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Case Reports

Native Hip Septic Arthritis in the Setting of Postpartum Gynecologic Infection

A Case Report

Maier, Stephen P. II MD1,a; Wixted, John J. MD2

Author Information
doi: 10.2106/JBJS.CC.20.00979
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  • Disclosures


Septic arthritis frequently occurs secondary to bacteremia, most commonly in the setting of intravenous drug use or acute endocarditis with active seeding. Direct extension of infection or traumatic contamination of the joint space can also cause this pathology, requiring emergent pathogen evacuation with concurrent irrigation/debridement of the capsular/articular anatomy. Obstetric associations with septic arthritis have been detailed with exceptionally rare frequency1-12. This report describes a case of atraumatic septic hip arthritis in the postpartum setting without documented hematologic infection, creating a delay in identifying its source.

The patient was informed that data concerning her case would be submitted for publication, and she provided consent.

Case Report

A 34-year-old healthy gravida-3-parity-3 woman presented with right hip pain, fever, and a full-body rash. Eleven days earlier, she delivered a healthy boy through an uncomplicated, spontaneous, vaginal delivery, and she had been discharged after an uneventful postpartum stay. Four days before presentation, she experienced vaginal bleeding accompanied by shaking chills, with subsequent progressive hip pain that began as weakness/locking, culminating in a limitation of ambulatory capacity (Fig. 1). She denied recent travel, past surgeries, throat pain, respiratory symptoms/cough, tobacco/alcohol/drug use, and lived with her husband and 3 children. Notably, the patient reported that her 5-year-old son was diagnosed with streptococcal pharyngitis 5 days earlier, for which he was receiving medical treatment.

Fig. 1:
Relative timeline of symptom onset before presentation to the emergency department.

The patient spiked a high-grade fever (103°F/39.4°C) on the day of presentation, prompting evaluation at an outside hospital. Workup included plain radiographs (Fig. 2), computed tomography (CT) hip/pelvis (Table I), lower extremity noninvasive studies (Table I), and laboratory studies (including negative blood cultures before the initiation of antibiotics, Table II). Given the triad of fever, short-arc range-of-motion, pain, and elevated inflammatory markers, a CT-guided hip aspiration was performed, yielding 13 cc of purulent fluid (22,000 nucleated white blood cells and 100% polymorphonuclear leukocytes, with Gram-positive cocci). She was initiated on ampicillin/sulbactam + vancomycin and transferred to our institution for higher acuity care.

Fig. 2:
AP and frog-leg lateral views of the right hip without evidence of osseous abnormalities.
TABLE I - Imaging Collected During Evaluation and Management of the Patient's Septic Arthritis Workup*
Imaging Modality Results
XR right hip No evidence of fracture or dislocation
CT abdomen/pelvis 1. Postpartum uterus
2. No evidence of fluid collection or abscess
3. Right hip effusion
Ultrasound pelvis 1. Enlarged heterogeneous uterus c/w postpartum state
2. Endometrial thickness of 0.9 cm
3. Trace fluid and few echogenic foci in the endometrial canal, the latter which may reflect small mild gas
Lower extremity noninvasive studies (bilateral) No evidence of superficial or deep venous thrombosis of bilateral lower extremities
Transesophageal echocardiogram Normal left ventricular wall thickness, cavity size, and regional/global systolic function (EF 55%-60%). Mildly dilated right ventricular cavity with normal systolic function. Mild mitral regurgitation. No 2D echocardiographic evidence for endocarditis. If clinically suggested, the absence of discrete vegetation on echocardiography does not exclude the diagnosis of endocarditis
XR right hip (3-4 weeks postop) No evidence of fracture or dislocation without obvious osseous abnormalities
*CT = computed tomography.

TABLE II - Microbiologic Data Table*,
Source Type and Number Result
Hip (aspirate)
Culture (OSH) +Group A streptococcus
Hip (intraoperative)
Swab 1 +Group A streptococcus
Swab 2 +Group A streptococcus
Swab 3 +Group A streptococcus
Biopsy 1 +Group A streptococcus
Culture 1 (OSH) Negative
Culture 2 (OSH) Negative
Culture 1 Negative
Culture 2 Negative
Culture 3 Negative
Culture 4 Negative
Culture 5 Negative
Culture 6 Negative
Swab 1 +Group A streptococcus
Culture 1 (OSH) +Group A streptococcus
+Citrobacter koseri
Culture 2 Negative
Culture 3 Negative
*Cultures, biopsy, and swabs were collected at our home institution unless otherwise noted.
OSH = outside hospital.

On arrival, she was afebrile and tachycardic (117 bpm), but otherwise stable (121/69 mm Hg, 18 breaths/minute, and 97% on room air), in no acute distress, appeared generally uncomfortable, exhibited a diffuse maculopapular rash on her chest/abdomen/back/bilateral proximal thighs (centrifugally spread), and demonstrated severe pain with hip short-arc range-of-motion. Laboratory tests were abnormal, including an elevated white blood cells count (11.2 × 103 µL), C-reactive protein (CRP 172 mg/L), and erythrocyte sedimentation rate (ESR 45 mm/hr). Blood and urine cultures were collected, and she was transitioned to a broader regimen of vancomycin + ceftazidime + clindamycin.

The patient was diagnosed with septic arthritis and taken urgently to the operating room for hip irrigation and debridement through a posterior approach. A viscous, purulent fluid was evacuated from the hip, which was subsequently irrigated with copious saline. Three separate wound culture swabs were sent for microbiologic examination.

During positioning on the operating table, thin, milky, vaginal discharge was noted. The obstetrics/gynecology team was consulted for formal evaluation, which noted a well-healing second-degree laceration with minimal perineal involvement, sutures in place and intact, without erythema/purulence. A small quantity of normal nonmalodorous serous lochia was noted, with a normal-appearing cervix. Vaginal mucosal wound cultures and group B streptococcal (GBS) swabs were collected. Notably, the patient's prenatal labs were normal.

Postoperatively, the patient was evaluated by the Infectious Disease Service who recommended admission to the intensive care unit. Symptoms were concerning for early onset of Streptococcal toxic shock syndrome (TSS), particularly given the intimate exposure to her child with group A streptococcus (GAS) pharyngitis. She was treated with intravenous penicillin G and clindamycin, with scarlet fever and invasive streptococcal infections atop the differential diagnosis. Postpartum invasive GAS infections have been described involving myonecrosis of the uterus with an associated fulminant course1; thus, the gynecology-oncology team was consulted for an endometrial biopsy to investigate possible gynecologic etiologies of the primary infection.

The patient was monitored in the intensive care unit for 48 hours, with improvement in her rash and hip pain. Intraoperative wound and vaginal cultures grew GAS, as well as the endometrial tissue biopsy and the urine culture collected at the outside hospital; however, all blood cultures and the urine cultures collected at our institution were negative (Table II). An echocardiogram demonstrated no cardiac source of infection (Table I).

She was discharged on postoperative day 5 with a peripherally inserted central catheter in place for a 6-week course of ceftriaxone. Posttreatment inflammatory blood markers were normal (ESR 11 and CRP 0.8). At the 6-month follow-up, the patient made a near full recovery, and by 1-year and 2-year follow-ups, she had returned to her baseline level of function without restrictions, recurrences, or complications, with full, painless range-of-motion.


In the absence of risk factors for septic arthritis, the diagnosis in this patient remained dubious; however, the concordance between intraoperative hip cultures, vaginal swabs, urine culture, and endometrial biopsy presents a convincing unifying process explaining the septic hip. In the setting of negative blood cultures before and after initiating antibiotics, explanation regarding the route of transfer is less clear. The most likely explanation is that of a transient bacteremia unifying all infected systems by hematogenous spread. Given the patient’s excellent health, she may have immunologically cleared the hematologic infection before hip/urine/vaginal/endometrial culture collection, exhibiting the confusing discordant infectious picture, although a quiescent collection of microbes may have settled in various locations. Furthermore, an atypical pathogen such as GAS in the setting of an infected close contact raises suspicion that infectivity originated with the patient’s child.

The literature is limited in its description of postpartum orthopaedic pathology, seemingly all publications are limited to single case reports of esoteric findings, consistent with the case we present. Previous authors have discussed postpartum topics including septic sacroiliitis2, osteomyelitis3, retroperitoneal fasciitis4, periarticular hip abscess and coxitis5, and retroperitoneal abscess/fistula6; however, the infectious microbe most frequently described is GBS. In our case, the patient’s cultures were unanimously positive for GAS, which has not been previously described in the literature to the best of our knowledge. It is plausible that the patient contracted a GAS infection from her son, which systemically spread causing the constellation of positive cultures.

Pudendal nerve anesthesia has been described as an alternative means of septic inoculation in the peripartum patient7. Our patient experienced a second-degree perineal laceration at the time of her delivery, requiring perineal anesthetization before repair, presenting a potential source of infection. However, she would likely have exhibited a local cellulitic/necrotic reaction at the injection/repair site. Our patient was formally examined by our obstetrics/gynecology and gynecology/oncology colleagues, who described the laceration as well-healing without infectious signs.

In our literature review, we identified 2 previously described cases of septic arthritis in the postpartum hip, however, neither of which was caused by GAS. Phuah and Mehta described cases of postpartum Mycoplasma hominis8 and postpartum GBS septic arthritis of the hip9, respectively. Cases of M. hominis septic hips are exceedingly rare because only 26 cases were described in the literature until 2007, of which 15.4% occurred in postpartum women8.

Gluteal pyomyositis has also been described in the postpartum patient10,11. Despite the anatomical difference in location and affected tissue, these cases have presented similarly to septic arthritis in the postpartum woman, confusing the diagnoses. Their pathophysiologies share common themes—that is, hematogenously spread, local hip/buttock pain, and signs/symptoms of sepsis—however, hip cultures and CT scanning are used to differentiate the diagnoses. In our patient, the data definitively ruled out gluteal pyomyositis and confirmed an infected femoral-acetabular joint.

Transient osteoporosis of pregnancy is also a known phenomenon that may predispose pregnant women to unilateral hip pathology, classically occurring during the third trimester—or in the nongravid patient’s fifth/sixth decade of life—and may subject individuals to an increased risk of fracture. Wood described a case of a displaced subcapital fracture in the postpartum period that caused hip pain notably with ambulation12. Similarly, our patient presented postpartum with unilateral hip pain and antalgic gait; however, imaging studies ruled out fracture, and septic signs/symptoms were indicative of an infectious process.

TSS is not a well-described entity in the orthopaedic literature; however, given its potentially devastating effects, it may be worth recognizing the associated symptomatology should a toxic-appearing young women present with monoarthritic pain. Our patient did not develop a fulminant course—symptoms were limited to fever/rash/classic pathogen—but ominous features include hypotension, acute kidney injury, coagulopathy, liver dysfunction, acute respiratory distress syndrome, and soft-tissue necrosis. Rheumatic fever was less suspected in our patient; however, symptoms developed in the aftermath of her child’s GAS pharyngitis with arthralgia—2 main features of the diagnosis; the additional classic features of carditis/valvulitis, subcutaneous nodules, erythema marginatum, and Sydenham chorea were absent. Similarly, the absence of a sandpaper-like rash or strawberry tongue made scarlet fever less likely.

In summary, the case presented demonstrates bacterial arthritis of the hip, likely caused by hematogenous spread despite negative blood cultures, and concurrently positive vaginal+urine cultures and endometrial biopsy, all unified by the same pathogen. Septic arthritis with its sequela renders the disease a life-threatening illness, which should be treated with prompt surgical decompression, irrigation and debridement, and antibiosis, as was enacted for this patient. The etiology of infection is less straightforward and will ultimately remain speculative without definitive evidence of a source. It can be concluded beyond reasonable doubt that the processes are interconnected, and the source of GAS infection in this postpartum mother is likely her offspring, supported by her son’s case of bacterial pharyngitis. The patient made a full recovery.

Fig. 3:
Magnetic resonance imaging of right hip performed postoperatively at 3 to 4 weeks with coronal (Fig. 3-A) T1 and (Fig. 3-B) T2 sequences, as well as axial (Fig. 3-C) STIR and (Fig. 3-D) PDFS sequences showing changes in the femoral head and acetabulum with residual intracapsular fluid, demonstrating the rapidity with which cartilage changes may occur in the setting of septic arthritis.


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septic arthritis; postpartum, hip; obstetrics/gynecology; Group A streptococcus

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