Sepsis and septic shock US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Sepsis and septic shock. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Sepsis and septic shock US Medical PG Question 1: A 7-year-old boy is brought to the emergency room because of severe, acute diarrhea. He is drowsy with a dull, lethargic appearance. He has sunken eyes, poor skin turgor, and dry oral mucous membranes and tongue. He has a rapid, thready pulse with a systolic blood pressure of 60 mm Hg and his respirations are 33/min. His capillary refill time is 6 sec. He has had no urine output for the past 24 hours. Which of the following is the most appropriate next step in treatment?
- A. Start IV fluid resuscitation by administering colloid solutions
- B. Provide oral rehydration therapy to correct dehydration
- C. Give initial IV bolus of 2 L of Ringer’s lactate, followed by packed red cells, fresh frozen plasma, and platelets in a ratio of 1:1:1
- D. Start IV fluid resuscitation with normal saline or Ringer’s lactate, along with monitoring of vitals and urine output (Correct Answer)
- E. Give antidiarrheal drugs
Sepsis and septic shock Explanation: ***Start IV fluid resuscitation with normal saline or Ringer's lactate, along with monitoring of vitals and urine output***
- This patient presents with **severe dehydration** and **hypovolemic shock** (lethargy, sunken eyes, poor skin turgor, dry mucous membranes, rapid thready pulse, hypotension [systolic BP 60 mmHg], tachypnea, prolonged capillary refill >5 seconds, and anuria).
- According to **PALS guidelines**, the immediate priority is rapid intravenous administration of **isotonic crystalloids** (normal saline or Ringer's lactate) given as **20 mL/kg boluses** over 5-20 minutes, repeated as needed based on clinical response.
- Close monitoring of vital signs, mental status, perfusion (capillary refill), and urine output is essential to assess response to resuscitation and guide further fluid management.
*Start IV fluid resuscitation by administering colloid solutions*
- While colloids (albumin, synthetic colloids) can expand intravascular volume, **isotonic crystalloids** are preferred for initial resuscitation in severe dehydration per **WHO and PALS guidelines**.
- Crystalloids are equally effective, more readily available, less expensive, and have fewer potential adverse effects compared to colloids in pediatric dehydration.
- There is no proven survival benefit of colloids over crystalloids in this clinical scenario.
*Provide oral rehydration therapy to correct dehydration*
- **Oral rehydration therapy (ORT)** is the appropriate first-line treatment for **mild to moderate dehydration** in children who can tolerate oral intake.
- However, ORT is **contraindicated** in patients with **severe dehydration** or **hypovolemic shock**, particularly those with altered mental status, inability to drink, or hemodynamic instability.
- This patient's drowsiness, hypotension, and signs of shock require immediate IV resuscitation; ORT would be too slow and potentially dangerous.
*Give initial IV bolus of 2 L of Ringer's lactate, followed by packed red cells, fresh frozen plasma, and platelets in a ratio of 1:1:1*
- A 2-liter bolus is **excessive and dangerous** for a 7-year-old child (average weight ~23 kg); the appropriate initial bolus is **20 mL/kg** (~460 mL), which can be repeated based on response.
- The **1:1:1 massive transfusion protocol** (packed RBCs, FFP, platelets) is indicated for **hemorrhagic shock** with significant blood loss, not for hypovolemic shock from dehydration.
- There is no evidence of bleeding or coagulopathy in this patient; blood products are not indicated.
*Give antidiarrheal drugs*
- **Antidiarrheal agents** (loperamide, diphenoxylate) are **contraindicated** in young children with acute infectious diarrhea, as they can prolong illness, increase risk of complications (toxic megacolon, bacterial overgrowth), and mask serious underlying conditions.
- The priority in severe dehydration is **fluid and electrolyte resuscitation**, not stopping the diarrhea.
- The diarrhea typically resolves once the underlying infection is controlled and hydration is restored.
Sepsis and septic shock US Medical PG Question 2: A 57-year-old man is admitted to the burn unit after he was brought to the emergency room following an accidental fire in his house. His past medical history is unknown due to his current clinical condition. Currently, his blood pressure is 75/40 mmHg, pulse rate is 140/min, and respiratory rate is 17/min. The patient is subsequently intubated and started on aggressive fluid resuscitation. A Swan-Ganz catheter is inserted to clarify his volume status. Which of the following hemodynamic parameters would you expect to see in this patient?
- A. Cardiac output: ↓, systemic vascular resistance: ↔, pulmonary artery wedge pressure: ↔
- B. Cardiac output: ↑, systemic vascular resistance: ↑, pulmonary artery wedge pressure: ↔
- C. Cardiac output: ↑, systemic vascular resistance: ↓, pulmonary artery wedge pressure: ↔
- D. Cardiac output: ↓, systemic vascular resistance: ↑, pulmonary artery wedge pressure: ↓ (Correct Answer)
- E. Cardiac output: ↔, systemic vascular resistance: ↔, pulmonary artery wedge pressure: ↔
Sepsis and septic shock Explanation: ***Cardiac output: ↓, systemic vascular resistance: ↑, pulmonary artery wedge pressure: ↓***
- The patient's **hypotension (75/40 mmHg)** and **tachycardia (140/min)**, combined with severe burns, indicate **hypovolemic shock** due to massive fluid loss from damaged capillaries.
- In response to decreased cardiac output and hypovolemia, the body compensates by increasing **systemic vascular resistance (SVR)** to maintain perfusion to vital organs, and **pulmonary artery wedge pressure (PAWP)** will be low due to reduced intravascular volume.
*Cardiac output: ↓, systemic vascular resistance: ↔, pulmonary artery wedge pressure: ↔*
- This option incorrectly suggests that systemic vascular resistance and pulmonary artery wedge pressure would be normal, which is inconsistent with **hypovolemic shock**.
- In shock, the body's compensatory mechanisms would lead to significant changes in SVR and PAWP, not maintain them at baseline.
*Cardiac output: ↑, systemic vascular resistance: ↑, pulmonary artery wedge pressure: ↔*
- Increased cardiac output is usually seen in **distributive shock** (e.g., septic shock) where vasodilation leads to reduced SVR, not increased SVR as suggested here.
- An elevated SVR coupled with an increased cardiac output would typically result in a higher blood pressure unless there is a compensatory drop in other parameters.
*Cardiac output: ↑, systemic vascular resistance: ↓, pulmonary artery wedge pressure: ↔*
- This pattern (high cardiac output, low SVR) is characteristic of **distributive shock**, such as **septic shock** or anaphylactic shock, rather than the hypovolemic shock expected in a burn patient.
- Severe burns primarily cause massive fluid shifts, leading to hypovolemia and a reduced cardiac output, not an elevated one.
*Cardiac output: ↔, systemic vascular resistance: ↔, pulmonary artery wedge pressure: ↔*
- This scenario represents **normal hemodynamic parameters**, which would not be expected in a patient experiencing severe shock from extensive burns.
- The patient's clinical presentation (hypotension, tachycardia) clearly indicates a state of hemodynamic instability.
Sepsis and septic shock US Medical PG Question 3: A 37-year-old man presents to the emergency department for a persistent fever. The patient states he has felt unwell for the past week and has felt subjectively febrile. The patient has a past medical history of a suicide attempt and alcohol abuse. He is not currently taking any medications. The patient admits to using heroin and cocaine and drinking 5-8 alcoholic drinks per day. His temperature is 103°F (39.4°C), blood pressure is 92/59 mmHg, pulse is 110/min, respirations are 20/min, and oxygen saturation is 96% on room air. Cardiopulmonary exam is notable for a systolic murmur heard best along the left sternal border. Dermatologic exam reveals scarring in the antecubital fossa. Which of the following is the next best step in management?
- A. CT scan
- B. Ultrasound
- C. Chest radiograph
- D. Blood cultures (Correct Answer)
- E. Vancomycin and gentamicin
Sepsis and septic shock Explanation: ***Blood cultures***
- The patient's history of **intravenous drug use (IVDU)**, persistent fever, and a **new systolic murmur** strongly suggest **infective endocarditis**.
- **Blood cultures** are crucial for identifying the causative organism and guiding appropriate antibiotic therapy, serving as the cornerstone of diagnosis in suspected endocarditis.
*CT scan*
- While CT scans can be useful for identifying complications of endocarditis (e.g., septic emboli in the brain or lungs), they are **not the initial diagnostic step** for identifying the source of infection.
- CT scans expose the patient to **radiation** and are more expensive, making them less suitable as a first step compared to blood cultures.
*Ultrasound*
- An **echocardiogram** (a type of ultrasound) is essential for visualizing vegetations on heart valves, but it is typically performed *after* blood cultures reveal bacteremia to confirm the diagnosis and assess severity.
- A general ultrasound of other body areas would be non-specific and **unlikely to pinpoint the cause** of persistent fever in this clinical context.
*Chest radiograph*
- A chest radiograph can identify **pulmonary infiltrates** or **septic emboli in the lungs**, which are potential complications of right-sided endocarditis (common in IVDU).
- However, a chest radiograph **does not identify the causative organism** or confirm the primary diagnosis of endocarditis, making it a secondary investigation.
*Vancomycin and gentamicin*
- This combination represents a broad-spectrum antibiotic regimen often used for **empiric treatment of infective endocarditis**, particularly in IVDU patients due to concerns for MRSA or resistant streptococcal species.
- While ultimately necessary, administering antibiotics *before* obtaining **blood cultures** can significantly reduce the yield of cultures and hinder definitive diagnosis and tailored treatment.
Sepsis and septic shock US Medical PG Question 4: A 72-year-old male is brought from his nursing home to the emergency department for fever, chills, dyspnea, productive cough, and oliguria over the past 72 hours. He was in his normal state of health and slowly developed breathing problems and fever. His past medical history is significant for hepatitis C, hypertension, and hypercholesterolemia. His medications include bisoprolol, hydrochlorothiazide, and atorvastatin. Upon arrival to the ED, his blood pressure is 80/48 mm Hg, pulse is 120/min, a respiratory rate of 28/min, and body temperature of 39.0°C (102.2°F). Physical examination reveals decreased breathing sounds in the base of the left lung, along with increased vocal resonance, and pan-inspiratory crackles. The abdomen is mildly distended with a positive fluid wave. The patient's level of consciousness ranges from disoriented to drowsiness. He is transferred immediately to the ICU where vasoactive support is initiated. Laboratory tests show leukocytosis, neutrophilia with bands. Since admission 6 hours ago, the patient has remained anuric. Which of the following additional findings would you expect in this patient?
- A. Urine sodium > 40 mEq/L
- B. Urinary osmolality > 500 mOsmol/kg
- C. Urinary osmolality < 350 mOsmol/kg
- D. Blood urea nitrogen (BUN):Serum creatinine (Cr) ratio <15:1
- E. Blood urea nitrogen (BUN):Serum creatinine (Cr) ratio > 20:1 (Correct Answer)
Sepsis and septic shock Explanation: ***Blood urea nitrogen (BUN):Serum creatinine (Cr) ratio > 20:1***
- This patient is presenting with signs of **septic shock** (fever, hypotension, altered mental status, oliguria, leukocytosis) likely due to **pneumonia**. The prolonged hypotension and poor perfusion lead to **prerenal acute kidney injury (AKI)** that may be progressing to **acute tubular necrosis (ATN)**.
- In **prerenal AKI**, reduced renal perfusion leads to increased reabsorption of urea and water in the renal tubules, resulting in a **BUN:creatinine ratio greater than 20:1**. This elevated ratio persists even as the patient transitions to ATN.
- Given **6 hours of anuria** despite vasoactive support, this suggests significant renal injury, but the BUN:Cr ratio remains the most reliable finding at this stage.
*Urine sodium > 40 mEq/L*
- A urine sodium concentration greater than 40 mEq/L is typically seen in **intrinsic AKI** (e.g., acute tubular necrosis), where tubular damage impairs sodium reabsorption.
- While this patient may be developing ATN given the prolonged anuria, in the **early phase** of septic AKI with recent hypotension, the kidneys initially attempt to conserve sodium, resulting in **low urine sodium (<20 mEq/L)**.
*Urinary osmolality > 500 mOsmol/kg*
- A urinary osmolality above 500 mOsmol/kg indicates appropriately concentrated urine, which is a compensatory mechanism in **early prerenal AKI** as the kidneys try to conserve water.
- However, given this patient has been **anuric for 6 hours** despite ICU-level vasoactive support, the kidney injury has likely progressed beyond pure prerenal state. In established ATN, the concentrating ability is impaired, and urinary osmolality would be **closer to isotonic (<350 mOsmol/kg)** rather than highly concentrated.
- The **elevated BUN:Cr ratio** is more reliable in this mixed clinical picture.
*Urinary osmolality < 350 mOsmol/kg*
- A urinary osmolality less than 350 mOsmol/kg indicates inappropriately diluted urine, which is characteristic of **established intrinsic AKI (acute tubular necrosis)**, where the kidney's concentrating ability is impaired.
- While the patient may be progressing toward ATN, the **BUN:Cr ratio elevation** develops earlier and is the most expected finding at this presentation stage.
*Blood urea nitrogen (BUN):Serum creatinine (Cr) ratio <15:1*
- A BUN:creatinine ratio less than 15:1 is typically seen in **intrinsic AKI after several days**, **normal renal function**, or conditions with decreased urea production.
- In this patient with septic shock and acute hypoperfusion leading to AKI, the ratio would be **elevated (>20:1)** due to enhanced urea reabsorption in the setting of decreased renal blood flow.
Sepsis and septic shock US Medical PG Question 5: A 55-year-old woman with type 2 diabetes mellitus is admitted to the hospital because of a 2-day history of fever, breathlessness, and cough productive of large quantities of green sputum. She drinks 8 beers daily. Her temperature is 39°C (102.2°F), pulse is 110/min, respirations are 28/min, and blood pressure is 100/60 mm Hg. Blood and sputum cultures grow gram-negative, catalase-positive, capsulated bacilli. Which of the following components of the causal organism is the most likely cause of this patient's hypotension?
- A. Poly-D-glutamate
- B. Teichoic acid
- C. Lipid A (Correct Answer)
- D. Lecithinase
- E. Lipooligosaccharide
Sepsis and septic shock Explanation: ***Lipid A***
- The patient's presentation with **fever**, **hypotension**, and gram-negative bacterial infection suggests **sepsis** and **septic shock**.
- **Lipid A** is the endotoxic component of **lipopolysaccharide (LPS)** found in the outer membrane of gram-negative bacteria, directly responsible for mediating the systemic inflammatory response and hypotension in septic shock.
- Lipid A is recognized by **TLR4** on immune cells, triggering the release of **TNF-α**, **IL-1**, and other cytokines that cause vasodilation, increased vascular permeability, and shock.
*Poly-D-glutamate*
- This is a component of the **capsule of *Bacillus anthracis***, which is a gram-positive rod, not the gram-negative, catalase-positive, capsulated organism described.
- While it contributes to virulence by inhibiting phagocytosis, it does not directly cause the profound hemodynamic changes seen in sepsis from gram-negative bacteria.
*Teichoic acid*
- **Teichoic acids** are components of the **cell wall of gram-positive bacteria** (e.g., *Staphylococcus*, *Streptococcus*) and are not found in gram-negative bacteria.
- While they can stimulate an inflammatory response, they are not the primary cause of septic shock in gram-negative infections.
*Lecithinase*
- **Lecithinase** (also known as **alpha-toxin** or **phospholipase C**) is an **exotoxin** produced by various bacteria, notably *Clostridium perfringens*.
- While it can cause tissue damage and contribute to virulence, it is not an integral structural component of the bacterial cell wall responsible for generalized vasodilation and hypotension in gram-negative sepsis.
*Lipooligosaccharide*
- **Lipooligosaccharide (LOS)** is a structural variant of LPS found in certain gram-negative bacteria (particularly **Neisseriaceae** like *N. meningitidis* and *N. gonorrhoeae*), consisting of **Lipid A** plus a short oligosaccharide core without the O-antigen repeats.
- While **Lipid A within LOS** is endotoxic, the question asks for the specific **component** causing hypotension, which is **Lipid A itself**, not the larger LOS molecule.
- The likely pathogen here (*Klebsiella pneumoniae* given clinical context) contains **LPS**, not LOS, making Lipid A the most precise answer.
Sepsis and septic shock US Medical PG Question 6: A 68-year-old woman is brought to the emergency department by ambulance after she was found down by her daughter. She lives alone in her apartment so it is unclear when she began to develop symptoms. Her medical history is significant for cardiac arrhythmias, diabetes, pericarditis, and a stroke 2 years ago. On presentation her temperature is 98.1°F (36.7°C), blood pressure is 88/51 mmHg, pulse is 137/min, and respirations are 18/min. On physical exam her skin is cold and clammy. If special tests were obtained, they would reveal dramatically decreased pulmonary capillary wedge pressure, increased systemic vascular resistance, and mildly decreased cardiac output. Which of the following treatments would most directly target the cause of this patient's low blood pressure?
- A. Vasopressors
- B. Intravenous fluids (Correct Answer)
- C. Antibiotic administration
- D. Relieve obstruction
- E. Intravenous inotropes
Sepsis and septic shock Explanation: ***Intravenous fluids***
- The patient exhibits signs of **hypovolemic shock**, including **hypotension** (BP 88/51 mmHg), **tachycardia** (pulse 137/min), and **cold, clammy skin**. The dramatically decreased **pulmonary capillary wedge pressure (PCWP)** indicates low preload, which is characteristic of hypovolemia.
- Administration of intravenous fluids directly addresses the underlying cause of this patient's low blood pressure by increasing intravascular volume, thereby improving **cardiac preload** and ultimately **cardiac output** and blood pressure.
*Vasopressors*
- While vasopressors can temporarily increase blood pressure by causing **vasoconstriction**, they do not address the root cause of hypovolemic shock, which is insufficient circulating blood volume.
- Using vasopressors without adequate fluid resuscitation in hypovolemic shock can lead to further **organ hypoperfusion** due to increased afterload on an already compromised heart.
*Antibiotic administration*
- Although the patient's presentation with hypotension and tachycardia could raise suspicion for **sepsis**, there is no explicit evidence of infection presented (e.g., fever, focal source).
- The **decreased PCWP** points more strongly towards hypovolemic shock rather than septic shock, where PCWP can be variable or even normal/elevated.
*Relieve obstruction*
- Obstruction, such as in **cardiac tamponade** or **pulmonary embolism**, can cause obstructive shock, which presents with hypotension.
- However, the dramatically **decreased PCWP** is not typically seen in obstructive shock, where PCWP would likely be normal or elevated due to impedance to cardiac filling or outflow.
*Intravenous inotropes*
- **Inotropes** like dobutamine increase myocardial contractility and are primarily indicated in **cardiogenic shock** or severe heart failure with reduced ejection fraction to improve cardiac output.
- While cardiac output is mildly decreased, the primary issue is reduced preload as indicated by the very low PCWP, making fluid resuscitation a more appropriate initial step than directly increasing contractility.
Sepsis and septic shock US Medical PG Question 7: A 27-year-old man is brought to the emergency department by emergency medical services. The patient was an unrestrained passenger in a head-on collision that occurred 15 minutes ago and is currently unresponsive. His temperature is 99.5°F (37.5°C), blood pressure is 60/33 mmHg, pulse is 180/min, respirations are 17/min, and oxygen saturation is 95% on room air. A FAST exam demonstrates fluid in Morrison’s pouch. Laboratory values are drawn upon presentation to the ED and sent off. The patient is started on IV fluids and an initial trauma survey is started. Twenty minutes later, his blood pressure is 95/65 mmHg, and his pulse is 110/min. The patient is further stabilized and is scheduled for emergency surgery. Which of the following best represents this patient’s most likely initial laboratory values?
- A. Hemoglobin: 10 g/dL, Hematocrit: 30%, MCV: 110 µm^3
- B. Hemoglobin: 19 g/dL, Hematocrit: 55%, MCV: 95 µm^3
- C. Hemoglobin: 7 g/dL, Hematocrit: 21%, MCV: 75 µm^3
- D. Hemoglobin: 11 g/dL, Hematocrit: 33%, MCV: 88 µm^3 (Correct Answer)
- E. Hemoglobin: 15 g/dL, Hematocrit: 45%, MCV: 90 µm^3
Sepsis and septic shock Explanation: ***Hemoglobin: 11 g/dL, Hematocrit: 33%, MCV: 88 µm^3***
- The patient experienced significant trauma and is experiencing **hemorrhagic shock**, as evidenced by his initial **hypotension** (BP 60/33 mmHg), **tachycardia** (pulse 180/min), and positive **FAST exam** for fluid in Morrison's pouch, indicating intra-abdominal bleeding.
- The initial hemoglobin and hematocrit could be mildly decreased due to acute blood loss, but significant drops are often *not immediately apparent* as plasma volume has not yet moved into the intravascular compartment to dilute the remaining red blood cells. A hemoglobin of 11 g/dL and hematocrit of 33% are consistent with **acute blood loss** before significant hemodilution occurs. MCV of 88 µm^3 is within the normal range for **normocytic anemia** seen in acute hemorrhage.
*Hemoglobin: 10 g/dL, Hematocrit: 30%, MCV: 110 µm^3*
- While a hemoglobin of 10 g/dL and hematocrit of 30% are consistent with anemia due to blood loss, an **MCV of 110 µm^3** (macrocytic) is not typically seen in acute hemorrhage.
- Macrocytic anemia usually results from conditions like **B12 or folate deficiency**, alcoholism, or liver disease, which are not suggested by the acute traumatic scenario.
*Hemoglobin: 19 g/dL, Hematocrit: 55%, MCV: 95 µm^3*
- This indicates **polycythemia** (abnormally high red blood cell count), which is the opposite of what would be expected in a patient experiencing acute hemorrhagic shock.
- These values would suggest conditions like **polycythemia vera** or severe dehydration, which are not relevant in this acute trauma setting.
*Hemoglobin: 7 g/dL, Hematocrit: 21%, MCV: 75 µm^3*
- While a hemoglobin of 7 g/dL and hematocrit of 21% represent significant anemia consistent with major blood loss, these values are typically seen *later* as **hemodilution** occurs, or in cases of chronic blood loss.
- An **MCV of 75 µm^3** (microcytic) is generally indicative of **iron deficiency anemia** or thalassemia, which develops over time and is not characteristic of acute traumatic blood loss.
*Hemoglobin: 15 g/dL, Hematocrit: 45%, MCV: 90 µm^3*
- These values are within the **normal range** for hemoglobin and hematocrit, which would not be expected in a patient presenting with signs of **hemorrhagic shock** and a positive FAST exam indicating significant internal bleeding.
- This would suggest either very minor blood loss or that the values were taken before any bleeding had occurred or before hemodilution had a chance to manifest.
Sepsis and septic shock US Medical PG Question 8: A 55-year-old man with a history of IV drug abuse presents to the emergency department with an altered mental status. He was found unconscious in the park by police. His temperature is 100.0°F (37.8°C), blood pressure is 87/48 mmHg, pulse is 150/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for multiple scars and abscesses in the antecubital fossa. His laboratory studies are ordered as seen below.
Serum:
Na+: 139 mEq/L
Cl-: 105 mEq/L
K+: 4.3 mEq/L
HCO3-: 19 mEq/L
BUN: 20 mg/dL
Glucose: 95 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
Which of the following is the most appropriate treatment for this patient’s blood pressure and acid-base status?
- A. Ringer lactate (Correct Answer)
- B. Dextrose 5% normal saline
- C. Sodium bicarbonate
- D. Hypertonic saline
- E. Normal saline
Sepsis and septic shock Explanation: ***Ringer lactate***
- This patient presents with **hypotension** (BP 87/48 mmHg) and **metabolic acidosis** (HCO3- 19 mEq/L, with an elevated anion gap if calculated). Ringer lactate is a **balanced crystalloid solution** that contains lactate, which is metabolized to bicarbonate in the liver, helping to correct metabolic acidosis while providing fluid resuscitation.
- The patient's history of **IV drug abuse**, fever, and altered mental status suggests a possible underlying infection (e.g., sepsis), which often presents with hypotension and metabolic acidosis requiring aggressive fluid resuscitation with a balanced solution.
*Dextrose 5% normal saline*
- While it provides fluids and some sodium, Dextrose 5% normal saline contains **free water**, which is not ideal for a patient with hypotension and may exacerbate cerebral edema if present.
- It does not contain bicarbonate precursors and therefore would not directly address the patient's **metabolic acidosis**.
*Sodium bicarbonate*
- Administering sodium bicarbonate directly might be considered for severe metabolic acidosis, but **fluid resuscitation with a balanced solution** like Ringer lactate is usually the initial step to address both hypotension and acidosis.
- Excessive or rapid administration of sodium bicarbonate can lead to **alkalosis**, worsening intracellular acidosis, and fluid overload.
*Hypertonic saline*
- **Hypertonic saline** is primarily used to treat severe **hyponatremia** or to reduce intracranial pressure.
- It would not be appropriate for a patient with normal sodium levels and hypotension, as it could lead to further dehydration or worsen hypernatremia.
*Normal saline*
- **Normal saline (0.9% NaCl)** is an isotonic crystalloid often used for fluid resuscitation, but it has a high chloride content.
- Large volumes of normal saline can worsen or induce **hyperchloremic metabolic acidosis**, which would be detrimental to a patient who already has metabolic acidosis.
Sepsis and septic shock US Medical PG Question 9: A 50-year-old man with a history of stage 4 kidney disease was admitted to the hospital for an elective hemicolectomy. His past medical history is significant for severe diverticulitis. After the procedure he becomes septic and was placed on broad spectrum antibiotics. On morning rounds, he appear weak and complains of fatigue and nausea. His words are soft and he has difficulty answering questions. His temperature is 38.9°C (102.1°F), heart rate is 110/min, respiratory rate is 15/min, blood pressure 90/65 mm Hg, and saturation is 89% on room air. On physical exam, his mental status appears altered. He has a bruise on his left arm that spontaneously appeared overnight. His cardiac exam is positive for a weak friction rub. Blood specimens are collected and sent for evaluation. An ECG is performed (see image). What therapy will this patient most likely receive next?
- A. Send the patient for hemodialysis (Correct Answer)
- B. Perform a STAT pericardiocentesis
- C. Prepare the patient for renal transplant
- D. Treat the patient with aspirin
- E. Treat the patient with cyclophosphamide and prednisone
Sepsis and septic shock Explanation: ***Send the patient for hemodialysis***
- This patient presents with symptoms of **uremic encephalopathy** and **uremic pericarditis** in the context of **stage 4 kidney disease**. The altered mental status, weakness, fatigue, nausea, and the development of a bruise (which could indicate uremic coagulopathy) are suggestive of severe uremia. The ECG shows widespread **ST elevation and PR depression**, particularly noticeable in leads like II, V2-V6, which is a classic finding for pericarditis. The **weak friction rub** confirms this clinical suspicion. Hemodialysis is crucial to rapidly remove uremic toxins and resolve both uremic encephalopathy and pericarditis.
- The ECG findings, including diffuse **ST elevation** with **PR depression**, are characteristic of **pericarditis**. In a patient with end-stage renal disease, **uremia** is a common cause of pericarditis, which can be life-threatening if not promptly treated with dialysis.
*Perform a STAT pericardiocentesis*
- While the patient has pericarditis, there are no immediate signs of **cardiac tamponade**, such as muffled heart sounds, jugular venous distension, or pulsus paradoxus, that would necessitate an emergency pericardiocentesis.
- The primary treatment for **uremic pericarditis** is typically **hemodialysis** to resolve the underlying uremic state, not direct fluid removal unless tamponade is present.
*Prepare the patient for renal transplant*
- **Renal transplant** is a long-term solution for end-stage renal disease, but it is not an acute intervention for immediate life-threatening uremic complications like uremic pericarditis and encephalopathy.
- The patient needs urgent stabilization and treatment of his current acute medical issues before transplant consideration.
*Treat the patient with aspirin*
- While aspirin can be used for some forms of pericarditis, it is generally **contraindicated** in patients with **uremic pericarditis** due to the increased risk of **gastric bleeding** and potential exacerbation of uremic coagulopathy.
- The primary treatment for uremic pericarditis is **dialysis**, not anti-inflammatory medications, as the inflammation is driven by uremic toxins.
*Treat the patient with cyclophosphamide and prednisone*
- **Immunosuppressants** like cyclophosphamide and prednisone are used for autoimmune or inflammatory conditions causing pericarditis, such as systemic lupus erythematosus.
- This patient's pericarditis is clearly linked to **uremia** from kidney disease, not an autoimmune condition, making immunosuppressive therapy inappropriate and potentially harmful.
Sepsis and septic shock US Medical PG Question 10: Five days after admission into the ICU for drug-induced acute kidney injury, a 27-year-old woman develops fever. She is currently on a ventilator and sedatives. Hemodialysis is performed via a catheter placed in the right internal jugular vein. Feeding is via a nasogastric tube. An indwelling urinary catheter shows minimum output. Her blood pressure is 85/45 mm Hg, the pulse is 112/min, the respirations are 32/min, and the temperature is 39.6°C (103.3°F). The examination of the central catheter shows erythema around the insertion site with no discharge. Lung auscultation shows rhonchi. Cardiac examination shows no new findings. A chest CT scan shows bilateral pleural effusions with no lung infiltration. Empirical antibiotic therapy is initiated. Blood cultures obtained from peripheral blood and the catheter tip show S. aureus with a similar antibiogram. Urinary culture obtained from the indwelling catheter shows polymicrobial growth. Which of the following best explains this patient’s recent findings?
- A. Catheter-associated urinary tract infection
- B. Central catheter-related bacteremia (Correct Answer)
- C. Endocarditis
- D. Ventilator-associated pneumonia
- E. Naso-gastric tube sinusitis
Sepsis and septic shock Explanation: ***Central catheter-related bacteremia***
- The presence of **erythema at the catheter insertion site** and the isolation of **_S. aureus_ with a similar antibiogram from both peripheral blood and the catheter tip** are highly indicative of a catheter-related bloodstream infection.
- This type of infection is common in critically ill patients with central venous catheters due to the direct access provided for bacteria to enter the bloodstream.
*Catheter-associated urinary tract infection*
- While a **polymicrobial growth** in the urinary culture suggests a urinary tract infection, the isolation of **_S. aureus_ in blood cultures** with signs of local catheter infection points away from the urinary tract as the primary source of bacteremia.
- The patient has an **indwelling urinary catheter**, which is a risk factor for UTIs, but the systemic infection with _S. aureus_ is better explained by the central line.
*Endocarditis*
- Although **_S. aureus_ bacteremia** can lead to endocarditis, the case states that the **cardiac examination shows no new findings**, making endocarditis less likely as the primary explanation for the acute deterioration without other supporting evidence like a new murmur or imaging findings.
- Endocarditis is a potential complication of bacteremia, not typically the initial source, especially with a clear source like a central line.
*Ventilator-associated pneumonia*
- Pulmonary symptoms like **rhonchi** and **bilateral pleural effusions** are present, but the **lack of lung infiltration on CT** and the **isolation of _S. aureus_ from blood and catheter tip** (not respiratory samples) make VAP unlikely to be the primary cause of this systemic infection.
- The patient is also on a ventilator, which is a risk factor for VAP, but the microbiologic and imaging evidence does not fully support it as the main diagnosis.
*Naso-gastric tube sinusitis*
- While nasogastric tubes can cause sinusitis, which could manifest with fever, it is less likely to result in **_S. aureus_ bacteremia with a positive catheter tip culture**.
- Sinusitis would explain fever, but not the specific microbiological findings of _S. aureus_ in blood and catheter tip, nor the local erythema at the catheter site.
More Sepsis and septic shock US Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
