Questions, Board Review

Board Review Questions: April 2024

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1. Which medication would treat spontaneous bacterial peritonitis for a patient developing hepatorenal syndrome?

A. Albumin
B. Cefotaxime
C. N-acetylcysteine
D. Octreotide

The correct answer is B, Cefotaxime.

Why is this the correct answer?
One of the most common risk factors (up to 25%-30% of patients) for developing hepatorenal syndrome is spontaneous bacterial peritonitis (SBP). Cefotaxime is the recommended empiric antibiotic because it covers most of the organisms that cause SBP and has high ascitic fluid concentrations. Correcting the underlying cause of hepatorenal syndrome may reverse the process, but liver transplant is the definitive treatment if no etiology is found or renal function worsens despite therapies.

Hepatorenal syndrome can arise spontaneously, but hepatorenal syndrome associated with cirrhosis has a significant morbidity rate and 2-week mortality rate if left untreated. A paracentesis should be performed to rule this out, and treatment should be started if there is clinical suspicion. Type 1 hepatorenal syndrome, marked by oliguria and rapidly increasing serum creatinine (more than doubling within 2 weeks), is more critical than type 2. Type 2 hepatorenal syndrome progresses more gradually and may advance less insidiously.

Why are the other choices wrong?
Use of albumin decreases electrolyte imbalances in patients undergoing paracentesis and helps maintain cardiac output. Large-volume paracentesis performed without albumin can cause type 1 hepatorenal syndrome as well as hemodynamic compromise. This patient should undergo diagnostic paracentesis for SBP, but albumin by itself does not treat SBP, nor does it reverse hepatorenal syndrome. However, albumin is recommended to treat SBP when it is associated with azotemia.

N-acetylcysteine is usually used to treat acetaminophen overdose. It has been shown to improve renal function, but the mechanism is unclear. N-acetylcysteine has no role in treatment of liver failure that is not drug related.

Somatostatin analogues such as octreotide aid in splanchnic vasoconstriction and are a mainstay for variceal bleeding. There is a potential for benefit in hepatorenal patients due to regulation of splanchnic vasodilation that secondarily causes renal circulatory perfusion problems. However, this possibility has not yet been validated by clinical trials.

REFERENCES
Medscape article on hepatorenal failure https://emedicine.medscape.com/article/178208-overview

Wolfson AB. Renal failure. In: Walls RM, Hockberger RS, Gausche-Hill M, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Vol 2. 10th ed. Elsevier; 2023:1163-1181.

O'Mara SR, Wiesner L. Hepatic disorders. In: Tintinalli JE, Ma OJ, Yealy DM, et al, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020:516-523.

European Association for the Study of the Liver. EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. J Hepatol. 2010 Sep;53(3):397-417. https://www.journal-of-hepatology.eu/article/S0168-8278(10)00478-2/fulltext

UpToDate article on hepatorenal syndrome, available in full with a subscription https://www.uptodate.com/contents/hepatorenal-syndrome


2. Which laboratory abnormality is expected in primary adrenal insufficiency?

A. Hyperglycemia
B. Hypocalcemia
C. Hypokalemia
D. Hyponatremia

The correct answer is D, Hyponatremia.

Why is this the correct answer?
Destruction of the adrenal cortex in primary adrenal insufficiency (Addison disease) manifests with signs and symptoms of steroid deficiency (mineralocorticoids, glucocorticoids, gonadocorticoids) and increased adrenocorticotropic hormone (ACTH). The mineralocorticoid aldosterone stimulates the kidneys to reabsorb sodium and to excrete potassium. Aldosterone deficiency contributes to the presence of hyponatremia (seen 90% of the time), and hyperkalemia (seen 60% of the time). Deficiency in the glucocorticoid cortisol can lead to hypoglycemia, a common finding in children and infants.

Signs and symptoms of gonadocorticoid deficiency are more common in women and include decreased axillary and pubic hair and decreased libido. Increased ACTH leads to skin hyperpigmentation. Causes of primary adrenal insufficiency include autoimmune disease (most common cause in Western countries), congenital conditions, drugs, hemorrhage, infections (tuberculosis is traditionally a common cause but is now uncommon in Western countries), infiltrative diseases (such as amyloidosis and sarcoidosis), and metastatic cancer.

Why are the other choices wrong?
Cortisol is involved with maintaining euglycemia. Cortisol deficiency in primary adrenal insufficiency leads to hypoglycemia, not hyperglycemia.

Hypercalcemia, not hypocalcemia, is seen in primary adrenal insufficiency. The hypercalcemia is thought to be a result of increased mobilization from bone and diminished renal excretion. It generally corrects quickly with hydration.

Aldosterone causes sodium reabsorption and potassium excretion. Aldosterone deficiency in primary adrenal insufficiency causes hyperkalemia, not hypokalemia.

REFERENCES

Idrose AM. Adrenal insufficiency. In: Tintinalli JE, Ma OJ, Yealy DM, et al, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020:1457-1460.

Field AG. Adrenal and pituitary disorders. In: Wolfson AB, Cloutier RL, Hendey GW, Ling LJ, Rosen CL, Schaider JJ, eds. Harwood-Nuss’ Clinical Practice of Emergency Medicine. 7th ed. Wolters Kluwer; 2021:1072-1080.

UpToDate article on adrenal insufficiency in adults, available in full with a subscription https://www.uptodate.com/contents/clinical-manifestations-of-adrenal-insufficiency-in-adults


3. A mother brings in her 5-month-old baby because he has been constipated for the past week. She says he has been eating less for the past 3 days and seems "sluggish and weak." He has had no fever, vomiting, rash, or other concerns. His vital signs are BP 107/74, P 111, R 22, and T 36.6°C (97.9°F); SpO2 is 100% on room air. The child is awake and interactive but lies still during the examination. Examination findings are otherwise negative except for diffuse decreased tone. Deep tendon reflexes are normal. What pharmacotherapy should the treatment include?

A. Botulism immune globulin 0.5 mL/kg/hr
B. Dexamethasone 0.6 mg/kg
C. Normal saline bolus 10 mL/kg
D. Vancomycin 15 mg/kg

The correct answer is A, Botulism immune globulin 0.5 mL/kg/hr.

Why is this the correct answer?
The classic presentation of infant botulism includes a history of constipation followed by altered neuromuscular examination findings, with cranial nerve issues noted initially. This is sometimes described as “floppy baby” presentation. According to the CDC, any of the following symptoms can be observed: constipation, poor feeding, ptosis, sluggish pupils, flattened facial expression, diminished suck and gag reflexes, weak and altered cry, respiratory difficulty, and respiratory arrest. Infant botulism is caused by ingestion of Clostridium botulinum, which can be attributed to ingestion of honey or corn syrup. The mortality rate is 5% to 10%. It is more common in breastfed infants because breastfeeding can affect the gastric acid or bile acids that would otherwise minimize the growth of Clostridium. C. botulinum can also be ingested on a fomite when local construction has caused it to be mobilized from the soil.

The primary concern in infant botulism is paralysis of musculature related to breathing; deep tendon reflexes are spared and remain normal. Treatment includes supportive care, frequent evaluation of the respiratory status, and empiric treatment with intravenous botulism immune globulin. The time it takes to get results from stool sample testing is often too long given how difficult it is to obtain the sample in a constipated infant.

Why are the other choices wrong?
Dexamethasone is a steroid that is often used to treat croup, and there is evidence for its use in treating asthma in one or two doses (depending on the study). However, steroids have no role in the treatment of infant botulism.

Normal saline is best used as a volume expander and is only dosed at 10 mL/kg when the normal 20 mL/kg could cause harm (ie, increased intracranial pressure, congestive heart failure, renal dysfunction). This child has normal mentation and vital signs and does not warrant a fluid bolus at this time.

Vancomycin can be important in the treatment of wound botulism, but penicillin is still the preferred first-line agent. However, vancomycin has no role in the treatment of infant botulism.

REFERENCES
Srinivasan S, Velasco Masson JL. Constipation. In: Shaw KN, Bachur EG, Chamberlain J, Lavelle J, Nagler J, Shook JE, eds. Fleisher & Ludwig's Textbook of Pediatric Emergency Medicine. 8th ed. Wolters Kluwer; 2021:127-133.

Mostafa AMT, McKeever RG. Botulism. In: Wolfson AB, Cloutier RL, Hendey GW, Ling LJ, Rosen CL, Schaider JJ, eds. Harwood-Nuss’ Clinical Practice of Emergency Medicine. 7th ed. Wolters Kluwer; 2021:1536-1539.

CDC article on infant botulism https://www.cdc.gov/botulism/infant-botulism.html


4. A 41-year-old woman presents via ambulance after being found down on the sidewalk. She is cooperative but somnolent and confused. Her vital signs include BP 110/70, P 95, and R 12; SpO2 is 96% on room air. An empty bottle of lorazepam, filled the day before with 60 tablets, is found in her pocket. What is the most appropriate initial step in management?

A. Administer flumazenil 0.2 mg IV
B. Administer naloxone 0.2 mg IV
C. Order a head CT scan without contrast
D. Perform a capillary blood glucose check

The correct answer is D, Perform a capillary blood glucose check.

Why is this the correct answer?
Any patient who presents with altered mental status should have a capillary blood glucose level checked as part of the initial assessment. This is a high-yield, minimally invasive test that can be performed rapidly at the bedside and provides immediately actionable information. Even when the cause of altered mental status appears obvious (such as in cases of trauma, stroke, or overdose), hypoglycemia should still be ruled out. This step can prevent more expensive, invasive, and time-consuming interventions.

Why are the other choices wrong?
Empiric treatment with flumazenil should be avoided for most patients, even those with known or suspected benzodiazepine overdose. Flumazenil is a selective central benzodiazepine antagonist. Seizure activity can occur after administration of flumazenil to patients who are physically dependent on benzodiazepines. Furthermore, flumazenil is contraindicated in patients with possible increased intracranial pressure because of its adverse effects on cerebral hemodynamics.

Significant opioid toxicity typically manifests with respiratory depression. This patient is cooperative and breathing at a normal rate with good oxygenation. Administration of naloxone, a competitive antagonist at opioid receptors, is likely unnecessary and may precipitate withdrawal symptoms. In this case, diagnosing possible hypoglycemia is a higher priority.

Emergency physicians should have a low threshold for performing head CT on patients with altered mental status in the setting of possible trauma. This patient was found down and cannot give a reliable history. Unless additional history that clearly rules out head trauma becomes available, she should probably undergo CT scanning after having her blood glucose level measured.

REFERENCES
Quan D. Benzodiazepines. In: Tintinalli JE, Ma OJ, Yealy DM, et al, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020:1215-1219.

UpToDate article on benzodiazepine poisoning and withdrawal, available in full with a subscription https://www.uptodate.com/contents/benzodiazepine-poisoning-and-withdrawal


5. A 68-year-old man presents with lower abdominal pain and a distended abdomen. He has been unable to void for the past 6 hours. He denies previous hematuria. Bedside ultrasonography reveals an enlarged bladder with 250 mL of fluid. The nurse is unable to pass a 14-Fr Foley catheter. Placement of which catheter is the best next step in management?

A. 12-Fr Foley catheter
B. 14-Fr Foley catheter over guidewire
C. Coudé catheter
D. Suprapubic catheter

The correct answer is C, Coudé catheter.

Why is this the correct answer?
Given his age and medical history, this patient's urinary retention is most likely caused by a urethral obstruction that is significant enough to prevent passage of a 14-Fr catheter. The best next step is to try to place a coudé catheter. A coudé catheter has a semirigid curved tip that allows for passage past the urethral obstruction, generally an enlarged prostate gland. A coudé catheter is placed in a similar manner to that used for a Foley catheter, with sterile technique. The shaft of the patient's penis is held vertically and taut with the physician's nondominant hand. After urethral anesthesia with lidocaine is achieved, the tip of the coudé catheter is placed cephalad and advanced until urine is returned. To ensure the tip of the catheter stays cephalad as the catheter is advanced, the physician should reference the position of the balloon port, which faces the same direction. The balloon is then inflated using 5 to 10 mL of sterile water, depending on the manufacturer's specifications.

Why are the other choices wrong?
A smaller catheter is unlikely to provide enough rigidity to pass by the urethral obstruction. A larger Foley catheter (18 Fr) is sometimes used because it is stiffer; it can be tried if a coudé catheter is unavailable.

The use of a catheter over a filiform or hydrophilic guidewire can be considered if the passage of a coudé catheter is unsuccessful. Metal or vascular guidewires should never be used for urethral procedures.

Placement of a suprapubic catheter should be considered if other techniques have failed and urology consultation is unavailable. Suprapubic catheter placement is not the next step; a coudé catheter should be tried next.

REFERENCES
Davis JE, Silverman MA. Urologic procedures. In: Roberts JR, Custalow CB, Thomsen TW, et al, eds. Roberts and Hedges’ Clinical Procedures in Emergency Medicine and Acute Care. 7th ed. Elsevier; 2019:1141-1185.

Manthey DE, Story DJ. Acute urinary retention. In: Tintinalli JE, Ma OJ, Yealy DM, et al, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020:586-581.

UpToDate article on managing urinary catheters in adults, available in full with a subscription https://www.uptodate.com/contents/placement-and-management-of-urinary-bladder-catheters-in-adults

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