A case report of toxic shock syndrome in a patient with underlying chronic liver disease associated with multiple satellite abscesses in elbow, perinephric region, psoas, and neck


Toxic shock syndrome is an acute febrile illness, which leads to multi-organ dysfunction and has a high mortality and morbidity. We report a case of toxic shock syndrome in a patient with underlying chronic liver disease associated with multiple satellite abscesses in elbow, peri-nephric region, psoas and neck.

Keywords: Chronic liver disease, peri-nephric region, Staphylococcus aureus, superantigen, toxic shock syndrome

How to cite this article:
Nandwani S, Pande A, Saluja M. A case report of toxic shock syndrome in a patient with underlying chronic liver disease associated with multiple satellite abscesses in elbow, perinephric region, psoas, and neck. Ann Trop Med Public Health 2013;6:358-60


How to cite this URL:
Nandwani S, Pande A, Saluja M. A case report of toxic shock syndrome in a patient with underlying chronic liver disease associated with multiple satellite abscesses in elbow, perinephric region, psoas, and neck. Ann Trop Med Public Health [serial online] 2013 [cited 2020 Aug 3];6:358-60. Available from: https://www.atmph.org/text.asp?2013/6/3/358/121009



Although classically associated with tampon use, toxic shock syndrome is also known to be associated with a variety of non-menstrual related conditions. [1] A 40-year-old patient presented to the hospital with complaints of high grade fever (102°F) and progressively increasing breathlessness since 3 days and decreased urinary output since one day. Patient was not known to have any underlying chronic illness and had no habits like smoking, alcohol or any addiction. The patient was hypotensive with a B.P. = 80/60 mm of Hg, RR = 40/min, HR=140/min, SPO 2 =90% and bilateral basal crepitations were present on chest examination. Abdominal examination revealed ascites and generalized tenderness. Patient had a pus discharge from a wound following trivial injury on the right elbow for which open arthroplasty was done. There was a boggy swelling of 2 cm × 2 cm on the right side of the neck from which pus was aspirated and sent for culture. Blood and urine cultures were sent along with the routine investigations, which showed pancytopenia (Hb = 8gm %, TLC 3500/mm 3 , Platelet count 60,000/mm 3 ), random blood glucose = 413 mg/dl,urine ketones = -ve, BUN = 162 mg/dl, Sr. creatinine = 2.7 mg/dl, Sr. Bilirubin = 2.7 mg/dl predominantly direct, hypo­albuminemia with reversal of A:G ratio, SGOT = 73 u/l, SGPT = 24u/l, and SALP = 1310 U/l (13 times the normal, PT = 25.6sec with control 12.5 sec. ABG showed severe metabolic acidosis,blood and urine cultures were negative, pus culture grew Staphylococcus aureus (MSSA) which was sensitive to piperacillin, amoxycillin, oxcallin, clindamycin, linezolid, vancomycin. Abdominal ultrasound revealed a nodular liver with features consistent with chronic liver disease, portal hypertension, ascites (diagnostic tapping = transudate, cultures negative,

ADA = 7U/L). An upper GI endoscopy showed Grade 2 esophageal varicies. Considering a very high value of Serum alkaline phosphatase and negative reports of HAV, HBV, HCV and HIV, a CECT abdomen was done which revealed a peri-nephric abscess on the right side [Figure 1]a and a psoas abscess on the left side.In view of multi organ dysfunction syndrome (MODS) and underlying chronic liver disease (CLD) an exploratory laparotomy was not done and the patient was conservatively managed using piperacillin,tazobactum, clindamycin and linezolid. A repeat CECT abdomen after 60 days of in-hospital treatment showed complete resolution of the peri-nephric [Figure 1]b and psoas abscess and the patient fully recovered. The patient is still under evaluation for the cause of CLD.

Figure 1: (a) A CECT abdomen showing right sided peri-nephric abscess (b) A CECT abdomen 2 months later shows resolution of the peri-nephric abscess

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Toxic shock syndrome was first coined in 1978 by Todd et al., [2] who reported the symptom complex in a group of 7 children aged 8 to 17 years with an acute febrile illness. It is a potentially fatal multisystem disorder associated with fever, hypotension, myalgia, vomiting, diarrhea, mucosal hyperemia and an erythematous rash that desquamates subsequently during convalence. This is also associated with infection of mucosal or sequestered sites by toxic shock syndrome toxin (TSST)- producing Staphylococcus aureus strains usually belonging to bacteriophage group 1 (TSST-1). Staphylococcus enterotoxins and TSST-1 are superantigens which are potent activators of T Lymphocytes. [3] The term “superantigen” was adopted to describe the ability of these toxins to cause a remarkable expansion of T lymphocytes displaying specific b chain variable regions of the T-cell antigen receptor. [4] Superantigens bypass normal antigen presentation and can stimulate over 20% of all T cells, whereas a conventional antigen stimulates only in the order of 1 in 10,000 T cells. The remarkable feature of superantigen activity is the expansion of lymphocyte populations bearing the particular Vβ chains that bind the superantigen. In the case of TSST-1, this is Vβ2.Being Vβ restricted T cell mitogen, these superantigens stimulate a very large number of T cells without any relation to their epitope specificity. [5]

Diagnosis of TSS still depends on a constellation of findings rather than one specific finding

Case Definition

Case definition of staphylococcusaureus toxic shock syndrome

  1. Fever: temperature of 38.9°C (102°F).
  2. Hypotension: Systolic blood pressure of 90 mmHg, or orthostatic hypotension. (orthostatic drop in diastolic blood pressure by 15 mmHg, orthostatic syncope, or orthostatic dizziness)
  3. Diffuse macular rash with subsequent desquamation in 1- 2 weeks after onset (including the palms and soles).
  4. Multisystem involvement (3 or more of the following):
    1. Hepatic: Bilirubin or aminotransferase levels 2 times normal.
    2. Hematologic: Platelet count 100,000/L.
    3. Renal: Blood urea nitrogen or serum creatinine level 2 times the normal upper limit.
    4. Mucous membranes: Vaginal, oropharyngeal, or conjunctival hyperemia.
    5. Gastrointestinal: Vomiting or diarrhea at onset of illness.
    6. Muscular: Severe myalgias or serum creatinine phosphokinase level 2 times the upper limit.
    7. Central nervous system: Disorientation or alteration in consciousness without focal neurologic signs and in the absence of fever and hypotension.
  5. Negative serologic or other tests for measles, leptospirosis, and Rocky Mountain spotted fever as well as negative blood or cerebrospinal fluid cultures for organisms other than Staphylococcus aureus.

Case classification

Probable:A case with 5 of the 6 clinical findings above.

Confirmed:A case with all 6 of the findings described above, including desquamation, unless the patient dies before desquamation can occur. [6]


In India the incidence of Staphylococcus infection is high. Staphylococcus TSS has been usually associated with tampon use. The present case is of a male patient who had an undiagnosed chronic liver disease in whom a trivial injury to the elbow lead to absess formation along with multiple satellite abscesses in neck,psoas and kidney which responded to conservative management with appropriate antibiotics.Since such a presentation is common with other diseases like dengue, leptospira, malaria etc, TSS shoud be kept as a possible differential diagnosis in patients presenting with similar features.


The present case report is an original work conducted at the Subharti Institute of Medical Sciences, Subhartipuram, Meerut, India. There is no funding agency for this work and approval is taken from the ethical committee of the institute for the case report.



1. Herzer CM. Toxic shock syndrome: Broadening the differential diagnosis. J Am Board Fam Pract 2001;14:131-6.
2. Todd J, Fishaut M, Kapral F, Welch T. Toxic-shock ­syndrome associated with phage-group 1 Staphylococci. Lancet 1978;2:1116-8.
3. Ananthanarayan R, Paniker CKJ.Textbook of microbiology. 6 th ed. Hyderabad: Orient Longman Private Limited; 2002. p. 182.
4. White J, Herman A, Pullen AM, Kubo R, Kappler JW, Marrack P. The V-beta Specific superantigen staphylococcal enterotoxin B: Stimulation of mature T Cells and clonal deletion in neonatal mice. Cell 1989;56:27-35.
5. Llewelyn M, Cohen J. Superantigens: Microbial agents that corrupt immunity.Lancet Infect Dis 2002;2:156-62.
6. M Wharton et al.: Case definitions for public health surveillance. MMWR 39:1, 1990.

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.121009


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