8 A 45‐year‐old man is recovering in the surgical ICU after an exploratory laparotomy and small bowel resection for small bowel obstruction. On postoperative day 7, he is still unable to tolerate enteral nutrition and is started on total parenteral nutrition through his existing central line. Due to leukocytosis and persistent fevers, blood cultures demonstrating Candida glabrata fungemia were obtained on postoperative day 12.What is the next best step?Remove the central line and immediately start fluconazole.Remove the central line, start fluconazole, and initiate peripheral parenteral nutrition.Remove the central line, start micafungin, obtain ophthalmology consultation.Repeat blood cultures.Obtain a CT scan.Candidemia is usually the result of a central line‐associated bloodstream infection. The Infectious Diseases Society of America (IDSA) currently recommends that all patients with documented candidemia undergo at least one dilated eye examination to rule out intraocular involvement. Intraocular candidiasis may require intravitreal antifungal therapy and/or vitrectomy. Candida glabrata is intrinsically resistant to azoles such as fluconazole (choice A), thus the antifungals of choice for Candida glabrata are echinocandins such as micafungin. Removal of the central line is appropriate, but appropriate treatment for candidemia (micafungin) is also required (choice B). Repeat cultures are also appropriate, but not the next best step as it does not treat the candidemia (choice D). A CT scan may be warranted to exclude an intra‐abdominal source, but would not be the next best step (choice E).Answer: CRodrigues CF, Silva S, Henriques M. Candida glabrata: a review of its features and resistance. Eur J Clin Microbiol Infect Dis. 2014; 33(5):673–688.Pappas, PG, Kauffman, CA, Andes, D, et al. Clinical practice guidelines for the management of candidiasis: 2009 update by the Infectious Diseases Society of America. Clin Infect Dis. 2009; 48:503–535.
9 A 65‐year‐old woman with infected necrotizing pancreatitis and hypotension requires 6 L of crystalloid in her resuscitation. On physical exam, she is edematous and remains hypotensive.The major cause of vasodilation in sepsis appears to be mediated by:Up‐regulating fibrinolysis.ATP‐sensitive potassium channels in smooth muscle.ATP‐sensitive calcium channels in smooth muscle.Increase in vasopressin.G‐arginine.The major cause of vasodilation in sepsis appears to be mediated by ATP‐sensitive potassium channels in smooth muscle. The result of their activation is increased permeability of vascular smooth muscle cells to potassium, and hyperpolarization of the cell membranes, preventing muscle contraction, leading to vasodilation. There is a relative deficiency of vasopressin in early sepsis. The endothelium is an endocrine organ, capable of regulating the function of the microcirculation and producing nitric oxide (NO), an endogenous vasodilator. Its major effects are to cause local vasodilation and inhibition of platelet aggregation. NO is produced from l‐arginine by nitric oxide synthetase (NOS), and its actions are mediated by cGMP. There are two forms of the enzyme NOS, a constitutive form, produced as part of the normal regulatory mechanisms, and an inducible form, whose production appears to be pathologic. Inducible NOS (iNOS) is an offshoot of the inflammatory response, by TNF and other cytokines. It results in massive production of NO, causing widespread vasodilation (due to loss of vasomotor tone) and hypotension, which is hyporeactive to adrenergic agents. NO has a physiological antagonist, endothelin‐1, a potent vasoconstrictor whose circulating level is increased in cardiogenic shock and following severe trauma.Answer: BJackson WF Ion channels and vascular tone. Hypertension. 2000; 35(1 Pt 2):173–178.Quayle, JM, Nelson, MT, Standen, NB ATP sensitive and inwardly rectifying potassium channels in smooth muscle. Physiol Rev. 1997; 77(4):1165–1232.
10 The removal of a central venous catheter alone could be effective in the treatment of a central line‐associated bloodstream infection in which of the following organisms?PseudomonasE. coliStaphylococcus aureusKlebsiella pneumoniaStaphylococcus epidermidisWhen treating catheter‐related bloodstream infections (CLABSI), several factors are important to consider in the treatment algorithm. Staphylococcus epidermidis is often a contaminate and tends to behave in a nonvirulent manner. However, it is known to cause biofilms, so catheters must be removed. The use of antibiotics in a short course may be beneficial depending on the clinical condition of the patient.Answer: EPérez Parra A, Cruz Menárquez M, Pérez Granda MJ A simple educational intervention to decrease incidence of central line‐associated bloodstream infection (CLABSI) in intensive care units with low baseline incidence of CLABSI. Infect Control Hosp Epidemiol. 2010; 31(9):964–967.Pronovost P, Needham D, Berenholtz S, et al. An intervention to decrease catheter‐related bloodstream infections in the ICU. N Engl J Med. 2006; 355(26):2725–2732. Erratum in: New England Journal of Medicine (2007) 356 (25), 2660.
11 A 60‐year‐old woman is admitted to the ICU from the operating room after undergoing an emergent right colectomy and end ileostomy for a perforated gangrenous cecum. Over the next 12 hours, she has escalating vasopressor requirements despite being adequately fluid resuscitated and is started on stress dose steroids. Despite all these measures, she remains in refractory shock. The addition of which therapeutic can best improve this patient's arterial pressure?Nitric oxide synthase inhibitor 546C88Angiotensin IIFludrocortisoneVitamin CHypertonic salineThe ATHOS‐3 trials found that in patients with severe vasodilatory shock on high‐dose catecholamine‐based vasopressors and vasopressin, the administration of angiotensin II is associated with a 45% absolute increase in MAP response when compared to placebo. It has subsequently been approved for the treatment of refractory vasodilatory shock. Angiotensin II is a naturally occurring hormone secreted as part of the renin‐angiotensin system that results in powerful systemic vasoconstriction. Angiotensin II is contraindicated in patients on ACE inhibitors. Nitric oxide synthase inhibitor 546C88 increased blood pressure in patients with septic shock but was associated with more frequent cardiovascular side effects and increased 28‐day mortality (choice A). Fludrocortisone when used in conjunction with hydrocortisone has been demonstrated in the APROCCHSS trial to reduce mortality; however, it did not show an increase in MAP and subsequent trials questioned fludrocortisone's efficacy (choice C). Vitamin C has been shown to decrease organ dysfunction and mortality when administered early in combination with hydrocortisone and thiamine for patients with septic shock; however, it has not been shown to directly increase MAP (choice D). Hypertonic saline would increase intravascular volume, but would have no benefit in a patient who has been adequately resuscitated (choice E).Answer: BKhanna A, English SW, Wang XS, et al. Angiotensin II for the treatment of vasodilatory shock. N Engl J Med. 2017; 377(5):419–430. doi: https://doi.org/10.1056/NEJMoa1704154. Epub 2017 May 21. PMID: 28528561.López A, Lorente JA, Steingrub J, et al. Multiple‐center, randomized, placebo‐controlled, double‐blind study of the nitric oxide synthase inhibitor 546C88: effect on survival in patients with septic shock. Crit Care Med. 2004; 32:21–30.Annane D, Renault A, Brun‐Buisson C, et al. Hydrocortisone plus fludrocortisone for adults with septic shock. N Engl J Med. 2018; 378(9):809–818. doi: https://doi.org/10.1056/NEJMoa1705716. PMID: 29490185.Marik PE, Khangoora V, Rivera R, et al. Hydrocortisone, vitamin C, and thiamine for the treatment of severe sepsis and septic shock: a retrospective before‐after study. Chest. 2017; 151(6):1229–1238. doi: