Ascites diagnosis and management US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Ascites diagnosis and management. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Ascites diagnosis and management US Medical PG Question 1: A 42-year-old man with chronic hepatitis C is admitted to the hospital because of jaundice and abdominal distention. He is diagnosed with decompensated liver cirrhosis, and treatment with diuretics is begun. Two days after admission, he develops abdominal pain and fever. Physical examination shows tense ascites and diffuse abdominal tenderness. Paracentesis yields cloudy fluid with elevated polymorphonuclear (PMN) leukocyte count. A drug with which of the following mechanisms is most appropriate for this patient's condition?
- A. Free radical creation within bacterial cell
- B. Inhibition of bacterial 50S subunit
- C. Inhibition of bacterial RNA polymerase
- D. Inhibition of bacterial peptidoglycan crosslinking (Correct Answer)
- E. Inhibition of bacterial DNA gyrase
Ascites diagnosis and management Explanation: ***Inhibition of bacterial peptidoglycan crosslinking***
- The patient's symptoms (fever, abdominal pain, diffuse tenderness, cloudy ascitic fluid with elevated PMN count) are highly suggestive of **spontaneous bacterial peritonitis (SBP)**, a common complication of decompensated cirrhosis.
- The most appropriate treatment for SBP is **broad-spectrum antibiotics**, typically a third-generation cephalosporin like **cefotaxime** or **ceftriaxone**, which work by inhibiting bacterial peptidoglycan crosslinking in the cell wall (beta-lactam mechanism).
- These agents provide excellent coverage against the common gram-negative enteric pathogens (especially *E. coli*) that cause SBP.
*Free radical creation within bacterial cell*
- This mechanism is characteristic of **nitroimidazoles** (e.g., metronidazole), which are effective against anaerobic bacteria and certain protozoa.
- While anaerobes can occasionally be involved in secondary peritonitis, empiric treatment for SBP typically targets gram-negative enteric bacteria, for which nitroimidazoles are not first-line choices.
*Inhibition of bacterial 50S subunit*
- This mechanism is common to **macrolides** (e.g., azithromycin) and **lincosamides** (e.g., clindamycin).
- These antibiotics are generally not first-line empiric treatment for SBP, which primarily requires coverage of gram-negative aerobes.
*Inhibition of bacterial RNA polymerase*
- This is the mechanism of action for **rifampin**, which is primarily used for tuberculosis and prophylaxis against certain bacterial meningitis (e.g., *N. meningitidis*).
- Rifampin is not suitable as empiric monotherapy for SBP given the typical causative pathogens.
*Inhibition of bacterial DNA gyrase*
- This is the mechanism of **fluoroquinolones** (e.g., ciprofloxacin, levofloxacin), which inhibit DNA gyrase (topoisomerase II) and topoisomerase IV, preventing bacterial DNA replication.
- Fluoroquinolones can be used for SBP treatment and prophylaxis, but third-generation cephalosporins remain the preferred first-line empiric therapy for acute SBP in most clinical guidelines.
Ascites diagnosis and management US Medical PG Question 2: A 49-year-old woman with a history of hepatitis C cirrhosis complicated by esophageal varices, ascites, and hepatic encephalopathy presents with 1 week of increasing abdominal discomfort. Currently, she takes lactulose, rifaximin, furosemide, and spironolactone. On physical examination, she has mild asterixis, generalized jaundice, and a distended abdomen with positive fluid wave. Diagnostic paracentesis yields a WBC count of 1196/uL with 85% neutrophils. Which of the following is the most appropriate treatment?
- A. Cefotaxime (Correct Answer)
- B. Transjugular intrahepatic portosystemic shunt placement
- C. Large volume paracentesis with albumin
- D. Increased furosemide and spironolactone
- E. Metronidazole
Ascites diagnosis and management Explanation: ***Cefotaxime***
- The patient presents with classic signs of **spontaneous bacterial peritonitis (SBP)**: increasing abdominal discomfort in a cirrhotic patient with ascites, and a diagnostic paracentesis showing **ascitic fluid neutrophil count >250 cells/mm³** (1196 × 0.85 = 1016 neutrophils/μL).
- **Third-generation cephalosporins** like cefotaxime or ceftriaxone are the **first-line treatment** for SBP due to their broad-spectrum coverage against common enteric gram-negative bacteria (especially E. coli and Klebsiella).
- Treatment should be initiated promptly once SBP is diagnosed to reduce mortality.
*Transjugular intrahepatic portosystemic shunt placement*
- TIPS is primarily used for **refractory ascites** or **recurrent variceal bleeding** that is not responsive to medical management.
- It is **not indicated** for the acute treatment of SBP and would be inappropriate in the setting of active infection.
*Large volume paracentesis with albumin*
- Large volume paracentesis is used to relieve symptoms of **tense ascites** causing respiratory compromise or severe discomfort, not as a primary treatment for SBP.
- While albumin is often given with large volume paracentesis (>5L removed) to prevent post-paracentesis circulatory dysfunction, it does not treat the underlying bacterial infection.
*Increased furosemide and spironolactone*
- Diuretics like furosemide and spironolactone are used to manage **chronic ascites** by promoting fluid excretion.
- Increasing their dose will not address the active bacterial infection causing SBP and may worsen renal function in an acutely ill patient.
*Metronidazole*
- Metronidazole is primarily effective against **anaerobic bacteria** and some protozoa.
- While it might be considered in specific polymicrobial intra-abdominal infections, it is **not sufficient as monotherapy** for SBP, which commonly involves gram-negative aerobic bacteria like E. coli and Klebsiella species.
Ascites diagnosis and management US Medical PG Question 3: A 50-year-old woman presents with esophageal varices, alcoholic cirrhosis, hepatic encephalopathy, portal hypertension, and recent onset confusion. The patient’s husband does not recall her past medical history but knows her current medications and states that she is quite disciplined about taking them. Current medications are spironolactone, labetalol, lactulose, and furosemide. Her temperature is 38.3°C (100.9°F), heart rate is 115/min, blood pressure is 105/62 mm Hg, respiratory rate is 12/min, and oxygen saturation is 96% on room air. On physical examination, the patient is disoriented, lethargic, and poorly responsive to commands. A cardiac examination is unremarkable. Lungs are clear to auscultation. The abdomen is distended, tense, and mildly tender. Mild asterixis is present. Neurologic examination is normal. The digital rectal examination reveals guaiac negative stool. Laboratory findings are significant for the following:
Basic metabolic panel Unremarkable
Platelet count 95,500/µL
Leukocyte count 14,790/µL
Hematocrit 33% (baseline is 30%)
Which of the following would most likely be of diagnostic value in this patient?
- A. Therapeutic trial of lactulose
- B. Abdominal paracentesis (Correct Answer)
- C. Noncontrast CT of the head
- D. Serum ammonia level
- E. Esophagogastroduodenoscopy
Ascites diagnosis and management Explanation: ***Abdominal paracentesis***
- The patient presents with **fever, abdominal tenderness, distension, and new-onset confusion** in the setting of **cirrhosis and ascites**, which are highly suggestive of **spontaneous bacterial peritonitis (SBP)**.
- An **abdominal paracentesis** with analysis of ascitic fluid (cell count with differential, culture) is necessary to diagnose SBP and guide appropriate antibiotic treatment.
*Therapeutic trial of lactulose*
- While the patient has **hepatic encephalopathy** and is on lactulose, her current presentation with **fever and abdominal tenderness** suggests an acute infectious process rather than worsening encephalopathy unresponsive to current therapy.
- A therapeutic trial of lactulose alone would delay the diagnosis of a potentially life-threatening infection like SBP.
*Noncontrast CT of the head*
- Although the patient has new-onset confusion, her presentation also includes **fever, abdominal tenderness, and signs of infection** in a patient with cirrhosis.
- A CT head would be more appropriate if there were focal neurological deficits, acute head trauma, or if SBP was ruled out and other causes of altered mental status were suspected.
*Serum ammonia level*
- The patient has known **hepatic encephalopathy**, and her current confusion is likely multifactorial.
- While an elevated ammonia level supports the diagnosis of hepatic encephalopathy, it is not diagnostic for the *cause* of her acute deterioration and would not rule out SBP, which requires urgent diagnosis and treatment.
*Esophagogastroduodenoscopy*
- The patient has a history of esophageal varices, but there is no evidence of active gastrointestinal bleeding (e.g., melena, hematemesis, guaiac positive stool).
- An **EGD** would be indicated for acute variceal bleeding, but it is not the most immediate or relevant diagnostic step for her current acute presentation of fever, abdominal pain, and confusion.
Ascites diagnosis and management US Medical PG Question 4: A 65-year-old Caucasian man visits the nephrology outpatient clinic for a follow-up appointment. He was previously diagnosed with stage G3a chronic kidney disease (CKD) and albuminuria stage A2. He follows strict dietary recommendations and takes enalapril. He has a history of benign prostatic hyperplasia which has been complicated by urinary tract obstruction. His vitals are stable, and his blood pressure is within the recommended limits. His most recent laboratory studies are as follows:
Serum sodium 140 mEq/L
Serum potassium 5.8 mEq/L
Serum chloride 102 mEq/L
Serum phosphate 4.0 mg/dL
Hemoglobin 11.5 mg/dL
Albumin excretion rate (AER) 280 mg/day
Which of the following is the best strategy in the management of this patient?
- A. Observation
- B. Addition of furosemide
- C. Addition of patiromer (Correct Answer)
- D. Addition of sevelamer
- E. Removal of enalapril
Ascites diagnosis and management Explanation: ***Addition of patiromer***
- The patient has **hyperkalemia** (serum potassium 5.8 mEq/L) which is exacerbated by his enalapril use and CKD; **patiromer** is a potassium binder that can effectively lower serum potassium without necessitating discontinuation of essential medications like ACE inhibitors.
- Patiromer is a good choice for chronic hyperkalemia in patients with **CKD** who require drugs that can increase potassium, such as **ACE inhibitors**, helping to maintain the benefits of these renoprotective agents.
*Observation*
- The patient's **serum potassium is elevated at 5.8 mEq/L**, which is a potentially dangerous level requiring intervention, not just observation.
- Hyperkalemia can lead to **life-threatening cardiac arrhythmias**, necessitating active management rather than a wait-and-see approach.
*Addition of furosemide*
- While furosemide can promote potassium excretion, its primary role is fluid removal and relief of congestion, and it may not be sufficient to address significant hyperkalemia in a patient on an **ACE inhibitor** with CKD.
- Furosemide would not directly counteract the potassium-retaining effect of **enalapril** as effectively as a potassium binder would, especially in the context of controlled blood pressure and no overt fluid overload.
*Addition of sevelamer*
- **Sevelamer** is a phosphate binder primarily used to manage **hyperphosphatemia** in CKD patients, which this patient does not have (serum phosphate 4.0 mg/dL is within normal limits).
- Its mechanism of action does not involve **potassium binding** or excretion, making it ineffective for the patient's hyperkalemia.
*Removal of enalapril*
- **Enalapril** is crucial for its **renoprotective effects**, including reducing proteinuria (AER 280 mg/day) and controlling blood pressure in CKD patients.
- Discontinuing enalapril would remove these benefits and could worsen kidney disease progression and proteinuria, while there are other strategies (like **patiromer**) to manage the side effect of hyperkalemia.
Ascites diagnosis and management US Medical PG Question 5: A 26-year-old male is brought into the emergency room because he collapsed after working out. The patient is a jockey, and he states that he feels dehydrated and has an upcoming meet for which he needs to lose some weight. On exam, the patient has dry mucosa with cracked lips. His temperature is 98.9 deg F (37.2 deg C), blood pressure is 115/70 mmHg, pulse is 105/min, and respirations are 18/min. The patient's blood pressure upon standing up is 94/65 mmHg. His serum Na+ is 125 mEq/L and K+ is 3.0 mEq/L. His urinalysis reveals Na+ of 35 mEq/L and K+ of 32 mEq/L. The abuse of which of the following is most likely responsible for the patient's presentation?
- A. Metoprolol
- B. Polyethylene glycol
- C. Furosemide (Correct Answer)
- D. Spironolactone
- E. Amiloride
Ascites diagnosis and management Explanation: ***Furosemide***
- The patient's **hyponatremia** (Na+ 125 mEq/L), **hypokalemia** (K+ 3.0 mEq/L), and signs of **dehydration** (dry mucosa, cracked lips, orthostatic hypotension, tachycardia) are consistent with the overuse of a **loop diuretic**.
- **Furosemide** inhibits the Na-K-2Cl cotransporter in the **thick ascending limb of the loop of Henle**, leading to significant excretion of sodium, potassium, and water.
- The **high urinary sodium (35 mEq/L) and potassium (32 mEq/L)** confirm **renal wasting**, which is the hallmark of diuretic abuse (as opposed to GI losses or poor intake, which would show low urinary electrolytes).
*Metoprolol*
- **Metoprolol** is a beta-blocker that primarily reduces heart rate and blood pressure, but it does not cause significant electrolyte disturbances like **hyponatremia** or **hypokalemia**, or profound dehydration.
- While it can lower blood pressure, it would not typically cause the combination of **orthostatic hypotension** and electrolyte abnormalities seen here.
*Polyethylene glycol*
- **Polyethylene glycol** is an osmotic laxative used for constipation or bowel preparation, which can cause fluid and electrolyte imbalances but typically presents with **diarrhea** and more pronounced gastrointestinal symptoms.
- Importantly, GI losses would result in **low urinary electrolytes** (kidney conserving electrolytes), not the high urinary Na+ and K+ seen here.
*Spironolactone*
- **Spironolactone** is a potassium-sparing diuretic, which would typically cause **hyperkalemia** rather than the **hypokalemia** observed in this patient.
- It also does not usually cause severe **hyponatremia** or profound dehydration to the extent seen here.
*Amiloride*
- **Amiloride** is a potassium-sparing diuretic, similar to spironolactone, and would lead to **potassium retention** (hyperkalemia) rather than severe **hypokalemia**.
- It has a mild diuretic effect and would not typically cause the profound **electrolyte imbalances** and dehydration observed.
Ascites diagnosis and management US Medical PG Question 6: A 54-year-old woman comes to the physician with abdominal distention and mild diffuse abdominal discomfort. She has not had nausea, vomiting, fever, or chills. She was diagnosed with alcoholic liver cirrhosis 2 years ago. Examination shows a protruding, distended abdomen that is dull to percussion with a positive fluid wave. Ultrasonography shows mild to moderate ascites. Appropriate treatment of the patient's condition is started. Four days later, the patient experiences palpitations and chest pain at home. She is brought to the emergency department, where her temperature is 37.3°C (99.1°F), pulse is 182/min, respirations are 18/min, and blood pressure is 82/50 mm Hg. An ECG shows ventricular tachycardia. Initial laboratory studies show:
Serum
Na+ 131 mEq/L
K+ 2.9 mEq/L
Cl- 92 mEq/L
Bicarbonate 34 mEq/L
Urea nitrogen 42 mg/dL
Creatinine 4.8 mg/dL
Glucose 90 mg/dL
Ca2+ 8.1 mg/dL
Mg2+ 1.5 mg/dL
Phosphate 4.7 mg/dL
Arterial Blood Gas
pH 7.52
pCO2 45 mm Hg
pO2 90.2 mm Hg
She is successfully cardioverted to normal sinus rhythm. Which of the following treatments is most likely responsible for this patient's presentation?
- A. Lisinopril
- B. Acetazolamide
- C. Mannitol
- D. Furosemide (Correct Answer)
- E. Hydrochlorothiazide
Ascites diagnosis and management Explanation: ***Furosemide***
- The patient's **hypokalemia (2.9 mEq/L)**, **hypomagnesemia (1.5 mg/dL)**, and **metabolic alkalosis (pH 7.52, bicarbonate 34 mEq/L)** are characteristic side effects of **loop diuretics** like furosemide.
- These electrolyte imbalances, particularly **hypokalemia** and **hypomagnesemia**, can predispose to serious cardiac arrhythmias such as **ventricular tachycardia**, which the patient experienced.
- Loop diuretics are commonly used in combination with spironolactone for management of cirrhotic ascites.
*Lisinopril*
- Lisinopril is an **ACE inhibitor** and would typically cause **hyperkalemia**, not hypokalemia, due to its effect on aldosterone.
- It works by vasodilation and could potentially worsen hypotension, but it doesn't explain the patient's specific electrolyte disturbances or arrhythmia profile.
*Acetazolamide*
- Acetazolamide is a **carbonic anhydrase inhibitor** that can cause **metabolic acidosis** and hypokalemia but would not lead to the metabolic alkalosis observed here.
- It increases bicarbonate excretion, which is the opposite of this patient's acid-base status.
*Mannitol*
- Mannitol is an **osmotic diuretic** primarily used for cerebral edema or acute glaucoma.
- Its main effects relate to fluid shifts, and while it could cause electrolyte disturbances, it's not typically associated with this specific constellation of hypokalemia, hypomagnesemia, and metabolic alkalosis.
*Hydrochlorothiazide*
- Hydrochlorothiazide is a **thiazide diuretic** that can cause hypokalemia, hypomagnesemia, and metabolic alkalosis, similar to loop diuretics.
- However, **thiazides are not used for cirrhotic ascites** because they are ineffective in treating significant fluid overload and can worsen complications of cirrhosis. The standard treatment is spironolactone (aldosterone antagonist) with or without a loop diuretic like furosemide for refractory cases.
Ascites diagnosis and management US Medical PG Question 7: A 75-year-old woman is brought to a physician’s office by her son with complaints of diarrhea and vomiting for 1 day. Her stool is loose, watery, and yellow-colored, while her vomitus contains partially digested food particles. She denies having blood or mucus in her stools and vomitus. Since the onset of her symptoms, she has not had anything to eat and her son adds that she is unable to tolerate fluids. The past medical history is unremarkable and she does not take any medications regularly. The pulse is 115/min, the respiratory rate is 16/min, the blood pressure is 100/60 mm Hg, and the temperature is 37.0°C (98.6°F). The physical examination shows dry mucous membranes and slightly sunken eyes. The abdomen is soft and non-tender. Which of the following physiologic changes in glomerular filtration rate (GFR), renal plasma flow (RPF), and filtration fraction (FF) are expected?
- A. Decreased GFR, decreased RPF, decreased FF
- B. Decreased GFR, decreased RPF, no change in FF
- C. Increased GFR, increased RPF, increased FF
- D. Increased GFR, decreased RPF, increased FF
- E. Decreased GFR, decreased RPF, increased FF (Correct Answer)
Ascites diagnosis and management Explanation: ***Decreased GFR, decreased RPF, increased FF***
- Due to **dehydration** from diarrhea and vomiting, there is a decrease in blood volume leading to decreased renal blood flow and **renal plasma flow (RPF)**.
- The body responds to hypovolemia by activating the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system, which cause **preferential efferent arteriolar constriction** (more than afferent constriction). This helps maintain glomerular hydrostatic pressure despite reduced renal perfusion.
- As a result, **GFR decreases** but proportionally **less than RPF decreases**, causing the **filtration fraction (FF = GFR/RPF) to increase**.
- In this patient with significant dehydration (tachycardia, hypotension, dry mucous membranes), both GFR and RPF are reduced, but FF is elevated due to compensatory mechanisms.
*Decreased GFR, decreased RPF, decreased FF*
- While GFR and RPF will decrease due to dehydration, the **filtration fraction is expected to increase**, not decrease.
- A decreased FF would imply GFR fell proportionally more than RPF, which contradicts the physiologic response where efferent arteriolar constriction helps preserve GFR relative to RPF.
*Decreased GFR, decreased RPF, no change in FF*
- With significant fluid loss and compensatory mechanisms (efferent arteriolar constriction via angiotensin II), a change in **filtration fraction** is expected.
- The body actively alters arteriolar tone to prioritize GFR maintenance, which directly increases FF.
*Increased GFR, increased RPF, increased FF*
- This pattern suggests **hypervolemia** or increased renal perfusion, which directly contradicts the patient's severe dehydration.
- Both GFR and RPF are expected to decrease in volume depletion, not increase.
*Increased GFR, decreased RPF, increased FF*
- An increase in GFR is physiologically impossible given the patient's severe volume depletion and reduced renal perfusion.
- While FF does increase in dehydration, this occurs in the context of **both GFR and RPF being decreased**, not with an increased GFR.
Ascites diagnosis and management US Medical PG Question 8: A 67-year-old man is brought to the emergency department when he was found obtunded at the homeless shelter. The patient is currently not responsive and smells of alcohol. The patient has a past medical history of alcohol use, IV drug use, and hepatitis C. His temperature is 99°F (37.2°C), blood pressure is 95/65 mmHg, pulse is 95/min, respirations are 13/min, and oxygen saturation is 95% on room air. The patient is started on IV fluids, and his pulse decreases to 70/min. On physical exam, the patient has an abdominal exam notable for distension and a positive fluid wave. The patient displays mild yellow discoloration of his skin. The patient has notable poor dentition and poor hygiene overall. A systolic murmur is heard along the left sternal border on cardiac exam. Pulmonary exam is notable for mild bibasilar crackles. Laboratory values are ordered, and return as below:
Hemoglobin: 10 g/dL
Hematocrit: 32%
Leukocyte count: 7,500 cells/mm^3 with normal differential
Platelet count: 227,000/mm^3
Serum:
Na+: 125 mEq/L
Cl-: 100 mEq/L
K+: 5.0 mEq/L
HCO3-: 24 mEq/L
BUN: 51 mg/dL
Glucose: 89 mg/dL
Creatinine: 2.2 mg/dL
Ca2+: 10.0 mg/dL
AST: 22 U/L
ALT: 19 U/L
Urine:
Color: Amber
Nitrites: Negative
Sodium: 12 mmol/24 hours
Red blood cells: 0/hpf
Over the next 24 hours, the patient produces very little urine. Which of the following best explains this patient’s renal findings?
- A. Liver failure (Correct Answer)
- B. Nephrotoxic agent
- C. Dehydration
- D. Postrenal azotemia
- E. Congestive heart failure
Ascites diagnosis and management Explanation: ***Liver failure***
- The patient's history of **alcohol use**, **hepatitis C**, **ascites** (abdominal distension with fluid wave), and **jaundice** (yellow skin discoloration) are all signs of severe liver disease/cirrhosis.
- In the context of advanced liver failure, this patient has developed **hepatorenal syndrome (HRS)**, a critical complication characterized by **functional renal failure** due to severe renal vasoconstriction without intrinsic kidney damage.
- Key diagnostic features of HRS include: elevated **BUN** and **creatinine**, markedly **low urine sodium (<20 mEq/L)**, **oliguria** that does not improve with volume expansion, and absence of other causes of renal failure.
- The urine sodium of **12 mmol/24 hours** is pathognomonic for HRS, indicating maximal sodium retention by the kidneys in response to decreased effective arterial blood volume.
*Nephrotoxic agent*
- While IV drug use can be associated with certain nephrotoxic exposures, there is no direct evidence in the clinical presentation (e.g., specific drug use leading to toxicity, muddy brown casts on urinalysis) to support this.
- **Acute tubular necrosis (ATN)** from nephrotoxins typically presents with urine sodium **>40 mEq/L** and granular casts, which are absent here.
- The patient's underlying liver disease with characteristic low urine sodium provides a more comprehensive explanation for the renal dysfunction.
*Dehydration*
- The patient's **blood pressure** is low, but he responded to IV fluids with a decreased pulse, suggesting some improvement in volume status, yet his renal function worsened with persistent oliguria.
- While dehydration can cause **prerenal azotemia**, the lack of improvement after IV fluid resuscitation, extreme oliguria, very low urine sodium in the context of advanced cirrhosis with ascites point strongly towards hepatorenal syndrome rather than simple hypovolemia.
- True prerenal azotemia from dehydration typically improves with fluid administration, which did not occur here.
*Postrenal azotemia*
- This condition is caused by an **obstruction** to urine outflow, such as a kidney stone, enlarged prostate, or tumor.
- There are no clinical signs or symptoms (e.g., flank pain, difficulty urinating, hydronephrosis on imaging) in the patient's presentation to suggest an obstructive cause.
- Postrenal obstruction typically requires **bilateral** obstruction or obstruction in a single functioning kidney to cause significant azotemia.
*Congestive heart failure*
- While the patient has **bibasilar crackles** and a cardiac murmur, these are non-specific findings that might be related to volume overload from liver disease or endocarditis from IV drug use.
- **Cardiorenal syndrome** can cause renal dysfunction, but typically presents with more prominent signs of heart failure and urine sodium is often higher (>40 mEq/L) when diuretics are used.
- The patient's profound liver failure with ascites, jaundice, and the characteristic very low urine sodium provide a much stronger and more direct explanation for the progressive renal dysfunction as hepatorenal syndrome.
Ascites diagnosis and management US Medical PG Question 9: A 55-year-old patient who immigrated from the Middle East to the United States 10 years ago presents to the emergency department because of excessive weakness, abdominal discomfort, and weight loss for the past 10 months. He has had type 2 diabetes mellitus for 10 years for which he takes metformin. He had an appendectomy 12 years ago in his home country, and his postoperative course was not complicated. He denies smoking and drinks alcohol socially. His blood pressure is 110/70 mm Hg, pulse is 75/min, and temperature is 37.1°C (98.7°F). On physical examination, the patient appears exhausted, and his sclerae are yellowish. A firm mass is palpated in the right upper abdominal quadrant. Abdominal ultrasonography shows liver surface nodularity, splenomegaly, and increased diameter of the portal vein. Which of the following is the most common complication of this patient condition?
- A. Hepatopulmonary syndrome
- B. Ascites (Correct Answer)
- C. Hepatic encephalopathy
- D. Hepatorenal syndrome
- E. Hepatic osteodystrophy
Ascites diagnosis and management Explanation: ***Ascites***
- The patient presents with classic signs of **portal hypertension** (splenomegaly, increased portal vein diameter, liver surface nodularity suggesting cirrhosis), and **ascites** is the most common and often the earliest major complication.
- The presence of **abdominal discomfort** and an **RUQ mass** could be related to severe liver disease and its complications, including fluid accumulation or an underlying liver malignancy often associated with cirrhosis.
*Hepatopulmonary syndrome*
- This involves **intrapulmonary vascular dilatations** in the setting of liver disease leading to oxygenation defects, typically marked by platypnea and orthodeoxia, which are not described here.
- While a complication of **cirrhosis**, it is less common than ascites and typically presents with respiratory symptoms not highlighted in this case.
*Hepatic encephalopathy*
- Characterized by **neuropsychiatric symptoms** due to the accumulation of toxins (e.g., ammonia) that the liver cannot detoxify.
- The patient's presentation mainly focuses on physical weakness, abdominal issues, and jaundice, without mention of confusion, asterixis, or altered mental status.
*Hepatorenal syndrome*
- This is a form of **functional renal failure** that occurs in patients with advanced liver disease, presenting with rapidly progressive azotemia due to severe splanchnic vasodilation.
- It is a **later and more severe complication** of liver failure, and while possible, ascites is typically seen much earlier and more frequently.
*Hepatic osteodystrophy*
- This refers to a group of **metabolic bone disorders** (osteoporosis, osteomalacia) that can occur in chronic liver disease.
- While it can manifest as bone pain, it is not a direct or immediate complication of portal hypertension and would not explain the acute abdominal findings.
Ascites diagnosis and management US Medical PG Question 10: A 45-year-old homeless man is brought to the emergency department. He was found unconscious at the park. The patient has a past medical history of IV drug abuse, hepatitis C, alcohol abuse, schizophrenia, and depression. He does not receive normal medical follow up or care. His temperature is 102°F (38.9°C), blood pressure is 97/68 mmHg, pulse is 120/min, respirations are 22/min, and oxygen saturation is 98% on room air. Physical exam demonstrates a diffusely distended abdomen that is dull to percussion with a notable fluid wave. The abdominal exam causes the patient to contract his extremities. Cardiac and pulmonary exam are within normal limits. The patient responds to painful stimuli and smells heavily of alcohol. Which of the following is the best next step in management?
- A. Ceftriaxone
- B. CT abdomen
- C. Paracentesis (Correct Answer)
- D. Cefotaxime
- E. Ultrasound
Ascites diagnosis and management Explanation: ***Paracentesis***
- The patient's **distended abdomen**, **dullness to percussion**, and **fluid wave** are classic signs of **ascites**. Given his history of **alcohol abuse** and **hepatitis C**, he is at high risk for cirrhosis-related ascites, which can become infected (spontaneous bacterial peritonitis, or **SBP**).
- A **paracentesis** is crucial for diagnosing SBP by analyzing the ascitic fluid for **cell count (especially PMNs)**, culture, and other parameters. It's the most appropriate first step in a patient with new-onset ascites or suspected SBP, especially if they are febrile.
*Ceftriaxone*
- While **antibiotics** are indicated for **spontaneous bacterial peritonitis (SBP)**, initiating empiric antibiotics like **ceftriaxone** before diagnostic paracentesis could mask the causative organism and make diagnosis difficult.
- Paracentesis is necessary to confirm SBP and guide specific antibiotic therapy, though empiric antibiotics should be started promptly after fluid collection if SBP is highly suspected.
*CT abdomen*
- A **CT scan** would provide detailed anatomical information but is not the most urgent or appropriate first step for diagnosing **SBP** or guiding immediate management in this setting.
- While it can confirm ascites, it cannot establish the diagnosis of infection or determine the fluid's cellular content, which is critical for treatment decisions.
*Cefotaxime*
- Similar to ceftriaxone, **cefotaxime** is an appropriate **antibiotic** for treating **spontaneous bacterial peritonitis (SBP)**.
- However, performing a **diagnostic paracentesis** to confirm SBP and obtain fluid for analysis is the priority before initiating empiric antibiotic therapy, just as with ceftriaxone.
*Ultrasound*
- An **ultrasound** can confirm the presence of **ascites** and rule out other causes of abdominal distension, and can also guide paracentesis.
- However, in a patient with suspected **spontaneous bacterial peritonitis (SBP)** and clear signs of ascites, performing the **diagnostic paracentesis** is the most direct and urgent next step to identify infection, making it more critical than just imaging.
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