Tugas Kepaniteraan Ilmu Kesehatan Anak RS Bhakti Yudha

Maria Donata Keli

11 2015 058

1 a. Tanda-tanda Sepsis Neonatorum

Berdasarkan kejadiannya, infeksi sepsis neonatorum berlangsung dalam dua awitan berikut
Awitan dini :
a. Gejala klinisnya tampak secara dini yaitu sekitar/sejak semula (rata-rata 48 jam
pertama).
b. Infeksi berkaitan dengan sumber pada ibunya saat proses persalinan.
c. Kumannya: stafilokokus (E. Coli, H. Infuenzae, Klebsiella, Monilia).
Awitan lanjut :
a. Gejala klinisnya tampak setelah7 hari, saat penderita telah pulang.
b. Sumber infeksinya: faktor lingkungan yang kotor dan infeksius, infeksi
nosokomial di rumah sakit.
c. Penyebab infeksinya : S. Aureus, stafilokokus grup beta, E. Coli monositogen.
d. Komplikasi berat : komplikasi susunan saraf pusat.
Diagnosis sepsis nenoatorum sulit ditetapkan karena gejalanya tidak khas. Setiap perubahan
keadaan fisik atau gambaran darah neonatus dianggap terjadi infeksi sepsis neonatorum.
Diagnosis ditegakkan jika terdapat lebih dari satu kumpulan gejala berikut ini :
Gejala umum infeksi : tampak sakit, tidak man ruinum, suhu naik atau turun,
sklerena/skerederna.
Gejala gastrointestinal : terdapat diare, muntah, hepatomegali, splenomegali, atau
perut kembung.
Gejala paru : sianosis, apnea, atau takipnea.
Gejala kardiovaskular : terdapat takikardia, edema atau dehidrasi.
Gejala neurologic : letargi (tampak seperti mayat), peka rangsang atau kejang.
Gejala hematologis-laboratorium : ikterus, pendarahan bawah kulit, leukopenia, dan
leukosit kurang dari 5.000/mm3.

1.b.Etiologi
Semua infeksi pada neonatus dianggap oportunisitik dan setiap bakteri mampu
menyebabkan sepsis.
 Mikroorganisme berupa bakteri, jamur, virus atau riketsia. Penyebab paling sering
dari sepsis : Escherichia Coli dan Streptococcus grup B (dengan angka kesakitan
sekitar 50 70 %. Diikuti dengan malaria, sifilis, dan toksoplasma. Streptococcus
grup A, dan streptococcus viridans, patogen lainnya gonokokus, candida alibicans,
virus herpes simpleks (tipe II) dan organisme listeria, rubella, sitomegalo, koksaki,
hepatitis, influenza, parotitis.
Pertolongan persalinan yang tidak higiene, partus lama, partus dengan tindakan.
Kelahiran kurang, BBLR, cacat bawaan

Etiologi terjadinya sepsis pada neonatus adalah dari bakteri, virus, jamur dan protozoa
(jarang). Penyebab yang paling sering dari sepsis awitan awal adalah Streptokokus grup B
dan bakteri enterik yang didapat dari saluran kelamin ibu. Sepsis awitan lanjut dapat
disebabkan oleh SGB, virus herpes simplek (HSV), enterovirus dan E.coli. Pada bayi dengan
berat badan lahir sangat rendah, Candida dan Stafilokokus koagulase-negatif (CONS),
merupakan patogen yang paling umum pada sepsis awitan lanjut.

Jika dikelompokan maka didapat:

Bakteri gram positif

Streptokokus grup B penyebab paling sering.

Stafilokokus koagulase negatif merupakan penyebab utama bakterimia
nosokomial.
Streptokokus bukan grup B.

Bakteri gram negatif

Escherichia coli Kl penyebab nomor 2 terbanyak.

H. influenzae.
Listeria monositogenes.
Pseudomonas
Klebsiella.
Enterobakter.
Salmonella.
Bakteria anaerob.
Gardenerella vaginalis.

Walaupun jarang terjadi,terhisapnya cairan amnion yang terinfeksi dapat menyebabkan

pneumonia dan sepsis dalam rahim, ditandai dengan distres janin atau asfiksia neonatus.
Pemaparan terhadap patogen saat persalinan dan dalam ruang perawatan atau di masyarakat
merupakan mekanisme infeksi setelah lahir.

1.c Penanganan Sepsis Neonatorum

Prinsip pengobatan sepsis neonatorum adalah mempertahankan metabolisme tubuh dan

memperbaiki keadaan umum dengan pemberian cairan intravena termasuk kebutuhan nutrisi.
Menurut Yu Victor Y.H dan Hans E. Monintja pemberian antibiotik hendaknya memenuhi
kriteria efektif berdasarkan hasil pemantauan mikrobiologi, murah, dan mudah diperoleh,
tidak toksik, dapat menembus sawar darah otak atau dinding kapiler dalam otak yang
memisahkan darah dari jaringan otak dan dapat diberi secara parenteral. Pilihan obat yang
diberikan ialah ampisilin dan gentamisin atau ampisilin dan kloramfenikol, eritromisin atau
sefalasporin atau obat lain sesuai hasil tes resistensi.

Dosis antibiotik untuk sepsis neonatorum : Ampisislin 200 mg/kgBB/hari, dibagi 3 atau 4 kali
pemberian; Gentamisin 5 mg/kg BB/hari, dibagi dalam 2 pemberian; Kloramfenikol 25
mg/kg BB/hari, dibagi dalam 3 atau 4 kali pemberian; Sefalasporin 100 mg/kg BB/hari,
dibagi dalam 2 kali pemberian;Eritromisin500 mg/kg BB/hari, dibagi dalam 3 dosis.

2. Penanganan Pasien MAS (Meconium Aspiration Syndrom}

Nilai konsistensi mekonium. Kejadian MAS meningkat seiring dengan peningkatan

konsistensi mekonium.
Rekomendasi bahwa dokter kebidanan harus membersihkan hidung dan orofaring
bayi sebelum melahirkan bahu atau dada, tidak dianjurkan lagi.
Jika ditemukan mekonium pada cairan ketuban, bayi harus segera diserahkan kepada
dokter anak untuk dibersihkan.
Pada penilaian awal sebuah persalinan dengan ketuban bercampur mekonium, dokter
anak harus menentukan apakah bayi bugar atau tidak. Bayi dikatakan bugar bila
frekuensi denyut jantung >100 kali/menit, bernapas spontan, dan tonus baik (bergerak
spontan atau fleksi ekstremitas).
a. Bila bayi bugar, berikan perawatan rutin tanpa memandang konsistensi mekonium.
b. Bila terdapat distres pernapasan, lakukan laringoskopi direk dan pengisapan
intratrakeal (menggunakan aspirator mekonium).
Bayi yang dilahirkan dengan ketuban bercampur mekonium, sebanyak 20-30% akan
mengalami depresi saat melalui perineum. Pada kasus ini, intubasi menggunakan
laringoskop sebaiknya dilakukan sebelum usaha napas dimulai. Setelah intubasi, pipa
 endotrakeal dihubungkan dengan mesin pengisap. Prosedur ini diulangi sampai trakea
bersih atau bila resusitasi harus dimulai. Visualisasi pita suara tanpa melakukan
pengisapan tidak dianjurkan karena mekonium masih mungkin berada di bawah pita
suara. Ventilasi tekanan positif sebisa mungkindihindari sampai pengisapan trakea
selesai. Kondisi umum bayi tidak boleh diabaikan selama melakukan pengisapan
trakea. Pengisapan trakea harus dilakukan dengan cepat dan ventilasi harus segera
dimulai sebelum terjadi bradikardi.

Walaupun telah dilakukan pengisapan trakea, bayi yang mengalami distres intrapartum masih
berisiko mengalami MAS dan harus dipantau secara ketat.
o Perawatan rutin. Distres sering mengakibatkan abnormalitas metabolik seperti
hipoksia, asidosis, hipoglikemia, dan hipokalsemia. Koreksi abnormalitas metabolik
bila diperlukan. Cairan harus direstriksi untuk mencegah edema serebri dan paru.
o Pemantauan saturasi oksigen. Pulse oxymetri dapat dijadikan pemeriksaan
awal untuk mendeteksi PPHN dengan membandingkan saturasi oksigen pada
lengan kanan dengan saturasi oksigen pada ekstremitas bawah.
o Obstruksi. Pada bayi dengan aspirasi mekonium berat, dapat terjadi obstruksi mekanik
saluran napas danbpneumonitis kimia. Atelektasis dan inflamasi yang terus berjalan
serta terbentuknya pirau ekstrapulmonar akan memperburuk mismatch ventilasi-
perfusi dan mengakibatkan hipoksemia berat.
o Hipoksemia. Tata laksana hipoksemia adalah meningkatkan konsentrasi oksigen
inspirasi dengan pemantauan analisis gas darah dan pH. Bayi harus mendapat oksigen
yang adekuat karena hipoksia berulang mengakibatkan vasokonstriksi
paru dan selanjutnya dapatbmenyebabkan PPHN.
o Ventilasi mekanik. Ventilasi mekanik terindikasi bila PaCO2 >60 mmHg atau terdapat
hipoksemia persisten (PaO2 <50 mmHg). Pada kasus berat, seringkali dibutuhkan
inspiratory pressure yang lebih tinggi dibandingkan kasus sindrom gawat napas.
Waktu ekspirasi yang cukup harus diberikan untuk mencegah air trapping akibat
obstruksi parsial saluran napas. Bayi dengan MAS berat yang tidak
berespons dengan ventilator konvensional dan yang mengalami air leak syndrome
mungkin membutuhkan high frequency oscillatory ventilator.
Medikamentosa.
o Antibiotik. Seringkali sulit untuk membedakan antara pneumonia bakterial dan MAS
hanya berdasarkan temuan klinis dan foto toraks. Walaupun beberapa bayi dengan
 MAS juga mengalami infeksi, penggunaan antibiotik spektrum luas terindikasi hanya
pada kasus dengan infiltrat pada foto toraks. Kultur darah darus dilakukan untuk
mengidentifikasi etiologi dan mengevaluasi keberhasilan terapi antibiotik.
o Surfaktan. Mekonium menghambat aktivitas surfaktan endogen. Terapi surfaktan
dapat meningkatkan oksigenasi, menurunkan komplikasi pulmonal, dan menurunkan
kebutuhan ECMO (extracorporeal membrane oxygenation). Surfaktan tidak rutin
diberikan untuk kasus MAS, tetapi dapat dipertimbangkan untuk kasus yang berat dan
tidak berespons terhadap terapi standar.
o Kortikosteroid. Penggunaan kortikosteroid pada MAS tidak dianjurkan.

3. Penanganan Pasien HMD (Hialin Membran Disease)

Antibiotika untuk mencegah infeksi sekunder
Setiap penderita PMH perlu mendapat antibiotika untuk mencegah terjadinya infeksi
sekunder. Antibiotik diberikan adalah yang mempunyai spektrum luas penisilin
(50.000 U-100.000 U/KgBB/hari) atau ampicilin (100 mg/KgBB/hari) dengan
gentamisin (3-5 mg/KgBB/hari).
Antibiotik diberikan selama bayi mendapatkan cairan intravena sampai gejala
gangguan nafas tidak ditemukan lagi.
Furosemid untuk memfasilitasi reduksi cairan ginjal dan menurunkan cairan paru.
Fenobarbital.
Vitamin E untuk menurunkan produksi radikal bebas oksigen.
Metilksantin ( teofilin dan kafein ) untuk mengobati apnea dan untuk pemberhentian
dari pemakaian ventilasi mekanik.
Pemberian Surfaktan Buatan
Surfaktan artifisial sebanyak 25 mg dosis tunggal dengan menyemprotkan ke dalam
trakea penderita.
Surfaktan eksogen adalah derivate dari sumber alami misalnya manusia ( di dapat dari
cairan amnion atau paru sapi,tetapi bisa juga berbentuk surfakatan buatan ).Surfaktan
ini disemprotkan ke dalam trakea dengan dosis 60 mg/KgBB.
Pemberian Oksigen
Oksigen mempunyai pengaruh yang kompleks terhadap bayi baru lahir. Pemberian O2
yang terlalu banyak dapat menimbulkan komplikasi yang tidak diinginkan seperti
fibrosis paru, kerusakan retina (retrolental fibroplasta) dan lain-lain.
Untuk mencegah timbulnya komplikasi ini, pemberian O2 sebaiknya diikuti dengan :
 Pemeriksaan tekanan O2 arterial (PaO2) secara teratur.
Konsentrasi O2 yang diberikan harus dijaga agar cukup untuk
mempertahankan tekanan PaO2 antara 80 100 mmHg.
Bila fasilitas untuk pemeriksaan tekanan gas arterial tidak ada, O2 dapat
diberikan sampai gejala cyanosis menghilang.

4. Penanganan Pasien DIC (Disseminated Intravascular Coagulation)

Atasi penyakit primer yang menimbulkan DIC
Pemberian heparin. Heparin dapat diberikan 200 U/KgBB iv tiap 4-6 jam. Kenaikan
kadar fibrinogen plasma nyata dalam 6-8 jam, setelah 24-48 jam sesudah mencapai
harga normal.
Terapi pengganti darah atau PRC diberikan untuk mengganti darah yang keluar. Bila
dalam pengobatan yang baik, jumlah trombosit tetap rendah dalam waktu sampai
seminggu, berarti tetap mungkin terjadi perdarahan terus atau ulangan, sehingga
dalam keadaan ini perlu diberikan platelet concentrate.
Obat penghambat fibrinolitik. Bila perlu sekali, baru boleh diberikan sesudah heparin
disuntikkan. Lama pengobatan tergantung dari perjalanan penyakit primernya. Bila
penyakit primernya dapat diatasi cepat, misalnya komplikasi kehamilan dan sepsis,
pengobatan DIC hanya perlu untuk 1-2 hari. Pada keganasan leukemia dan penyakit-
penyakit lain dimana pengobatan tidak efektif, heparin perlu lebih lama diberikan.
Pada keadaan ini sebaiknya diberikan heparin subkutan secara berkala. Antikoagulan
lain jarang diberikan. Sodium warfarin kadang-kadang memberikan hasil baik yaitu:
Masa Protombin.
Partial Thrombin Time (PTT).
PTT diaktifkan seharusnya juga memanjang pada DIC fulminan karena
berbagai sebab sehingga parameter ini lebih berguna pada masa protrombin.
Mekanisme terjdinya PTT normal atau memendek pada 40-50% pasien DIC
sama seperti pada masa protrombin.
Kadar Faktor Pembekuan

Pemeriksaan kadar faktor pada pembekuan memberikan sedikit informasi

yang berarti pada pasien DIC. Sebagaimana sudah disebutkan sebelumnya
pada kebanyakan pasien DIC fulminan faktor pembekuan yang aktif beredar
dalam sirkulasi terutama F Xa, IXa dan trombin. Sebagai contoh jika F VIII
diperiksa dengan pasien DIC dengan disertai peningikata F Xa, jelas F VIII
yang dicatat akan tinggi karena dalam uji sistem F Xa melintas kebutuhan F
 VIII sehingga terjadi perubahan fibrinogen menjadi fibrin dengan cepat
dengan waktu yang dicatat dalam kurva standar pendek, dan ini akan
diinterpretasi sebagai kadar F VIII yang tinggi.
FDP
Kadar FDP akan meningkat pada 85-100% kasus DIC. Hasil degradasi ini
akibat biodegradasi fibrinogen atau fibrin oleh plasmin, jadi secara tidak
langsung menunjukkan bahwa jumlah plasmin melebihi jumlah normal dalam
darah. Tes protamin sulfat atau etanol biasanya positif bila dalam sirkulasi
darah ada fibrin monomer soluble.
D- Dimer
Suatu test terbaru untuk DIC adalah D-Dimer.D-Dimer merupakan hasil
degradasi fibrin ikat silang yaitu fibrinogen yang diubah menjadi fibrin
kemudian diaktifkan oleh factor XIII. D-Dimer tamapaknya merupakan tes
yang paling dapat dipercaya untuk menilai kemungkinan DIC, Menunjukkan
adanya D-Dimer apnormal pada 93% kasus, kadar AT III apnorml pada 89%
kasus, kadar fibri nopeptida apnormal pada 88% kasus, dan titer FDP
abnormal pada 75 % kasus.

5. Dosis Obat
Rifampisin: 10-20 mg/kgBB/hari, dosis maksimal 600 mg/hari.
Etambutol: 15-20 mg/kgBB/hari, dosis maksimal 1 250 mg/hari

Ranitidin : 2-4 mg/kg bb dua kali sehari. Dosis maksimal untuk anak-anak ialah 300
mg sehari.

Dopamin: 1-20 mcg/kg/menit, maksimum 50 mcg/kg/menit, titrasi sampai respon

yang diharapkan.

Digoksin : Untuk digitalisasi cepat : 25 mcg/kg berat badan dengan selang waktu
tertentu sampai kompensasi tercapai. Pemeliharaan : 10-20 mcg/kg berat badan/hari.

Imunoglobulin : Intra vena imunodefisiensi primer dan atau sekunder dosis bulanan :
100 - 200 mg/kg BB. Maksimal : 300 - 400 mg/kg BB. Purpura trombositopenia
idiopatik (Idiopathic Thrombocytopenic Purpura) induksi : 400 mg mg/kg BB per hari
selama 5 hari. pemeliharaan : 400 mg/kg BB, 1 kali seminggu. sindrom kawasaki : 2
g/kg BB
 Cefadroxil: 30 mg / kg BB / hari dalam dosis terbagi tiap 12 jam

Metronidazole: 10-15 mg/kgBB/hari

Background

Postpartum hemorrhage (PPH) is the leading cause of maternal mortality. All women who
carry a pregnancy beyond 20 weeks gestation are at risk for PPH and its sequelae. Although
maternal mortality rates have declined greatly in the developed world, PPH remains a leading
cause of maternal mortality elsewhere.

Postpartum hemorrhage. Maternal morbidity by subre

Postpartum hemorrhage. Maternal morbidity by subregion, 1995.

The direct pregnancy-related maternal mortality rate in the United States is approximately 7-
10 women per 100,000 live births. National statistics suggest that approximately 8% of these
deaths are caused by PPH.[1] In industrialized countries, PPH usually ranks in the top 3
causes of maternal mortality, along with embolism and hypertension. In the developing
world, several countries have maternal mortality rates in excess of 1000 women per 100,000
live births, and World Health Organization statistics suggest that 25% of maternal deaths are
due to PPH, accounting for more than 100,000 maternal deaths per year.[2] The most recent
Practice Bulletin from the American College of Obstetricians and Gynecologists places the
estimate at 140,000 maternal deaths per year or 1 woman every 4 minutes.[3]

The rate of PPH increased from 1.5% in 1999 to 4.1% in 2009, and the rate of atonic PPH
rose from 1% in 1999 to 3.4% in 2009. The risk of total PPH with a morbidly adherent
placenta was markedly higher.[4]

Problem
The definition of PPH is somewhat arbitrary and problematic. PPH is defined as blood loss of
more than 500 mL following vaginal delivery or more than 1000 mL following cesarean
delivery.[5, 6] A loss of these amounts within 24 hours of delivery is termed early or primary
PPH, whereas such losses are termed late or secondary PPH if they occur 24 hours after
delivery. This article focuses on early PPH.

Estimates of blood loss at delivery are subjective and generally inaccurate. Studies have
suggested that caregivers consistently underestimate actual blood loss. Another proposal
suggests using a 10% fall in hematocrit value to define PPH, but this change is dependent on
the timing of the test and the amount of fluid resuscitation given.[7] More importantly, the
diagnosis would be retrospective, perhaps useful for research but not so in the clinical setting.

Another consideration is the differing capacities of individual patients to cope with blood
loss. A healthy woman has a 30-50% increase in blood volume in a normal singleton
pregnancy and is much more tolerant of blood loss than a woman who has preexisting
anemia, an underlying cardiac condition, or a volume-contracted condition secondary to
dehydration or preeclampsia. For these reasons, various authors have suggested that PPH
should be diagnosed with any amount of blood loss that threatens the hemodynamic stability
of the woman.

The diagnosis of PPH is usually reserved for pregnancies that have progressed beyond 20
weeks gestation. Deliveries at less than 20 weeks gestational age are spontaneous abortions.
Bleeding related to spontaneous abortion may have etiologies and management in common
with those for PPH.

Epidemiology

Frequency
United States and industrialized countries

The frequency of PPH is related to the management of the third stage of labor. This is the
period from the completed delivery of the baby until the completed delivery of the placenta.
Data from several sources, including several large randomized trials performed in
industrialized countries, indicate that the prevalence rate of PPH of more than 500 mL is
approximately 5% when active management is used versus 13% when expectant management
is used. The prevalence rate of PPH of more than 1000 mL is approximately 1% when active
management is used versus 3% when expectant management is used.[8, 9] See Medscape
Reference article Management of the Third Stage of Labor.

Developing countries

The increased frequency of PPH in the developing world is more likely reflected by the rates
given above for expectant management because of the lack of widespread availability of
medications used in the active management of the third stage.[2] A number of factors also
contribute to much less favorable outcomes of PPH in developing countries. The first is a
lack of experienced caregivers who might be able to successfully manage PPH if it occurred.
Additionally, the same drugs used for prophylaxis against PPH in active management of the
third stage are also the primary agents in the treatment of PPH. Lack of blood transfusion
services, anesthetic services, and operating capabilities also plays a role. Finally, the
previously mentioned comorbidities are more commonly observed in developing countries
and combine to decrease a woman's tolerance of blood loss.

Etiology

PPH has many potential causes, but the most common, by a wide margin, is uterine atony, ie,
failure of the uterus to contract and retract following delivery of the baby. PPH in a previous
pregnancy is a major risk factor and every effort should be made to determine its severity and
cause. In a recent randomized trial in the United States, birthweight, labor induction and
augmentation, chorioamnionitis, magnesium sulfate use, and previous PPH were all
positively associated with increased risk of PPH.[10]

In a large, population-based study, significant risk factors, identified using multivariable

analysis, were as follows:

Retained placenta (OR 3.5, 95% CI 2.1-5.8)

Failure to progress during the second stage of labor (OR 3.4, 95% CI 2.4-4.7)

Placenta accreta (OR 3.3, 95% CI 1.7-6.4)

Lacerations (OR 2.4, 95% CI 2.0-2.8)

Instrumental delivery (OR 2.3, 95% CI 1.6-3.4)

Large-for-gestational-age (LGA) newborn (OR 1.9, 95% CI 1.6-2.4)

Hypertensive disorders (OR 1.7, 95%CI 1.2-2.1)

Induction of labor (OR 1.4, 95%CI 1.1-1.7)

Augmentation of labor with oxytocin (OR 1.4, 95% CI 1.2-1.7). [11]

PPH is also associated with obesity. In a study by Blomberg, the risk of atonic uterine
hemorrhage rapidly increased with increasing BMI; in women with a BMI over 40, the risk
was 5.2% with normal delivery and 13.6% with instrumental delivery.[12]

A study by Hanley et al reported that serotonin-norepinephrine reuptake inhibitor exposure in

late pregnancy was associated with a 1.6- to 1.9-fold increased risk of postpartum
hemorrhage.[13, 14]

As a way of remembering the causes of PPH, several sources have suggested using the 4 T
s as a mnemonic: tone, tissue, trauma, and thrombosis.[15]
Tone

Uterine atony and failure of contraction and retraction of myometrial muscle fibers can lead
to rapid and severe hemorrhage and hypovolemic shock. Overdistension of the uterus, either
absolute or relative, is a major risk factor for atony. Overdistension of the uterus can be
caused by multifetal gestation, fetal macrosomia, polyhydramnios, or fetal abnormality (eg,
severe hydrocephalus); a uterine structural abnormality; or a failure to deliver the placenta or
distension with blood before or after placental delivery.

Poor myometrial contraction can result from fatigue due to prolonged labor or rapid forceful
labor, especially if stimulated. It can also result from the inhibition of contractions by drugs
such as halogenated anesthetic agents, nitrates, nonsteroidal anti-inflammatory drugs,
magnesium sulfate, beta-sympathomimetics, and nifedipine. Other causes include placental
implantation site in the lower uterine segment, bacterial toxins (eg, chorioamnionitis,
endomyometritis, septicemia), hypoxia due to hypoperfusion or Couvelaire uterus in abruptio
placentae, and hypothermia due to massive resuscitation or prolonged uterine exteriorization.
Recent data suggest that grand multiparity is not an independent risk factor for PPH.

Tissue

Uterine contraction and retraction leads to detachment and expulsion of the placenta.
Complete detachment and expulsion of the placenta permits continued retraction and optimal
occlusion of blood vessels.

Retention of a portion of the placenta is more common if the placenta has developed with a
succenturiate or accessory lobe. Following delivery of the placenta and when minimal
bleeding is present, the placenta should be inspected for evidence of fetal vessels coursing to
the placental edge and abruptly ending at a tear in the membranes. Such a finding suggests a
retained succenturiate lobe.

The placenta is more likely to be retained at extreme preterm gestations (especially < 24 wk),
and significant bleeding can occur. This should be a consideration in all deliveries at very
early gestations, whether they are spontaneous or induced. Recent trials suggest that the use
of misoprostol for second trimester termination of pregnancy leads to a marked reduction in
the rate of retained placenta when compared to techniques using the intrauterine instillation
of prostaglandin or hypertonic saline.[16] One such trial reported rates of retained placenta
requiring D&C of 3.4% with oral misoprostol compared to 22.4% using intra-amniotic
prostaglandin (p=0.002).[17]

Failure of complete separation of the placenta occurs in placenta accreta and its variants. In
this condition, the placenta has invaded beyond the normal cleavage plane and is abnormally
adherent. Significant bleeding from the area where normal attachment (and now detachment)
has occurred may mark partial accreta. Complete accreta in which the entire surface of the
placenta is abnormally attached, or more severe invasion (placenta increta or percreta), may
not initially cause severe bleeding, but it may develop as more aggressive efforts are made to
remove the placenta. This condition should be considered possible whenever the placenta is
implanted over a previous uterine scar, especially if associated with placenta previa.

All patients with placenta previa should be informed of the risk of severe PPH, including the
possible need for transfusion and hysterectomy.

Finally, retained blood may cause uterine distension and prevent effective contraction.

Trauma
Damage to the genital tract may occur spontaneously or through manipulations used to
deliver the baby. Cesarean delivery results in twice the average blood loss of vaginal delivery.
Incisions in the poorly contractile lower segment heal well but are more reliant on suturing,
vasospasm, and clotting for hemostasis.

Uterine rupture is most common in patients with previous cesarean delivery scars. Routine
transvaginal palpation of such scars is no longer recommended. Any uterus that has
undergone a procedure resulting in a total or thick partial disruption of the uterine wall should
be considered at risk for rupture in a future pregnancy. This admonition includes
fibroidectomy; uteroplasty for congenital abnormality; cornual or cervical ectopic resection;
and perforation of the uterus during dilatation, curettage, biopsy, hysteroscopy, laparoscopy,
or intrauterine contraceptive device placement.

Trauma may occur following very prolonged or vigorous labor, especially if the patient has
relative or absolute cephalopelvic disproportion and the uterus has been stimulated with
oxytocin or prostaglandins. Using intrauterine pressure monitoring may lessen this risk.
Trauma also may occur following extrauterine or intrauterine manipulation of the fetus. The
highest risk is probably associated with internal version and extraction of a second twin;
however, uterine rupture may also occur secondary to external version. Finally, trauma may
result secondary to attempts to remove a retained placenta manually or with instrumentation.
The uterus should always be controlled with a hand on the abdomen during any such
procedure. An intraumbilical vein saline/oxytocin or saline/misoprostol injection may reduce
the need for more invasive removal techniques.[8]

Cervical laceration is most commonly associated with forceps delivery, and the cervix should
be inspected following all such deliveries. Assisted vaginal delivery (forceps or vacuum)
should never be attempted without the cervix being fully dilated. Cervical laceration may
occur spontaneously. In these cases, mothers have often been unable to resist bearing down
before full cervical dilatation. Rarely, manual exploration or instrumentation of the uterus
may result in cervical damage. Very rarely, the cervix is purposefully incised at the 2- and/or
10-oclock positions to facilitate delivery of an entrapped fetal head during a breech delivery
(Dhrssen incision).

Vaginal sidewall laceration is also most commonly associated with operative vaginal delivery,
but it may occur spontaneously, especially if a fetal hand presents with the head. Lacerations
may occur during manipulations to resolve shoulder dystocia. Lacerations often occur in the
region overlying the ischial spines. The frequency of sidewall and cervical lacerations has
probably decreased in recent years because of the reduction in the use of midpelvic forceps
and, especially, midpelvic rotational procedures.

Lower vaginal trauma occurs either spontaneously or because of episiotomy. Spontaneous

lacerations usually involve the posterior fourchette; however, trauma to the periurethral and
clitoral region may occur and can be problematic.

Thrombosis

In the immediate postpartum period, disorders of the coagulation system and platelets do not
usually result in excessive bleeding; this emphasizes the efficiency of uterine contraction and
retraction for preventing hemorrhage.[5] Fibrin deposition over the placental site and clots
within supplying vessels play a significant role in the hours and days following delivery, and
abnormalities in these areas can lead to late PPH or exacerbate bleeding from other causes,
most notably, trauma.

Abnormalities may be preexistent or acquired. Thrombocytopenia may be related to

preexisting disease, such as idiopathic thrombocytopenic purpura, or acquired secondary to
HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count), abruptio
placentae, disseminated intravascular coagulation (DIC), or sepsis. Rarely, functional
abnormalities of platelets may also occur. Most of these are preexisting, although sometimes
previously undiagnosed.
Preexisting abnormalities of the clotting system, such as familial hypofibrinogenemia and
von Willebrand disease, may occur and should be considered. An expert panel recently issued
guidelines to aid in the diagnosis and management of women with such conditions.[18] An
underlying bleeding disorder should be considered in a woman with any of the following:
menorrhagia since menarche, family history of bleeding disorders, personal history of notable
bruising without known injury, bleeding from the oral cavity or GI tract without obvious
lesion, or epistaxis of longer than 10 minutes duration (possibly requiring packing or
cautery). If a bleeding disorder is suspected, consultation is suggested.

Acquired abnormalities are more commonly problematic. DIC related to abruptio placentae,
HELLP syndrome, intrauterine fetal demise, amniotic fluid embolism, and sepsis may occur.
Fibrinogen levels are markedly elevated during pregnancy, and a fibrinogen level that would
be in the reference range in the nonpregnant state should be viewed with suspicion in the
aforementioned clinical scenarios.

Finally, dilutional coagulopathy may occur following massive PPH and resuscitation with
crystalloid and packed red blood cells (PRBCs).

Risk factors and associated conditions for PPH are listed above; however, a large number of
women experiencing PPH have no risk factors. Different etiologies may have common risk
factors, and this is especially true of uterine atony and trauma of the lower genital tract. PPH
usually has a single cause, but more than one cause is also possible, most likely following a
prolonged labor that ultimately ends in an operative vaginal birth.

Prevention

High-quality evidence suggests that active management of the third stage of labor reduces the
incidence and severity of PPH.[9] Active management is the combination of (1) uterotonic
administration (preferably oxytocin) immediately upon delivery of the baby, (2) early cord
clamping and cutting, and (3) gentle cord traction with uterine countertraction when the
uterus is well contracted (ie, Brandt-Andrews maneuver).

The value of active management in the prevention of PPH cannot be overstated (see
Management of the Third Stage of Labor). The use of active versus expectant management in
the third stage was the subject of 5 randomized controlled trials (RCTs) and a Cochrane meta-
analysis.[19, 8, 9] These trials included more than 6000 women, and the findings are
summarized in Table 1.

Table 1. Benefits of Active Management Versus Expectant Management (Open Table in a

new window)

The findings show a conclusive benefit for active management, with an approximate 60%
reduction in the occurrence of PPH greater than or equal to 500 mL and 1000 mL,
hemoglobin concentration of less than 9 g/dL at 24-48 hours after delivery, and the need for
blood transfusion. An 80% reduction in the need for therapeutic uterotonic agents was noted.
These results were all highly significant as indicated by the 95% confidence interval figures.
The results indicate that for every 12 patients receiving active rather than physiological
management, one PPH would be prevented. For every 67 patients so treated, one patient
would avoid transfusion with blood products.

One concern regarding active management is that retained placenta may occur more
frequently. This concern is not supported by the trials. This is especially true if oxytocin is
used as the uterotonic.[20, 21] The US RCTs mentioned above compared the use of active
management protocols in which the oxytocin was administered either immediately after
delivery of the baby or immediately after delivery of the placenta. The authors stated that no
statistically significant difference was noted in the PPH rate and that delaying administration
until after placental delivery was justified.

Noteworthy is the finding that early administration of oxytocin (before placental delivery) did
not increase the rate of retained placenta. Additionally, the trial showed trends toward a
benefit for early administration of oxytocin, including a 25% reduction in PPH and a 50%
reduction in the need for transfusion.[10] These findings are clearly consistent with the
previous RCTs and the early administration of oxytocin with delivery of the baby is strongly
recommended.

They also stated that administration with delivery of the baby did not increase the rate of
retained placenta, but they did not point out that this finding clearly supports early
administration. Additionally, the trial showed trends toward a benefit for early administration
of oxytocin, including a 25% reduction in PPH and a 50% reduction in the need for
transfusion.[10] These differences may be due to chance, but, given the results of the
previous RCTs, the administration of oxytocin with delivery of the baby would seem to be
strongly warranted.

Following delivery, administering a uterotonic drug that lasts at least 2-3 hours is reasonable.
[3] This could be 10 U of oxytocin in 500 mL of intravenous fluid by continuous drip, 200-
250 mcg of ergonovine intramuscularly, or 250 mcg of 15-methyl prostaglandin F2-alpha
(carboprost [Hemabate]) intramuscularly. The use of misoprostol and a long-acting oxytocin
analogue (carbetocin) is being studied for this use.[22] It has been suggested that distribution
of misoprostol ahead of childbirth in communities where home birth is unavoidable can be an
effective approach. However, there is insufficient evidence to support this and there are
concerns that the drug might be used for starting labor or terminating pregnancy.[23]

The presence of significant antepartum or intrapartum risk factors warrants delivery in

maternity units that have readily available resources to deal with massive obstetric
hemorrhage. All medical facilities should have protocols for dealing with PPH and obstetric
hemorrhage.

Pathophysiology

Over the course of a pregnancy, maternal blood volume increases by approximately 50%
(from 4 L to 6 L). The plasma volume increases somewhat more than the total RBC volume,
leading to a fall in the hemoglobin concentration and hematocrit value. The increase in blood
volume serves to fulfill the perfusion demands of the low-resistance uteroplacental unit and
to provide a reserve for the blood loss that occurs at delivery.[7]

At term, the estimated blood flow to the uterus is 500-800 mL/min, which constitutes 10-15%
of cardiac output. Most of this flow traverses the low-resistance placental bed. The uterine
blood vessels that supply the placental site traverse a weave of myometrial fibers. As these
fibers contract following delivery, myometrial retraction occurs. Retraction is the unique
characteristic of the uterine muscle to maintain its shortened length following each successive
contraction. The blood vessels are compressed and kinked by this crisscross latticework, and,
normally, blood flow is quickly occluded. This arrangement of muscle bundles has been
referred to as the "living ligatures" or "physiologic sutures" of the uterus.[5]

Uterine atony is a failure of the uterine myometrial fibers to contract and retract. This is the
most important cause of PPH and usually occurs immediately following delivery of the baby,
up to 4 hours after the delivery. Trauma to the genital tract (ie, uterus, uterine cervix, vagina,
labia, clitoris) in pregnancy results in significantly more bleeding than would occur in the
nonpregnant state because of increased blood supply to these tissues. The trauma specifically
related to the delivery of the baby, either vaginally in a spontaneous or assisted manner or by
cesarean delivery, can also be substantial and can lead to significant disruption of soft tissue
and tearing of blood vessels.

Presentation
Although the presentation of PPH is most often dramatic, bleeding may be slower and
seemingly less noteworthy but may still ultimately result in critical loss and shock. This is
more likely to be true of bleeding secondary to retained tissue or trauma. Nursing practices
for routine care in the postpartum period should include close observation and documentation
of maternal vital signs and condition, vaginal blood loss, and uterine tone and size. The uterus
should be periodically massaged to express any clots that have accumulated in the uterus or
vagina.[24]

The usual presentation of PPH is one of heavy vaginal bleeding that can quickly lead to signs
and symptoms of hypovolemic shock. This rapid blood loss reflects the combination of high
uterine blood flow and the most common cause of PPH, ie, uterine atony. Blood loss is
usually visible at the introitus, and this is especially true if the placenta has delivered. If the
placenta remains in situ, then a significant amount of blood can be retained in the uterus
behind a partially separated placenta, the membranes, or both.

Even after placental delivery, blood may collect in an atonic uterus. For this reason, the
uterine size and tone should be monitored throughout the third stage and in the so-called
fourth stage, following delivery of the placenta. This is accomplished by gently palpating the
uterine fundus. If the cause of bleeding is not uterine atony, then blood loss may be slower
and clinical signs and symptoms of hypovolemia may develop over a longer time frame.
Bleeding from trauma may be concealed in the form of hematomas of the retroperitoneum,
broad ligament or lower genital tract, or abdominal cavity. The clinical findings in
hypovolemia are listed in Table 2.

Table 2. Clinical Findings in Obstetric Hemorrhage[25] (Open Table in a new window)

Two important facts are worth bearing in mind. The first is that caregivers consistently
underestimate visible blood loss by as much as 50%. The volume of any clotted blood
represents half of the blood volume required to form the clots. The second is that most
women giving birth are healthy and compensate for blood loss very well. This, combined
with the fact that the most common birthing position is some variant of semirecumbent with
the legs elevated, means that symptoms of hypovolemia may not develop until a large volume
of blood has been lost.[26]

Rapid recognition and diagnosis of PPH is essential to successful management. Resuscitative

measures and the diagnosis and treatment of the underlying cause must occur quickly before
sequelae of severe hypovolemia develop. The major factor in the adverse outcomes
associated with severe hemorrhage is a delay in initiating appropriate management.

Contraindications

Other than nonconsent, absence of surgical expertise or allergy to specific agents, the
techniques used in the management of PPH have no absolute contraindications. The vast
majority of cases (>99%) are handled without what would traditionally be considered surgical
intervention. In most cases, surgical intervention is a last resort. An exception is those cases
in which uterine rupture or genital tract trauma has occurred and surgical repair is clearly
indicated.

Transfusion of packed RBC and other blood products may be necessary in the management
of severe PPH. Some women may refuse such an intervention on personal or religious
grounds. The most widely known group that does not accept blood transfusion are Jehovahs
Witnesses. The wishes of the patient must be respected in this matter. Significant increased
risk of maternal mortality due to obstetric hemorrhage has been noted in the Jehovahs
Witness population. The increased risk of death was found to be 6-fold in a recent national
review of 23 years experience in the Netherlands and 44-fold in a much smaller study of 391
deliveries in a US tertiary level center.[27, 28] Discussion regarding the implications of such
prohibitions should be undertaken early in the pregnancy whenever possible and
subsequently reviewed.

In almost all cases in which surgical management is chosen after medical management has
failed, not attempting surgery would lead to maternal death. Even an unstable condition
cannot be considered a true contraindication. One type of surgery may be chosen over
another, but when medical management has failed, surgery is most likely the only life-saving
option.

Workup

RELATED REFERENCE TOPICS

Postpartum Hemorrhage in Emergency Medicine

Normal and Abnormal Puerperium

Bakri Balloon Placement

RELATED NEWS AND ARTICLES

Oxytocin Without Misoprostol Best for Postpartum Hemorrhage Prevention

ACOG Urges Immediate Postpartum LARCs

Maternal Mortality Rates on the Rise in Most US States

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