiac surgery?
- A. Cefazolin (Correct Answer)
- B. Penicillin
- C. Clindamycin
- D. Vancomycin
Explanation: ***Cefazolin*** - **Cefazolin** is a first-generation cephalosporin that provides excellent coverage against **Staphylococcus aureus** and **Streptococcus species**, which are common pathogens in surgical site infections in cardiac surgery. - It has a favorable safety profile, long half-life allowing for convenient dosing, and good tissue penetration, making it the preferred choice for **preoperative antibiotic prophylaxis** in most cardiac surgery cases. *Penicillin* - **Penicillin** has a narrow spectrum of activity compared to cefazolin and does not adequately cover all potential pathogens in cardiac surgery, particularly **methicillin-susceptible Staphylococcus aureus (MSSA)**. - Due to its limited spectrum, penicillin is generally not recommended for routine **surgical prophylaxis**, especially in complex procedures like cardiac surgery. *Clindamycin* - **Clindamycin** is an alternative for patients with **beta-lactam allergies**, providing coverage against gram-positive organisms and anaerobes. - However, for routine prophylaxis without a specific allergy or high risk of resistant organisms, **clindamycin** is less effective than cefazolin against the most prevalent surgical pathogens. *Vancomycin* - **Vancomycin** is reserved for patients with a known **penicillin allergy** or a high risk of **methicillin-resistant Staphylococcus aureus (MRSA)** colonization or infection. - Its routine use as a primary prophylactic agent in cardiac surgery is discouraged to prevent the development of **vancomycin resistance**.
Question 4: When do we have to start antibiotics to prevent post-operative infection?
- A. 1 week before surgery
- B. 2 days before surgery
- C. After surgery
- D. 30-60 minutes before incision (up to 24 hours post-op) (Correct Answer)
Explanation: ***30-60 minutes before incision (up to 24 hours post-op)*** - Surgical antibiotic prophylaxis (SAP) should be administered **30-60 minutes before surgical incision** to ensure adequate tissue and serum concentrations at the time of incision. - This timing allows optimal drug distribution to surgical tissues, which is crucial for preventing surgical site infections (SSIs). - For most clean and clean-contaminated surgeries, prophylaxis should be limited to a **single dose** or continued for **maximum 24 hours post-operatively** as per WHO and CDC guidelines. - Prolonged post-operative antibiotics beyond 24 hours do **not** reduce infection rates and increase the risk of **antibiotic resistance** and **adverse effects**. *1 week before surgery* - Administering antibiotics this far in advance is **unnecessary** and **ineffective** for surgical prophylaxis. - It increases the risk of **antibiotic resistance** and does not guarantee adequate drug levels at the time of incision. - Pre-operative antibiotic use should be avoided unless treating an active infection. *2 days before surgery* - This timeframe is too early to achieve prophylactic benefit during the surgical procedure. - Prolonged pre-operative use promotes **bacterial resistance** without providing additional protection. - Drug levels will not be optimal at the time of incision due to metabolism and excretion. *After surgery* - Starting antibiotics **after surgical incision** is **too late** for prophylaxis as contamination has already occurred. - Post-operative initiation is considered **therapeutic treatment** for established infection, not prevention. - The critical window for prophylaxis is the period from skin incision to wound closure.
Question 5: Preferred time for prophylactic antibiotic administration for surgery?
- A. 1 day before surgery
- B. At the time of induction of anaesthesia (Correct Answer)
- C. I.V. during surgery
- D. I.M. 6 hrs before surgery
Explanation: ***At the time of induction of anaesthesia*** - This timing ensures that a **therapeutic concentration** of the antibiotic is present in the tissues at the time of the initial surgical incision, when the risk of bacterial contamination is highest. - Administering the antibiotic too early or too late can reduce its effectiveness in preventing **surgical site infections (SSIs)**. *1 day before surgery* - Administering antibiotics a day before surgery would lead to the drug being **metabolized and eliminated** from the body before the surgical incision is made, rendering it ineffective for prophylaxis. - This timing also increases the risk of **antibiotic resistance** development without providing adequate protection against SSIs. *I.V. during surgery* - Administering the antibiotic intravenously during surgery means that the drug will not have reached sufficient **tissue concentrations** at the crucial moment of the initial incision. - The protective effect is largely dependent on adequate tissue levels **prior to contamination**, which would not be achieved by administration only during the procedure. *I.M. 6 hrs before surgery* - While closer to the optimal timing than 1 day before, administering intramuscularly 6 hours prior may result in **suboptimal drug levels** at the time of incision, especially for drugs with shorter half-lives. - Intramuscular administration can also have variable absorption rates compared to intravenous, potentially delaying peak tissue concentration and reducing reliability for **prophylactic efficacy**.
Question 6: In postoperative intensive care unit, five patients developed postoperative wound infection on the same day. The best method to prevent cross infection occurring in other patients in the same ward is to:
- A. Practice proper hand washing (Correct Answer)
- B. Disinfect the ward with sodium hypochlorite
- C. Fumigate the ward
- D. Give antibiotics to all other patients in the ward
Explanation: ***Correct: Practice proper hand washing*** - **Proper hand hygiene** is the **single most effective method** for preventing the transmission of **healthcare-associated infections (HAIs)**, including surgical site infections - It physically removes or inactivates **transient microorganisms** from the hands of healthcare workers, thereby stopping their spread between patients - This is the **gold standard** recommended by **WHO, CDC**, and all major infection control guidelines for preventing **cross-infection** in healthcare settings *Incorrect: Disinfect the ward with sodium hypochlorite* - While disinfection with **sodium hypochlorite** is important for **environmental cleaning**, it is **less effective than hand hygiene** in preventing direct patient-to-patient transmission - Environmental disinfection alone **cannot interrupt the main routes of transmission**, which often involve **direct contact** or contaminated hands of healthcare personnel - This is a **secondary measure**, not the primary prevention strategy *Incorrect: Fumigate the ward* - **Fumigation** is typically used for **terminal disinfection** in specific situations, such as after highly contagious outbreaks, and is **not a routine** or primary method for preventing cross-infection in an active ward - Its effectiveness in preventing day-to-day cross-infection is **limited compared to immediate infection control practices** like hand hygiene - This practice is largely **outdated** in modern infection control protocols *Incorrect: Give antibiotics to all other patients in the ward* - **Prophylactic antibiotic use** in all other patients is **discouraged** due to the risk of **antimicrobial resistance (AMR)** and potential adverse effects - It does **not address the source of infection** or the transmission pathways, and can lead to wider public health issues - This is an **inappropriate primary prevention strategy** that violates antimicrobial stewardship principles
Question 7: The Henderson-Jones classification is used for:
- A. Diabetic foot
- B. Prosthetic joint infection (Correct Answer)
- C. Pressure ulcers
- D. Burns
Explanation: ***Prosthetic joint infection*** - The **Henderson-Jones classification** is a system used to categorize **prosthetic joint infections (PJI)** based on their **timing** of onset, distinguishing between early, delayed, and late infections. - This classification aids in guiding **treatment strategies**, as the approach for PJI varies depending on when the infection develops after surgery. *Diabetic foot* - **Diabetic foot ulcers** are typically classified using systems like the **Wagner classification** or the **University of Texas Wound Classification System**, which focus on wound depth, presence of infection, and ischemia. - These classifications specifically address the unique pathology and progression of **foot complications** in diabetic patients. *Pressure ulcers* - **Pressure ulcers (bedsores)** are commonly classified using the **National Pressure Ulcer Advisory Panel (NPUAP)** staging system or the **International Pressure Ulcer Classification System**, which categorize ulcers by depth of tissue damage. - These systems are crucial for assessing severity, guiding treatment, and predicting outcomes for **skin and underlying tissue injury** caused by sustained pressure. *Burns* - **Burns** are traditionally classified by **depth** (e.g., first, second, third, and fourth-degree burns) and **total body surface area (TBSA)** affected, using tools like the Rule of Nines. - This classification helps determine the **severity** of the burn and guides initial management, fluid resuscitation, and surgical intervention.
Question 8: All of the following factors affect osseointegration EXCEPT:
- A. Biocompatibility of implant material.
- B. Implant design.
- C. Patient's blood type (Correct Answer)
- D. Status of the host bed.
Explanation: ***Patient's blood type*** - A patient's **blood type** (e.g., A, B, AB, O) is determined by antigens present on red blood cells and plays no direct role in the biological processes of bone healing or the integration of a dental implant with bone. - While systemic factors can influence osseointegration, blood type itself does not affect the cellular and molecular mechanisms required for direct bone-to-implant contact. *Biocompatibility of implant material* - The **biocompatibility** of the implant material (e.g., **titanium**) is crucial for osseointegration, as it must not elicit adverse reactions and must permit host bone growth on its surface. - Materials that are cytotoxic or inflammatory will prevent bone apposition and lead to fibrous encapsulation rather than direct bone contact. *Implant design* - **Implant design**, including features like **surface roughness**, thread pitch, and macro-geometry, significantly influences the initial stability and long-term success of osseointegration. - A greater surface area and appropriate surface treatments can enhance bone cell attachment and differentiation, promoting faster and stronger bone integration. *Status of the host bed* - The **status of the host bone bed** refers to its quality and quantity (e.g., bone density, vascularity), which are critical for the biological processes of osseointegration. - Adequate bone volume and good bone quality provide a stable foundation and sufficient blood supply for bone regeneration around the implant.
Question 9: Osteosclerosis of bone occurs due to?
- A. Decreased host resistance
- B. Increase in the virulence of organisms causing infection
- C. Increased host response (Correct Answer)
- D. Occurs in immunocompromised patients
Explanation: ### Explanation **Concept Overview:** Osteosclerosis refers to an abnormal increase in bone density, characterized by thickening of the trabeculae and narrowing of the medullary canal. In the context of infections (like chronic osteomyelitis), it represents a **productive or formative bone response** rather than a destructive one. **Why Option C is Correct:** Osteosclerosis occurs when the **host’s immune response is strong** and the infecting organism’s virulence is relatively low. This balance allows the body to contain the infection by stimulating osteoblastic activity, leading to the formation of dense, sclerotic bone. A classic clinical example is **Garré’s Sclerosing Osteomyelitis**, where the body reacts to a low-grade chronic infection by producing massive subperiosteal new bone and sclerosis without significant suppuration or sequestration. **Why Other Options are Incorrect:** * **Options A & D:** Decreased host resistance or an immunocompromised state typically leads to rapid, aggressive bone destruction (osteolysis) and systemic spread, rather than the organized, dense bone formation seen in sclerosis. * **Option B:** High virulence of an organism usually results in acute suppuration, abscess formation, and bone necrosis (sequestrum). Sclerosis is a hallmark of a chronic, low-grade process where the host is "winning" the battle or maintaining a stalemate. **High-Yield Clinical Pearls for NEET-PG:** * **Garré’s Sclerosing Osteomyelitis:** Most common in the mandible and tibia; characterized by "onion-skin" periosteal reaction and dense sclerosis. * **Brodie’s Abscess:** Another form of high host resistance where a subacute infection is localized and walled off by a rim of sclerotic bone. * **Radiological Sign:** On X-ray, osteosclerosis appears as increased radiopacity (whiteness) and loss of the normal trabecular pattern.
Question 10: What is the usual site of tuberculous bursitis?
- A. Prepatellar
- B. Subacromial
- C. Subdeltoid
- D. Trochanteric (Correct Answer)
Explanation: ### Explanation **Correct Option: D. Trochanteric** Tuberculous bursitis is a chronic granulomatous inflammation caused by *Mycobacterium tuberculosis*. Among all the bursae in the human body, the **Trochanteric bursa** (located between the greater trochanter and the gluteus maximus/tensor fasciae latae) is the **most common site** of involvement. The pathogenesis usually involves the hematogenous spread of the bacilli or direct extension from an underlying focus of osteomyelitis in the greater trochanter. Clinically, it presents as a "cold abscess" over the lateral aspect of the hip, often associated with a limp and local tenderness, though hip joint movements usually remain preserved in the early stages. **Why other options are incorrect:** * **A. Prepatellar:** While the prepatellar bursa is a common site for *septic* (pyogenic) or *traumatic* bursitis (Housemaid’s knee), it is rarely affected by tuberculosis. * **B & C. Subacromial and Subdeltoid:** These bursae are occasionally involved in TB, often secondary to tuberculosis of the shoulder joint (Caries Sicca), but they are statistically less common than trochanteric involvement. **Clinical Pearls for NEET-PG:** * **Pathognomonic Sign:** The presence of **"Rice bodies"** (fibrin masses) within the bursal fluid is a classic finding in tuberculous bursitis and rheumatoid arthritis. * **Radiology:** X-rays may show soft tissue swelling and irregular erosions of the greater trochanter (the "hidden" primary focus). * **Treatment:** Management involves a combination of Anti-Tubercular Therapy (ATT) and surgical excision (bursectomy) if the disease is extensive or recalcitrant. * **Differential Diagnosis:** Must be distinguished from "Snapping Hip Syndrome" and Trochanteric Pain Syndrome.
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