PerinatologiPerinatologi

Bambang Mulyawan

FK - UMM

Asfiksia Asfiksia NeonatorumNeonatorum

Asfiksia Asfiksia NeonatorumNeonatorum

Dr.Bambang Mulyawan SpADr.Bambang Mulyawan SpA

Fakultas KedokteranFakultas Kedokteran

Universitas MuhammadiyahUniversitas Muhammadiyah

M a l a n gM a l a n g

Pendahuluan (1)

Asfiksia Bayi Baru Lahir (BBL) : 15% kematian BBL (5 juta) /tahun

Angka kejadian asfiksia di RS Propinsi : 25,2% (Jawa Barat)

Angka kematian asfiksia di RS Pusat Rujukan Propinsi di Indonesia : 41%

10% BBL membutuhkan bantuan untuk mulai bernafas ( bantuan ringan res.lanjut yg ekstensif)

5% BBL membutuhkan tindakan resusitasi ringan 1% - 10% BBL di RS perlu bantuan ventilasi, hanya

sedikit yg perlu intubasi dan kompresi dada15/06/1999 Dr.Bambang M 3

Pendahuluan (2)

“Sebagian besar bayi yaitu sekitar 90% tidak membutuhkan atau hanya sedikit memerlukan bantuan untuk memantap-kan pernafasannya setelah lahir dan akan melalui masa transisi dari kehidup-an intrauterin ke ekstrauturin tanpa ma-salah.”

15/06/1999 Dr.Bambang M 4

Pendahuluan (3)

Infant resuscitation required in 6% of all births. Asphyxia usually not anticipated. All labor and delivery units required to be

skilled in neonatal resuscitation (Standard of Practice)

NALS (Neonatal Advanced Life Support)

Definisi (1)

Asfiksia neonatorum : BBL yang tidak dapat bernafas secara spontan dan teratur pada saat lahir atau beberapa saat setelah lahir.

BBL : Bayi Baru Lahir pada menit-menit pertama sp beberapa jam selanjutnya

Periode neonatal : lahir 28 hari

15/06/1999 Dr.Bambang M 6

Definisi (2)

Asfiksia BBL ditandai dg keadaan : *hipoksemia *hiperkarbia *asidosis

15/06/1999 Dr.Bambang M 7

Definisi (3)

Karakteristik asfiksia BBL /Perinatal (menurut AAP dan ACOG -2004 ) : 1. asidemia metabolik atau campuran (metabolik dan respiratorik) yang jelas, yaitu ph<7, pada sampel darah yang diambil dari a.umbilikal 2. nilai Apgar 0-3 pada menit ke 5 3. manifestasi neurologi pd periode BBL segera, termasuk kejang,hipotonia,koma atau ensefalopati hipoksisk isemik 4. terjadi disfungsi sistem multiorgan segera pada periode BBL

15/06/1999 Dr.Bambang M 8

Definisi (3-a)

Inconsistent Definitions Criteria for Neonatal Asphyxia (APA and ACOG,

1992)– Profound metabolic (or mixed) acidosis (ph < 7.0)– Persistence of Apgar score 0 - 3 for > 5 minutes– Clinical neurological sequelae– Evidence of multi-organ system dysfunction

Definisi (4)

This is pathologic condition referred to neonate who have no spontaneous breathing or represented irregular breathing movement after birth. Usually caused by perinatal hypoxia. It is emergency condition and need quickly treatment (resuscitation).

birth asphyxia is defined simply as the failure to initiate and sustain breathing at birth

The common worry of health professionals and parents is the permanent brain damage that birth

asphyxia can cause.

Definisi (4-a)

Patofisiologi asfiksia (1) BBL mempunyai karakteristik yg unik. Alveoli paru janin dalam rahim berisi cairan paru lahir

nafas pertama udara masuk alveolicairan paru diabsorpsi oleh jaringan paru dstseluruh alveoli berisi udara oksigen. Paru membutuhkan tek.puncak inspirasi dan tek.akhir ekspirasi yg tinggialiran darah paru meningkat.

Kegagalan penurunan resistensi vaskuler paru hipertensi pulmonal persisten pada BBL (Persisten pulmonary Hypertension of the neonate ) aliran drh paru inadekuat dan hipoksemia relatifekspansi par < gagal nafas ! ! !

15/06/1999 Dr.Bambang M 12

Patofisiologi (1-a)

Production of lung fluid diminishes 2-4 days before delivery

80-100 ml remain in the passageway of a full term infant

during the birth, fetal chest is compressed and squeezes fluid

Patofisiologi (1-b)

First breath is inspiratory gasp Changes trigger aortic and caratoid chemo

receptors that trigger brain’s respiratory center

Natural result of a normal vaginal delivery

Patofisiologi (1-c)

Significant decrease in environmental temperature after birth– Stimulates skin nerve endings– Newborn responds with rhythmic respirations– Excessive cooling may lead to profound

depression of cold stress

Patofisiologi (1-d)

Onset of respiration stimulates cardiovascular changes– As air enter the lungs, oxygen content rises in

alveoli and stimulates relaxation of pulmonary arteries

Patent ductus arteriosus closes– With increased oxygenated pulmonary blood flow

and loss of placenta, systemic blood flow increases, foreaman ovale closes, and PDA begins to close

– Leads to decrease in pulmonary vascular resistance-allows complete vascular flow to the lungs

Patofisiologi (1-e)

Patofisiologi (2)

When fetal asphyxia happens, the body will show a self-defended mechanism which redistribute blood flow to different organs called “inter-organs shunt” in order to prevent some important organs including brain, heart and adrenal from hypoxic damage.

Patofisiologi (3)

Hypoxic cellular damage : _reversible ( early stage ) _unreversible damage

Primary apnea Secondary apnea Other damage :

persisten pulmonary hypertension, hypo/hyperglicemia, hyperbilirubinemia

15/06/1999 Dr.Bambang M. 19

Etiologi / Faktor resiko (1)

Maternal factor: hypoxia, anemia, diabetes, hypertension, smoking, nephritis,

heart disease, too old or too young,etc Delivery condition:Abruption of placenta, placenta previa, prolapsed cord,

premature rupture of membranes,etc Fetal factor:Multiple birth, congenital or malformed fetus,etc

Etiologi / faktor resiko (2) Anticipate Asphyxia

– Preterm delivery– Thick meconium– Acute fetal or placental hemorrhage– Use of narcotics in labor– Maternal infection– Polyhydramnios: GI obstruction– Oligohydramnios: Hypoplastic lungs

Manifestasi klinis (1)

Fetal asphyxia

fetal heart rate: tachycardia bradycardia

fetal movement: increase decrease

amniotic fluid: meconium-stained

Manifestasi klinis (2)

Apgar score:

A: appearance(skin color)

P: pulse(heart rate)

G: grimace(reactive ability)

A: activity(muscular tension)

R: respiration

manifestasi klinis (2-a)

Assign Apgar Score at 1, 5, and 10 Minutes. Apgar Score more useful in Term than Preterm

Infant, but not specific for diagnosis of neonatal asphyxia.

Cord Arterial Blood Gases: Ph (< 7) and Base Deficit ( > - 4 ).

Manifestasi klinis (2-b)

Degree of asphyxia:

Apgar score 8~10: no asphyxia

Apgar score 4~8: mild/cyanosis asphyxia

Apgar score 0~3: severe/pale asphyxia

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LOW BIRTH WEIGHT BABIES

Low birth weight

Definition : < 2500 g

Incidence : 30% neonates

Importance

LBW babies account for 25% neonatal deaths and 50% infant deaths.

LBW babies are more prone to :

- malnutrition.

- recurrent infections.

- neurodevelopmental delay.

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Two types of LBW neonates

Preterm ( 1/3 )

Small – for – dates ( 2/3 )

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LBW (Preterm) : Problems

Birth asphyxia

Hypothermia

Feeding difficulties

Infections

Hyperbilirubinemia

Respiratory distress

Apneic spells Intraventricular

hemorrhage Hypoglycemia Metabolic

acidosis

30

LBW (SFD) : Problems

Birth asphyxiaMeconium aspiration syndromeHypothermiaHypoglycemia InfectionsPolycythermia

Causation : IUGR / SFD

Poor nutritional status of mother.Hypertension, toxemia, anemia.Multiple pregnancy, postmaturity.Chronic malaria, chronic illness.Tobacco use.

Causation : Prematurity

Low maternal weight, teenage pregnancy, multiple pregnancy.

Previous preterm baby, cervical incompetence.

Antepartum hemorrhage, acute systemic disease.

Induced premature delivery.Majority unknown.

Identification of preterm LBW

Date of LMPPhysical features

- breast nodule, genitalia, sole creases,

ear cartilage / recoil.

Ideal place for delivery of LBW

Transfer mother before delivery to a well-equipped centre.

Prevention of hypothermia topmost priority.

Skilled person needed for effective resuscitation.

Indications for hospitalisation

Birth weight < 1800 gGestation < 34 wksUnable to feed*Sick neonate*

* Irrespective of birth weight and gestation

Sindroma Aspirasi MekoniumSindroma Aspirasi Mekonium

Meconium Aspiration SyndromeMeconium Aspiration Syndrome( MAS )( MAS )

Bambang Mulyawan

FK-UMM

Pendahuluan

MAS merupakan masalah kegawatan yg sering dijumpai di ruang bersalin ( hipoksiahipoksia intrauterine aspirasi pneumoni BBL )

Biasanya pd bayi cukup bulan dan lebih bulan ( : Kecil untuk Masa Kehamilan / KMK )

Waspada : jika BBL lahir dg cairan ketuban campur mekonium dg gejala RDS

Patogenesis dan patofisiologi

Stress intrauterin mekonium in-utero ke dlm cairan ketuban, terhisap janin ketika inspirasi o.k hipoksi dan stimulasi vagal fetal distres / sebelum persa-linan

Mekanisme keluarnya mekonium in-utero masih belum jelas

Patogenesis dan patofisiologi ( lanj.)

BBL dg cairan ketuban mekonial asfiksia antepartum atau intrapartum obstruksi jalan nafas, turunnya kapasitas paru, pe> expiratory large airway resistancxe

Obstruksi total : atelektasis. Partial : trapping udara dan hiperekspansi alveolar

Mekonium pd alveolar me< fungsi surfaktan kolaps RDS

Patogen . . . . . ( lanj. )

Hipoksia intrauterin aspirasi mekonium obstruksi mekanik / keradangan kimiawi air trapping / atelektasis ventilasi tidak seimbang / intrapulmonal shunting kebocoran udara hipoksemia asidosis sirkulasi fetal persistent

47

SINDROM ASPIRASI MEKONIUM (SAM)

Hipoksia janinHipoksia janin

Mekonium keluar & janin gaspingMekonium keluar & janin gasping

Cairan amnion yang terkontaminasi mekonium Cairan amnion yang terkontaminasi mekonium terhirup ke larings dan trakheaterhirup ke larings dan trakhea

Mekonium masuk saluran napas lebih kecil dan Mekonium masuk saluran napas lebih kecil dan alveolus alveolus

Kerusakan paru Kerusakan paru

Pembersihan sal. napas Pembersihan sal. napas tidak adekuat tidak adekuat

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Kerusakan paru

Mekonium mengandung enzim merusak epitel bronkus, bronkiolus dan alveolus

Mekonium menyumbat sal. napas secara total/parsial beberapa bagian paru kolaps, bagian paru lain hiperinflasi

What Is Meconium?

Odorless, thick, blackish green material First seen during the third month of

gestation Accumulation of desquamated cells from

GI tract, skin, lanugo, fatty material from the vernix, amniotic fluid

Manifestasi klinis

Bervariasi : tergantung keparahan serangan hipoksik dan jumlah viskositas mekonium teraspirasi

Sering pada gestasi post matur : warna meko. pd kuku, rambut, tali pusat

Gejala RDS ( takipnea, NCH, retraksi interkostal, diameter AP dada >, sianosis

Pada gejala MAS lambat : distres nafas awal ringan. Semakin parah bbrp jam : atelektasis dan pneumonitis kimia

Auskultasi : vesikular lemag, ronki/rales, wheezing/mengi

Pemeriksaan radiologis

Foto polos dada : infiltrat kasar menyebar pd kedua lap.paru, dapat disertai pneumotoraks, atelektasis, emfisema

Chest X-Ray

Hyperinflation Coarse, patchy densities

representing scattered areas of atelectasis and consolidation mixed with air trapping

Faktor predisposisi

Insufisiensi plasenta, hipertensi, oligohidramnion, ibu kecanduan ( rokok, kokain), infeksi (chorio-amnionitis) hipoksia, manajemen jalan nafas tidak adekuat, defisiensi surfaktan, hipertensi pulmonal

Risk Factors for Meconium Passage

Postterm pregnancy Preeclampsia-eclampsia Maternal hypertension Maternal diabetes mellitus Abnormal fetal heart rate IUGR Abnormal biophysical profile Oligohydramnios Maternal heavy smoking

Infant ActiveInfant Depressed

Intrapartum suctioning of mouth, nose, pharynx

Intubate and suction trachea

Other resuscitation as indicated

Observe

Meconium in Amniotic FluidMeconium in Amniotic Fluid

Langkah diagnostik

Riwayat : PJT ( pertumbuhan janin terhambat ), kesulitan persalinan / gawat janin, persalinan dg air ketuban mekonial, asfiksia berat

Pemerksaan fisik : cair ketuban mekonial/ bayi diliputi mekonium, tl pusat/kulit bayi warna hijau, asfiksia berat bbrp jam gangguan nafas/RDS, td bayi lebih bulan

Foto toraks : AP dan Lateral Laboratorium: Hb, Ht, darah tepi, kultur Analisa Gas Darah : hipoksemia, asidemia : asidosis

metabolik, respiratorik,/kombinasi

58

Diagnosis

Cukup/lebih bulan, jarang sekali kurang bulan Cairan amnion terkontaminasi mekonium Mekonium tampak/dapat dihisap dari saluran napas

atas (bantuan laringoskop) Kulit bayi diwarnai mekonium Sesak napas Foto toraks : hiperinflasi paru disertai banyak daerah

paru yang kolaps

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Pencegahan

Pembersihan saluran napas atas sebelum bayi bernapas saat lahir

– Penghisapan saluran napas sebelum bahu dilahirkan

– Penghisapan saluran napas (larings dan trakea) secara langsung dengan bantuan laringoskop

penatalaksanaan

Prevensi slm periode prenatal, antenatal, tindaka tepat slm intrapartum

Diagram Alur Resusitasi Neonatus

Pengobatan / terapi

Suportif : oksigen, suhu lingkungan, perawatan pernafasan, kadar gas darah arteri, terapi surfaktan, ventilasi mekanik, cairan infus glukosa 10%

Antibiotik spektrum luas Tindakan bedah :pd pneumotoraks, pneumomediastinum,

empisema subkutan : pungsi toraks, drainase

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Perjalanan Penyakit

SAM : sesak napas sejak lahir

SAM ringan : SAM ringan : membaik membaik secara bertahap secara bertahap dalam beberapa dalam beberapa hari – beberapa hari – beberapa minggu minggu

Memburuk Memburuk secara secara progresif progresif tidak tidak tertolong tertolong

Tertolong Tertolong kerusakan paru kerusakan paru perlu waktu perlu waktu lama untuk lama untuk sembuh sembuh sempurna sempurna

SAM SAM berat berat

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Komplikasi

1. Pneumotoraks / pneumomediastinum

2. Kerusakan akibat hipoksia pada organ lain

Pemantauan/Monitoring

Tumbuh kembang pd bayi yg selamat, hidup tanpa komplikasi (survival intact) baik

Pada bayi dg komplikasi hipoksi serebri, gagal ginjal, efek tosik O2, epilepsi, palsi serebral gangguan tumbuh kembang

Ikterus neonatorumIkterus neonatorum

-Pewarnaan kuning pada sklera dan kulit yang disebabkan oleh penumpukan bilirubin

-Terlihat pada kulit bila kadar >5 mg/dl-Terlihat pada >50% neonatus- Pada bayi prematur > bayi cukup bulan

Neonatal Hyperbilirubinemia

Jaundice is common in the first week of life and may be missed in dark skinned babies

Blanch the tip of the nose or hold baby up and gently tip forward and backward to get the eyes to open.

Teach mother to do the same at home in the first week and report to hospital if significant jaundice is observed.

Clinical assessmentJaundice

Blanching the tip of the nose

Two infants with jaundice; note yellow sclerae

Metabolisme bilirubin

HemoglobinGlobinHemeBilirubin indirek1 gram HB 34 mg bilirubin

Bil.ind terikat Albumin diangkut ke hati Diambil oleh ligandin masuk kehati Dikonyugasi oleh enzim glucoronil transferase

bilirubin direk

Metabolisme bilirubin

Bilirubin direk (empedu) disalurkan melalui duktus biliaris ke usus

Di dalam usus oleh bakteriasterkobilin dikeluarkan dengan sisa makanan sebagai feses

Sebagian diuraikan oleh enzim B-glucoronidase Bilirubin indirek diserap kembali ke darah terikat albumin hati (sirkulasi enterohepatik)

Sifat dan bahaya hiperbilirubinemia

Bilirubin indirek mudah larut dalam lemak bila kadar tinggi, tidak terikat albumin, sawar darah otak rusak melalui sawar darah – otak terikat sel otak kernikterus

Bilirubin direk larut dalam air. Bila ada atresia atau obstruksi duktus biliaris ber tumpuk dfi dalam hati merusak sel hati sirosis hepatis

Penilaian klinis ikterus

Daerah tubuh Kadar bilirubin mg/dl

Muka 4 - 8

Dada/punggung 5 -12

Perut dan paha 8 -16

Tangan dan kaki 11-18

Telapal tangan/kaki >15

Indirect Serum Bilirubin ConcentrationIndirect Serum Bilirubin Concentrationand Its Relation To The Progressionand Its Relation To The Progressionof Dermal Icterus in Full-Term Infants*of Dermal Icterus in Full-Term Infants*

11

22

44

33

55

55 55

DermalDermalZoneZone

Bilirubin (mg/100 mL)Bilirubin (mg/100 mL)

Mean ± SD Range Observations Mean ± SD Range Observations

5.9 ± 0.35.9 ± 0.38.9 ± 1.78.9 ± 1.7

11.8 ± 1.811.8 ± 1.815 ± 1.715 ± 1.7

4.3 ± 7.9 4.3 ± 7.9 5.4 ± 12.25.4 ± 12.28.1 ± 16.58.1 ± 16.5

11.1 ± 18.3711.1 ± 18.37>15 >15

13134949525245452929

1122334455

*Includes all infants whose rate of serum bilirubin rise was 0.7*Includes all infants whose rate of serum bilirubin rise was 0.7 mg/dL/h or less. mg/dL/h or less.

Dermal Zones of J aundiceDermal Zones of J aundice

Mengapa terjadi ikterus pada neonatus

Peningkatan bilirubun karena hemolisis Tidak cukup albumin sebagai pengangkut Kurang ligandin untuk mengambil ke hati Kurang konyugasi di dalam hati Ekskresi yang tidak cukup Meningkat sirkulasi entero-hepatik

Ikterus fisiologik

Timbul setelah 24 jam Kadar tertinggi pada hari ke 5 pada BCB;

pada hari ke 7 pada BKB Kadar bilirubin < 15 mg/dl Hilang dalam 14 hari Hilang tanpa perlu pengobatan

Mechanism of Physiologic Jaundice

Increased rbc’s

Shortened rbc lifespan

Immature hepatic uptake & conjugation

Increased enterohepaticCirculation

Ikterus patologik

Timbul dalam 24 jam pertama Kenaikan kadar bilirubin > 5 mg / dl / hari Bilirubin serum >15 mg / dl Ikterus berlangsung lebih dari 14 hari Warna feses dempul dan urin kuning tua Bilirubin direk > 2 mg / dl

Penyebab ikterus

Timbul dalam 24 jam pertama

* Penyakit hemolitik pada BBL: Inkompatibilitas Rh,ABO* Infeksi ; TORCH, malaria, bakteri* Defisiensi enzim G6PD

Penyebab ikterus

Timbul antara 24-72 jam* Fisiologik* Sepsis* Polisitemia* Perdarahan tertutup* Perdarahan intraventrikular* Peningkatan sirkulasi entero-hepatik

Penyebab ikterus

Timbul setelah 72 jam* Sepsis* Hematoma sefal* Hepatitis neonatal* Atresia biliaris* Breastmilk jaundice* Kelainan metabolik

Pendekatan bayi dengan ikterus

Perlu diketahui* Berat lahir* Masa gestasi* Usia dalam jam* Apakah ikterus fisiologik atau patologik* Bila ikterus adalah fisiologik dan keadaan bayi baik hanya perlu diobservasi* Bila ikterus berat periksa kemungkinan telah

terjadi kernikterus

Pemeriksaan untuk ikterus patologik

Riwayat kehamilan dan persalinan * Riwayat keluarga adanya penyakit hati * Adanya riwayat inkompatilitas darah * Penyakit ibu selama hamil * Trauma lahir, asfiksia, * Penundaan pengikatan tali pusat * Penundaan makanan per os, pengeluaran mekoneum * Pemberian ASI

Pemeriksaan untuk ikterus patologik

Pemeriksaan fisik* Prematuritas* KMK : polisitemia* Trauma lahir* Pucat : hemolisis

* Petekhie* Hepatosplenomegali Iso-imunisasi, sepsis

Pemeriksaan untuk ikterus patologik

Pemeriksaan laboratorium* Bilirubin serum total dan direk* Golongan darah dan Rhesus ibu dan bayi* Uji Coombs* Hematokrit* Hapusan darah tepi* Skrining sepsis* Fungsi hati dan tiroid untuk ikterus lanjut

Tatalaksana ikterus neonatorum

Tujuan : Mencegah keracunan oleh bilirubin

Cara1. Pencegahan hiperbilirubinemia

- Pemberian makan dini- Hidrasi adekwat

2. Penurunan kadar bilirubin- Terapi sinar- Transfusi tukar

Terapi Sinar

Prinsip : Bilirubin oleh cahaya dengan gelombang 450-460 nanometer photoisomer

yang larut dalam air Perlengkapan

lampu neon 6-8 buahtempat tidur atau inkubatoralat penutup mata

Indikasi terapi sinar

Kadar bil mg/dl Berat lahir Usia

5-9 bila hemolisis semua < 24 jam

10-14 < 2500 g >24 jam

> 2500 g (observasi)

15-19 > 2500 g >48 jam

Terapi sinar

Letakkan bayi dalam keadaan telanjang dibawah lampu dengan jarak 45 cm

Tutup mata Setiap 2 jam bayi disusui Ubah posisi bayi setiap selesai menyusui Ukur suhu setiap 4 jam Timbang bayi setiap hari Periksa kadar bilirubin setiap 12 jam Hentikan terapi sinar bila kadar < 10 mg/dl

Efek samping terapi sinar

Meningkatkan kehilangan cairan insensibel Defekasi encer Warna kemerahan pada kulit Bronze baby syndrome Hipertermia

Transfusi tukar

Indikasi :

kadar bil Berat lahir Usia

10-14 mg/dl <2500 g <24 jam

15- 19 semua <48 jam

>20 semua 0 - >72 jam

Transfusi tukar

Pilihan darah untuk transfusi tukarInkompatilitas ABO

darah golongan O +ve dalam plasma ABIsoimujjnisasi Rhesus

darah gol O –ve atau

darah golongan bayi yang Rhesus negatif

Untuk lain darah golongan bayi

Hiperbilirubinemia indirek yang memanjang

Sindrom Crigler Najjar Breastmilk jaundice Hipothiroidism Stenosis pilorus Hemolisis yang berlangsung terus Malaria

Hiperbilirubinemia direk yang memanjang

Hepatitis neonatal idiopatik Inspissated bile syndrome Infeksi Malformasi- atresia biliaris, kista kholedokus Penyakit metabolisme- galaktosemia Nutrisi parenteral total yang lama

Thanks….

But it’s not the end !!!

Brief History

A 45-year-old man was seen in the emergency department for persistent night sweats, headache, intermittent fever, and severe chills, which occurred approximately every 48 h. The patient was born in Asia and had moved to the United States 5 years earlier. At that time, he had suffered a similar illness, was treated, and appeared to make a good recovery. Blood was drawn for laboratory studies including a hemoglobin determination and thick and thin blood smears for parasites.

Brief History

The patient was slightly anemic, with a hemoglobin level of 9.5 g/dl. Examination of Giemsa-stained blood films revealed the presence of enlarged red blood cells contain ing trophozoite forms (Fig. 23.1). Several irregular ameboid trophozoites containing brown granules were seen. Eosinophilic stippling was visible in the cytoplasm of the erythrocytes. A few round to oval gametocytes were seen. Based on these findings, a diagnosis of infection with a blood parasite was made.

enlarged red blood cells contain ing trophozoite forms (Fig. 23.1).

Plasmodium falciparum and P. malariae are encountered in all shaded areas of the map (with P. falciparum by far the most prevalent). Plasmodium vivax and P. ovale are traditionally thought to occupy complementary niches, with P. ovale predominating in Sub-Saharan Africa and P. vivax in the other areas; however these two species are not always distinguishable on the basis of morphologic characteristics alone; the use of molecular tools will help clarify their exact distribution.

Features in Blood P. falciparum P. vivax P. malariae P. ovale

affected RBC normal size enlarged, a few ovalocytes

normal size normal to increased; ovalocytosis

forms in peripheral blood

ring trophozoites and gametocytes only

all forms all forms all forms

immature trophozoites (ring forms)

2 chromatin dots; 2+ rings per RBC; applique forms; rings delicate

rarely may have 2 chromatin dots or multiple rings per RBC

mature trophozoites not seen ameboid band or bayonet forms

schizonts not seen 12-24 merozoites in mature schizonts

6-12 merozoites in mature schizont, may form a circle ("daisy")

8-12 merozoites in mature schizont

gametocytes banana shaped

stippling Mauer's dots or clefts (occasional)

Schuffner's dots (usual)

Ziemann's dots (rare; if overstain)

James's stippling

                                                                         

Diagnostic points:-  1.Red cells containing parasites are usually enlarged.  2.Schuffner's dots are frequently present in the red cells as shown above.  3.The mature ring forms tend to be large and coarse. 4.Developing forms are frequently present. 

Complications Most complications are caused by P falciparum, and they may include the following:

– Coma (cerebral malaria) • Defined as coma, altered mental status, or multiple seizures with P falciparum in the blood,

cerebral malaria is the most common cause of death in malaria patients. If untreated, this complication is lethal.

• Even with treatment, 15% of children and 20% of adults who develop cerebral malaria die. • The symptoms of cerebral malaria are similar to those of toxic encephalopathy.

– Seizures– Renal failure: As many as 30% of nonimmune adults infected with P falciparum suffer acute renal

failure.– Hemoglobinuria (blackwater fever)

• Blackwater fever is the passage of dark, Madeira-colored urine. • Hemolysis, hemoglobinemia, and the subsequent hemoglobinuria and hemozoinuria cause

this condition.– Noncardiogenic pulmonary edema: This affliction is most common in pregnant women and results

in death in 80% of patients.– Profound hypoglycemia: Hypoglycemia often occurs in young children and pregnant women. It

often is difficult to diagnose since adrenergic signs are not always present and since stupor already may have occurred in the patient.

– Lactic acidosis: This occurs when the microvasculature becomes clogged with P falciparum. If the venous lactate level reaches 45 mg/dL, a poor prognosis is very likely.

– Hemolysis resulting in severe anemia and jaundice– Bleeding (coagulopathy)

BABESIOSIS

SymptomsBabesiosis is associated with hemolytic anemia, jaundice, fever and hepatomegaly, usually 1-2 weeks after infection

DiagnosisDiagnosis is based on symptoms, patient history and detection of intraerythrocytic parasite in the patient or transfer of blood in normal hamsters which can be heavily parasitized.

Chloroquine (Aralen HCl, Aralen Phosphate) -- Inhibits parasite growth by concentrating within acid vesicles of the parasite and increasing its internal pH. In addition, inhibits hemoglobin utilization and metabolism by the parasite. Adult Dose10 mg base/kg PO, not to exceed 600 mg; then 5 mg base/kg PO; not to exceed 300 mg at 6-h, 24-h, and 48-h intervals (total 25 mg/kg)

QUESTIONS1. Which infection does this patient have? Which parasite is

infecting him?2. Describe the typical appearance of this parasite in thick and thin

Giemsa-stained smears.3. Which blood protozoan parasite morphologically resembles this

parasite?4. Comment on the size of the erythrocytes. What do we call the

eosinophilic stippling seen in these cells? Which other species causes this characteristic?

5. Describe the clinical illness caused by this parasite. Which serious complicationmay occur with this infection?

6. How does the life cycle of different species of this parasite vary? How does this fact relate to this patient's infection?

7. How would this patient be treated?