Septic Shock in an Elderly Patient With Gout and Toe Pain

Peter Gibbs, DO, and Dean Gianakos, MD, FACP

In elderly patients, soft-tissue infections can be devastating. What initially appears as a superficial skin ulcer or a simple furuncle can, under certain circumstances, rapidly progress to life-threatening myositis or necrotizing fasciitis. Prompt treatment with broad-spectrum antibiotics and surgical drainage of abscesses are required in any patient who shows early signs of severe illness or sepsis.1 The problem is that many of these patients initially appear less ill than they really are, and the physical findings do not substantiate the level of pain that is being reported.2,3 Therefore, multiple, careful evaluations and close monitoring are critical to ensuring the appropriate treatment of these patients.

Case Presentation

A 67-year-old, morbidly obese, white woman with a history of gout, hypertension, type 2 diabetes mellitus, and hypothyroidism presented to the emergency department (ED) with a 3-day history of fever, shortness of breath, sore throat, and diarrhea. She also reported pain in her right great toe, which she said was her most bothersome symptom. The pain had been present for months, but it had started to feel worse in the last 3 to 4 days. The patient had seen her primary care physician for her toe pain 1 month earlier, at which time the pain was mild, and was told that the pain was probably related to her chronic gout. No treatment regimen was prescribed at that time. During the physical examination, the patient was in mild distress, and her right toe was swollen and erythematous, with minimal drainage from the plantar surface. The patient had a temperature of 101.6°F, blood pressure of 103/63 mm Hg, pulse of 93 beats per minute, and O2 saturation of 94% on room air. She rated her pain at 9 out of 10 on a comparative pain scale. Because the toe was incised, with very little drainage, the ED physician was not sure that the toe was the source of her fever, and he considered deferring antibiotic administration. Initial Gram stain revealed many gram-positive cocci. The patient’s white blood cell count at the time of presentation was 20,600/µL with 79% neutrophils and 17% bands. Serum chemistries were remarkable for a potassium of 3.2 mEq/L, glucose of 180 mg/dL, creatinine of 1.9 mg/dL, and glomerular filtration rate estimated at 27 mL/min/1.73m2. The patient’s thyroid-stimulating hormone level was 6.83 mIU/L with a normal free thyroxine level. A catheterized urine sample that was collected for analysis demonstrated a hazy appearance, trace protein, small leukocyte esterase, and two hyaline casts. An influenza swab test and a rapid strep assay were both negative for respiratory pathogens, with cultures pending, and chest radiography was normal. An x-ray of the patient’s right foot did not show any acute bone abnormality of the great toe or soft-tissue gas. Intravenous fluids, piperacillin/tazobactam, and vancomycin were initiated. The next morning, the patient reported severe pain in her right toe and foot. On examination, she was found to be in mild respiratory distress. Her blood pressure was 85/60 mm Hg. An examination of her lungs revealed bibasilar rales. An examination of her right toe revealed a drainage of pus from the plantar surface. Arterial blood gas levels were as follows: pH, 7.2; PCO2, 42.1 mm Hg; PO2, 74 mm Hg; HCO3, 16.9 mEq/L; and O2 saturation of 91% on 5 liters of oxygen. A throat culture demonstrated group A beta-hemolytic streptococci. The toe wound culture grew the same organism. Blood cultures were negative. Intensivists were consulted to manage the patient’s septic shock, pulmonary edema, and acute renal failure.


Changes in skin texture and immunity, underlying skin conditions (eczema and venous stasis), and comorbid diseases (eg, diabetes mellitus) place older adults at a higher risk for soft-tissue infections.4-6 Pathogen virulence is also a major factor; even previously healthy young adults can be overwhelmed by severe infection caused by group A beta-hemolytic streptococci.7 Staphylococcus aureus, particularly methicillin-resistant S. aureus, is the most common cause of skin and soft-tissue infections.1 Other significant organisms include group A beta-hemolytic streptococci, Clostridium perfringens, and other anaerobes. In the case patient, group A beta-hemolytic streptococci were identified. This organism can produce a myriad of dermatological and systemic presentations.8

Beginning at the dermal layer, group A beta-hemolytic streptococci may cause erysipelas, which is characterized by several specific signs; for example, lesions are usually raised and well delineated from surrounding, noninfected tissue. The skin appears bright and salmon-colored. Streptococcal cellulitis, on the other hand, usually does not have the above-mentioned characteristics, and often spreads into the subcutaneous tissues.8 Necrotizing fasciitis is an infection that involves deeper subcutaneous tissue or fascia. Initially described in 1924 as “hemolytic streptococcal gangrene,” necrotizing fasciitis originates from an area of mild erythema, and then develops progressively over the next 24 to 72 hours into severe inflammation of subcutaneous fascia, giving the skin a purple appearance.8 Ecchymoses and bullae may also develop, as well as necrosis and skin sloughing.

Despite advancements in medicine and radiographic imaging, mortality from this condition remains at 20% or higher today.8 Even patients who survive necrotizing fasciitis have an increased risk of death due to infections such as pneumonia and pyelonephritis.9 Myositis or myonecrosis is another serious complication of group A beta-hemolytic streptococci. Following nonpenetrating trauma to muscle, bacteria from the throat can travel hematogenously to the injured muscle, causing intense infection and inflammation. If severe, compartment syndrome may also develop at the site. Mortality from myonecrosis may be as high as 80%.8 This condition can be difficult to distinguish from necrotizing fasciitis; distinction requires surgical exploration.8,10 When a group A beta-hemolytic streptococci soft-tissue or skin infection overwhelms the body’s immune system, streptococcal toxic shock syndrome (STSS) may also develop.5 STSS is any known streptococcal infection that results in shock and organ failure. Immunocompromised states, such as poorly controlled diabetes mellitus and malignancy, predispose patients to this systemic response to localized infection. Management of STSS includes aggressive fluid resuscitation to maintain a mean arterial pressure of more than 60 mm Hg and the early administration of antibiotics. Early control and elimination of the infection source is necessary to hinder progression of the infection. Therefore, immediate surgical debridement and exploration of a suspected infection site is critical.10,11

The use of computed tomography or magnetic resonance imaging scans is limited in diagnosing the extent and progression of infection since group A beta-hemolytic streptococci do not form gas or frank abscesses. Optimal treatment of known group A beta-hemolytic streptococci includes high-dose penicillin and clindamycin.3 Although there are some reports of resistance to clindamycin, it demonstrates unique antibiotic properties against streptococci, including suppression of exotoxin and M protein production, and an increased half-life. Clindamycin also does not antagonize the effects of penicillin.8,12 Patients should be carefully monitored for the need for cardiovascular, respiratory, and renal support. The incidence of acute respiratory distress syndrome has been reported in 55% of patients.8 It is not unusual for these patients to need intubation and ventilatory support. Also, approximately 50% of patients will develop acute renal failure that will require dialysis.8 Intractable hypotension may require high doses of pressor agents such as norepinephrine.8

Outcome of the Case

The patient was treated for STSS, which presumably developed from a superficial, group A beta-hemolytic streptococcal toe infection. It is also possible that group A beta-hemolytic streptococci from the patient’s throat hematogenously seeded a chronically inflamed, gouty toe. The day after admission, the patient’s antibiotics were switched to penicillin and clindamycin. The patient’s great right toe was surgically explored, and no evidence of abscess or necrotizing fasciitis was found. After a 1-month hospitalization that included the use of ventilator support, pressors, and hemodialysis, the patient returned to her baseline health. She was transferred to a rehabilitation facility for physical therapy and general reconditioning prior to returning home. She was recently seen for a follow-up visit and was found to be doing quite well.


Elderly patients are at increased risk of overwhelming skin and soft-tissue infections caused by group A beta-hemolytic streptococci. A patient’s report of skin or soft-tissue pain may be significantly greater than what is evident on physical examination. Therefore, frequent monitoring and re-examination of these patients are required. Patients who develop STSS require aggressive fluid resuscitation, antibiotics (penicillin and clindamycin), pressor agents to support blood pressure, and early surgical exploration and debridement of the infectious site.

The authors report no relevant financial relationships.

Dr. Gibbs is a Resident, and Dr. Gianakos is Associate Director, Lynchburg Family Medicine Residency, Lynchburg, VA.


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