Archives of Gynecology and Obstetrics

, Volume 277, Issue 6, pp 579–581

Necrotizing fasciitis after cesarean section


    • Intensive Care DepartmentUniversitary Marques de Valdecilla Hospital
  • J. Carlos Rodriguez-Borregan
    • Intensive Care DepartmentUniversitary Marques de Valdecilla Hospital
  • Tomas Obeso
    • Intensive Care DepartmentUniversitary Marques de Valdecilla Hospital
  • Alvaro Castellanos
    • Intensive Care DepartmentUniversitary Marques de Valdecilla Hospital
  • Amelia Perez-Ceballos
    • Intensive Care DepartmentUniversitary Marques de Valdecilla Hospital
  • José Ramón de Miguel Sesmero
    • Gynecology and Obstetrics DepartmentHospital Marqués de Valdecilla
Case Report

DOI: 10.1007/s00404-007-0509-z

Cite this article as:
Castro, A.G., Rodriguez-Borregan, J.C., Obeso, T. et al. Arch Gynecol Obstet (2008) 277: 579. doi:10.1007/s00404-007-0509-z


We report a case of monomicrobial necrotizing fasciitis affecting a healthy woman after caesarean section. On day 1 post-partum she started taking a non-steroidal anti-inflammatory drug. The patient developed an acute fulminant infection and died from sepsis. The causative bacterium was Streptococcus pyogenes.


Necrotizing fasciitisCesareanNon-steroidal anti-inflammatory


The term necrotizing fasciitis (NF) was first used by Wilson in 1952 to describe necrosis of the fascia and subcutaneous tissue with relative sparing of the underlying muscle [1]. Fortunately, NF is rare. Mortality rates for necrotizing soft-tissue infections can reach 76% [2]. Most patients who develop NF have pre-existing conditions that render them susceptible to infection (advanced age, chronic renal failure, peripheral vascular disease, diabetes mellitus…) [3]. The symptoms of NF may initially be non-specific, and certain diagnostic signs that we have come to associate with NF are not always present. Having established the diagnosis, treatment should be instituted immediately [4].

We report a rare case of post-caesarean NF. The patient developed an acute fulminant infection and died from sepsis. The causative bacterium was Streptococcus pyogenes.

Case report

A 34-year-old woman, at 41 weeks’ gestation, presented with a 5-day history of dysuria and fever. Her medical history was unremarkable except for penicillin allergy. She had mild fever (37.7°C), a heart rate of 119 beats per minute with normal peripheral pulses, and a blood pressure of 95/65 mmHg. Blood and urine cultures were negative on admission and she had a normal white cell count. She was not in labour, but emergency caesarean section was performed due to the presence of foetal tachycardia and type II dips or late decelerations of the foetal heart rate. The antibiotic prophylaxis used was erythromycin. (Erythromycin 1 g IV, as a single dose).

The newborn infant presented an Apgar score of 8/9/9 (first, fifth and tenth minutes) and was admitted to the low-risk neonatal observation unit. The white cell count was 18,300, with a blood pH of 7.40 and a C reactive protein (CRP) of 18.3 mg/dl.

The patient was asymptomatic on the first day after delivery, with a blood pressure of 90/60 mmHg, a heart rate of 90 beats per minute, and normal pulses. On day 1 post-partum, she started taking a non-steroidal anti-inflammatory drug (NSAID) for non-specific abdominal pain. On day 2 post-partum, she developed fever associated with tachycardia of 156 beats per minute, a blood pressure of 85/50 mmHg, and a respiratory rate of 28 breaths per minute. Physical examination revealed erythema, tenderness, oedema and induration of the skin of the abdominal wall in the area of the incision. At that time, the white cell count was 1,400/μl, and there were signs of renal impairment (creatinine 1.7 mg/dl) and early disseminated intravascular coagulation, with a CRP of 36.9 mg/dl and a serum pH of 7.24.

She was transferred to the intensive care unit (ICU). On arrival she was distressed, had poor peripheral perfusion, a pulse rate of 150 beats/min, and a blood pressure of 75/45 mmHg. She was oliguric. The blood tests on admission to the ICU revealed a white cell count of 2,000/μl, creatinine 2.32 mg/dl, CRP 22.8 mg/dl, and procalcitonin >10 ng/ml.

Treatment was started with intravenous fluids, aztreonam, and ciprofloxacin. However, the hypotension and the signs of sepsis persisted and the patient required intubation for shock and respiratory failure. Arterial blood gases prior to intubation revealed a pH of 7.10, pCO2 of 26 mmHg and pO2 of 64 mmHg.

At this time, after examination, debridement was performed of an extensive area of necrosis of the fascia of the abdominal wall in the area of the incision. Both the surgical specimens and the blood cultures grew Streptococcus pyogenes serotype A.

In refractory and irreversible shock, the patient presented a sudden episode of cardiorespiratory arrest and died two hours later.

The diagnosis of NF was confirmed in the autopsy study.


The exact incidence of NF is unknown; fortunately it is uncommon. However, it is often a fulminant infection involving extensive areas of soft tissue necrosis.

NF can affect any part of the body, but the limbs, perineum and abdominal wall are the sites most commonly involved [4]. In our case, the region affected was the area of the incision in the abdominal wall for caesarean section. Exceptionally NF can affect the head and neck region, being of odontogenic origin in this case [5, 6].

The triggering event is usually a minor penetrating injury or a surgical wound. Approximately 20% are post-operative infections [7, 8].

Group A streptococcus is the most common monomicrobial bacterial isolate, as in this case, though, overall, polymicrobial infection with a variety of Gram-positive, Gram-negative, aerobic, and anaerobic bacteria is more common [8].

With regard to the antibiotic prophylaxis administered, it is known that S. pyogenes has a mechanism of resistance to the macrolides that is acquired via plasmids and transposons bearing one of the erm (erythromycin ribosomal methylase) genes. In our country, as in many other regions throughout the world, the strains of S. pyogenes are almost uniformly sensitive to all the macrolides. The frequency of resistance to erythromycin in the late eighties and early nineties was in the range 0–3%. However, numerous studies performed in different regions of Spain during the nineties provided evidence of a significant increase in the resistance of S. pyogenes to erythromycin, principally in strains with the M phenotype. The majority of resistant strains belong to a few clones, or even to the same clone. The M phenotype is characterised by sensitivity to clindamycin and resistance to erythromycin. There is no evidence that a single dose of erythromycin is responsible for bacterial selection.

The aetiology of NF is not fully understood, and sometimes no individual factor can be found [4]; the major risk factors are summarised in Table 1. Diabetes mellitus, age over 50 years, and peripheral vascular disease are the most common factors and appear to be associated with even greater morbidity and a higher mortality [8, 9]. None of these risk factors was present in our case. Similarly, Goepfert and cols., in a series of nine patients with NF after caesarean section, showed that none of the women had any of these three predisposing factors [10].
Table 1

Predisposing factors for necrotizing fasciitis

Comorbid conditions



Chronic disease

Drugs—for example, steroids


Age > 60

Intravenous drug misuse

Peripheral vascular disease

Aetiological factors

Blunt or penetrating trauma

Soft tissue infections


Intravenous drug use



Muscle injuries

Underlying malignancy


Renal failure

We would like to draw attention to the administration of an NSAID on the first day post-partum. In the literature, NF following caesarean section has occurred in a number of cases in which NSAIDs were administered in the immediate post-operative period [11, 12]. Several hypotheses regarding a possible association between NSAIDs and the onset of NF have been published in the literature. One of these is that, due to their antipyretic and anti-inflammatory properties, the NSADIs simply cause masking of the signs and symptoms of infection or sepsis, leading to a delay in the diagnosis. Another mechanism that has been postulated is an impairment of natural host defence mechanisms [12]. Proposed mechanisms for this come from in vitro studies in which non-steroidal anti-inflammatory drugs have been shown to impair granulocyte chemotaxis, phagocytosis, and bactericidal activity, which are important in early defence. Lymphocyte transformation has been shown to be depressed in vivo. However, the clinical significance of these observations is not known [13].

The use of non-steroidal anti-inflammatory drugs as the initial treatment of pain in these patients adheres to the recommendations of the pain scale of the World Health Organisation. The association of NSAIDs and NF remains controversial as this situation has only been reported in a few cases in the medical literature.

Most patients present with signs of inflammation such as erythema, swelling, and pain at the affected site. Severe pain disproportionate to local findings and associated with systemic toxicity should raise the suspicion of NF. Patients presenting at an advanced stage may show signs of systemic shock and sepsis, but these patients can often cause diagnostic difficulties as they may be confused, agitated, or even have a reduced level of consciousness [4].

Radiographic studies reveal gas on plain films in approximately 35% of cases. The use of CT or magnetic resonance imaging has reportedly been helpful is distinguishing between NF and cellulitis and may help to guide management [1416].

Once suspicion is high for NF, the patient should undergo surgical exploration and debridement. Resuscitation should be performed according to the clinical state, and intensive care support may even be required. Intravenous antibiotics should be started immediately on diagnosis and then changed according to microbiological sensitivities. The role of hyperbaric oxygen in the treatment of NF remains controversial [4].

In our opinion, we believe it is difficult to describe the case presented here as a preventable death. First, the rapid and devastating progression of NF, the diagnostic difficulty in its early stages, its association with systemic toxicity and the high mortality are well recognised [17]. Secondly, our patient did not develop evident symptoms of sepsis during the early stages of the illness. Thirdly, there was no relevant past medical history. And finally, when the signs and symptoms clearly suggested clinical sepsis, aggressive therapy was initiated to correct the course of the disease, though unfortunately without success.

Copyright information

© Springer-Verlag 2007