|
 
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| CASE REPORT |
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| Year : 2021 | Volume
: 11
| Issue : 2 | Page : 48-49 |
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A case of ovarian hyperstimulation syndrome with diffuse cortical necrosis
Sweety Kakoti, Dhruvajyoti Choudhury, Tonmoy Das
Department of Nephrology, Apollo Hospital Guwahati, Ganeshguri, Guwahati, Assam, India
| Date of Submission | 23-Jul-2021 |
| Date of Acceptance | 27-Jul-2021 |
| Date of Web Publication | 05-Oct-2021 |
Correspondence Address:
Dr. Sweety Kakoti
Department of Nephrology, Apollo Hospital Guwahati, Ganeshguri, Guwahati, Assam
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/ajoim.ajoim_6_21
Ovarian hyperstimulation syndrome is an iatrogenic, serious complication of controlled ovarian hyperstimulation, usually self-limited, but occasionally life threatening and typically occurs with gonadotropin. A 32-year-old married female [Para 0+1, 30 weeks (intra-uterine death)—2016], who underwent ovum pick up procedure for secondary infertility, presented to the Department of Nephrology, Apollo Hospital, Guwahati with the complaints of pain in the abdomen, anuria, breathing difficulty, bleeding per vagina on the next day. On investigating the case, the patient had thrombocytopenia, leucocytosis, anemia, normal morphology in peripheral blood smear, raised inflammatory markers, hepatic transaminases, lactate dehydrogenase, and rapidly progressive renal failure, metabolic acidosis with negative serological markers for connective tissue disease. Radio imaging suggested bilaterally enlarged ovaries with multiple hemorrhagic cysts, pleural effusion, and ascites. Ultrasound showed normal sized kidneys with increased echotexture and hypoechoeic cortical rim. Renal biopsy showed diffuse renal cortical necrosis. Supportive management started with a target to correct volume depletion, monitoring, and electrolyte abnormalities. Patient was hemodynamically stabilised and discharged on thrice weekly maintenance dialysis. Keywords: Infertility, in-vitro fertilization, OHSS, ovum pickup
How to cite this article:
Kakoti S, Choudhury D, Das T. A case of ovarian hyperstimulation syndrome with diffuse cortical necrosis. Assam J Intern Med 2021;11:48-9 |
| Background | |  |
Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic, serious complication of controlled ovarian hyperstimulation, usually self-limited but occasionally life-threatening, and typically occurs with gonadotropin.[1] It manifests as increased capillary permeability and fluid retention, with inflammatory mediators (e.g., VEGF).[2]
Clinical manifestations of OHSS can vary from mild to moderate forms with enlarged ovaries, symptoms of nausea, vomiting, sudden increase in weight of >3 kg, abdominal discomfort to severe forms with ascites, pleural or pericardial effusion, hypovolemia, hemoconcentration, acute kidney injury, abnormal liver function test (LFT), hypoalbuminemia, hyponatremia, hypokalemia, etc.[3]
| Case Presentation | | |
A 32-year-old married female [Para 0+1, 30 weeks (intra-uterine death)—2016], who was undergoing treatment for secondary infertility with Inj. FSH, Inj. LH and Inj. HCG, underwent ovum pick-up procedure under general anesthesia on February 2, 2019. Following that, on the next day, she developed pain in the abdomen, anuria, breathing difficulty, bleeding per vagina without any history of fever, ecchymosis, petechiae, melena, rash, hair fall, joint pain, photosensitivity, and oral lesions. Past history revealed that she was a known case of hypothyroidism on treatment. Clinical examination showed normal vitals except tachycardia of 110/min, pallor, and bipedal edema. There was diffuse guarding and tenderness in the abdomen.
On investigating the case, the patient had thrombocytopenia (30,000/mm3), leucocytosis (23,780/mm3), hemoglobin 8.8 g/dL, normal morphology in peripheral blood smear, inflammatory markers such as C-reactive protein and procalcitonin raised, raised hepatic transaminases (aspartate transaminase 962 U/L and alanine transaminase 430 U/L) in LFT, D-dimer >1000 ng/mL, lactate dehydrogenase 3551 U/L, and creatinine rapidly rose from 2.6 to 14.2 mg/dL. Coagulation profile was normal, viral-negative, tropical fever panel-negative. Arterial blood gases showed metabolic acidosis, antinuclear and antiphospholipid antibodies, and vasculitic serological markers were negative. Blood cultures showed no growth. Abdominal ultrasound showed normal sized kidneys with increased echotexture and thin hypoechoeic cortical rim, ascites, and bilaterally enlarged ovaries with multiple cysts of varying sizes with hemorrhagic contents. Chest X-ray showed bilateral minimal pleural effusion. Renal biopsy showed diffuse renal cortical necrosis.
Hence, the patient was diagnosed as a case of OHSS with diffuse cortical necrosis. Immediately after admission, infusion therapy was started, consisting of normal saline infusion 0.9% and human albumin 20%. Fluid intake and urine outputs, ultrasonography, and laboratory studies were monitored strictly daily. The patient was treated initially with steroid pulse keeping in view of rapidly progressive renal failure. There were no serious changes in serum electrolytes. Renal function was supported by hemodialysis, and 2 U of packed red blood cells transfused. Gradually, creatinine decreased to 4.2 mg/dL, but anuria persisted. The patient was hemodynamically stabilized and was discharged with the advice of three-times-weekly maintenance hemodialysis.
| Conclusion | | |
Physicians can reduce the risk of OHSS by monitoring gonadotropin therapy and by “coasting” which is withholding exogenous gonadotropins and postponing the hCG trigger until a patient’s E2 level has declined to a “safer” pre-defined level (usually ~3000 pg/nL).[4],[5]
The renal complications secondary to OHSS most commonly include prerenal AKI, which, if left untreated, leads to ischemic damage to the kidney leading to acute tubular necrosis, which is frequently reversible.[6]
The Society of Obstetricians and Gynaecologists of Canada (SOGC) recommends the following clinical practice guidelines[7]:
- The addition of metformin should be considered in patients with polycystic ovarian syndrome who are undergoing in-vitro fertilization, because it may reduce the incidence of OHSS.
- Gonadotropin dosing should be carefully individualized, taking into account the patient’s age, body mass, antral follicle count, and previous response to gonadotropins.
- Cycle cancellation before administration of hCG is an effective strategy for the prevention of OHSS, but the emotional and financial burden it imposes on patients should be considered before the cycle is cancelled.
- GnRH antagonist stimulation protocols are recommended in patients at high risk for OHSS, and the risk of severe OHSS can be reduced by using a GnRH agonist as a substitute for hCG to trigger final oocyte maturation.
- Progesterone, rather than hCG, should be used for luteal-phase support.
In in-vitro fertilization, it can be advantageous to postpone the embryo transfer by freezing the embryos.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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| 2. | Zheng HH, Song Y, Wu JY. Critical ovarian hyperstimulation syndrome after in vitro fertilization treatment in a renal transplant recipient: A case report. Transplant Proc 2016;48:267-70. |
| 3. | Golan A, Ron-el R, Herman A, Soffer Y, Weinraub Z, Caspi E. Ovarian hyperstimulation syndrome: An update review. Obstet Gynecol Surv 1989;44:430-40. |
| 4. | Abdallah R, Kligman I, Davis O, Rosenwaks Z. Withholding gonadotropins until human chorionic gonadotropin administration. Semin Reprod Med 2010;28:486-92. |
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| 7. | Corbett S, Shmorgun D, Claman P; Reproductive Endocrinology Infertility Committee; Special Contributor. The prevention of ovarian hyperstimulation syndrome. J Obstet Gynaecol Can 2014;36:1024-33. |
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