Surgical Infections — MCQs

A 34-year-old female patient presented with left leg pain. On examination, the area was erythematous, warm, and tender with indistinct borders. The doctor suspected cellulitis and started her on IV oxacillin. The doctor noted that the pain was disproportionate to the level of cellulitis, and hence admitted the patient. During the night, the patient developed hypotension, deranged renal function tests, and a deranged coagulation profile. X-ray and CT of the leg were conducted. Which is the most common organism causing the condition described?

Q74Medium

What is the most common cause of a cold abscess of the chest wall?

Q75Easy

What is the recommended treatment for streptococcal necrotizing fasciitis?

Q76Easy

What is the best treatment to prevent gas gangrene?

Q77Easy

Post-splenectomy sepsis is common in patients with which of the following conditions?

Q78Medium

Chronic thick-walled pyogenic abscess may be due to the following, except?

Q79Easy

What is the primary objective in the management of septic shock?

Q80Medium

What are the most common types of infections following splenectomy?

Surgical Infections Indian Medical PG Practice Questions and MCQs

Question 71: Hypotension in a case of gas gangrene is best treated by?

A. Ringer's Lactate (Correct Answer)
B. Normal Saline
C. Plasma
D. Whole Blood

Explanation: **Explanation:** In gas gangrene (clostridial myonecrosis), hypotension is primarily driven by a massive shift of fluid from the intravascular to the extravascular space (third-spacing) and the systemic effects of alpha-toxins. This leads to **hypovolemic shock**. **1. Why Ringer’s Lactate (RL) is the Correct Choice:** RL is the preferred crystalloid for initial resuscitation in surgical infections and trauma. It is an **isotonic, balanced salt solution** that closely mimics the electrolyte composition of extracellular fluid. Unlike Normal Saline, RL contains lactate, which acts as a buffer against the metabolic acidosis often seen in septic/toxic shock. Large-volume resuscitation with RL is essential to restore circulating volume and maintain renal perfusion. **2. Why the Other Options are Incorrect:** * **Normal Saline (NS):** While isotonic, large volumes of NS can lead to **hyperchloremic metabolic acidosis**, which can exacerbate the existing acidotic state in a critically ill gas gangrene patient. * **Plasma:** While plasma can expand volume, it is not the first-line treatment for acute hypotension. It carries risks of transfusion-related lung injury (TRALI) and infections, and is reserved for correcting coagulopathies. * **Whole Blood:** This is indicated for hemorrhagic shock. In gas gangrene, the primary issue is fluid loss and toxemia, not acute blood loss (unless secondary to extensive debridement). **Clinical Pearls for NEET-PG:** * **Causative Agent:** *Clostridium perfringens* (most common). * **Pathognomonic Sign:** Crepitus on palpation and "gas shadows" along muscle planes on X-ray. * **Management Priority:** 1. Aggressive fluid resuscitation (RL); 2. High-dose Penicillin + Clindamycin; 3. **Emergency surgical debridement** (most definitive). * **Hyperbaric Oxygen (HBO):** Useful adjunct to inhibit the growth of anaerobic bacteria and stop toxin production.

Question 72: Which of the following statements is NOT true regarding a carbuncle?

A. It is an infective gangrene of the subcutaneous tissue.
B. It is primarily caused by Staphylococcus.
C. Individuals with diabetes are more susceptible.
D. It is typically caused by Streptococcus. (Correct Answer)

Explanation: ### Explanation A **carbuncle** is a deep-seated infective gangrene of the subcutaneous tissue, typically involving a cluster of interconnected hair follicles. **1. Why Option D is the correct (False) statement:** The primary causative organism for a carbuncle is **Staphylococcus aureus**, not Streptococcus. While Streptococcus is the classic cause of spreading infections like cellulitis or erysipelas, Staphylococcus is known for producing coagulase, which leads to localized suppuration, abscess formation, and tissue necrosis—the hallmarks of a carbuncle. **2. Analysis of other options:** * **Option A (True):** A carbuncle is defined as **infective gangrene** of the subcutaneous fat. The infection spreads horizontally under the dense deep fascia and reaches the surface through multiple hair follicles, creating a characteristic "sieve-like" appearance. * **Option B (True):** As mentioned, *Staphylococcus aureus* is the most common pathogen. * **Option C (True):** **Diabetes mellitus** is the most significant predisposing factor. High blood sugar levels impair neutrophil function and provide a favorable environment for bacterial growth. Other risk factors include malnutrition and immunosuppression. ### NEET-PG High-Yield Pearls * **Common Site:** The **nape of the neck** and the **back** are the most common sites because the skin is thick and the subcutaneous tissue is dense and fibrous. * **Clinical Feature:** It presents as a painful, brawny, inflammatory induration that eventually discharges pus through multiple openings (**Cribriform appearance**). * **Management:** * Control of blood sugar is mandatory. * Antibiotics (anti-staphylococcal). * Surgical intervention: A **cruciate incision** is made to excise all necrotic tissue (debridement) until healthy bleeding edges are reached.

Question 73: A 34-year-old female patient presented with left leg pain. On examination, the area was erythematous, warm, and tender with indistinct borders. The doctor suspected cellulitis and started her on IV oxacillin. The doctor noted that the pain was disproportionate to the level of cellulitis, and hence admitted the patient. During the night, the patient developed hypotension, deranged renal function tests, and a deranged coagulation profile. X-ray and CT of the leg were conducted. Which is the most common organism causing the condition described?

A. Group A Streptococcus (Correct Answer)
B. Staphylococcus aureus
C. Pseudomonas aeruginosa
D. Group D Streptococcus

Explanation: ### Explanation The clinical presentation describes a classic case of **Necrotizing Fasciitis (Type II)**. The key diagnostic "red flag" mentioned is **pain disproportionate to clinical findings**, which distinguishes necrotizing infections from simple cellulitis. The rapid progression to systemic inflammatory response syndrome (SIRS), hypotension (septic shock), and multi-organ dysfunction (renal and coagulation derangement) further confirms a necrotizing soft tissue infection (NSTI). **1. Why Group A Streptococcus is correct:** * **Group A Beta-hemolytic Streptococcus (Streptococcus pyogenes)** is the most common cause of **Type II (monomicrobial)** necrotizing fasciitis. * It is often referred to as the "flesh-eating bacteria." It can affect healthy individuals after minor trauma and is frequently associated with **Streptococcal Toxic Shock Syndrome (STSS)**, explaining the patient's rapid hemodynamic collapse. **2. Why other options are incorrect:** * **Staphylococcus aureus:** While it can cause cellulitis and occasionally monomicrobial necrotizing fasciitis (especially MRSA), it is less common than Group A Strep in the monomicrobial type. * **Pseudomonas aeruginosa:** Typically seen in immunocompromised patients, burn victims, or as part of a **Type I (polymicrobial)** infection, but it is not the most common overall. * **Group D Streptococcus (Enterococci):** These are usually part of the mixed flora in Type I necrotizing fasciitis (often post-abdominal surgery or in diabetics) but are rarely the primary causative agent. **Clinical Pearls for NEET-PG:** * **Classification:** Type I is polymicrobial (aerobes + anaerobes; common in diabetics/Fournier’s gangrene); Type II is monomicrobial (Group A Strep). * **Diagnosis:** Primarily clinical. Imaging (X-ray/CT) may show **gas in soft tissues** (crepitus), but its absence does not rule out the diagnosis. * **Finger Test:** A positive test involves lack of bleeding, "dishwater pus," and easy blunt dissection of the fascia. * **Treatment:** Immediate **surgical debridement** is the definitive treatment; antibiotics alone are insufficient.

Question 74: What is the most common cause of a cold abscess of the chest wall?

A. Pott's spine (Correct Answer)
B. Tuberculous abscesses of the chest wall
C. Tuberculosis of the ribs
D. Intercostal lymphadenitis

Explanation: **Explanation:** The most common cause of a cold abscess of the chest wall is **Pott’s spine** (tuberculosis of the thoracic vertebrae). A "cold abscess" is characterized by a collection of pus without the classic signs of inflammation (heat, redness, or pain), typically caused by *Mycobacterium tuberculosis*. **Why Pott's Spine is Correct:** In the thoracic region, tuberculosis of the vertebral bodies leads to the formation of paravertebral debris. This pus tracks along the path of least resistance, specifically following the **intercostal nerves and vessels**. It travels laterally and anteriorly along the neurovascular bundle to point at the **lateral or anterior cutaneous branches** of the intercostal nerves, eventually presenting as a fluctuant swelling on the chest wall. **Analysis of Incorrect Options:** * **Tuberculous abscesses of the chest wall:** This is a general descriptive term for the presentation, not the primary anatomical source. * **Tuberculosis of the ribs:** While TB can affect the ribs (causing a localized cold abscess), it is statistically less common than secondary involvement from a spinal source. * **Intercostal lymphadenitis:** This refers to the infection of lymph nodes between the ribs. While these nodes can break down to form an abscess (collar-stud abscess), it is a less frequent cause compared to the tracking of pus from the spine. **NEET-PG High-Yield Pearls:** * **Most common site of presentation:** The abscess usually points in the **mid-axillary line** (where the lateral cutaneous branch emerges) or the **parasternal region** (where the anterior cutaneous branch emerges). * **Investigation of choice:** MRI is the gold standard for evaluating Pott’s spine and the extent of the abscess. * **Management:** Treatment involves Anti-Tubercular Therapy (ATT). Surgical aspiration or drainage is reserved for cases with neurological deficit or failure of medical therapy. Always look for a primary focus in the spine or lungs when a cold abscess is found on the chest wall.

Question 75: What is the recommended treatment for streptococcal necrotizing fasciitis?

A. Surgical debridement
B. Penicillin
C. Clindamycin
D. All of the above (Correct Answer)

Explanation: **Explanation:** Streptococcal necrotizing fasciitis (Type II NF), often caused by *Streptococcus pyogenes* (Group A Strep), is a surgical emergency characterized by rapid, full-thickness destruction of fascia and fat. Management requires a multi-modal approach involving aggressive surgery and synergistic antibiotic therapy. 1. **Surgical Debridement (Option A):** This is the **most critical step**. Antibiotics cannot penetrate necrotic tissue due to thrombosed end-arteries. Early, aggressive, and often repeated surgical debridement is mandatory to source control the infection and prevent mortality. 2. **Penicillin (Option B):** Penicillin remains the drug of choice for *S. pyogenes* due to its bactericidal action against the cell wall. 3. **Clindamycin (Option C):** This is added for two specific reasons: * **The Eagle Effect:** Penicillin is less effective against bacteria in the stationary phase (high bacterial load). Clindamycin, a protein synthesis inhibitor, is not affected by the growth phase. * **Toxin Suppression:** It inhibits the production of bacterial exotoxins (superantigens) responsible for Streptococcal Toxic Shock Syndrome (STSS). **Why "All of the above" is correct:** Monotherapy is insufficient. The gold standard is **Emergency Debridement + Penicillin + Clindamycin.** **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Sign:** "Pain out of proportion to physical findings" is the earliest hallmark. * **LRINEC Score:** Used to differentiate NF from cellulitis (includes CRP, WBC, Hemoglobin, Sodium, Creatinine, and Glucose). * **Type I vs. Type II:** Type I is polymicrobial (diabetics/elderly); Type II is monomicrobial (Strep/Staph, often in healthy individuals). * **Finger Test:** Lack of bleeding, "dishwater pus," and easy blunt dissection of fascia during surgery confirm the diagnosis.

Question 76: What is the best treatment to prevent gas gangrene?

A. Thorough debridement (Correct Answer)
B. Antiserum
C. Vaccination
D. Antibiotics

Explanation: **Explanation:** The primary pathophysiology of **Gas Gangrene (Clostridial Myonecrosis)** involves the proliferation of anaerobic *Clostridium perfringens* in devitalized, ischemic tissues. These bacteria thrive in low-oxygen environments (anaerobic conditions) created by necrotic debris, foreign bodies, and compromised blood supply. **1. Why Thorough Debridement is the Correct Answer:** The most effective way to prevent gas gangrene is to eliminate the environment where the bacteria grow. **Thorough debridement** (removal of all dead, devitalized tissue and foreign material) restores an aerobic environment and reduces the bacterial load. Since *Clostridia* cannot survive in well-oxygenated, viable tissue, surgical toilet and debridement remain the "gold standard" for prevention. **2. Why Other Options are Incorrect:** * **Antiserum:** Polyvalent antitoxins are largely ineffective for prophylaxis and have a high risk of serum sickness/anaphylaxis. They are not used routinely. * **Vaccination:** There is currently no effective human vaccine available for *Clostridium perfringens*. * **Antibiotics:** While intravenous Penicillin G or Clindamycin are used as *adjuncts*, they cannot reach the site of infection if the tissue is necrotic and lacks blood supply. Antibiotics alone cannot prevent gas gangrene without surgical intervention. **Clinical Pearls for NEET-PG:** * **Incubation Period:** Very short, typically **1–6 hours** (up to 3 days). * **Clinical Sign:** "Dishwater pus" (thin, serosanguinous discharge) and **crepitus** (gas in tissues). * **X-ray Finding:** Feather-like appearance of muscle fibers due to gas. * **Management Priority:** 1. Aggressive Debridement, 2. High-dose Penicillin, 3. Hyperbaric Oxygen (HBO) therapy.

Question 77: Post-splenectomy sepsis is common in patients with which of the following conditions?

A. Immune thrombocytopenic purpura (ITP)
B. Thalassemia
C. Hereditary spherocytosis
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Overwhelming Post-Splenectomy Infection (OPSI)** is a life-threatening medical emergency characterized by a rapid, fulminant clinical course. The spleen plays a critical role in filtering encapsulated bacteria and producing opsonins (like tuftsin and properdin). While any splenectomized patient is at risk, the incidence of sepsis is significantly higher when the spleen is removed for **hematologic disorders** compared to trauma. **Why "All of the Above" is Correct:** The risk of OPSI is directly related to the underlying condition for which the splenectomy was performed: * **Thalassemia (Option B):** Carries the highest risk among the options. These patients often have underlying iron overload and immune dysfunction, making them highly susceptible to post-operative sepsis. * **Hereditary Spherocytosis (Option C):** As a chronic hemolytic anemia, it carries a significant risk, though generally lower than Thalassemia. * **ITP (Option A):** While the risk is lower compared to Thalassemia, patients with ITP are still at a higher risk of OPSI than the general population or trauma patients due to the loss of splenic clearance of opsonized pathogens. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Organism:** *Streptococcus pneumoniae* (50-90% of cases), followed by *Haemophilus influenzae* type B and *Neisseria meningitidis*. * **Timing:** The risk is highest in the first **2 years** post-surgery, but the risk remains lifelong. * **Prevention (Vaccination):** Ideally administered **2 weeks before** elective surgery or **2 weeks after** emergency surgery (to ensure adequate antibody response). * **Prophylaxis:** Daily oral penicillin is often recommended, especially in children, for at least 2 years post-splenectomy. * **Age Factor:** The risk of OPSI is highest in children under the age of 5.

Question 78: Chronic thick-walled pyogenic abscess may be due to the following, except?

A. Presence of a foreign body
B. Prolonged antibiotic therapy
C. Virulent strains of organism (Correct Answer)
D. Inadequate drainage

Explanation: **Explanation:** The development of a **chronic thick-walled pyogenic abscess** (often referred to as an "Antibioma" in specific contexts) occurs when an acute infection fails to resolve and the body attempts to wall off the infection with dense fibrous tissue. **Why "Virulent strains of organism" is the correct answer:** Virulence refers to the severity or harmfulness of a pathogen. **Highly virulent organisms** typically cause acute, rapidly spreading infections (like cellulitis or gas gangrene) or acute abscesses with systemic toxicity. They are less likely to result in a chronic, thick-walled, indolent abscess because they either overwhelm the host's defenses quickly or provoke a massive immune response that leads to rapid suppuration and rupture. Chronic, thick-walled abscesses are more commonly associated with **low-virulence organisms** that the body can contain but not fully eliminate. **Analysis of Incorrect Options:** * **Presence of a foreign body:** A foreign body acts as a nidus for persistent infection and prevents the collapse of the abscess cavity, leading to chronic inflammation and wall thickening. * **Prolonged antibiotic therapy:** Inadequate or "blind" antibiotic use can suppress the infection without sterilizing the cavity. This leads to the formation of a sterile but thick-walled mass known as an **Antibioma**. * **Inadequate drainage:** The gold standard for abscess treatment is *Ubi pus, ibi evacua* (where there is pus, evacuate it). If drainage is incomplete, the residual infection persists, leading to chronic inflammation and progressive fibrosis of the wall. **NEET-PG High-Yield Pearls:** * **Antibioma:** A firm, non-tender, thick-walled mass resulting from treating a pyogenic abscess with antibiotics without surgical drainage. * **Pathology:** The "thick wall" is composed of mature fibroblasts and collagen (fibrosis), which limits antibiotic penetration, making surgical excision or formal drainage necessary. * **Common Site:** Often seen in the breast (chronic breast abscess) or gluteal region.

Question 79: What is the primary objective in the management of septic shock?

A. Maintaining myocardial function.
B. Ensuring sufficient fluid volume.
C. Locating and eradicating the source of infection. (Correct Answer)
D. Identifying and removing the allergen.

Explanation: In the management of septic shock, the primary objective is **source control** (locating and eradicating the source of infection). While supportive measures are vital, the underlying pathophysiology of septic shock is a systemic inflammatory response triggered by a pathogen. Unless the nidus of infection—such as an abscess, necrotic tissue, or an infected catheter—is removed or drained, the inflammatory cascade will continue, leading to irreversible multi-organ dysfunction syndrome (MODS) and death. **Analysis of Options:** * **Option C (Correct):** Source control is the definitive treatment. Without it, fluid resuscitation and vasopressors are merely "buying time" rather than curing the patient. * **Option A (Incorrect):** Myocardial dysfunction can occur in late sepsis (septic cardiomyopathy), but maintaining it is a supportive goal, not the primary curative objective. * **Option B (Incorrect):** Fluid resuscitation is the *initial* step in the "Surviving Sepsis" bundles to restore perfusion, but it does not address the root cause of the shock. * **Option D (Incorrect):** This refers to the management of **Anaphylactic shock**, not septic shock. **High-Yield NEET-PG Pearls:** * **The "Golden Hour":** Antibiotics should be administered within **1 hour** of recognition. * **Fluid Resuscitation:** The standard initial bolus is **30 mL/kg** of crystalloids. * **Vasopressor of Choice:** **Norepinephrine** is the first-line agent if fluid resuscitation fails to maintain a Mean Arterial Pressure (MAP) ≥ 65 mmHg. * **Source Control Rule:** "Ubi pus, ibi evacua" (Where there is pus, evacuate it). This includes debridement, drainage, or removal of infected hardware.

Question 80: What are the most common types of infections following splenectomy?

A. Unencapsulated bacteria
B. Encapsulated bacteria (Correct Answer)
C. Gram-positive sepsis
D. Gram-negative bacteria

Explanation: ### Explanation **1. Why Encapsulated Bacteria is Correct:** The spleen is the body’s largest lymphoid organ and plays a critical role in filtering the blood. It contains **macrophages** and **B-lymphocytes** (in the marginal zone) that are essential for clearing **opsonized bacteria**. Encapsulated bacteria possess a polysaccharide capsule that resists phagocytosis unless they are coated with antibodies (opsonins). In a splenectomized patient, there is a deficiency in IgM production and a lack of splenic macrophages to clear these opsonized pathogens, leading to **Overwhelming Post-Splenectomy Infection (OPSI)**. **2. Analysis of Incorrect Options:** * **Option A (Unencapsulated bacteria):** These are generally easier for the systemic immune system (neutrophils and non-splenic macrophages) to clear without the specialized filtering architecture of the spleen. * **Option C (Gram-positive sepsis):** While some encapsulated organisms are Gram-positive (e.g., *S. pneumoniae*), this is a clinical syndrome rather than a specific category of pathogen. OPSI can also be caused by Gram-negative encapsulated organisms. * **Option D (Gram-negative bacteria):** While *H. influenzae* and *N. meningitidis* are Gram-negative, the defining characteristic that makes them dangerous post-splenectomy is their **capsule**, not their Gram stain status. **3. NEET-PG High-Yield Pearls:** * **Most Common Organism:** *Streptococcus pneumoniae* (causes ~50-90% of OPSI cases). * **Other Key Organisms:** *Haemophilus influenzae* type B, *Neisseria meningitidis*, and *Capnocytophaga canimorsus* (following dog bites). * **Vaccination Protocol:** Ideally, vaccines should be given **2 weeks before** elective splenectomy or **2 weeks after** emergency splenectomy. * **Prophylaxis:** Daily oral penicillin is often recommended, especially in children, for at least 2 years post-surgery or until age 5. * **Peripheral Smear Findings:** Look for **Howell-Jolly bodies**, Pappenheimer bodies, and Heinz bodies post-splenectomy.

Practice by Chapter

Surgical Site Infections

Practice Questions

Intra-abdominal Infections

Practice Questions

Soft Tissue Infections

Practice Questions

Necrotizing Soft Tissue Infections

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Surgical Sepsis

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Tetanus Prophylaxis

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Antimicrobial Prophylaxis

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Antimicrobial Therapy in Surgical Infections

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Surgical Drainage Procedures

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Infection Control in Operating Room

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Biofilms and Implant-Related Infections

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Prevention Strategies

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