Grand Rounds

Man, 32, With Severe Scrotal Pain and Swelling

Clinician Reviews. 2017 September;27(9):34-39

References

1. Norton KS, Johnson LW, Perry T, et al. Management of Fournier’s gangrene: an eleven-year retrospective analysis of early recognition, diagnosis, and treatment. Am Surg. 2002;68(8):709-713.
2. Agostini T, Mori F, Perello R, et al. Successful combined approach to a severe Fournier’s gangrene. Indian J Plast Surg. 2014;47(1):132-136.
3. Cabrera G, March P. Fournier’s gangrene. Glendale, CA: Cinahl Information Systems; 2016.
4. Czymek R, Kujath P, Bruch HP, et al. Treatment, outcome and quality of life after Fournier’s gangrene: a multicentre study. Colorectal Dis. 2013;15(12):1529-1536.
5. Sugihara T, Yasunaga H, Horiguchi H, et al. Impact of surgical intervention timing on the case fatality rate for Fournier’s gangrene: an analysis of 379 cases. BJU Int. 2012;110(11c):E1096-1100.
6. Tuncel A, Keten T, Aslan Y, et al. Comparison of different scoring systems for outcome prediction in patients with Fournier’s gangrene: experience with 50 patients. Scand J Urol. 2014;48(4):393-399.
7. Taken K, Oncu MR, Ergun M, et al. Fournier’s gangrene: causes, presentation and survival of sixty-five patients. Pak J Med Sci. 2016;32(3):746-750.
8. Palvolgyi R, Kaji AH, Valeriano J, et al. Fournier’s gangrene: a model for early prediction. Am Surg. 2014;80(10):926-931.
9. Pais V, Santora T. Fournier gangrene. http://emedicine.medscape.com/article/2028899-overview. Accessed August 16, 2017.
10. Cottrill RR. A demonstration of clinical reasoning through a case of scrotal infection. Urol Nurs. 2013;33(1):33-37.
11. Summers A. Fournier’s gangrene. J Nurse Pract. 2014;10(8):582-587.
12. Miller LG, Perdreau-Remington F, Rieg G, et al. Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureus in Los Angeles. N Engl J Med. 2005;352(14):1445-1453.
13. Gupta N, Zinn K, Bansal I, Weinstein R. Fournier’s gangrene: ultrasound or computed tomography? A letter to the editor. Med Ultrason. 2014;16(4):389-390.
14. Bjurlin MA, O’Grady T, Kim DY, et al. Causative pathogens, antibiotic sensitivity, resistance patterns, and severity in a contemporary series of Fournier’s gangrene. Urol. 2013;81(4):752-758.
15. Goh T, Goh LG. Pitfalls in diagnosing necrotizing fasciitis. https://psnet.ahrq.gov/webmm/case/329/pitfalls-in-diagnos ing-necrotizing-fasciitis. Accessed August 16, 2017.
16. Kale P, Dhawan B. The changing face of community-acquired methicillin-resistant Staphylococcus aureus. Indian J Med Microbiol. 2016;34(3):275-285.
17. CDC. Necrotizing fasciitis. www.cdc.gov/Features/NecrotizingFasciitis/index.html. Accessed August 16, 2017.
18. Barnes BE, Sampson DA. A literature review on community-acquired methicillin-resistant Staphylococcus aureus in the United States: clinical information for primary care nurse practitioners. J Am Acad Nurse Pract. 2011;23(1):23-32.
19. Madjid M, Vela D, Khalili-Tabrizi H, et al. Systemic infections cause exaggerated local inflammation in atherosclerotic coronary arteries. Clues to the triggering effect of acute infections on acute coronary syndromes. Tex Heart Inst J. 2007;34(1):11-18.
20. Devereaux PJ, Chan MTV, Alonso-Coello PA, et al; VISION Study Investigators. Association between postoperative troponin levels and 30-day mortality among patients undergoing noncardiac surgery. JAMA. 2012;307(21):2295-2304.
21. Corrales-Medina VF, Fatemi O, Serpa J, et al. The association between Staphylococcus aureus bacteremia and acute myocardial infarction. Scand J Infect Dis. 2009;41(6-7):511-514.
22. Romero-Bermejo FJ, Ruiz-Bailen M, Gil-Cebrian J, Huertos-Ranchal MJ. Sepsis-induced cardiomyopathy. Curr Cardiol Rev. 2011;7(3):163-183.
23. Smilowitz NR, Gupta N, Guo Y, Bangalore S. Comparison of outcomes of patients with sepsis with versus without acute myocardial infarction and comparison of invasive versus noninvasive management of the patients with infarction. Am J Cardiol. 2016;117(7):1065-1071.
24. Mattson M. Sepsis and cardiac disease: improving outcomes through recognition and management. Prog Cardiovasc Nurs. 2009;24(4):199-201.
25. Papadakis MA, McPhee SJ. Current Medical Diagnosis & Treatment. 54th ed. New York, NY: McGraw Hill Education; 2015:137-138, 151-152, 937.
26. Eyre RC. Evaluation of the acute scrotum in adults. www.uptodate.com/contents/evaluation-of-the-acute-scrotum-in-adults. Accessed August 16, 2017.

Etiology

About 83% of FG cases are polymicrobial infections comprised of enterobacter, enterococci, Escherichia coli, group A streptococci, pseudomonas, and clostridium, with symptoms evolving two to four days following the initial insult.^4,7,11,14,15 Monomicrobial infections are much less common, but the symptoms progress even more rapidly.¹⁵ Methicillin-resistant Staphylococcus aureus (MRSA) necrotizing fasciitis infections occur in about 3% of monomicrobial cases.¹² MRSA emerged in the early 2000s as an additional causative pathogen for polymicrobial necrotizing fasciitis infections.^12,14,15 Prior to that time, S aureus strains were almost uniformly susceptible to penicillinase-resistant ß lactams.¹²

A distinction should be made between health care-associated (HA) MRSA and community-acquired (CA) MRSA due to treatment considerations. HA-MRSA infections are contracted through previous health care exposure (within the past year) and are less resistant to treatment.^16,17 In contrast, CA-MRSA, which comprises 29% of MRSA cases, causes infections in previously healthy young patients without prior health care contact within the past year.¹⁶ CA-MRSA strains are more robust than HA-MRSA strains and can cause sepsis and other invasive, rapidly progressive, and possibly life-threatening infections due to the amount of tissue destruction and necrosis.^16,18 Transmission of CA-MRSA is often associated with crowded environments, frequent skin-to-skin contact, compromised skin integrity, contaminated items or surfaces, and lack of cleanliness.¹⁶ Over the years, CA-MRSA has developed resistance to multiple antimicrobials; providers should therefore consider CA-MRSA on initial evaluation of necrotizing infections, to ensure appropriate initiation of treatment.^12,16

CASE CONTINUED

Extensive debridement was completed down to healthy tissue in all affected areas (see Figure 1b). The necrotizing fasciitis had spared the left testicle and spermatic cord, and a colostomy was not required.

The patient’s initial postoperative vital signs were unremarkable, except for his BP (86/54 mm Hg). The patient was taken postoperatively to the surgical intensive care unit (SICU) with the diagnosis of FG. Aggressive IV fluids were administered for resuscitation, and he was closely monitored for increasing sepsis. Metronidazole was added for anaerobic and gram-positive coverage. His postoperative lab results can also be found in Table 1.

His ECG showed a normal sinus rhythm without ST changes, and he denied any cardiac symptoms. His physical exam was significant for mild pallor, dry mucus membranes, and a left scrotal and pelvic packed dressing. He was given two units of packed red blood cells for acute postoperative blood-loss anemia. The preliminary tissue culture results showed gram-positive cocci consistent with a staphylococcal infection; his antibiotics were then changed to IV ampicillin/sulbactam and clindamycin.

Approximately five hours postoperatively, an ECG suddenly showed acute ST elevation in leads II, II, and aVF, with reciprocal changes. The patient was diagnosed with an acute myocardial infarction (AMI). He denied any chest pain, shortness of breath, or diaphoresis. The SICU team initiated aspirin therapy and immediately contacted cardiology for an emergent coronary angiogram.

The angiogram and cardiac catheterization revealed an elevated left ventricular end diastolic (LVED) volume, inferior wall hypokinesis, a low-normal ejection fraction, and a 30% lesion in the first diagonal of his left anterior descending artery. A postprocedure echocardiogram demonstrated left ventricular (LV) ejection fraction of 50%, with LV hypokinesis in the inferior base and mild left atrial enlargement. The patient was started on metoprolol for myocardial protection and recovery.

Complications

Perioperative complications of FG, including AMI, must be considered due to the physiologic stress on the body.¹⁹ Most patients with perioperative AMI after noncardiac surgery do not experience ischemic symptoms.²⁰

Growing evidence suggests the pivotal role of acute inflammation (postoperatively or from infection) as a precipitating event in AMI.^20,21 Chemical mediators, such as inflammatory cytokines, endotoxins, and nitric oxide, may play a role in the development of an AMI.²²

If cardiovascular disease and/or significant cardiovascular risk factors (ie, older age, male, cigarette smoking, cardiac family history, acute kidney injury) are present, the risk for AMI increases in the first two days following surgery.^21,23 Acute infections and sepsis also initiate or increase systemic inflammatory activity via these same chemical mediators.²¹

Most suspected infectious agents also produce coronary artery sheer stress and destabilization of vulnerable plaques, leading to plaque rupture and thrombosis.^19,24 Proinflammatory cytokines promote enhanced platelet activation and contribute to this thrombotic environment.^21,23 Thrombus leads to obstructed coronary blood flow, myocardial ischemia, and finally, infarction.²¹

A reversible myocardial depression, cardiomyopathy, or myocardial ischemia may occur in patients with acute systemic infection or sepsis when the myocardium is functionally and structurally injured by these inflammatory chemical mediators.^19,22-24 Characteristics of such a cardiomyopathy include left ventricle dilation with a low filling pressure, an abnormal increase in LVED volume, and a depressed ejection fraction.²²

An acute infectious or septic process can raise troponin levels in 43% to 85% of patients.^22,24 Troponin biomarkers can assist in predicting myocardial injury and events after surgery with nearly absolute myocardial tissue specificity.²⁰ Cardiovascular involvement caused by myocardial injury–related sepsis is observed in up to 70% of patients in the ICU for these reasons.²³ Therefore, providers should consider measuring troponin biomarkers during such infectious and septic processes, as this team did for the case patient. The providers were able to diagnose his AMI early and institute appropriate treatment measures to avoid extensive myocardial tissue damage.

Several studies have already demonstrated a correlation between pneumococcal pneumonia and an increased risk for AMI, and the same mechanisms are presumed responsible for any severe acute infectious state.²¹ More research is needed to understand the pathophysiology of AMI in sepsis and acute systemic infections.²³

References

Hypogonadism after testicular cancer treatment can have lifelong impact

Man, 32, With Severe Scrotal Pain and Swelling

References

Etiology

CASE CONTINUED

Complications

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