Journal of Obstetrics and Gynaecology
ISSN: 0144-3615 (Print) 1364-6893 (Online) Journal homepage: http://www.tandfonline.com/loi/ijog20
Surgical treatment of late-onset amniotic fluid pulmonary embolism J. Yao, G.-G. Shao, W. Song, R.-G. Yang, D.-X. Yin, L.-M. Zhang & Y.-P. Liu To cite this article: J. Yao, G.-G. Shao, W. Song, R.-G. Yang, D.-X. Yin, L.-M. Zhang & Y.-P. Liu (2014) Surgical treatment of late-onset amniotic fluid pulmonary embolism, Journal of Obstetrics and Gynaecology, 34:2, 209-211 To link to this article: http://dx.doi.org/10.3109/01443615.2013.853729
Published online: 02 Dec 2013.
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Date: 13 September 2015, At: 08:02
Gynaecology Case Reports 209 out using desmin, actin and S100 staining. Desmin is a 52 kd protein that is a subunit of intermediate filaments in skeletal, smooth and cardiac muscle. Actin is a major protein component of thin filaments that together with motor protein myosin combine to form myofibrils. S100 is a marker of melanoma, malignant peripheral nerve sheath tumour, schwannoma, paraganglioma stromal cells, histiocytoma and clear cell sarcomas. The presence of desmin and actin and the absence of S100 confirmed this was a leiomyoma which was classified as benign due to the low mitotic count that was completely excised. A follow up review at 3 months showed a well-healed operation site with complete resolution of the mass.
Downloaded by [UNSW Library] at 08:02 13 September 2015
Discussion Benign neoplasms of the urethra may arise from any of the constituent tissues including glandular, transitional and squamous epithelium, and also from smooth and striated muscle tissue. They may also exhibit unusual growth patterns, including benign metastasising leiomyoma, disseminated peritoneal leiomyomatosis, intravenous leiomyomatosis, parasitic leiomyoma (Putran et al. 2010) and retroperitoneal growth (Fasih et al. 2008). Urethral leiomyomas are more common in females than males (Jalde et al. 2012): this is possibly due to spread from the most common site, namely the uterus, which may have happened in this case. Urethral leiomyomas are reported to enlarge during pregnancy and regress after delivery, suggesting a possible hormonal dependence (Fry et al. 1988) which is thought to be oestrogen and more prevalent in the fourth decade (Ghadian and Hoseini 2013). Most tumours present with a palpable lump but can also present with urinary irritative or obstructive voiding symptoms dependent upon its size and position (Bai et al. 2007). The differential diagnoses include urethrocele, urethral diverticulum, urethral malignancy, paraurethral cysts and vaginal paraurethral myxoid leiomyoma (Costantini et al. 2008). Urethral leiomyomas are very uncommon lesions (Fry et al. 1988) but should be excised to exclude malignancy, but prognosis is excellent, since there are no recorded cases of recurrence or malignant transformation (Merrel and Brown 1981; Oderda et al. 2013) to leiomyosarcoma. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References Bai SW, Jung HJ, Jeon MJ et al. 2007. Leiomyomas of the female urethra and bladder: a report of five cases and review of the literature. International Urogynecology Journal 18:913–917. Costantini E, Cochetti G, Porena M. 2008. Vaginal para-urethral myxoid leiomyoma: case report and review of the literature. International Urogynecology Journal 19:1183–1185. Fasih N, Prasad Shanbhogue AK, Macdonald DB et al. 2008. Leiomyomas beyond the uterus: usual locations, rare manifestations. Radiographics 28:1931–1948. Fry M, Wheeler JS, Mata JA et al. 1988. Leiomyoma of the female urethra. Journal of Urology 140:613–614. Ghadian A, Hoseini SY. 2013. Transvesical enucleation of multiple leiomyoma of bladder and urethra. Nephro-urology 5:709–711. Jalde DD, Godhi SA, Uppin SM et al. 2012. A case of urethral leiomyoma – a rare presentation. World Journal of Science and Technology 2:27–28. Merrel RW, Brown HE. 1981. Recurrent urethral leiomyoma presenting as stress incontinence. Urology 17:588–589. Oderda M, Mondaini N, Bartoletti R et al. 2013. Leiomyomata of the genitourinary tract: a case series from the ‘rare urological neoplasm’ registry. Scandinavian Journal of Urology 47:158–162. Putran J, Khaled K. 2010. Parasitic leiomyomas: two case reports and review of literature. Gynecological Surgery 7:383–384.
Surgical treatment of late-onset amniotic fluid pulmonary embolism J. Yao1,2, G.-G. Shao1, W. Song3, R.-G. Yang2, D.-X. Yin4, L.-M. Zhang2 & Y.-P. Liu1
Departments of 1Thoracic Surgery, The First Hospital of Jilin University, 2Jilin Province People’s Hospital, 3Obstetrics and Gynecology, The First Clinical Hospital of Jilin University and 4Vascular Surgery, China-Japan Union Hospital of Jilin University, Changchun, China DOI: 10.3109/01443615.2013.853729 Correspondence: G.-G. Shao, Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, China
Introduction Pulmonary embolism (PE) refers to a group of diseases and clinical syndromes resulting from the occlusion of the pulmonary artery by a variety of emboli, including pulmonary thromboembolism (PTE), amniotic fluid pulmonary embolism, fat embolism syndrome and air embolism. Amniotic fluid pulmonary embolism is a rare obstetric emergency, with a mortality rate as high as 80%, and late-onset amniotic fluid pulmonary embolism is an even rarer clinical entity. Late-onset amniotic fluid pulmonary embolism, which was first reported in 1926 (Meyer 1926), occurs when amniotic fluid components enter the maternal blood circulation during childbirth. Pathologically, fetal components, including lanugo, vermix, meconium and keratinised epithelia, are found in the pulmonary circulation of the pregnant woman, although hypersensitivity triggered by invisible components in amniotic fluid (e.g. surface-active substance, thromboxane A2, endothelin, leukotrienes) is thought to be an important cause of this condition (Gei and Hankins 2000; Clark et al. 1995; Clark 2010). Late-onset amniotic fluid pulmonary embolisms are characterised by an acute onset, a short course and a poor prognosis. Most patients are managed with symptomatic treatment, including anti-shock, anti-spasmodic, and vasoactive drugs, with surgical treatment being extremely rare. We describe here a patient with late-onset amniotic fluid embolism in the middle and lower lobes of the right lung.
Case report A 22-year-old primipara was admitted to our hospital on 13 February, 2009, with a 3-day history of haemoptysis associated with dyspnoea, starting 6 days after a caesarean section. At 40 weeks of pregnancy, on her expected date of delivery, she checked into a local hospital, where she underwent a caesarean section after failure to trigger the onset of labour. She received epidural anaesthesia and showed stable vital signs during the operation, with blood pressure, heart rate and blood oxygen saturation within normal ranges. She was conscious intraoperatively and did not receive postoperative pain pump therapy. The surgery was uneventful, and both she and her baby were in generally good condition. The patient experienced no potent uterine contractions before delivery or bleeding during delivery, and she was discharged 4 days after caesarean section. On the third morning after discharge from the hospital, or 6 days after the caesarean section, she developed haemoptysis with no obvious trigger, coughing up about 100 ml of bright red blood, along with chest tightness and shortness of breath. A chest examination upon admission to our hospital revealed a narrowed right intercostal space, dullness on percussion, a faint trachea conduction sound in the right upper lung, and no breath sounds in the right middle and lower lobes. Three-dimensional chest CT scans showed atelectasis in the right middle and lower lobes and right pulmonary embolism (Figures 1 and 2). Fibreoptic bronchoscopy showed rich blood clots and fresh blood at the opening of the right main bronchus. Following thorough aspiration and rinsing to remove fresh blood and blood clots, the patient’s symptoms were alleviated. Anteroposterior chest radiography showed re-expansion of her right upper lobe and atelectasis of the right middle and lower lobes (Figure 3). The main symptom of the patient on admission was hemoptysis, of a subacute nature, with the lesion site identical to the bleeding site. Given the failure of bronchoscopy therapy, her right middle and lower lobes were resected to prevent the development of life-threatening haemoptysis. During the lobectomy, we
Downloaded by [UNSW Library] at 08:02 13 September 2015
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Gynaecology Case Reports
Figure 1. Three-dimensional reconstruction of a preoperative chest CT scan of our patient, showing that the right pulmonary arteries were significantly smaller than the left pulmonary arteries, indicating a right pulmonary embolism.
Figure 2. Preoperative enhanced chest CT scan, shows atelectasis of the middle and lower lobes of the right lung of our patient, as well as a right pulmonary embolism.
Downloaded by [UNSW Library] at 08:02 13 September 2015
Gynaecology Case Reports 211
Figure 3. Anteroposterior chest radiograph following removal of blood clots by fibreoptic bronchoscopy, showing re-expansion of the right upper lobe and atelectasis of the right middle and lower lobes.
observed atelectasis of her right middle and lower lobes, as well as tracheal occlusion by blood clots. The excised tissue was sent for pathological examination, which showed an amniotic fluid embolism in the right middle and lower lobes (Figure 4). The patient was administered antibiotics and symptomatic treatment after surgery. She recovered well, and her stitches were removed 10 days after surgery. The clean incision healed uneventfully and the patient was discharged.
Discussion It is difficult to find clinical explanations to account for all the reactions triggered by amniotic fluid pulmonary embolism. Amniotic fluid embolisms may occur when visible pollutants in the amniotic fluid, including lanugo, keratinised epithelium, vernix and meconium, as well as procoagulant substances, enter the maternal blood circulation (Gei and Hankins 2000). In contrast, others have suggested that amniotic fluid embolisms are triggered primarily
by anaphylactic reactions, proposing to replace the phrase ‘amniotic fluid embolism’ with ‘anaphylactoid syndrome of pregnancy’ (Clark et al. 1995; Clark 2010). Findings in our patient, however, suggest that these embolisms are not triggered solely by anaphylactic reactions that occur when amniotic fluid enters the maternal bloodstream. Our findings also suggest that visible components in amniotic fluid can form emboli, which cause pulmonary embolism, resulting in a range of symptoms. In addition, our results supplement the clinical staging standards for amniotic fluid embolism (Sisodia et al. 2012). Late-onset amniotic fluid pulmonary embolism is extremely rare clinically. Our patient did not experience any of the traditional triggers of amniotic fluid embolism, including multipara, premature rupture or artificial rupture of membranes, strong uterine contractions, improper application of oxytocin or poor uterine contractions after surgery. However, she developed this condition 6 days after delivery by caesarean section, with clinical manifestations of haemoptysis with breathing difficulties. Our findings suggest that spiral CT and digital subtraction pulmonary angiography are important tools in the diagnosis of pulmonary embolism. A systematic review of literature published between 1995 and 2004 found that multi-slice spiral CT may be the gold standard for the diagnosis of pulmonary embolism, as it has a sensitivity of 87–94% and a specificity of 94–100% (Russo et al. 2005). Our findings also indicate the importance of obtaining a detailed medical history of the patient prior to diagnosis and treatment, to avoid any misdiagnosis or missed diagnosis due to a traditional understanding of amniotic fluid embolism. Amniotic fluid embolism may be the cause of pulmonary embolism after childbirth. The entrance into the maternal bloodstream of small amounts of visible components in the amniotic fluid may not necessarily trigger anaphylactic reactions and may instead form emboli. Accordingly, treatment strategies should not be confined to a single treatment modality; rather, pulmonary re-expansion, as well as thrombolytic and anticoagulant therapy, should be administered, in addition to surgical treatment of pulmonary embolisms. These treatments may prevent small scattered emboli in the blood from again causing embolisms and late-onset hypersensitivity. The findings in this patient indicate that amniotic fluid embolisms and pulmonary embolisms have various clinical manifestations and low specificity. If a patient’s medical history and clinical manifestations suggest amniotic fluid embolism, the patient should be examined and diagnosed as quickly as possible to provide comprehensive treatment and avoid adverse consequences. Amniotic fluid pulmonary embolism is suggested when respiratory symptoms such as hemoptysis develop suddenly in women after labour, making it necessary to perform pulmonary angiography in a timely fashion. Following a definitive diagnosis, thrombolysis should be withheld until thoracic surgeons are consulted to deal with the diseased lungs as early as possible, in order to prevent pulmonary embolism from inducing other life-threatening side-effects. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
Figure 4. Pathologic examination, showing amniotic fluid components in the blood vessels of our patient.
Clark SL, Hankins GDV, Dudley DA et al. 1995. Amniotic fluid embolism: analysis of the national registry. American Journal of Obstetrics and Gynecology 172:1158–1169. Clark SL. 2010. Amniotic fluid embolism. Clinical Obstetrics and Gynecology 53:322–328. Gei G, Hankins GDV. 2000. Amniotic fluid embolism: an update. Contemporary Obstetrics and Gynecology 45:53–66. Meyer JR. 1926. Embolia pulmonar amino caseosa. Brasil Medico 2:301–303. Russo V, Piva T, Lovato L et al. 2005. Multidetector CT: a new gold standard in the diagnosis of pulmonary embolism? State of the art and diagnostic algorithms. La Radiologia Medica 109:49–61. Sisodia SM, Bendale KA, Khan WA. 2012. Amniotic fluid embolism: a cause of sudden maternal death and police inquest. American Journal of Forensic Medicine and Pathology 33:330–334.
ISSN: 0144-3615 (Print) 1364-6893 (Online) Journal homepage: http://www.tandfonline.com/loi/ijog20
Surgical treatment of late-onset amniotic fluid pulmonary embolism J. Yao, G.-G. Shao, W. Song, R.-G. Yang, D.-X. Yin, L.-M. Zhang & Y.-P. Liu To cite this article: J. Yao, G.-G. Shao, W. Song, R.-G. Yang, D.-X. Yin, L.-M. Zhang & Y.-P. Liu (2014) Surgical treatment of late-onset amniotic fluid pulmonary embolism, Journal of Obstetrics and Gynaecology, 34:2, 209-211 To link to this article: http://dx.doi.org/10.3109/01443615.2013.853729
Published online: 02 Dec 2013.
Submit your article to this journal
Article views: 104
View related articles
View Crossmark data
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ijog20 Download by: [UNSW Library]
Date: 13 September 2015, At: 08:02
Gynaecology Case Reports 209 out using desmin, actin and S100 staining. Desmin is a 52 kd protein that is a subunit of intermediate filaments in skeletal, smooth and cardiac muscle. Actin is a major protein component of thin filaments that together with motor protein myosin combine to form myofibrils. S100 is a marker of melanoma, malignant peripheral nerve sheath tumour, schwannoma, paraganglioma stromal cells, histiocytoma and clear cell sarcomas. The presence of desmin and actin and the absence of S100 confirmed this was a leiomyoma which was classified as benign due to the low mitotic count that was completely excised. A follow up review at 3 months showed a well-healed operation site with complete resolution of the mass.
Downloaded by [UNSW Library] at 08:02 13 September 2015
Discussion Benign neoplasms of the urethra may arise from any of the constituent tissues including glandular, transitional and squamous epithelium, and also from smooth and striated muscle tissue. They may also exhibit unusual growth patterns, including benign metastasising leiomyoma, disseminated peritoneal leiomyomatosis, intravenous leiomyomatosis, parasitic leiomyoma (Putran et al. 2010) and retroperitoneal growth (Fasih et al. 2008). Urethral leiomyomas are more common in females than males (Jalde et al. 2012): this is possibly due to spread from the most common site, namely the uterus, which may have happened in this case. Urethral leiomyomas are reported to enlarge during pregnancy and regress after delivery, suggesting a possible hormonal dependence (Fry et al. 1988) which is thought to be oestrogen and more prevalent in the fourth decade (Ghadian and Hoseini 2013). Most tumours present with a palpable lump but can also present with urinary irritative or obstructive voiding symptoms dependent upon its size and position (Bai et al. 2007). The differential diagnoses include urethrocele, urethral diverticulum, urethral malignancy, paraurethral cysts and vaginal paraurethral myxoid leiomyoma (Costantini et al. 2008). Urethral leiomyomas are very uncommon lesions (Fry et al. 1988) but should be excised to exclude malignancy, but prognosis is excellent, since there are no recorded cases of recurrence or malignant transformation (Merrel and Brown 1981; Oderda et al. 2013) to leiomyosarcoma. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References Bai SW, Jung HJ, Jeon MJ et al. 2007. Leiomyomas of the female urethra and bladder: a report of five cases and review of the literature. International Urogynecology Journal 18:913–917. Costantini E, Cochetti G, Porena M. 2008. Vaginal para-urethral myxoid leiomyoma: case report and review of the literature. International Urogynecology Journal 19:1183–1185. Fasih N, Prasad Shanbhogue AK, Macdonald DB et al. 2008. Leiomyomas beyond the uterus: usual locations, rare manifestations. Radiographics 28:1931–1948. Fry M, Wheeler JS, Mata JA et al. 1988. Leiomyoma of the female urethra. Journal of Urology 140:613–614. Ghadian A, Hoseini SY. 2013. Transvesical enucleation of multiple leiomyoma of bladder and urethra. Nephro-urology 5:709–711. Jalde DD, Godhi SA, Uppin SM et al. 2012. A case of urethral leiomyoma – a rare presentation. World Journal of Science and Technology 2:27–28. Merrel RW, Brown HE. 1981. Recurrent urethral leiomyoma presenting as stress incontinence. Urology 17:588–589. Oderda M, Mondaini N, Bartoletti R et al. 2013. Leiomyomata of the genitourinary tract: a case series from the ‘rare urological neoplasm’ registry. Scandinavian Journal of Urology 47:158–162. Putran J, Khaled K. 2010. Parasitic leiomyomas: two case reports and review of literature. Gynecological Surgery 7:383–384.
Surgical treatment of late-onset amniotic fluid pulmonary embolism J. Yao1,2, G.-G. Shao1, W. Song3, R.-G. Yang2, D.-X. Yin4, L.-M. Zhang2 & Y.-P. Liu1
Departments of 1Thoracic Surgery, The First Hospital of Jilin University, 2Jilin Province People’s Hospital, 3Obstetrics and Gynecology, The First Clinical Hospital of Jilin University and 4Vascular Surgery, China-Japan Union Hospital of Jilin University, Changchun, China DOI: 10.3109/01443615.2013.853729 Correspondence: G.-G. Shao, Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, China
Introduction Pulmonary embolism (PE) refers to a group of diseases and clinical syndromes resulting from the occlusion of the pulmonary artery by a variety of emboli, including pulmonary thromboembolism (PTE), amniotic fluid pulmonary embolism, fat embolism syndrome and air embolism. Amniotic fluid pulmonary embolism is a rare obstetric emergency, with a mortality rate as high as 80%, and late-onset amniotic fluid pulmonary embolism is an even rarer clinical entity. Late-onset amniotic fluid pulmonary embolism, which was first reported in 1926 (Meyer 1926), occurs when amniotic fluid components enter the maternal blood circulation during childbirth. Pathologically, fetal components, including lanugo, vermix, meconium and keratinised epithelia, are found in the pulmonary circulation of the pregnant woman, although hypersensitivity triggered by invisible components in amniotic fluid (e.g. surface-active substance, thromboxane A2, endothelin, leukotrienes) is thought to be an important cause of this condition (Gei and Hankins 2000; Clark et al. 1995; Clark 2010). Late-onset amniotic fluid pulmonary embolisms are characterised by an acute onset, a short course and a poor prognosis. Most patients are managed with symptomatic treatment, including anti-shock, anti-spasmodic, and vasoactive drugs, with surgical treatment being extremely rare. We describe here a patient with late-onset amniotic fluid embolism in the middle and lower lobes of the right lung.
Case report A 22-year-old primipara was admitted to our hospital on 13 February, 2009, with a 3-day history of haemoptysis associated with dyspnoea, starting 6 days after a caesarean section. At 40 weeks of pregnancy, on her expected date of delivery, she checked into a local hospital, where she underwent a caesarean section after failure to trigger the onset of labour. She received epidural anaesthesia and showed stable vital signs during the operation, with blood pressure, heart rate and blood oxygen saturation within normal ranges. She was conscious intraoperatively and did not receive postoperative pain pump therapy. The surgery was uneventful, and both she and her baby were in generally good condition. The patient experienced no potent uterine contractions before delivery or bleeding during delivery, and she was discharged 4 days after caesarean section. On the third morning after discharge from the hospital, or 6 days after the caesarean section, she developed haemoptysis with no obvious trigger, coughing up about 100 ml of bright red blood, along with chest tightness and shortness of breath. A chest examination upon admission to our hospital revealed a narrowed right intercostal space, dullness on percussion, a faint trachea conduction sound in the right upper lung, and no breath sounds in the right middle and lower lobes. Three-dimensional chest CT scans showed atelectasis in the right middle and lower lobes and right pulmonary embolism (Figures 1 and 2). Fibreoptic bronchoscopy showed rich blood clots and fresh blood at the opening of the right main bronchus. Following thorough aspiration and rinsing to remove fresh blood and blood clots, the patient’s symptoms were alleviated. Anteroposterior chest radiography showed re-expansion of her right upper lobe and atelectasis of the right middle and lower lobes (Figure 3). The main symptom of the patient on admission was hemoptysis, of a subacute nature, with the lesion site identical to the bleeding site. Given the failure of bronchoscopy therapy, her right middle and lower lobes were resected to prevent the development of life-threatening haemoptysis. During the lobectomy, we
Downloaded by [UNSW Library] at 08:02 13 September 2015
210
Gynaecology Case Reports
Figure 1. Three-dimensional reconstruction of a preoperative chest CT scan of our patient, showing that the right pulmonary arteries were significantly smaller than the left pulmonary arteries, indicating a right pulmonary embolism.
Figure 2. Preoperative enhanced chest CT scan, shows atelectasis of the middle and lower lobes of the right lung of our patient, as well as a right pulmonary embolism.
Downloaded by [UNSW Library] at 08:02 13 September 2015
Gynaecology Case Reports 211
Figure 3. Anteroposterior chest radiograph following removal of blood clots by fibreoptic bronchoscopy, showing re-expansion of the right upper lobe and atelectasis of the right middle and lower lobes.
observed atelectasis of her right middle and lower lobes, as well as tracheal occlusion by blood clots. The excised tissue was sent for pathological examination, which showed an amniotic fluid embolism in the right middle and lower lobes (Figure 4). The patient was administered antibiotics and symptomatic treatment after surgery. She recovered well, and her stitches were removed 10 days after surgery. The clean incision healed uneventfully and the patient was discharged.
Discussion It is difficult to find clinical explanations to account for all the reactions triggered by amniotic fluid pulmonary embolism. Amniotic fluid embolisms may occur when visible pollutants in the amniotic fluid, including lanugo, keratinised epithelium, vernix and meconium, as well as procoagulant substances, enter the maternal blood circulation (Gei and Hankins 2000). In contrast, others have suggested that amniotic fluid embolisms are triggered primarily
by anaphylactic reactions, proposing to replace the phrase ‘amniotic fluid embolism’ with ‘anaphylactoid syndrome of pregnancy’ (Clark et al. 1995; Clark 2010). Findings in our patient, however, suggest that these embolisms are not triggered solely by anaphylactic reactions that occur when amniotic fluid enters the maternal bloodstream. Our findings also suggest that visible components in amniotic fluid can form emboli, which cause pulmonary embolism, resulting in a range of symptoms. In addition, our results supplement the clinical staging standards for amniotic fluid embolism (Sisodia et al. 2012). Late-onset amniotic fluid pulmonary embolism is extremely rare clinically. Our patient did not experience any of the traditional triggers of amniotic fluid embolism, including multipara, premature rupture or artificial rupture of membranes, strong uterine contractions, improper application of oxytocin or poor uterine contractions after surgery. However, she developed this condition 6 days after delivery by caesarean section, with clinical manifestations of haemoptysis with breathing difficulties. Our findings suggest that spiral CT and digital subtraction pulmonary angiography are important tools in the diagnosis of pulmonary embolism. A systematic review of literature published between 1995 and 2004 found that multi-slice spiral CT may be the gold standard for the diagnosis of pulmonary embolism, as it has a sensitivity of 87–94% and a specificity of 94–100% (Russo et al. 2005). Our findings also indicate the importance of obtaining a detailed medical history of the patient prior to diagnosis and treatment, to avoid any misdiagnosis or missed diagnosis due to a traditional understanding of amniotic fluid embolism. Amniotic fluid embolism may be the cause of pulmonary embolism after childbirth. The entrance into the maternal bloodstream of small amounts of visible components in the amniotic fluid may not necessarily trigger anaphylactic reactions and may instead form emboli. Accordingly, treatment strategies should not be confined to a single treatment modality; rather, pulmonary re-expansion, as well as thrombolytic and anticoagulant therapy, should be administered, in addition to surgical treatment of pulmonary embolisms. These treatments may prevent small scattered emboli in the blood from again causing embolisms and late-onset hypersensitivity. The findings in this patient indicate that amniotic fluid embolisms and pulmonary embolisms have various clinical manifestations and low specificity. If a patient’s medical history and clinical manifestations suggest amniotic fluid embolism, the patient should be examined and diagnosed as quickly as possible to provide comprehensive treatment and avoid adverse consequences. Amniotic fluid pulmonary embolism is suggested when respiratory symptoms such as hemoptysis develop suddenly in women after labour, making it necessary to perform pulmonary angiography in a timely fashion. Following a definitive diagnosis, thrombolysis should be withheld until thoracic surgeons are consulted to deal with the diseased lungs as early as possible, in order to prevent pulmonary embolism from inducing other life-threatening side-effects. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
Figure 4. Pathologic examination, showing amniotic fluid components in the blood vessels of our patient.
Clark SL, Hankins GDV, Dudley DA et al. 1995. Amniotic fluid embolism: analysis of the national registry. American Journal of Obstetrics and Gynecology 172:1158–1169. Clark SL. 2010. Amniotic fluid embolism. Clinical Obstetrics and Gynecology 53:322–328. Gei G, Hankins GDV. 2000. Amniotic fluid embolism: an update. Contemporary Obstetrics and Gynecology 45:53–66. Meyer JR. 1926. Embolia pulmonar amino caseosa. Brasil Medico 2:301–303. Russo V, Piva T, Lovato L et al. 2005. Multidetector CT: a new gold standard in the diagnosis of pulmonary embolism? State of the art and diagnostic algorithms. La Radiologia Medica 109:49–61. Sisodia SM, Bendale KA, Khan WA. 2012. Amniotic fluid embolism: a cause of sudden maternal death and police inquest. American Journal of Forensic Medicine and Pathology 33:330–334.
