Abstract:

Septic complications following unsafe or poorly managed abortion remain a significant cause of maternal morbidity and mortality, particularly in resource-limited settings. This case highlights a young woman who developed severe sepsis and multi-organ involvement after undergoing dilatation and evacuation (D&E)/ dilatation and curettage (D&C) for incomplete abortion with post-procedure insertion of an intrauterine contraceptive device (Cu-T).

Introduction

Maternal sepsis is a severe and life-threatening condition that occurs when infection leads to organ dysfunction during pregnancy, abortion, or the postpartum period. Globally, maternal sepsis accounts for a significant proportion of maternal morbidity and mortality, particularly in low- and middle-income countries where timely access to safe abortion care and infection control practices may be limited.^1,2

A case of a young woman is reported in this study where the patient presented with post-abortal sepsis further complicated by emphysematous cystitis and septic shock following dilatation and evacuation (D&E) with intrauterine contraceptive device (IUCD) insertion.

Case Report

Patient Background

• Patient: Mrs. RK, 24 years old, housewife from underprivileged background.
• Obstetric history: Married for 4 years, 1 living child (2 years old).
• Index pregnancy: 2 months gestation, unplanned.
• No antenatal care.
• Past medical history: Recurrent urinary tract infections, prior indiscriminate antibiotic use.
• Contraceptive history: Barrier method before pregnancy.
• Immunization: Immunized against Tetanus.

Chronological Clinical Course

Step 1: Initial Event

• 4 Days Prior to Admission in the current hospital: Lower abdominal pain and vaginal bleeding.
• Diagnosed with incomplete abortion at a local hospital.
• Underwent dilatation and evacuation (D&E).
• Copper-T (IUCD) inserted immediately after the D& E as contraception.
• Discharged after 6 hours.

Step 2: Symptom Onset

• 24 Hours after D&E: Developed fever and diarrhea one day post-discharge.
• Condition worsened with shock (hypotension, tachycardia) on the 2^nd post-D&E day.
• Referred to tertiary hospital.

Tertiary Hospital Admission (Day 0 – November 30, 2022)

Presentation on admission

• Disoriented but conscious.
• Vitals: Temp 101°F, Pulse 134/min, BP 90/50 mmHg, RR 40/min, SpO₂ 90% (room air), improved to 95% with O₂.
• Examination:
  • Per abdomen: suprapubic tenderness.
  • External genitalia: desquamation.
  • Speculum: scanty foul-smelling blood-stained discharge, Cu-T thread visible (removed).
  • Bimanual exam: bulky uterus.
  • Per rectal exam: normal.

Transferred to Obstetrics ICU.

Step 3: Investigations

• Ultrasound (USG): Bulky uterus, scanty collection.
• CECT pelvis: Post-abortal uterus, no retained products, bladder with air-fluid level → suggestive of emphysematous cystitis.³
• Blood culture: Staphylococcus aureus positive.
• Cervical/vaginal swab & urine culture: Negative.
• ABG and procalcitonin: Raised (consistent with sepsis).
• Hematology: Anemia, leukocytosis.

Step 4: Diagnosis

• Post-abortal sepsis with septic shock.
• Emphysematous cystitis as complication.
• Multiorgan dysfunction (initial SOFA score: 10).^4,5

Step 5: Management and Clinical Course

ICU Management (Day 0–7)

• Airway & Breathing: Intubation and mechanical ventilation (Day 0–3). Extubated on Day 3 → oxygen support by mask.
• Circulation:
  • Fluid resuscitation under CVP guidance.
  • Inotropes (noradrenaline) for persistent hypotension → tapered off by Day 3.
• Antibiotics:
  • Initially ceftriaxone + metronidazole.
  • Switched to levofloxacin (based on sensitivity).
  • Later escalated to meropenem + amikacin (due to rising WBC).
• Adjuncts:
  • Hydrocortisone 100 mg BID.
  • Hypokalemia and metabolic acidosis corrected.
  • Blood transfusion for anemia (suspected transfusion reaction treated).
  • Albumin infusion for hypoalbuminemia.

Progression (Day 6–10)

• Oral fluids tolerated by Day 6.
• Improvement in hemodynamics.
• Developed oral ulcers and perioral skin peeling on Day 10.
• Tzanck smear → positive for herpes labialis → treated with acyclovir 200 mg TDS for 1 week.⁶  

Case Diagnosis

This case demonstrates maternal sepsis secondary to unsafe post-abortal care and IUCD insertion, further complicated by emphysematous cystitis and septic shock. Prompt ICU admission, aggressive resuscitation, targeted antibiotic therapy, and multidisciplinary care were essential for recovery.

Discussion:

Maternal sepsis remains a critical cause of morbidity and mortality, accounting for a significant proportion of maternal deaths worldwide. Estimates suggest that about 11% of maternal mortality is due to sepsis, underscoring its global importance.¹ In high-income countries, the incidence is relatively low, with U.S. data showing around 0.04% of deliveries complicated by sepsis, but in low- and middle-income countries the burden is far higher and linked to disproportionate mortality.⁷ Globally, puerperal sepsis alone leads to tens of thousands of maternal deaths annually, while unsafe abortion-related infections continue to pose a major public health challenge in resource-limited settings.⁸  

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection, typically marked by an acute increase of ≥2 points in the SOFA score, which is zero in otherwise healthy individuals.⁹ Septic shock represents sepsis’ most severe form, with circulatory collapse, tissue hypoperfusion, and persistent hypotension requiring vasopressors despite fluid resuscitation, often accompanied by elevated lactate levels.⁹ Progression is clinically significant: roughly 9% of sepsis cases become severe, 3% progress to septic shock, and mortality in shock can reach 40%.¹⁰ In pregnancy and postpartum, infection may arise from chorioamnionitis, endometritis, cesarean wound infection, septic abortion, or genital tract contamination, with urinary tract infections and pneumonia also major contributors.⁹  The most common pathogen is Escherichia coli, followed by streptococci, Staphylococcus aureus, anaerobes, and Listeria monocytogenes.¹¹ Group B streptococcus is linked to nearly half of maternal deaths in some studies.⁹

Risk is heightened by maternal factors such as impaired immunity, anemia, obesity, and diabetes, which facilitate bacterial spread and systemic inflammation.¹¹ Recurrent UTIs, inadequate antibiotic prophylaxis, and invasive procedures like IUD insertion or uterine evacuation in unsafe conditions further raise vulnerability.

Clinically, maternal sepsis may present with fever, tachycardia, hypotension, tachypnea, or more subtle complaints such as abdominal pain, diarrhea, urinary issues, or respiratory distress.¹¹  Diagnosis combines careful history, examination, laboratory tests (blood count, renal and liver function, coagulation, electrolytes, blood gases, lactate), and microbiological cultures. Biomarkers such as procalcitonin are being studied for their utility in pregnancy¹²,while imaging can identify retained products, abscesses, or pulmonary involvement.

Management depends on early recognition and immediate treatment. Timely empirical broad-spectrum antibiotics are crucial, as each hour of delay in hypotensive patients reduces survival by 7–8%.¹³ Alongside antibiotics, resuscitation includes airway support, oxygen, fluids, vasopressors, and correction of metabolic.⁹ disturbances Supportive strategies include thromboprophylaxis, glycemic control, and blood transfusion when necessary, while “source control”—such as uterine evacuation, abscess drainage, or device removal—is essential.¹⁴ Adjunctive corticosteroids may be used in refractory septic shock, though their role remains debated.⁹  

Maternal sepsis has grave implications for both mother and fetus. Maternal hyperpyrexia, inflammation, and hemodynamic instability can cause preterm labor, fetal growth restriction, intrauterine death, or neonatal sepsis.¹⁵ Mothers may suffer septic shock, multi-organ failure, ARDS, DIC, or chronic organ dysfunction.

Pathogenesis:

This case of post-abortal sepsis from Staphylococcus aureus most likely developed when bacteria gained entry through the traumatized process of the D&E and followed by the insertion of Cu-T at the same time without giving uterine tissue time to heal. Pathogenesis of the onset of sepsis began once S. aureus entered the bloodstream and started releasing toxins that triggered a dysregulated host immune response, characterized by excessive cytokine release and systemic inflammation. This cascading effect led to widespread endothelial dysfunction, capillary leakage with loss of albumin and fluid, and intravascular hypovolemia, while vasodilatory mediators reduced systemic vascular resistance and contribute to the shock.¹

The systemic process includes multi-organ involvement. The heart initially compensates with increased output, but septic cardiomyopathy may ensue, presenting as systolic dysfunction with ejection fraction below 45% or as diastolic dysfunction caused by myocardial edema and impaired ventricular compliance. These changes raise the risk of pulmonary edema during aggressive fluid resuscitation.¹⁶  In parallel, endothelial injury and toxin-mediated activation of the coagulation cascade promote microvascular thrombosis and disseminated intravascular coagulation, further impairing tissue oxygenation.¹⁷

At the metabolic level, tissue hypoxia and toxin-driven alterations in energy pathways result in hyperlactatemia. This is mediated by anaerobic glycolysis, inhibition of pyruvate dehydrogenase, and reduced lactate clearance, with the lungs identified as a major source of excess lactate. The resulting lactic acidosis exacerbates cellular dysfunction and disrupts acid–base balance, accelerating progression to hypotension, tissue hypoperfusion, and multi-organ failure.¹⁸

Conclusion:

Staphylococcus aureus is a recognized cause of toxic shock syndrome during labor, the early postpartum period, and following septic abortion. Even in the presence of septicemia, vaginal, cervical, or urine cultures may not always isolate the organism.¹⁹

This case underscores the life-threatening risks of post-abortion sepsis particularly when invasive procedures are followed by immediate intrauterine device insertion without proper aseptic measures or follow-up care. The recognition of the causative organism being S. aureus here might be due to the patient having recurrent urinary tract infections. The likely sequence involved ascending infection, toxin release, and subsequent dysregulated host response culminating in shock. Management hinges on aggressive multidisciplinary ICU management with immediate resuscitation, and initiation of broad-spectrum antibiotics soon after prompt recognition of sepsis. Steroids is considered when shock is refractory to fluids.¹⁷ It is important to note that IUCD insertion must be avoided soon after intrauterine procedures, it requires aseptic measures, and must be done after ruling out the presence of suspected genital tract infection.   

Overall, maternal sepsis is a preventable but devastating emergency. Global strategies must strengthen infection control, expand access to safe abortion and delivery care, and address maternal risk factors. When it occurs, survival hinges on rapid recognition, early antibiotics, aggressive hemodynamic support, and timely source control, safeguarding the lives of both mothers and their infants.

Author of this article

Dr. Kishuar Parveen
MBBS, FCPS, OBS & GYNAE
Senior Consultant
Mount Adora Hospital, Akhalia, Sylhet.

References

1.           Fact Sheets | Sepsis Alliance. Accessed October 7, 2025. https://www.sepsis.org/education/resources/fact-sheets/

2.           Runtime Error. Accessed October 7, 2025. https://www.who.int/news-room/fact-sheets/detail/sepsis.

3.           Balai M, Gupta L, Kumari A. Urethral caruncle in a perimenopausal female: Dramatic response to topical estrogen cream. Indian J Urol. 2018;34(4):308. doi:10.4103/IJU.IJU_200_18

4.           Page Not Found | CDC. Accessed October 7, 2025. https://www.cdc.gov/sepsis/what-is-sepsis.html

5.           404. Accessed October 7, 2025. https://www.who.int/reproductivehealth/publications/maternal_perinatal_health/sepsis/en/

6.           The resource cannot be found. Accessed October 7, 2025. https://www.cdc.gov/std/treatment-guidelines/herpes.htm.

7.           Hensley MK, Bauer ME, Admon LK, Prescott HC. Incidence of Maternal Sepsis and Sepsis-Related Maternal Deaths in the United States. JAMA. 2019;322(9):890. doi:10.1001/JAMA.2019.9818

8.           Gravett CA, Gravett MG, Martin ET, et al. Serious and Life-Threatening Pregnancy-Related Infections: Opportunities to Reduce the Global Burden. PLoS Med. 2012;9(10):e1001324. doi:10.1371/JOURNAL.PMED.1001324

9.           Shields AD, Plante LA, Pacheco LD, Louis JM. Society for Maternal-Fetal Medicine Consult Series #67: Maternal sepsis. Am J Obstet Gynecol. 2023;229(3):B2-B19. doi:10.1016/j.ajog.2023.05.019

10.        Liu P, Zhang X, Wang X, et al. Maternal sepsis in pregnancy and the puerperal periods: a cross-sectional study. Front Med (Lausanne). 2023;10:1126807. doi:10.3389/FMED.2023.1126807/FULL

11.        Nayak AH, Khade SA. Obstetric Sepsis: A Review Article. J Obstet Gynaecol India. 2022;72(6):470. doi:10.1007/S13224-022-01706-Y

12.        Behnia F, Omere CI, Clifford CC, Pacheco LD. Obstetric sepsis: Clinical pearls for diagnosis and management. Semin Perinatol. 2024;48(7):151975. doi:10.1016/J.SEMPERI.2024.151975

13.        Fan SR, Liu P, Yan SM, Huang L, Liu XP. New Concept and Management for Sepsis in Pregnancy and the Puerperium. Maternal-Fetal Medicine. 2020;2(4):231-239. doi:10.1097/FM9.0000000000000058

14.        Improving Diagnosis and Treatment of Maternal Sepsis.

15.        Fan SR, Liu P, Yan SM, Huang L, Liu XP. New Concept and Management for Sepsis in Pregnancy and the Puerperium. Maternal-Fetal Medicine. 2020;2(4):231-239. doi:10.1097/FM9.0000000000000058

16.        Mithoowani S, Laureano M, Crowther MA, Hillis CM. Investigation and management of erythrocytosis. CMAJ : Canadian Medical Association Journal. 2020;192(32):E913. doi:10.1503/CMAJ.191587

17.        Fonkalsrud EW, Cooper CB. Pectus Excavatum. Encyclopedia of Respiratory Medicine: Volume 1-4. 2023;1-4:V3-304-V3-309. doi:10.1016/B0-12-370879-6/00290-8

18.        Santos CL, Moraes L, Santos RS, et al. The biological effects of higher and lower positive end-expiratory pressure in pulmonary and extrapulmonary acute lung injury with intra-abdominal hypertension. Crit Care. 2014;18(3):1-11. doi:10.1186/CC13920/FIGURES/6

19.        Toxic shock syndrome – Symptoms & causes – Mayo Clinic. Accessed October 7, 2025. https://www.mayoclinic.org/diseases-conditions/toxic-shock-syndrome/symptoms-causes/syc-20355384