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Ovarian Hyperstimulation Syndrome
The Journal of Emergency Medicine, Vol. 33, No. 2, pp. 191–192, 2007 Copyright © 2007 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/07 $–see front matter
doi:10.1016/j.jemermed.2006.12.032
Visual Diagnosis in Emergency Medicine OVARIAN HYPERSTIMULATION SYNDROME Barry Hahn,
MD
Department of Emergency Medicine, Staten Island University Hospital, Staten Island, New York Reprint Address: Barry Hahn, MD, Department of Emergency Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305
CASE REPORT A 31-year-old woman, with no significant past medical or surgical history, presented to the Emergency Department (ED) with complaints of vomiting and severe lower abdominal pain. The patient had been receiving exogenous hormone therapy and underwent artificial insemination 3 days prior. On physical examination her vital signs were within normal limits and she displayed peritoneal signs. A urine pregnancy test was negative. Ultrasound revealed bilateral ovarian enlargement with multiple septated cysts (Figure 1). The right ovary measured 7.2 ⫻ 4.9 ⫻ 5.3 cm. The left ovary measured 10.9 ⫻ 6.5 ⫻ 5.6 cm and contained echogenic debris consistent with hemorrhage. Free fluid was present in the cul de sac (Figure 2). A diagnosis of ovarian hyperstimulation syndrome (OHSS) was made. Intravenous crystalloid fluid and narcotic analgesics were administered. An anteroposterior chest radiograph was unremarkable. Laboratory studies including a complete blood count, electrolyte panel, renal function, coagulation profile, and liver function tests were within normal limits. The patient was observed in the ED and seen by her gynecologist. Her pain was controlled in the ED and she was discharged home on oral analgesics, strict intake monitoring, and repeat ultrasound and examination by her gynecologist the following day.
Figure 1. Pelvic Ultrasound demonstrating ovarian enlargement with multiple septated cysts and echogenic debris.
spontaneous disease during pregnancy have been reported (1). Risk factors include age ⬍35 years, low body mass index, serum estradiol levels ⬎4000 pg/mL, or development of more than eight follicles in an ovary (2). The pathophysiology of this syndrome remains controversial. The manifestations of OHSS are believed to be the result of increased capillary permeability, which leads to a loss of protein-rich fluid from the intravascular compartment into the interstitial space (3). OHSS has traditionally been classified as mild, moderate, or severe, based on clinical and laboratory criteria. In mild OHSS, the ovaries are ⬍5 cm and mild abdominal discomfort is present. These patients have laboratory findings consistent with hyperstimulation (elevated estradiol and pro-
DISCUSSION OHSS is a complication of ovulation induction therapy for in vitro fertilization, although some case reports of
RECEIVED: 7 June 2006; FINAL ACCEPTED: 4 December 2006
SUBMISSION RECEIVED:
23 November 2006; 191
192
Figure 2. Pelvic Ultrasound of same patient demonstrating free fluid in the cul de sac.
gesterone levels). In moderate OHSS, the ovaries measure 5 to 10 cm and abdominal distention is present. Diarrhea and vomiting may be present. In severe OHSS, the ovaries are ⬎10 cm (4). Extravasation of protein-rich fluid results in extravascular fluid accumulation and intravascular volume depletion. The patient will have fluid and electrolyte disturbances. Pleural or pericardial effusions, ascites, hypovolemia, or shock may also be present. Oliguria occurs as a result of decreased vascular volume or tense ascites and secondary reduction in renal perfusion. The risk of thromboembolism and disseminated intravascular coagulation is increased due to hemoconcentration, increased blood viscosity, diminished peripheral blood flow, and patient inactivity. Acute respiratory distress syndrome and liver and kidney dysfunction may also develop (5). The severe form is rare, with an incidence of 0.5–5% among patients undergoing ovulation-induction therapy. Hospitalization for OHSS may be required based on the severity of symptoms, analgesic requirements, and other social considerations (availability of responsible adult supervision, support and assistance with child care). No single sign or symptom is an absolute indication, but hospitalization should be considered for severe abdominal pain, intractable vomiting, dehydration, tense ascites, dyspnea, severe electrolyte imbalance, or abnormal liver function tests (6). Patients with mild to moderate manifestations can generally be managed on an outpatient basis. Therapy for
B. Hahn
OHSS is mainly supportive until the condition resolves. The syndrome is self-limiting, and resolution parallels the decline in serum hCG levels. Mild disease symptoms typically resolve within 1 week, whereas moderate disease may last 2 to 3 weeks. Patients with the moderate form of OHSS may progress to severe disease rapidly, especially if pregnancy occurs. Therefore, outpatient treatment requires close monitoring for illness progression in addition to oral analgesics. In the setting of a maintained pregnancy, slow resolution of symptoms usually occurs over 1 to 2 months. In severe OHSS, management includes carefully monitoring blood volume, correcting electrolyte imbalances, and relieving secondary complications. Anticoagulant therapy is usually unnecessary if these therapies are promptly employed. Patients with severe disease should be admitted to an intensive care setting. CONCLUSION OHSS is an increasingly frequent complication as a result of the growth of ovulation induction therapy. The principal pathology is increased capillary permeability, which leads to extravascular fluid accumulation and intravascular volume depletion. Manifestations range from mild abdominal discomfort to severe, life-threatening illness. Therapy is mainly supportive and most patients can be managed on an outpatient basis if close follow-up is ensured. Hospitalization may be required based on the severity of symptoms, analgesic requirements, and other social considerations. REFERENCES 1. Smits G, Olatunbosun O, Delbaere A, Pierson R, Vassart G, Costagliola S. Ovarian hyperstimulation syndrome due to a mutation in the follicle-stimulating hormone receptor. N Engl J Med 2003;349: 760 – 6. 2. Budev M, Arroliga AC, Falcone T. Ovarian hyperstimulation syndrome. Crit Care Med 2005;33(10 suppl):S301– 6. 3. Avecillas JF, Falcone T, Arroliga AC. Ovarian hyperstimulation syndrome. Crit Care Clin 2004;20:679 –95. 4. Insler V, Lunenfeld B. Up to Date: Classification and treatment of ovarian hyperstimulation syndrome. Available at: http://www. uptodate.com. Accessed April 17, 2006. 5. Delvigne A, Rozenberg S. Review of clinical course and treatment of ovarian hyperstimulation syndrome (OHSS). Hum Reprod Update 2003;9:77–96. 6. The Practice Committee of the American Society for Reproductive Medicine. Ovarian hyperstimulation syndrome. Fertil Steril 2003; 80:1309 –14.
doi:10.1016/j.jemermed.2006.12.032
Visual Diagnosis in Emergency Medicine OVARIAN HYPERSTIMULATION SYNDROME Barry Hahn,
MD
Department of Emergency Medicine, Staten Island University Hospital, Staten Island, New York Reprint Address: Barry Hahn, MD, Department of Emergency Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305
CASE REPORT A 31-year-old woman, with no significant past medical or surgical history, presented to the Emergency Department (ED) with complaints of vomiting and severe lower abdominal pain. The patient had been receiving exogenous hormone therapy and underwent artificial insemination 3 days prior. On physical examination her vital signs were within normal limits and she displayed peritoneal signs. A urine pregnancy test was negative. Ultrasound revealed bilateral ovarian enlargement with multiple septated cysts (Figure 1). The right ovary measured 7.2 ⫻ 4.9 ⫻ 5.3 cm. The left ovary measured 10.9 ⫻ 6.5 ⫻ 5.6 cm and contained echogenic debris consistent with hemorrhage. Free fluid was present in the cul de sac (Figure 2). A diagnosis of ovarian hyperstimulation syndrome (OHSS) was made. Intravenous crystalloid fluid and narcotic analgesics were administered. An anteroposterior chest radiograph was unremarkable. Laboratory studies including a complete blood count, electrolyte panel, renal function, coagulation profile, and liver function tests were within normal limits. The patient was observed in the ED and seen by her gynecologist. Her pain was controlled in the ED and she was discharged home on oral analgesics, strict intake monitoring, and repeat ultrasound and examination by her gynecologist the following day.
Figure 1. Pelvic Ultrasound demonstrating ovarian enlargement with multiple septated cysts and echogenic debris.
spontaneous disease during pregnancy have been reported (1). Risk factors include age ⬍35 years, low body mass index, serum estradiol levels ⬎4000 pg/mL, or development of more than eight follicles in an ovary (2). The pathophysiology of this syndrome remains controversial. The manifestations of OHSS are believed to be the result of increased capillary permeability, which leads to a loss of protein-rich fluid from the intravascular compartment into the interstitial space (3). OHSS has traditionally been classified as mild, moderate, or severe, based on clinical and laboratory criteria. In mild OHSS, the ovaries are ⬍5 cm and mild abdominal discomfort is present. These patients have laboratory findings consistent with hyperstimulation (elevated estradiol and pro-
DISCUSSION OHSS is a complication of ovulation induction therapy for in vitro fertilization, although some case reports of
RECEIVED: 7 June 2006; FINAL ACCEPTED: 4 December 2006
SUBMISSION RECEIVED:
23 November 2006; 191
192
Figure 2. Pelvic Ultrasound of same patient demonstrating free fluid in the cul de sac.
gesterone levels). In moderate OHSS, the ovaries measure 5 to 10 cm and abdominal distention is present. Diarrhea and vomiting may be present. In severe OHSS, the ovaries are ⬎10 cm (4). Extravasation of protein-rich fluid results in extravascular fluid accumulation and intravascular volume depletion. The patient will have fluid and electrolyte disturbances. Pleural or pericardial effusions, ascites, hypovolemia, or shock may also be present. Oliguria occurs as a result of decreased vascular volume or tense ascites and secondary reduction in renal perfusion. The risk of thromboembolism and disseminated intravascular coagulation is increased due to hemoconcentration, increased blood viscosity, diminished peripheral blood flow, and patient inactivity. Acute respiratory distress syndrome and liver and kidney dysfunction may also develop (5). The severe form is rare, with an incidence of 0.5–5% among patients undergoing ovulation-induction therapy. Hospitalization for OHSS may be required based on the severity of symptoms, analgesic requirements, and other social considerations (availability of responsible adult supervision, support and assistance with child care). No single sign or symptom is an absolute indication, but hospitalization should be considered for severe abdominal pain, intractable vomiting, dehydration, tense ascites, dyspnea, severe electrolyte imbalance, or abnormal liver function tests (6). Patients with mild to moderate manifestations can generally be managed on an outpatient basis. Therapy for
B. Hahn
OHSS is mainly supportive until the condition resolves. The syndrome is self-limiting, and resolution parallels the decline in serum hCG levels. Mild disease symptoms typically resolve within 1 week, whereas moderate disease may last 2 to 3 weeks. Patients with the moderate form of OHSS may progress to severe disease rapidly, especially if pregnancy occurs. Therefore, outpatient treatment requires close monitoring for illness progression in addition to oral analgesics. In the setting of a maintained pregnancy, slow resolution of symptoms usually occurs over 1 to 2 months. In severe OHSS, management includes carefully monitoring blood volume, correcting electrolyte imbalances, and relieving secondary complications. Anticoagulant therapy is usually unnecessary if these therapies are promptly employed. Patients with severe disease should be admitted to an intensive care setting. CONCLUSION OHSS is an increasingly frequent complication as a result of the growth of ovulation induction therapy. The principal pathology is increased capillary permeability, which leads to extravascular fluid accumulation and intravascular volume depletion. Manifestations range from mild abdominal discomfort to severe, life-threatening illness. Therapy is mainly supportive and most patients can be managed on an outpatient basis if close follow-up is ensured. Hospitalization may be required based on the severity of symptoms, analgesic requirements, and other social considerations. REFERENCES 1. Smits G, Olatunbosun O, Delbaere A, Pierson R, Vassart G, Costagliola S. Ovarian hyperstimulation syndrome due to a mutation in the follicle-stimulating hormone receptor. N Engl J Med 2003;349: 760 – 6. 2. Budev M, Arroliga AC, Falcone T. Ovarian hyperstimulation syndrome. Crit Care Med 2005;33(10 suppl):S301– 6. 3. Avecillas JF, Falcone T, Arroliga AC. Ovarian hyperstimulation syndrome. Crit Care Clin 2004;20:679 –95. 4. Insler V, Lunenfeld B. Up to Date: Classification and treatment of ovarian hyperstimulation syndrome. Available at: http://www. uptodate.com. Accessed April 17, 2006. 5. Delvigne A, Rozenberg S. Review of clinical course and treatment of ovarian hyperstimulation syndrome (OHSS). Hum Reprod Update 2003;9:77–96. 6. The Practice Committee of the American Society for Reproductive Medicine. Ovarian hyperstimulation syndrome. Fertil Steril 2003; 80:1309 –14.