A 45-year-old woman with type 2 diabetes mellitus is hospitalized due to fever, chills, dysuria, flank pain, and lethargy. Temperature is 39.8 C (103.6 F), blood pressure is 86/42 mm Hg, and pulse is 118/min. Left costovertebral angle tenderness is present, and urinalysis reveals pyuria and bacteriuria. Urine and blood cultures are obtained, and intravenous fluids and empiric antibiotics are administered. Due to persistent hypotension, the patient requires norepinephrine therapy and is admitted to the intensive care unit. Two days later, the hypotension resolves, and the norepinephrine is tapered off. The patient's fever gradually improves, and the antibiotics are adjusted based on culture and sensitivity results. Repeat physical examination reveals discoloration in all the extremities as shown in the exhibit. Which of the following is the most likely underlying cause of the findings seen in this patient?
This patient with type 2 diabetes mellitus had acute pyelonephritis (eg, fever/chills, flank pain/costovertebral angle tenderness, pyuria/bacteriuria) complicated by septic shock. A type of distributive shock, septic shock is characterized by peripheral vasodilation that can lead to profound hypotension. As a result, vasopressors, which increase systemic vascular resistance, are often necessary following fluid resuscitation to restore adequate mean arterial pressure (MAP).
Norepinephrine, a first-line vasopressor for treatment of septic shock, acts on both alpha-1 and beta-1 adrenergic receptors, and its alpha-1 agonist properties produce potent vasoconstriction. This vasoconstriction increases MAP to provide circulation to critical organs (eg, brain); however, it also decreases perfusion to peripheral structures such as the distal digits. The resulting digital ischemia, which is typically bilateral and symmetric, can lead to tissue necrosis (eg, dry gangrene) if prolonged, as seen in this patient.
In a similar fashion, vasopressor-induced vasoconstriction can negatively impact the intestines (causing mesenteric ischemia) and/or kidneys (causing renal failure).
(Choice A) Endocarditis can spread septic emboli throughout the body but would not be expected to symmetrically affect all the extremities.
(Choice B) Some patients may form heparin-platelet factor 4 antibodies after receiving heparin, even at low doses (eg, as with thromboprophylaxis). Subsequent antibody activation of platelets can cause thrombosis; however, thrombosis is more commonly venous than arterial, and arterial thrombosis is not typically bilateral and symmetric. In addition, symptoms typically develop 5-10 days after heparin exposure.
(Choice D) Necrotizing infection of myofascia (ie, necrotizing fasciitis) can cause skin color changes (due to underlying soft tissue infection) and systemic toxicity (eg, fever, hypotension). However, the skin and soft tissue involvement is not typically bilateral and symmetric and would likely be rapidly progressive in the absence of surgical debridement.
(Choice E) Rupture of atherosclerotic plaques can form cholesterol emboli that may lodge within the distal peripheral vasculature, causing digital ischemia (eg, blue toe syndrome). However, bilateral and symmetrical involvement would be unusual.
Educational objective:
Vasopressors (eg, norepinephrine), which cause profound vasoconstriction, can also cause ischemia of peripheral structures such as the distal digits. The resulting digital tissue necrosis is usually bilateral and symmetric.