LO Tahun 2014 Blok 23

KEMENTERIAN PENDIDIKAN DAN KEBUDAYAAN
UNIVERSITAS SRIWIJAYA
FAKULTAS KEDOKTERAN
UNIT PENDIDIKAN KEDOKTERAN (UPK)
Zona F. Gedung I Kampus Unsri Indralaya OI Sumatera Selatan, Indonesia Telp. 0711 580061
atau / or Jl. dr. Muh. Ali Komplek RSUP Palembang 30126, Indonesia, Telp. 0711 352342, Fax. 0711
373438,
Skenario A Blok 23 Tahun 2014
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Learning outcome:
The graduated doctors capable of doing these following things:
Have the ability for anamnesis, general and obstetry physical examination and to plan supporting
examination as indicated, such as routine blood and urine.
Have the ability to conclude (diagnose) based on the data from physical and supporting examination.
Have the ability to make a good obstetry medical record.
Have the ability to plan a management (treatment) based on competence.
Have the ability to plan follow up and evaluation.
Have the ability to make evidence based medicine-prognosis and give good explanation (Informed
Consent) about the case.
Learning objectives:
In this tutorial, students should learn about:
Anatomy of reprodustion system
Obstetry physical examination, which include:
a Leopold (site, habitus, presentation and position)
b Fetal heart rate
Etiology, symptoms, clinical signs, physical examination and management of anemia
Terms in pregnancy
Interpretation of laboratory findings (haemoglobin value in pregnant woman)
Ideal pregnancy planning
A woman attends a routine antenatal appointment at 31 weeks gestation. She is 26 years old and this is her
fifth pregnancy. She has four children, all spontaneous vaginal deliveries at term. Her fourth child is 18
months old and the delivery was complicated by a postpartum haemorrhage (PPH) requiring a 4 unit blood
transfusion. She is reffered by midwife to doctor (public health centre) with possibility of breech
presentation. The mother complains of malaise and dizzy. Due to her economic condition, she admits that
during her pregnancy she only eats some food that she can afford to buy. She feels generally tired and
attributes this to caring for her four young children. She reports good fetal movements (more than 10 per
day).
In the examination findings:
Height = 150 cm; Weight 45 kg; Blood pressure = 126/73 mmHg; Pulse = 92 x/m; RR = 22 x/m.
Palpebral conjunctival looked pale
Outer examination: hard parts are palpabled in the right side of mothers abdomen.
Haemoglobin
7.8 g/dL
Mean cell volume
68 fL
Mean corpuscular hemoglobin concentration
28 g/dL
Serum iron level

Total iron binding capacity
White cell count
Platelets
Urinalysis: negative
Blood group: A negative
No atypical antibodies detected.
32 g/dL
510 mg/dL
11.200/L
237.000/L
You act as the doctor in public health centre and be pleased to analyse this case.
OBJECTIVES
Term Classification
a G5P4A0
b History of postpartum hemorrhage (PPH)
c Breech presentation
d Malaise
e Dizzy
f Poor
g Microcytic hypochrome anemia
h CBC (Complete Blood Count)
i MCV, MCHC, Serum iron, TIBC
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Problem Identification
A pregnant woman (31 years old) from poor family
G5P4A0
History of postpartum hemorrhage
31 weeks pregnancy with breech presentation
Complain of malaise and dizzy
Only eat some affordable food during pregnancy
The youngest child age is 18 months old
Problem Analysis
1.
A pregnant woman (31 years old) from poor family
a. What is the definition of poor?
b. What its connection with pregnancy and anemia?
2. G5P4A0
a. What are the risks for the 5th pregnancy (Grande Multipara)?
b. Possible complication from 5th pregnancy (Grande Multipara)?
3. History of postpartum hemorrhage
a. What are the causes of postpartum hemorrhage ?
b. What are the risk of pregnancy with previous postpartum hemorrhage?
4. 31 weeks pregnancy with breech presentation
a. What are the causes and the pathophysiology of breech presentation?
b. Epidemiology of breech presentation in Indonesia?
c. What is its relation with 31 weeks pregnancy?
d. What are the possible complication than can occur?
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e. How are the right and comprehensive management?

f. Outer version, knee chest position, reference, and screening.
5. Complain of malaise and dizzy
How is its relation with malaise and dizzy in this case (pathophysiology)?
How about the management and education?
6. Only eat some affordable food during pregnancy
How is the need of nutrition in pregnant woman?
What is the effect of eating affordable food only?
7. The youngest child age is 18 months old
How is ideal pregnancy range?
How if the pregnancy range is too close (clinical risk, caring pattern, etc)?
How to manage ideal pregnancy planning (contraception; conselling, methods and effectivity)?
Hypothesis:
A woman has a pregnancy with breech presentation complicated by anemia due to previous postpartum
hemorrhage, grande multipara and nutrients deficiency.
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Learning Issues:
Anatomy of reproduction system
Obstetry physical examination, which include:
Leopold (Site, habitus, presentation and position)
Fetal heart rate
Etiology, symptoms, clinical signs, physical examination and management of anemia
Examination of Nutrient Status and the needs of nutrients in pregnant woman
Epidemiology, etiology, management and also complication of transverse lie
Terms in pregnancy
Interpretation of laboratory findings (haemoglobin value in pregnant woman)
Ideal pregnancy planning
Concepts Framework:
Risk factors, etiology, predisposition breech presentation outcome, management, complication,
prevention.
Risk factors, etiology, predisposition anemia outcome, management, complication, prevention.
Theory Review.
BREECH PRESENTATION
a DEFINITION
Breech presentation defines as the condition in which the baby is in longitudinal lie and the podalic pole
presenting at the pelvic brim with the head occupying upper pole of uterus.
b ETIOLOGY
Certain factors can encourage a breech presentation. Prematurity is likely the chief cause. Twenty five
percent of fetuses are in the breech position at 32 weeks gestation; this drops to three percent at term.
1 All factors that inhibit the head decreasement into the pelvic, i.e. small pelvic, placenta previa, tumor previa,
uterine myom, and fetal anomaly.
2 All factors that ease fetal movement, i.e. untight abdominal wall (multiparity, abdomen pendulans),
hydramnion and prematurity.
3 Uterine cavum condition causes vertical axis approximately equal to the horizontal axis, i.e. bicornu uterus,
subseptus uterus and fundal position of placenta.
4 The shape of the uterus is a more likely determinant of the final fetal presentation as uterine shape anomalies
are strong predictors of breech presentation and other malpresentations.
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DIAGNOSIS
1 External examination
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Inspection : abdomen seemed widening to both sides.
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Palpation
a. Leopold I : ballotement is palpabled at the fundal site
b. Leopold II : hard parts are palpabled in the right side of mothers abdomen
c. Leopold III & IV: the babys bottom is palpabled near the symphisis, fetal heart rate clearly
auscultated at near umbilical area
2 Internal examination
After the membrane ruptured, in internal examination easily palpated:
a.
Sacrum as denominator
b.
Amniotic fluid greenish or meconeum
c.
Sometimes foot protruding into vagina or out to vulva.
d.
Umbilical cord prolapse may occur, particularly in the complete, footling, or kneeling breech.
3 Ultrasonography and radiology
Only performed if the internal examination is unclear.
d MANAGEMENT
1 External version; performed only no contraindication found, should be performed at > 32 weeks gestational
age.
2 For a woman with suspected breech presentation, pre- or early labour ultrasound should be performed to
assess type of breech presentation, fetal growth and estimated weight, and attitude of fetal head. If
ultrasound is not available, Caesarean section is recommended. (II-1A)
3 Contraindications to labour include
a. Cord presentation (II-3A)
b. Fetal growth restriction or macrosomia (I-A)
c. Any presentation other than a frank or complete breech with a flexed or neutral head attitude (III-B)
d. Clinically inadequate maternal pelvis (III-B)
e. Fetal anomaly incompatible with vaginal delivery (III-B)
4 Vaginal breech delivery can be offered when the estimated fetal weight is between 2500 g and 4000 g. (II2B)
5 Clinical pelvic examination should be performed to rule out pathological pelvic contraction. Radiologic
pelvimetry is not necessary for a safe trial of labour; good progress in labour is the best indicator of
adequate fetal-pelvic proportions. (III-B)
6 Continuous electronic fetal heart monitoring is preferable in the first stage and mandatory in the second
stage of labour. (I-A) When membranes rupture, immediate vaginal examination is recommended to
rule out prolapsed cord. (III-B)
7 In the absence of adequate progress in labour, Caesarean section is advised. (II-1A)
8 Induction of labour is not recommended for breech presentation. (II-3B) Oxytocin augmentation is
acceptable in the presence of uterine dystocia. (II-1A)
9 A passive second stage without active pushing may last up to 90 minutes, allowing the breech to descend
well into the pelvis. Once active pushing commences, if delivery is not imminent after 60 minutes,
Caesarean section is recommended. (I-A)
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The active second stage of labour should take place in or near an operating room with equipment and
personnel available to perform a timely Caesarean section if necessary. (III-A)
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A health care professional skilled in neonatal resuscitation should be in attendance at the time of
delivery. (III-A
ANEMIA
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The hematologic system undergoes significant change during pregnancy with expansion of the red cell mass
and blood volume resulting in a physiologic anemia of pregnancy.
Anemia is the most common medical complication of pregnancy.
Hematocrit levels <30% are abnormal in pregnancy and should trigger an evaluation for pathologic anemias.
In the reproductive age group, lymphomas are not infrequent while leukemias are rare. Treatment should
generally not be withheld because of pregnancy.
Changes occur in:
1 The plasma volume
2 The numbers of formed elements
3 The levels of coagulation factors during pregnancy
The upper and lower limits of these changes in the hematologic elements are somewhat variably defined, but
general ranges can be appreciated
TABLE Normal Pregnancy Values of the Different Blood Elements
Blood element
Pregnancy values
Red blood cells (hematocrit)
2nd trimester
31.235.5%
3rd trimester
31.936.5%
White blood cells
915 109 cells/liter
Platelets
140400 109 cells/liter
Coagulation factors
Fibrinogen
Increased up to 200%
Prothrombin
No change
V
No change
VII
VIII
IX
Slight increase
X
XI
Slight decrease
XIII
Slight decrease
Adapted from Anderson HM. Maternal Hematologic Disorders. In: Creasy RK, Resnik R eds. Maternalfetal medicine. 2nd ed. Philadelphia: Saunders, 1989.
DEFINITION
a The 1989 Centers for Disease Control and Prevention definition of anemia in pregnancy (modified from the
1968 World Health Organization definition) is as follows:
1 Hb less than 11.0 g/dl in the first and third trimesters and
2 Less than 10.5 g/dl in the second trimester, or
3 A hematocrit less than 32%.
Epidemiology 56% of pregnant women are anemic, depending on the geographic and socioeconomic
group studies. Four percent of white women and 13% of black women during the first trimester, rising to
19% of white women and 38% of black women in the third trimester.
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Signs and symptoms range from subclinical with mild anemia to

1 The presence of pallor
2 Fatigue
3 Anorexia
4 Weakness
5 Lassitude
6 Dyspnea
7 Edema in severe anemia.
At the first prenatal visit, questions relating to a history of anemia, bleeding diathesis, and other blood
disorders should be obtained.
Laboratory Tests
Routine prenatal laboratory studies should include a CBC.
It is important to note that in normal pregnancy, the hemoglobin/hematocrit tend to be low.
The RBC indices may be more helpful in deciding whether abnormalities such as iron deficiency (low mean
corpuscular volume [MCV]) or macrocytosis (high MCV) are present.
The hemoglobin/hematocrit should be repeated during the third trimester (about 28 to 32 weeks) and more
frequently if indicated.
Certain ethnicities should have screening tests for specific conditions.
1 African-American patients should have a Sickledex test or a hemoglobin electrophoresis to check for sickle
cell trait-disease and a determination for glucose 6-phosphate dehydrogenase deficiency.
2 Patients from the Mediterranean, the Middle East, India, and Southeast Asia are at risk for thalassemia,
which also can be identified on hemoglobin electrophoresis.
Further studies include
1 Urinalysis
2 Iron studies
3 Reticulocyte count
4 Peripheral blood smear
5 Stool for ova and parasites
6 Studies as indicated.
7 Bone marrow studies are rarely indicated in pregnancy.
Complications
Severe anemia can increase the risk of morbidity and mortality.
Blood loss during delivery ranges from
1 500 ml for a vaginal delivery to 1000 ml or more for cesarean section or vaginal delivery with
complications.
2 The anemic patient has a decreased margin of safety against these blood losses.
Past studies have suggested that severe maternal anemia (less than 6 gm per dl) is associated with poor
pregnancy outcomes, such as prematurity, low birth weight, abortion, and fetal death.
More recent studies have failed to confirm a significant association between maternal anemia and poor fetal
outcome (4).
Specific Anemias
Anemias Resulting from Inadequate Production of Hemoglobin
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Seen in nutritional deficiencies (e.g., iron deficiency) or inadequate production of hemoglobin chains
(e.g., thalassemia).
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Iron-deficiency Anemia
Oral iron intake may be inadequate to maintain iron stores as a result of menstrual blood loss during
reproductive life.
Pregnancy will exacerbate the loss of iron stores because of increased maternal blood production and fetal
growth needs.
The average menstruating woman requires between 10 and 13 mg of available iron in her daily diet to
compensate for an average daily loss of about 2 mg.
Pregnancy requires an increase to 15 to 18 mg per day of elemental iron (1).
In total, pregnancy requires about 1130 mg of elemental iron
1 450 mg for RBC expansion
2 360 mg for fetus-placenta
3 170 mg for basal loss
4 150 mg for delivery loss.
Iron not replaced by diet or the amount returned to storage after delivery leaves the mother with a deficit of
iron that is borrowed from maternal stores or must come from iron supplementation (4).
Factors contributing to iron deficiency include the following:
1 Inadequate iron intake caused by dietary insufficiency or inability to tolerate iron supplements
2 Bleeding during pregnancy, vaginally or from another source
3 Multiple gestation, which may increase the iron requirement and may be responsible for a greater blood loss
at delivery
4 Iron malabsorption
5 Concurrent antacid use, which may prevent iron absorption
6 Poor dietary habits or pica (an appetite for inedible substances, such as clay or dirt).
Mild iron deficiency anemia may not be manifested on the CBC until maternal iron stores are significantly
depleted. Thereafter, the following changes may be noted:
Initially a normochromic, normocytic anemia is seen
A microcytic, hypochromic anemia then occurs and the MCV falls to a level of 70 to 80 fL (normal = 90
10 fL)
Serum iron falls below 60 g per dl
Unsaturated iron-binding capacity rises above 350 g per dl
Serum ferritin correlates well with bone marrow stores, making a bone marrow examination rarely
necessary. Levels below 30 g per liter are diagnostic of iron deficiency.
Treatment Prophylaxis
Medications
Ferrous sulfate, 300 mg tablets, contain 60 mg (10 grains) of elemental iron.
Intestinal absorption permits absorption only up to 15 mg of iron without signs of iron intolerance or even
toxicity.
Given the limits of daily absorption and the well-recognized intolerance to iron, the thrice-daily dosing is
unnecessary.
Side Effects
Complications
Childhood poisoning. Note that maternal iron preparations are the second most common cause of childhood
poisoning in the United States (after aspirin).
These preparations should be kept away from children.
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Anemia of Chronic Illness

Laboratory Tests normochromic, normocytic (or microcytic) anemia unresponsive to iron therapy.
The diagnosis of a specific condition requires a high index of suspicion followed by careful history and
physical examination.
The treatment is determined by the specific cause.
Differential Diagnosis Includes intestinal disease, Parasitic disease (e.g., malaria, helminths), Chronic or
subclinical infection (e.g., chronic renal disease), Peptic ulcer disease, Neoplasia.
Anemia Resulting from Folic Acid Deficiency
In the nonpregnant woman, the recommended daily requirement for folic acid is 0.4 mg; this increases to 0.8
to 1.0 mg during pregnancy.
Folate stores are limited and easily depleted within a few months in times of increased demand (e.g.,
pregnancy and lactation).
All supplies of folate must come from external sources: Prime dietary sources are fruits and vegetables, of
which the best are
1 Spinach
2 Lettuce
3 Asparagus
4 Broccoli
5 Lima beans
6 Melons
7 Bananas.
Etiology Certain groups of pregnant women may be at risk for folic acid deficiency, namely those with
the following:
1 Ongoing hemolysis (e.g., hemoglobinopathies)
2 Seizure disorders on medication interfering with folic acid metabolism
3 Multiple gestation.
Folic acid deficiency is the most common cause of megaloblastic anemia.
The symptoms of anemia associated with folic acid deficiency are nonspecific.
Deficiencies in either folic acid or B12 can present with glossitis and roughness of skin.
However, the concomitant presence of neurologic symptoms is diagnostic of B 12 deficiency and is almost
never seen with folic acid deficiency.
The anemia of folic acid deficiency is megaloblastic with an MCV usually greater than 110 fL.
The macrocytosis can be masked by concomitant iron deficiency or thalassemia.
Neutropenia, thrombocytopenia, and hypersegmented granulocytes are usually present on the peripheral
blood smear.
The presence of an elevated serum iron and transferrin saturation also differentiates this from iron deficiency
anemia.
B12 deficiency is extremely rare in pregnancy, and therefore megaloblastic anemia is almost always due to
folic acid deficiency (1).
Folic acid deficiency has been associated with such pregnancy complications as
1 Low birth weight
2 Smaller maternal blood volume
3 Abruptio placentae
4 Prematurity.
These may also be explained, however, by the presence of other factors such as low socioeconomic status
and malnutrition.
Medications
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The daily dose of folic acid is 1.0 mg whether for prophylaxis or treatment.
This can be increased as necessary.
If given for megaloblastic anemia, an increased reticulocyte count should be seen within three to four days.
If neurologic symptoms are present, a B 12 level should be measured because folic acid will correct the
anemia but not the neurologic symptoms.
Oral folic acid is sufficient for treatment unless folic acid antagonists are being used, at which time
parenteral folic acid is indicated.
Patient Education
Prevention or reduction of neural tube defects.
Folic acid can be used preconceptionally for the prevention (or reduction) of both first-time and recurrent
neural tube defects (see Chapter 30, Teratogeus and Birth Defects).
Because the neural tube closes by 28 days of gestation, folic acid must be started months before conception
in order to attain this preventative effect.
The mechanism for this effect is unknown.
A risk of folic acid prophyaxis is masking B 12 deficiency (i.e., normalizing anemia but with ongoing
neurologic damage), although this is a very rare disorder in the reproductive age group.
Anemia from B12 Deficiency
Etiology
a B12 is absorbed in the ileum, bound to intrinsic factor.
b Intrinsic factor is secreted in the stomach by the fundic parietal cells.
These same cells are responsible for hydrochloric acid secretion.
c B12 deficiency is rarely due to inadequate ingestion, except in strict vegetarians.
Inadequate synthesis and production of intrinsic factor, or malabsorption syndromes are common causes.
Illustrations of these problems include
Pernicious anemia (rare in this age group)
Previous gastric or intestinal surgery
Inflammatory bowel disease
Helminth infestations.
These are uncommon in most pregnant women in the United States, making B 12 deficiency a much less
common cause for megaloblastic anemia than is folic acid deficiency.
Laboratory Tests
A radioimmunoassay is used to measure B12 serum levels.
Vitamin B12 levels may fall to 80 to 120 pg per ml during pregnancy; levels below 50 pg per ml are
indicative of B12 deficiency.
The Schilling test is used to measure B12 absorption but is contraindicated in pregnancy because of the use of
radioactive cobalt.
However, if vitamin B12 deficiency is present, then a Schilling test must be done at a safe time after
delivery.
Neurologic abnormalities are seen, as are elevated serum bilirubin and lactic dehydrogenase levels (4).
Clinical Manifestations
Neurologic symptoms are common in B12 deficiency and rare in folic acid deficiency.
Medications
If a deficiency is documented, 1 mg B 12 is given parenterally weekly for five to six weeks, then 100 mcg SQ
monthly.
Serum levels should respond within six weeks.
A brisk reticulocytosis should manifest within three to five days.
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Alpha-thalassemia
Etiology
The alpha-gene locus contains two structural genes.
The genotype of normal individuals is aa/aa.
The clinical severity increases as each allele is deleted.
1 The carrier state is represented by -a/aa and is clinically silent.
2 The heterozygous state is seen with -a/-a or /aa and is called -thalassemia minor.
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It is clinically asymptomatic, except during great stress.
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A mild microcytic, hypochromic anemia with poikilocytosis and anisocytosis is seen.
3
Newborns carry 2% to 10% of Bart hemoglobin (an abnormal tetramer of gamma-chains).
Hemoglobin H disease is seen with a deletion of three alpha-chains (/-a).
1 Splenomegaly and occasionally hepatomegaly are seen.
2 Chronic moderate hemolytic anemia is present with a reticulocytosis, microcytosis, hypochromasia, and
poikilocytosis.
3 Both hemoglobin H (a tetramer of beta-chains) and Bart hemoglobin are seen.
4 Hemoglobin H disease occurs mostly in Southeast Asians and is unusual in African Americans.
The absence of all four alpha-chains is incompatible with extrauterine life.
1 The fetus will generally experience second-trimester hydrops and will be lost.
2 A large amount of Bart hemoglobin will be present.
3 These pregnancies are notable for a high incidence of toxemia (1).
Evaluation
Improvements in prenatal diagnosis of the hemoglobinopathies and the thalassemias allow for early in utero
identification of the severely affected fetus.
Termination can then be offered for the severely affected fetus or reassurance if the fetus is unaffected or
mildly affected.
Those couples at risk must be identified early and offered genetic counseling (5).
Techniques for prenatal diagnosis include genetic counseling with a determination of risk based on
Mendelian inheritance patterns and direct determination of the fetal genotype by tissue sampling early in
pregnancy.
Fetal tissue can be obtained by chorionic villous sampling (CVS) performed between 10 and 12 weeks of
gestation, amniocentesis performed at 15 to 16 weeks of gestation for fetal amniocytes, or fetoscopy for
fetal blood after 19 to 20 weeks of gestation.
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Medications
In A--thalassemia minor, folate may need to be supplemented.
Iron-deficiency anemia must be ruled out as a cause of microcytic, hypochromic anemia.
In severe cases, transfusion may be required.
Complications
In A-thalassemia minor, the pregnancy may be complicated by anemia.
In silent carriers, no complications are seen.
In hemoglobin H disease, a more severe anemia can be seen, and transfusions are more often needed.
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Beta-thalassemia Minor
Etiology
In the United States, most -thalassemia is present in the African-American population.
03B2;-thalassemia minor is the heterozygous state.
Variable clinical severity is seen in -thalassemia minor.
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The condition is suspected when a patient is treated for iron-deficiency anemia and fails to respond.
Laboratory Tests
A moderate to severe microcytic, hypochromic anemia is seen associated with a relatively high red cell
count.
Hemoglobin A2 is elevated above 3.5%.
Serum iron and ferritin concentrations are elevated.
Mild to moderate splenomegaly may be present.
Except for mild anemia, most pregnancies are uncomplicated.
Medications
Folic acid supplementation may be necessary.
Transfusions are occasionally needed for the more severe anemia.
Beta-thalassemia Major
Etiology
-thalassemia major is the homozygous state.
This more severe disease is also known as Cooley anemia.
Pregnancy rarely occurs because individuals are so severely affected.
Infants who survive with this anemia have a course that is marked by profound, transfusion-dependent
anemia, growth retardation, and heart failure.
In children and adults, iron overload may be present from prior transfusions.
Excessive Destruction of Erythrocytes (Hemolytic Anemias)
Anemia results from an inability of the bone marrow to keep up with the destruction of RBCs.
Folic acid deficiency can also accompany hemolytic anemia because of increased erythrocyte synthesis.
Sickle Cell Anemia
Etiology
This group of diseases is caused by a hemoglobinopathy resulting from abnormal beta hemoglobin chains.
1 The substitution of glutamic acid to valine at the sixth position causes hemoglobin S.
2 This, in turn, arises from a single nucleotide change in the coding sequence for beta globins.
3 Other single amino acid substitutions also can cause abnormal hemoglobins that lead to instability, reduced
solubility, RBC cell wall rigidity, and a changed oxygen affinity.
The homozygous individual will have both abnormal beta-chains.
The heterozygote will have one abnormal and one normal beta-chain.
The homozygote generally has severe disease.
If the patient is heterozygous for more than one trait, the combination may be worse than either one
separately (e.g., hemoglobin SC).
Vaso-occlusions that lead to infarction occur because these rigid RBCs do not easily pass through the
microcirculation.
Sickle Cell Trait
Epidemiology
The frequency of sickle cell trait (hemoglobin SA) is 1 in 12 in the African-American population.
The frequency of sickle cell disease (hemoglobin SS) in the African-American population is 1 in 708.
Sickle cell trait is associated with morbidity in pregnancy, namely asymptomatic bacteriuria and
pyelonephritis.
Individuals of African ancestry should be screened, and those with the trait should have urine cultures
performed.
c Sickle cell trait may be associated with:
1 Vaso-occlusive disease
2 Sudden death at high altitudes (e.g., when exercising a mile above sea level, or when in a suddenly
depressurized aircraft)
3 Severe intercurrent illness.
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Sickle Cell Disease

Laboratory Tests
The diagnosis is made by the presence of irreversibly sickled RBCs on peripheral smear with normal, target,
fragmented, and nucleated cells.
The abnormal hemoglobin electrophoresis shows greater than 80% hemoglobin S.
Some patients have elevated levels of Hb F.
The family history and family studies are also important.
Beta-chain synthesis does not reach sufficient levels to cause symptoms until about six months of age.
Thereafter, the increased concentration of hemoglobin S makes the cells susceptible to sickling and
hemolysis, causing anemia and splenomegaly.
1 Major problems are
2 Infections
3 Vaso-occlusive episodes.
Children are at increased risk for certain infections, including
1 Sepsis
2 Meningitis
3 Pneumonia
4 Osteomyelitis
5 Urinary tract infections (UTIs).
The functional asplenia following vaso-occlusive microinfarctions compromises the immune system,
leading to infections caused by encapsulated organisms.
Vaso-occlusive crises occur because rigid RBCs are unable to pass in the microcirculation causing
infarctions.
Target areas include the
1 Extremities,
2 Lungs,
3 Spleen,
4 Splanchnic bed,
5 Brain, and
6 Eyes.
Pain resulting from these infarctions can mimic other conditions (e.g., pulmonary crises with fever mimic
pneumonia) and are a source of clinical confusion.
Other Abnormal Hemoglobins

a Sometimes implicated in hemolytic anemias.
b Hemoglobin SC disease usually is mild but can be subject to painful crises.
c The clinical syndrome, although milder, is similar to sickle cell anemia.
d Hemoglobin S/-thalassemia is similar in presentation.
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The course of hemoglobin S disease before pregnancy frequently predicts how the woman will do during the
pregnancy.
The spontaneous abortion rate does not appear to be increased unless associated with frequent crises and
severe anemia.
There is an increased incidence of perinatal mortality and low-birth-weight infants (6, 7), but fetuses have
generally good results.
Termination of the pregnancy because of maternal sickle cell anemia is largely unwarranted and should be
decided on an individual basis.
Generally, pregnancy proceeds normally except for an increased incidence of UTIs.
Occasionally, an inability to concentrate urine (hyposthenuria) occurs as a result of renal papillary necrosis
and loss of deep medullary nephrons.
Hematuria is uncommon, and other potential causes must be ruled out first before attributing it only to sickle
cell trait.
Medications
The pregnant woman with sickle cell anemia should be monitored by experienced physicians.
No medication will prevent sickling.
Blood transfusions may be needed to treat vaso-occlusive crises and anemia.
1 Partial exchange transfusions will increase the concentration of hemoglobin A.
2 This will decrease sickling and improve oxygen delivery to the fetus, providing an improved perinatal
outcome.
3 The target is a concentration of hemoglobin A greater than 25% and a hematocrit between 25% and 30%.
4 Transfusion therapy, however, can be complicated by fluid overload, iron overload, hepatitis, and human
immunodeficiency virus (HIV) infection and, therefore, must be used judiciously.
Iron supplementation is not necessary because of the increased iron stores secondary to the frequent
transfusions.
Folic acid supplementation of 1 mg per day is recommended.
Sickle cell crises must be treated with generous fluid support, oxygen supplementation, and blood
transfusions as necessary.
Procedures
Urinary tract infections occur more frequently.
Careful monitoring for asymptomatic bacteriuria and UTIs is necessary.
Fetal surveillance should be started in the late second to early third trimester by nonstress tests and
sonographic evaluation.
Labor and delivery are managed on the basis of obstetric principles: Cesarean section should be performed
only for obstetric indications. If abdominal delivery is necessary, regional anesthesia is preferred to
general anesthesia.
Genetic counseling is an important component of management.
Patient Education
Contraception is problematic in patients with severe hemoglobinopathies.
They are at increased risk for thromboembolic disorders; therefore, oral contraception may be relatively
contraindicated.
They are also at increased risk for infection, and so the intrauterine device also may not be a good choice if
they are not in a long-term, monogamous relationship.
Permanent sterilization should be considered when the patient is finished with childbearing.
FAKULTAS KEDOKTERAN
373438,
Skenario B Blok 23 Tahun 2014
Learning Outcomes:
1. Have the ability for anamnesis, general and obstetric physical examination of severe
preeclampsia/eclampsia and Graves disease to plan supporting examination as indicated, such as
routine blood and urine rutine, T3, T4,TSH and others.
2. Have the ability to conclude (diagnose) based on the data from physical and supporting examination.
3. Have the ability to make a good obstetric medical record.
4. Have the ability to plan a management (treatment) based on competence.
5. Have the ability to plan follow up and evaluation and referal system.
6. Have the ability to make evidence based medicine-prognosis and give good explanation (Informed
Learning Objectives:
At the end of this session, students should:
1. Understand the patophysiology of hypertension and Graves disease which may be occured
concomitantly in a pregnant woman.
2. Have the clinical skills to examine a pregnant woman who are suffering from hypertension, and
Graves disease and how to diagnose and manage it properly.
3. Known about symptoms and kind of seizure in a pregnant woman.
4. Have the ability to plan a management (treatment) emergency case in severe preeclampsia and
eclampsia.
5. Be able known complication severe preeclampsia/eclampsia and Graves disease based on
competence
6. Be able to prepare a plan for postnatal care. ( Family Planning & Rehabilitation )
Mrs. Mima, 38-year-old pregnant woman G4P3A0 39-weeks pregnancy, was brought by her husband to the
Puskesmas due to convulsion 2 hours ago. She has been complaining of headache and visual disturbance for
the last 2 days. According to her husband, she has been suffering from Graves disease since 3 years ago, but
was not well controlled.
Upon admission,
Height = 152 cm; Weight 65 kg;
BP: 180/110 mmHg. HR: 120 x/min, RR: 24 x/m.
Head and neck examination revealed exopthalmus and enlargement of thyroid gland.
Pretibial edema
Obstetric examination:
Outer examination: fundal height 32 cm, normal presentation.

FHR: 150 x/min.
Lab: Hb 11,2 g/dL; she had 2 + protein on urine, cylinder (-)
Term Clarification
G4P3A0
Convulsion
Exopthalmus
Graves Disease
Hypertension
Visual Disturbance
Pretibial edema
Headache.
Mrs. Mima, 38-year-old pregnant woman G4P3A0 39 weeks pregnancy
She had suffered convulsion 2 hours ago.
She has been complaining of headache and visual disturbance for the last 2 days.
She has been suffering from Graves disease since 3 years ago, but were not well controlled.
Physical exam: height: 152 cm, weight 65 kg, BP: 180/110 mmHg, HR: 120 x/min, RR: 24 x/m.
Head and neck examination revealed exopthalmus and enlargement of thyroid gland. Pretibial
edema.
Obstetrics finding: fundal height 32 cm, normal presentations. FHR: 150 x /min.
Laboratory finding: Hb 11,2 g/dL. She had 2 + protein on urine, cylinder (-)
Problem Analysis
Anatomy & physiology of reproduction system & thyroid gland
Correlation between Graves disease and hypertension, preeclampia/eclampsia in pregnancy.
Pathophysiology of convulsions, hypertension, exopthalmus, edema, proteinuria.
Diagnosis and management of eclampsia in pregnancy.
Diagnosis and management of Graves disease.
Additional examinations ( T3, T4, TSH)
Complications to mother and baby
Prognosis
Postnatal Management
Synthesis
Hypertension in Pregnancy
Definition
Hypertension in pregnancy is defined as a systolic blood pressure of 140 mmHg and/or a diastolic blood
pressure of 90 mmHg. The significance of any blood pressure measurement is related to the gestation of
the pregnancy and, in general terms, the earlier in pregnancy hypertension occurs the more likely it is to be
chronic hypertension.
Chronic hypertension
(CHT) describes all hypertension that exists pre-pregnancy. The majority of women in this group have
essential hypertension, though many will be diagnosed for the first time in pregnancy.
Renal hypertension can complicate renal disease of any underlying pathology. Its presence increases
maternal and perinatal morbidity and mortality though its management is as for other causes. The increased
morbidity is usually related to the underlying renal pathology and it is concern for the maternal kidneys that
usually precipitates delivery if problems arise.
Mild preeclampsia
Mild preeclampsia is specific syndrome in pregnancy with decreased perfusion of organs caused by
vasospasm and activity of endothelial cell
a. Blood presure 140/90 mmHg - < 160/110 mmHg.
b. Proteinuria: 300mg/ 24 hours with urine output, or dipstick: +1.
c. Local edema.
Severe preeclampsia
Severe preeclampsia is a complication in pregnancy women with sign hypertension 160/110 mmHg or
higher and there is proteinuria, edema and in 20 weeks gestasional age or more. Sign and simptom severe
preeclampsia:
Proteinuria: 5g with urine output for 24 hours, or dipstick: +4.
Oligouria: urine production < 400-500 ml/24 jam.
Increased creatinin serum.
Edema pulmonal and cyanosis.
Epigastrium pain and abdominal upper right pain
Disturbance of visus.
Disturbance of hepar function: increased alanine or aspartate amino transferase
Hemolisys microangiopatic.
Trombositopenia < 100.000/ml
Sindroma HELLP
Classification of severe preeclampsia
Severe preeclampsia without impending eclampsia
b. Severe preeclampsia with impending eclampsia, symptoms of impending eclampsia: headache,
disturbance of visus, nausea and vomitus, epigastrium pain, upper right abdominal pain.
Management for severe preeclampsia

1. Medicine for complication of severe preeclampsia
2. Plan about the pregnancy depend age of gestational age: expectative and active
Other causes of hypertension in pregnancy are:
Phaeochromocytoma: rare but maternal mortality is 50%
Coarctation of the aorta: high maternal mortality

Cushings syndrome: can be difficult to diagnose as features can be mimicked by normal pregnancy;
associated with a high fetal loss
Conns syndrome: hypertension is associated with hypokalaemia
Chronic Hypertension versus Pregnancy Induced Hypertension (PIH)
In the first trimester of pregnancy the marked vasodilatation and drop in vascular resistance sees
blood pressure fall in both normotensive and hypertensive women, (the drop being greater in the CHT
group). As such hypertension may not be seen until the third or late in the second trimester. CHT can
therefore only be diagnosed with reference to non-pregnant BP readings and this requires either prenatal BPs
or more commonly detailed postnatal follow-up. Pharmacological management of CHT and PIH is identical
and as a general rule if hypertension is present before 20 weeks CHT is more likely. Women with CHT tend
to be older, heavier and of higher parity.
COMPLICATIONS
Superimposed Pre-eclampsia
CHT is a major risk factor for pre-eclampsia. The signs of superimposed pre-eclampsia are similar in this
group but blood pressures (BP) will be higher or the BP picture will be difficult to interpret, due to CHT
treatment with antihypertensives. In women with CHT the development of proteinuria is diagnostic of preeclampsia and is almost universally associated with fetal growth restriction. Another very predictive feature
of pre-eclampsia in CHT is a high urate (uric acid). If pre-eclampsia does not develop then women with
CHT can expect a relatively uncomplicated pregnancy and outcome.
Fetal Growth Restriction
Even in the absence of other features of pre-eclampsia fetal growth restriction is more common in women
with CHT. The underlying aetiology is usually poor placentation. Routine assessment of fetal growth with
ultrasound scan (USS) from 28 weeks is commonplace.
Placental Abruption
Placental abruption is a rare but serious complication affecting 1% of CHT pregnancies. It is unlikely that
antihypertensive treatment would reduce this risk, but women should be advised of the risk and encouraged
to stop smoking.
Severe Hypertension
Episodes of acute hypertension can occur in this group of women, who may stop medication when they
conceive despite medical advice. The acute management is as for hypertension associated with severe preeclampsia and then oral therapy can be recommenced.
Hyperthyroidism in Pregnancy
Overview
Hyperthyroidism complicates approximately 12 in 1000 pregnancies. The overwhelming cause of
hyperthyroidism during pregnancy is Graves disease or autoimmune thyrotoxicosis. Pregnant women with
hyperthyroidism are at increased risk for congestive heart failure, thyroid storm, preterm labor,
preeclampsia, fetal growth restriction, and perinatal mortality. Treatment of hyperthyroid women to achieve
adequate metabolic control will result in improved pregnancy outcomes. However, overtreatment may result
in maternal or fetal hypothyroidism. Gestational transient thyrotoxicosis (GTT) is 10 times more prevalent
than Graves disease and may be caused by the elevated hCG values typically observed with hyperemesis
gravidarum. Subclinical hyperthyroidism effects 1.7% of pregnant women and has only recently been
introduced into clinical practice because of the development of extremely sensitive serum TSH assays.
Subclinical hyperthyroidism is not associated with any adverse maternal pregnancy outcomes. Treatment of
the latter two clinical entities has not been shown to be beneficial.
Graves disease is an organ-specific autoimmune process whereby thyroid-stimulating autoantibodies
attach to and activate TSH receptors. Other less common causes include toxic multinodular goiter, subacute
thyroiditis, adenoma, or iodine-induced thyrotoxicosis. Thyrotropin receptor activation by hCG, which has
some cross-reactivity with TSH, explains the biochemical and occasional clinical findings of thyrotoxicosis
in women with hyperemesis gravidarum and gestational trophoblastic decrease.
Presentation
As with hypothyroidism, clinical features of hyperthyroidism can be easily confused with
physiologic symptoms of pregnancy. Suggestive complaints or findings include nervousness, heat
intolerance, palpitations, goiter, failure to gain weight or weight loss, and exophthalmos. GTT usually occurs
in women with hyperemesis gravidarum. Subclinical hyperthyroidism defined as a serum TSH concentration
below the statistically defined lower limit of normal with a serum concentration of fT4 within the reference
range, is typically identified in asymptomatic women.
Complications
Thyrotoxicosis increases the risk of miscarriage. Diagnosis of thyrotoxicosis may be difficult
because some of the symptoms and signs are mimicked by normal pregnancy. Serum investigations are
necessary. Graves disease (GD) tends to improve in pregnancy, and may remit completely during the second
half of pregnancy. Fetal or neonatal thyrotoxicosis affects 210% of Graves disease pregnancies. This can
cause a small for dates baby, premature labour and intrauterine death or neonatal death. It is also associated
withcraniostenosis.
Overtreatment of maternal thyrotoxicosis will cause fetal hypothyroidism and goitre. If ultrasound
scans show a fetal goitre the differential diagnosis is fetal hypothyroidism or fetal thyrotoxicosis. This is an
indication for cordocentesis to measure fetal TSH and fT42.
Diagnosis
In women with a depressed serum TSH level (<0.4 mIU/L), clinical hyperthyroidism is confirmed by
an elevation in fT4 (>1.8 ng/dL) concentration. As is true for the diagnosis of hypothyroidism, one must
consider the impact of pregnancy on TSH and possibly fT4 (Table 22.1). Rarely, hyperthyroidism is caused
by abnormally high serum triiodothyronine values (T3 thyrotoxicosis). In women with depressed TSH yet
normal fT4, evaluation of fT3 or free T3 index may explain a patients hypermetabolic symptoms. Also,
evaluation of TSH receptor antibodies may be helpful in evaluation of women with Graves disease to
identify those at risk for delivery of an infant with fetal or neonatal hyperthyroidism.
Management and Treatment

Thyrotoxicosis during pregnancy can nearly always be controlled by thioamide drugs and treatment
has been associated with improved pregnancy outcomes. Some clinicians prefer propylthiouracil because it
inhibits peripheral conversion of T4 to T3 and it crosses the placenta less readily than methimazole.
Methimazole used in early pregnancy has also been associated with esophageal and choanal atresia as well
as aplasia cutis. Transient leukopenia occurs in approximately 10% of women treated with thioamides, but
this does not require cessation of therapy. In approximately 0.2%, agranulocytosis develops suddenly, is not
dose related, and, because of its acute onset, serial leukocyte counts during therapy are not helpful. Rather, if
fever or sore throat develops, patients should be instructed to discontinue medication immediately and report
for a complete blood count. The dose of propylthiouracil is empirical, and the American Thyroid Association
recommends an initial daily dose of 100 600 mg for propylthiouracil or 1040 mg for methimazole.
Women with overt hyperthyroidism diagnosed during pregnancy may require a higher initial dose
between 300 and 450 mg/day. The starting daily dose of methimazole is 2040 mg. The goal of therapy is
clinical euthyroidism with free thyroxine in the upper range of normal. The median time to normalization of
thyroid function tests is 68 weeks, but TSH levels may remain suppressed beyond normalization of fT4.
Once euthyroidism is achieved, serial measurement of TSH and fT4 during each trimester is recommended.
There is currently no convincing evidence that subclinical hyperthyroidism should be treated in
nonpregnant individuals. In fact, it should be considered contraindicated during pregnancy because maternal
antithyroid drugs cross the placenta and may cause fetal thyroid suppression. There are other alternatives for
treatment of overt hyperthyroidism which are rarely undertaken during pregnancy. For example, although
thyroidectomy is typically reserved for treatment outside of pregnancy, pregnant women who cannot adhere
to medical therapy or in whom therapy is toxic may benefit from surgical management . Ablative radioactive
iodine is contraindicated in pregnancy as it can cause fetal thyroid destruction.
REFERENCES:
1. Queenan JT, Spong CY, Lockwood CJ (eds). Management of High-Risk Pregnancy An EvidenceBased Approach, Blackwell Publishing, 5th ed, Victoria, 2007.
2. S. E. Robson and J. Waugh (eds). Medical Disorders in Pregnancy: A Manual for Midwives,
Blackwell Publishing. 1st ed, Iowa, 2008.

FAKULTAS KEDOKTERAN
373438,
Skenario C Blok 23 Tahun 2014
A female baby was born at Moh.Hoesin Hospital from a 19 years old woman. Her mother, Mrs.
Solehah was hospitalized at Moh.Hoesin Hospital due to contraction. It was her first pregnancy. She forgot
when her first day of last period, but she thought that her pregnancy was about 8 months. She said that she
never had hypertension or other illness during her pregnancy. Six hours after admitted, she delivered her
baby spontaneously. The labor process was 30 minutes, and rupture of membrane happened one hour before
delivery. The baby didnt cry spontaneously after birth, and resuscitation was done. APGAR score at 1
minute was 1, at 5 minute was 3, and at 10 minutes was 7. One hour later the baby still had grunting and
cyanosis.
On physical examination:
Body weight was 1400 gr, body length was 40 cm, and head circumference was 30 cm. The muscle tone
decreased, she poorly flexed at the limbs, she had thin skin, more lanugo over the body and plantar creased
at 1/3 anterior. At 10 minutes of age, she still had grunting and cyanosis on the whole body. The respiratory
rate was 70 x/min, heart rate was 150 bpm, the temperature was 36 oC. There was chest indrawing. Other
physical examinations were within normal limit.
As a general practitioner please analyze the problem and the management.

-----------------------------------------------------------------------------------------------------------Learning Objectives:
Students must be able to:
1.
2.
3.
4.
5.
6.
Explain the definition and classification of low birth weight infant.

Explain risk factors which predispose of low birth weight infant
Diagnose low birth weight infant
Manage low birth weight infant
Explain the definition, risk factor, diagnosis and management of asphyxia neonatorum
Explain the definition, risk factor, diagnosis and management of respiratory distress
Klarifikasi Istilah
1 Contraction (perut mules)

2 Rupture of membrane (pecah ketuban)
3 First day of last period (HPHT)
4 Apgar score
5 Lanugo
6 Plantar creased
7 Grunting (merintih)
8 Cyanosis (biru)
9 Chest indrawing (retraksi dinding dada)
Identifikasi Masalah
1.
2.
3.
4.
Bayi Ny. Solehah, perempuan, berat badan lahir 1400 gram

HPHT lupa dan usia kehamilan kira-kira 8 bulan.
Bayi lahir tidak langsung menangis, APGAR skor 1/3/7
Bayi merintih dan biru.
Analisis Masalah
1. Berat badan 1400 gram, berdasarkan berat badan lahir bayi ini diklasifikasikan
sebagai apa?
2. HPHT lupa dan ibu mengatakan usia kehamilannya kira-kira 8 bulan. Dengan menggunakan apa kita
dapat menentukan berapa minggu masa gestasinya?
3. Berdasarkan masa gestasi dan berat badan lahir bayi ini diklasifikasikan sebagai
apa? Apa yang digunakan untuk mengklasifikasikan bayi baru lahir berdasarkan berat lahir dan masa
gestasi baru baru lahir?
4.
5.
6.
7.
8.
9.
Bayi tidak langsung menangis setelah lahir, Apgar score rendah, apa diagnosisnya?
Bayi merintih dan biru, apa yang diderita bayi ini?
Apa diagnosis bandingnya?
Apa kemungkinan diagnosisnya?
Pemeriksaan apa yang diperlukan pada penderita ini?
Bagaimana tatalaksana penderita ini?
Hipotesis
Bayi Ny. Solehah, preterm, SGA (sesuai dengan usia kehamilan), BBLSR lahir spontan dengan asfiksia
perinatal dan respiratory distress. Kemungkinan penyebabnya (diagnosisnya) adalah penyakit membran
hialin.
Sintesis
1. Berat badan 1400 gram. Berdasarkan berat badan lahir, bayi ini diklasifikasikan
sebagai BBLSR
2. HPHT tidak diketahui. Pada penderita ini kita dapati kulit tipis, banyak lanugo dan plantar creased
hanya didapati 1/3 bagian depan telapak kaki, dari sini kita dapat memperkirakan bahwa bayi
termasuk bayi preterm. Lalu lakukan penentuan masa gestasi dengan menggunakan Ballards score.
3.
4.
5.
6.
7.
8.
Faktor risiko pencetus kehamilan prematur pada skenario ini adalah faktor usia ibu yang muda (<20
tahun)
Berdasarkan masa gestasi kira-kira 8 bulan dan berat badan lahir 1400, dengan menggunakan kurve
Lubchenco bayi ini diklasifikasikan sebagai AGA.
Bayi merintih dan biru, apa yang diderita bayi ini dengan menggunakan Downes score maka bayi
ini mengalami respiratory distress.
Diagnosis bandingnya adalah penyakit membran hialin dan transient tachypnea of the newborn
(TTN).
Kemungkinan diagnosisnya adalah penyakit membran hyalin.
Pemeriksaan yang diperlukan pada penderita ini:
a. Rontgen dada
b. Pemeriksaan darah (Hb, leukosit, hitung jenis, trombosit, CRP)
c. Kadar gula darah
d. Kultur darah
Tata laksana penderita ini:
a. Pertahankan suhu tubuh dalam batas normal (rawat dalam inkubator)
b. Beri vitamin K1 0,5 mg intramuskuler
c. Parenteral feeding
d. Beri oksigen
e. Beri antibiotika sampai kemungkinan infeksi dapat disingkirkan
f. Monitoring

FAKULTAS KEDOKTERAN
373438,
Skenario C Blok 23 Tahun 2014
A female baby was born at Moh.Hoesin Hospital from a 19 years old woman. Her mother, Mrs.
Solehah was hospitalized at Moh.Hoesin Hospital due to contraction. It was her first pregnancy. She forgot
when her first day of last period, but she thought that her pregnancy was about 8 months. She said that she
never had hypertension or other illness during her pregnancy. Six hours after admitted, she delivered her
baby spontaneously. The labor process was 30 minutes, and rupture of membrane happened one hour before
delivery. The baby didnt cry spontaneously after birth, and resuscitation was done. APGAR score at 1
minute was 1, at 5 minute was 3, and at 10 minutes was 7. One hour later the baby still had grunting and
cyanosis.
On physical examination:
Body weight was 1400 gr, body length was 40 cm, and head circumference was 30 cm. The muscle tone
decreased, she poorly flexed at the limbs, she had thin skin, more lanugo over the body and plantar creased
at 1/3 anterior. At 10 minutes of age, she still had grunting and cyanosis on the whole body. The respiratory
rate was 70 x/min, heart rate was 150 bpm, the temperature was 36 oC. There was chest indrawing. Other
physical examinations were within normal limit.
As a general practitioner please analyze the problem and the management.

FAKULTAS KEDOKTERAN
373438,
Skenario D Blok 23 Tahun 2014
Learning outcomes:
7. Have the ability for anamnesis, general and gynecology physical examination and to plan supporting
examination as indicated, such as routine blood, urine and ultrasound examination.
9. Have the ability to make a good gynecology medical record.
11. Have the ability to plan follow up and evaluation.
1. Anatomy of reproductive system
2. Gynecology physical examination, which include:
a. External examination (inspection, palpation, percussion, auscultation)
b. Internal examination (speculum & bimanual)
3. Etiology, symptoms, clinical signs, physical examination and management of bleeding in early
pregnancy and gynecologic disease
4. Terms in pregnancy
5. Differential diagnosis of bleeding in early pregnancy
6. Interpretation of laboratory findings (blood and urine)
7. Ideal pregnancy planning
Mrs. Tari, 37 years old, from middle income family comes to doctor at a public health centre with chief
complain of vaginal bleeding. Mrs. Tari also complains abdominal cramping. She missed her period for
about 8 weeks. She also feels nauseous, sometimes has vomit and breast tenderness. Since 1 year ago she
has been complaining about vaginal discharge with smelly odor and sometimes accompanied by vulvar
itchy. She already have 2 children before and the youngest child is 6 years old. Her husband is a truck driver.

Height: 155 cm, weight: 50 kg,
Blood pressure: 120/80 mmHg, pulse: 80 x/m, RR: 20 x/m.
Palpebral conjunctiva: normal
Breast: hyperpigmented
Abdomen: flat and souffl, symmetric, uterine fundus is not palpable, there are no mass, no painful
tenderness and no free fluid sign.
Internal examination:
Speculum examination: portio is livide, external os opens with blood come out from external os, there are no
cervical erotion, laceration or polyp.
Bimanual examination: cervix is soft, the external os opens, no cervical motion tenderness, uterine size is
about 8 weeks gestation, both adnexa and parametrium are within normal limit.
Hb 11 g/dL; WBC 12.000/mm3; ESR 15 mm/hour Peripheral Blood Image: WNL
Urine: pregnacy test (-HCG) positive
Objectives:
Terms Clarification
P2A1
Vaginal bleeding
Abdominal cramping
Missing period
Nausea and vomiting
Livide
Cervical motion tenderness
A pregnant woman (37 years old) from middle income family
P2A1
Vaginal bleeding
Abdominal cramping
Missing period about 8 weeks
Nausea and vomiting
Breast tenderness
Smelly vaginal discharge
Husband occupation truck driver
The youngest child is 6 years old
Portio livide with blood come from open external os
Uterine size about 8 weeks gestation
Pregnacy test (HCG) positive
Problem Analysis
A pregnant woman (37 years old) from middle income family
o What is the definition of middle income?
o What is its connection with pregnancy and abortion?
o What is the connection between middle income and abortion?

o What is the connection between age and abortion?
P2A1
o What is the meaning of P2A1?
o Possible complication from abortion?
8 weeks pregnancy with inevitable abortion
o What are the causes and the pathophysiology of abortion?
o How is the physical examination of 8 weeks pregnancy ?
o Epidemiology of abortion in Indonesia?
o What is its relation with 8 weeks pregnancy?
o What are the differential diagnosis?
o What are the possible complications that can occur?
o How are the right and comprehensive management?
Bedrest, sedation, evacuation product of conception, histopathologic examination,
laboratory screening, documentation.
Complain of vaginal bleeding and abdominal cramp

o How is its relation with vaginal bleeding and abdominal cramp in this case
(pathophysiology)?
o How about the management and education?
Missing period, nausea and vomiting, breast tenderness
o How to make diagnose whether a woman pregnant or not?
o What is the differential diagnosis?
Smelly vaginal discharge and husband a truck driver
o Is there any connection between vaginal discharge and husband occupation?
o Is there any connection between smelly discharge and abortion?
The youngest child age is 6 years old
o How is ideal pregnancy range?
o How if the pregnancy range is too long (clinical risk, caring pattern, outcome, etc)?
o How to manage ideal pregnancy planning (contaception; conselling, methods and
effectivity)?
Hypothesis:
Mrs. Tari has an inevitable abortion due to infection and advance maternal age.
Learning Issues:
1. Anatomy of reproduction system
a. External examination (inspection, palpation, percussion)
b. Internal examination ( speculum, bimanual)
3. Etiology, symptoms, clinical signs, physical examination and management of abortion
4. Determine the risk factors of abortion
5. Exclude the other differential diagnosis
7. Interpretation of laboratory findings (blood, urine) and ultrasound
Concepts Framework:
Risk factors, etiology, predisposition abortion outcome, management, complication,
prevention.
ABORTION
I.
DEFINITION
A spontaneous lost of pregnancy before 20 weeks
II.
INCIDENCE
15-25% of all pregnancy
III. CLASSIFICATION
1. Threatened abortion: fetus is still viable and cervical os is closed.
2. Inevitable abortion: fetus may still be alive but the cervical os is open
3. Incomplete abortion: some products of conception have been expelled already
4. Complete abortion: fetus and placental tissue have all been expelled
5. Missed abortion: the pregnancy has succumbed but has not been expelled
IV.
ETIOLOGY
The majority of abortion are due to chromosomal defects. If they are in the first trimester, it is not
necessarily helpful investigating women who misscarry- unless they had three consecutive
spontaneous misscarriages. The causes can be:
1. Abnormal conceptus (chromosomal and structural)
2. Immunological
3. Uterine abnormality
4. Cervical incompetence
5. Endocrine
6. Maternal disease (including systemic lupus erythematosus)
7. Infection
8. Toxin and cytotoxic drugs
9. Trauma
V.
CLINICAL FEATURES
Patients will present with amenorrhea followed by vaginal bleeding. Pain may be present. The
symptoms of pregnancy may have disappeared. On examination there may be lower abdominal
tenderness. The bleeding may vary from spotting to heavy bleeding. The uterine size may be smaller
(if products have been expelled), the same size, or larger than dates (if bleeding has occurred into the
uterine cavity). The cervix may be closed or open depending on the stages of abortion.
VI.
DIFFERENTIAL DIAGNOSIS
1. Ectopic pregnancy
2. Hydatidiform mole
3. Dysfunctional uterine bleedin
VII. INVESTIGATIONS
If the cervical os open, the pregnancy will not continue and no further investigations are needed. If
the os is closed, an ultrasound scan will determine whether a viable fetus is present in the uterine cavity.
VIII. MANAGEMENT
There is no proven treatment for threatened abortion. Inevitable, incomplete, complete and missed
abortions all require evacuation of the uterus.
REFERENCE
1. Rymer J, Fish A (eds). Early pregnancy problems. In: Gynaecology Infocus. 1 st ed, Elsevier
Limited, Edinburgh, 2005; 38-40
2. Stead LG, Stead SM, Kaufman MS (eds). Spontaneous abortion, ectopic pregnancy, and fetal
death. In: First Aid For The Obstetrics & Gynecology Clerckship. A Student to Student Guide.
Internantional ed. McGraw-Hill, Boston, 2002; 127-135

FAKULTAS KEDOKTERAN
373438,
Skenario E Blok 23 Tahun 2014
A male newborn was referred to Moh.Hoesin Hospital by a midwife - who helped his mother, Mrs Utamis
delivery - with chief complain of grunting. Mothers history was taken from the midwife. She said that Mrs
Utamis pregnancy was full term. The baby was born 3 hours ago with Apgar score 5 for 1st minute and 8 for
5th minutes, birth body weight was 3 kg. The mother had premature rupture of membrane 2 days ago and
had bad smell liquor. From the physical examination the baby was hypoactive and tachypnoe, no sucking
reflex, and there was chest indrawing.
As a general practitioner, please analyze the problems and the management.
------------------------------------------------------------------------------------------------------------
For Tutors Only

Learning Objectives:
-
Student must be able to understand the importance of neonatal infection

Student must be able to recognize risk factor which predispose new born infant to infection
Student must be able to diagnose neonatal infection
Student must be able to implement infection control to prevent infection
Klarifikasi Istilah
Dirujuk
Bayi merintih
Anamnesis
Nilai Apgar
Ketuban pecah
Air ketuban berbau busuk
Reflek isap
Napas cepat
Retraksi sela iga
Identifikasi Masalah
5. Bayi baru lahir dengan hamil cukup bulan dan berat lahir 3000 gram
6. Nilai Apgar 59
7. Merintih, napas cepat dan terdapat retraksi sela iga
8. Hipoaktif dan reflek isap tidak ada
9. Ketuban pecah 2 hari sebelum bayi lahir
10. Air ketuban berbau busuk
Analisis Masalah
10. Berat badan 3000 gram dan hamil cukup bulan. Berdasarkan berat badan lahir dan usia gestasi, bayi
ini diklasifikasikan sebagai apa?
11. Ketuban pecah 2 hari sebelum bayi lahir dan air ketuban berbau busuk. Apa yang mungkin terjadi
pada bayi ini?
12. a. Bayi merintih, napas cepat dan terdapat retraksi sela iga. Gejala apa yang
diderita bayi ini?
b. Penyakit apa yang mungkin menyebabkan gejala ini?
13. Hipoaktif dan reflek isap tidak ada. Dari gejala ini, adakah penyakit lain yang diderita bayi ini atau
apa diagnosis bandingnya?
14. Apa kemungkinan diagnosisnya?
15. Pemeriksaan apa yang diperlukan oleh penderita ini?
16. Bagaimana tatalaksana penderita ini?
17. Apa komplikasinya?
Hipotesis
Bayi baru lahir, cukup bulan, SMK (sesuai masa kehamilan), lahir spontan dengan gangguan pernapasan
(respiratory distress). Kemungkinan penyebabnya (diagnosisnya) adalah bronkopneumonia + sepsis
neonatorum (klinis sepsis)
Sintesis
9. Berdasarkan berat lahir 3000 gram dan usia kehamilan cukup bulan, bayi ini diklasifikasikan sebagai
bayi baru lahir cukup bulan sesuai dengan masa kehamilan.
10. Ketuban pecah 2 hari sebelum bayi lahir dan air ketuban berbau busuk. Kemungkinan bayi ini telah
mengalami infeksi intrauterin, karena ketuban pecah >18 jam dan ketuban berbau busuk merupakan
faktor risiko terjadinya infeksi intrauterin.
11. Bayi merintih, napas cepat dan terdapat retraksi sela iga. Dengan menggunakan Downes score maka
bayi ini mengalami respiratory distress. Kemungkinan penyakit penyebab respiratory distress ini
adalah bronkopneumonia
12. Hipoaktif dan reflek isap tidak ada. Dari gejala ini, penyakit lain yang mungkin pula diderita bayi ini
selain bronkopneumonia adalah sepsis neonatorum.
13. Kemungkinan diagnosis bayi ini adalah bronkopneumonia + sepsis neonatorum.
14. Pemeriksaan yang diperlukan pada penderita ini:
a. Rontgen dada
b. Pemeriksaan darah (Hb, leukosit, hitung jenis, trombosit, CRP)
c. Kadar gula darah
d. Pungsi lumbal (bila bayi mengalami sepsis neonatorum)
e. Kultur darah
15. Tatalaksana penderita ini:

a. Pertahankan suhu tubuh dalam batas normal (rawat dalam inkubator)
b. Beri vitamin K1 1 mg intramuskuler
c. Parenteral feeding
d. Beri oksigen
e. Beri antibiotika
f. Monitoring
9. Komplikasi yang paling sering adalah meningitis.

FAKULTAS KEDOKTERAN
373438,
Skenario F Blok 23 Tahun 2014
Learning outcome:
The graduated doctors:
13. Have the ability to do anamnesis, general and gynecology physical examination and to plan
supporting examination as indicated, such as routine blood, hormone assessment, sperm analysis,
urine, radiology and ultrasound examination.
16. Have the ability to make a good andrology medical record.
8. Anatomy & physiology of male and femele reproductive system
c. External examination (inspection, palpation, percussion)
d. Internal examination (speculum, bimanual)
10. Andrology and urology examination
11. Etiology, symptoms, clinical signs, physical examination and management of infertility
12. Terms in infertility
13. Differential diagnosis of infertility
14. Interpretation of laboratory findings (blood, urine, sperm analysis, post coital test) and ultrasound
(sonohysterography)
Mrs. Lina, 29 years old, attends the primary health centre with her husband. They have been trying to get
pregnant for 3 years but failed. She has regular menstrual cycles, every 28 days. There was no history of
intermenstrual or postcoital bleeding. There was no pain during her period, no contraception used, no history
of drug consumption (including alcohol and tobacco). She didnt have previous abdominal surgery, no
history of allergies, no pelvic infection and no chronic disease. Her husband (32 years old) is a bank
employee. He had no history of mumps and medication for any disease. He was not smoking and no alcohol
consumption. He also didnt have any allergies. This couple enjoyed regular intercourse.
You act as the doctor in the clinic and be pleased to analyse this case.

Wife
Height = 160 cm; Weight 55 kg; BMI = 21 kg/m2; Blood pressure = 110/70 mmHg; Pulse = 80 x/m; RR = 18
x/m.
Palpebral conjunctiva looked normal, no exophthalmus, no sign of hirsutism, no thyroid enlargement, no
galactorrhoea, secondary sexual characteristics are normal.
External examination: abdomen flat and souffl, symmetric, uterine fundal not palpable, there are no mass,
pain tenderness and free fluid sign.
Internal examination:
Speculum examination: portio not livide, external os closed, no fluor, no fluxus, there are no cervical
erotion, laceration or polyp.
Bimanual examination: cervix is firm, the external os closed, uterine size normal, both adnexa and
parametrium within normal limit.
Laboratory examination:
Hb 12 g/dL; WBC 8.000/mm3; RBC 4,3x106/mm3; Ht 36 vol%; Platelets 250.000/mm3; ESR 15 mm/hour;
Blood type A Rh (+); Blood film: Normal.
Urine: Normal
* Ultrasound: normal internal genitalia; Sonohysterography: normal uterine and both tubal patency.
Postcoital test: normal
Husband
Height = 176 cm; Weight 72 kg; BMI = 23 kg/m 2; Blood pressure = 120/80 mmHg; Pulse = 76 x/m; RR =
20 x/m.
Palpebral conjunctiva looked normal, no exopthalmus, no thyroid enlargement, no gynecomastia, secondary
sexual characteristics are normal.
External examination: abdomen flat and tender, symmetric, no sign of hepatomegaly and inguinal hernia
Genitalia examination:
Penis: normal; testes: normal size and volume; scrotum: no varicocele.
Laboratory examination:
Hb 14 g/dL; WBC 8.000/L; RBC 4,3x106/L; Ht 42 vol%; Platelets 350.000/L; ESR 6 mm/hour; Blood
type O Rh (+); Blood film: Normal. Blood chemistry: Normal. Hormonal: FSH, LH and testosterone level:
Normal
Urine: Normal
Semen analysis: volume 4.5 ml; sperm concentration 0.1x10 6/ml; motility 22% forward progression, 15%
rapid forward progression; morphology 5 % with normal forms.
OBJECTIVES
Term Clarification
Infertility
Regular menstrual cycles
Intermenstrual bleeding
Postcoital bleeding
Regular intercourse
Body mass index (BMI)
Exopthalmus
Hirsutism
Galactorrhoea
Secondary sexual characteristics
Gynecomastia
Varicocele
A couple trying to get pregnant for 3 years
Intermenstrual or postcoital bleeding
Pain during her period, no contraception used, no history of drug consumption (including alcohol and
tobacco)
She didnt have previous abdominal surgery, no history of allergies, no pelvic infection and no
chronic disease.
Her husband had no history of mumps and medication for any disease. He was not smoking and no
alcohol consumption. He also dont have any allergies.
The couple enjoyed regular intercourse.
BMI: Wife 21 kg/m2; Husband 23 kg/m2
She has no exopthalmus, no sign of hirsutism, no thyroid enlargement, no galactorrhoea, secondary
sexual characteristics is normal
The husband has no exophthalmus, no thyroid enlargement, no gynecomastia, secondary sexual
characteristics is normal.
Male external examination: abdomen flat and tender, symmetric, no sign of hepatomegaly, no
inguinal hernia
Male genitalia examination:
Penis: normal; testes: Normal size and volume; scrotum: no varicocele;
Semen analysis: volume 4.5 ml; sperm concentration 0.1x10 6/ml; motility 22% forward progression,
15% rapid forward progression; morphology 5% with normal forms
Problem Analysis
A couple trying to get pregnant for 3 years.
o What is the definition of infertility?

o What is the difference between primary and secondary infertility?
o What is the type of infertility for this couple?
o What is the probable cause of infertility in this couple?
o What is the criteria of regular menstrual cycle?
o What is the connection with infertility?
Intermenstrual or postcoital bleeding
o What is the definition of intermenstrual and postcoital bleeding?
o What are the conditions that may cause intermenstrual and postcoital bleeding?
o What is the relationships with infertility?
o What are the differential diagnosis?
No pain during the periods
o What is definition of dysmenorrhoea?
o What are the possible cause dysmenorrhoea?
o What is the proper management of dysmenorroea?
The couple have no history of drugs consumption (including alcohol and tobacco)
o What is the relationships between drugs consumption with infertility?
She has no history of abdominal surgery and pelvic infection
o What is the complication of previous abdominal surgery?
o How can abdominal surgery affect female fertility?
o What is the sign of pelvic infection?
o What is the possible complication of pelvic infection?
o What is the relationships of pelvic infection with infertility?
Her husband had no history of mumps during his childhood
o What is the complication of mumps?
o What is the relationships wit male fertility problem?
The couple dont have any allergies
o How can allergy affect the fertility?
o How to make diagnose of allergy?
The couple enjoyed regular intercourse
o What is the definition of intercourse?
o What is the criteria of regular intercourse?
o What is the relationship with infertility?
BMI: Wife 21 kg/m2; Husband 23 kg/m2
o What is the classification of BMI?
o What is the interpretation of BMI in this couple?
o What is the relationships with fertility?
She has no exopthalmus, no sign of hirsutism, no thyroid enlargement, no galactorrhoea, secondary
sexual characteristics is normal
o What is exopthalmus, hirsutism, galactorrhoea?
o What are the conditions that can cause them?
o What are the female secondary sexual characteristics?

o Why it is important to examine this characteristics in infertile patient?
The husband has no gynecomastia
o What is gynecomastia?
o In what conditions it can occur?
o What is the relationship with male fertility?
Male external examination: abdomen flat and souffl, symmetric, no sign of hepatomegaly, no
inguinal hernia
o What is inguinal hernia?
o How to make diagnosis of inguinal hernia?
o What is the relationship with male fertility?
Male genitalia examination:
Penis: normal; testes: normal size and volume; scrotum: no varicocele; prostate: no enlargement
o How to perform male genitalia examination?
o What is the criteria of normal male genitalia?
o What is the meaning of varicocele?
o How to diagnose varicocele?
o What is the cause of varicocele?
o What are their relationships with male infertility?
o How to manage the patient with varicocele?
Semen analysis: volume 4.5 ml; sperm concentration 0.1x10 6/ml; motility 22% forward progression,
15% rapid forward progression; morphology 5% with normal forms
o What are the steps of semen analysis?
o What are evaluates in this procedure?
o What is the interpretation of this patient semen analysis?
o How to manage the abnormality in semen analysis?
Hypothesis:
This couple has primary infertility due to male factor.
Learning Issues:
11. Etiology, symptoms, clinical signs, physical examination and management of primary infertility
12. Determine the risk factors of primary infertility
14. Terms in infertility
15. Interpretation of laboratory findings (blood, hormone profile, urine, postcoital test, semen analysis)
and ultrasound (sonohysterography)
16. Ideal pregnancy planning for infertile patient
Concepts Framework:
Risk factors, etiology, predisposition primary infertility management, outcome, complications
Theory Review
INFERTILITY
IX.
DEFINITION
The inability to conceive after 12 months of unprotected sexual intercouse
X.
INCIDENCE
Affects 15% of couples
XI.
CLASSIFICATION
There are two types:
1. Primary infertility: infertility in the absence of previous pregnancy
2. Secondary infertility: infertility after previous pregnancy
XII. ETIOLOGY
Three main causes of infertility:
1. Poor semen quality
2. Tubal disorder
3. Ovulatory disorder
Other rarer causes include mucus hostility and sperm antibodies, impotence and retrograde
ejaculation. This leaves a significant (10-20%) proportion with unexplained infertility, which includes
psychological factors.
XIII. CLINICAL FEATURES
Significant clues to the etiology can be achieved by a thorough history fromboth partners. In female,
evidence of ovulation can be gained from regularity of menstrual cycle and associated symptoms,e.g.
mittleschmerz pain, cervical mucuc changees and primary dys menorrhoea.
Tubal disorder are usually the result of scarring and adhesions secondary to infection or pelvic surgery,
e.g. ovarian cystectomy. In addition, endometriosis may cause pelvic scarring. If the distal portion of
the tube is blocked, a hydrosalphynx may developed. Tubal damage should be suspected if there is a
history of IUCD use, PID, pelvic surgery or pelvic pain.
Examination may also reveal endocrinal disorders, e.g. PCOS, or the tissue atrophy of premature
menopause, and physical signs of pelvic pathology, e.g. endometriotic scarring, ovarian cysts or
fibroids.
In the male, history may reveal previous operations or infections. Stress or recent intercurrent illnesses
may be associated with transitory reduced semen quality.
Examination should include testicles, looking for varicosities or the absence of vas deferens. Reduced
testicular size and increased firmness due to fibrosis may indicate spermatogenetic failure. A swollen
epididymis may indicate a blockage of the vas.
Rarely azoospermia may be due to hypogonadotrphic hypogonadism, indicated by lack of secondary
sexual development.
XIV. DIFFERENTIAL DIAGNOSIS
Defining the specific causes of infertility requires a proper history and examination and appropriate
investigations.
XV. INVESTIGATIONS
Male:
A semen analysis on two occasions is the basic investigation. The WHO criteria for normal semen
analysis is a sperm density of 20 million sperm per mL with 50% sperm with forward progression
and 50% normal morphology. The criteria are associated with a normal rate of conception. If the
value are reduced, serum LH, FSH and testosterone are indicated. High gonadotrophins are indicative
of testicular failure. Normal levels with reduced testosterone may indicated hypogonadotrophic
hypogonadism. In cases of non obstructive and some cases of obstructive azoospermia there may be
and indication for testicular biopsy to assess spermatogenesis and storage of any sperm found for
future use.
Female:
Simple test for ovulation shold be undertaken, i.e. mid-luteal phase serum progesterone, basal body
temprature charts for no more than two cycles. More sophisticated investigations include follicle
monitoring with ultrasound, serial LH measurement to detect the pre-ovulatory LH surge, and
laparoscopy in the luteal phase to confirm the presence of a corpus luteum.
Laparoscopy and dye instillation provide the optimum test of tubal patency or damage with the
additional benefit of visualization of the pelvis, i.e. ovarium, peritoneum to exclude endometriotic
deposits, and the uterus to assess anatomical abnormality. Hysterosalphyngography is used to assess
tubal patency and also to reveal intrauterine problems, e.g. adhesions, fibroids or anatomical
abnormalities such as bicornuate uterus. Other investigations include a postcoital test, which assess the
capacity of sperm to remain motile in the cervical mucus, and tests for antisperm antibodies in both
partners and the husbands seminal plasma.
XVI. MANAGEMENT
Male:
Poor semen quality previously had little opportunity for improvement unlessit was a transitory
problem, e.g. stress or viral infection. The value of varicocele repair is unsolved. Hormonal treatments
are unproven. With low counts, options that are now available include the preparation of a small
volume of the best sperm to place within uterus at ovulation (intrauterine insemination; IUI) or in vitro
fertilization (IVF) with oocyte collected from the patient. Intracytoplasmic sperm injection (ICSI) has
dramatically altered the treatment of severe male factor infertility. ICSI only requires low sperm
numbers and can be used in the treatment of both obstructive and non-obstructive azoospermia.
Antisperm antibodies have been successfully treated with steroids in the male. Donor semens remains
the only option for many infertile men.
Female:
Ovulatory disorders respond well to hormonal therapy, i.e. clomiphene or human menopausl
gonadotrophins. The later requires close monitoring to avoid hyperstimulation or high-order multiple
pregnancy. Tubal damage can be dealt with by surgery in selected cases, but the result rarely exceed
30%.
Bypassing the tube with IVF is successful in 20-25% of cycles. The involves ovarian stimulation to
produce multiple follicles, the aspiration of oocytes from these follicles, the IVF with partners semen
and transfer to the uterus 48-72 hours after fertilization.
Assisted conception techniques including IVF and gamete intrafallopian transfer are also applicable
where mucus hostility is possible cause or where no cause is found, e.g. unexplained infertility.
Success rate in these groups are 25-30%.
XVII. COMPLICATIONS
The major complication of infertility other than those associated with drugs and surgical intervention
is the psychological trauma of being unable to cocieve. Significant morbidity is present in many
coples, who require counselling and support to enable them to come to terms with childlessness.
REFERENCE
1. Rymer J, Fish A (eds). Infertility. In: Gynaecology Infocus. 1 st ed, Elsevier Limited, Edinburgh,
2005; 64-69
2. Stead LG, Stead SM, Kaufman MS (eds). Infertility. In: First Aid For The Obstetrics &
Gynecology Clerckship. A Student to Student Guide. Internantional ed. McGraw-Hill, Boston,
2002; 153-155
3. Doherty CM, Aliotta PJ. Infertility evaluation. In: Practical Guide to The Care of The
Gynecologic/Obstetric Patient. 2nd ed. Mosby Elsevier, USA, 2007; 137-166
4. Greer IA, Cameron IT, et al. Primary infertility. In: Problem-based in Obsterics And Gynaecology.
International ed. Churchill Livingstone, China, 2003; 3-5
UNDESCENDED TESTES
I.
DEFINITION
Cryptorchidism is the absence of one or both testes from the scrotum. This usually represents
failure of the testis to move, or "descend," during fetal development from an abdominal position,
through the inguinal canal, into the ipsilateral scrotum.
II.
INCIDENCE
About 3% of full-term and 30% of premature infant boys are born with at least one undescended
testis, making cryptorchidism the most common birth defect of male genitalia. However, most testes
descend by the first year of life (the majority within three months), making the true incidence of
cryptorchidism around 1% overall.
III.
CLASSIFICATION
A testis absent from the normal scrotal position can be:
1. found anywhere along the "path of descent" from high in the posterior (retroperitoneal)
abdomen, just below the kidney, to the inguinal ring;
2. found in the inguinal canal;
3. ectopic, that is, found to have "wandered" from that path, usually outside the inguinal canal and
sometimes even under the skin of the thigh, the perineum, the opposite scrotum, and femoral
canal;
4. found to be undeveloped (hypoplastic) or severely abnormal (dysgenetic);

5. found to have vanished (also see Anorchia)
IV.
ETIOLOGY
In most full-term infant boys with cryptorchidism but no other genital abnormalities, a cause cannot
be found, making this a common, sporadic, unexplained (idiopathic) birth defect.
Although severely premature infants can be born before descent of testes, there is a strong
association of cryptorchidism with low birthweight due to either prematurity or intrauterine growth
retardation. In these infants there is usually no evidence of hormonal malfunction. Associated
inguinal hernias are common.
Hormonal abnormalities (deficiency or insensitivity to androgens or anti-mllerian hormone) can be
demonstrated in a high proportion of those with evidence of undervirilization or ambiguity such as
hypospadias or micropenis.
A contributing role of environmental chemicals endocrine disruptors that interfere with normal
fetal hormone balance has been proposed as well, similar to the effects of diethylstilbestrol exposure.
It is rarely possible to implicate a specific chemical exposure for an individual child.
Occasional instances of other genetic defects involving development or function of the gubernaculum
have been reported. Homeobox gene mutations can cause cryptorchidism in animals but remain a
largely theoretical possibility in humans.
Rare iatrogenic cases have also been reported in which hernia repair or other surgery in the inguinal
area resulted in trapping of a testis above the scrotum.
A 2006 study showed that regular alcohol consumption during pregnancy (5 or more drinks per
week) is associated with a 3x increase in cryptorchidism, when compared to non-drinking mothers.
Other previously known risk factors include exposure to pesticides, low birth weight (including
premature birth), gestational diabetes and being a twin.
V.
CLINICAL FEATURES
The most common diagnostic dilemma in otherwise normal boys is distinguishing a retractile testis
from a testis that will not/cannot descend spontaneously into the scrotum. Retractile testes are more
common than truly undescended testes and do not need to be operated on. In normal males, as the
cremaster muscle relaxes or contracts, the testis moves lower or higher ("retracts") in the scrotum.
This cremasteric reflex is much more active in infant boys than older men. A retractile testis high in
the scrotum can be difficult to distinguish from a position in the lower inguinal canal. Though there
are various maneuvers used to do so, such as using a crosslegged position, soaping the examiner's
fingers, or examining in a warm bath, the benefit of surgery in these cases can be a matter of clinical
judgement.
In the minority of cases with bilaterally non-palpable testes, further testing to locate the testes, assess
their function, and exclude additional problems is often useful. Pelvic ultrasound or magnetic
resonance imaging can often, but not invariably, locate the testes while confirming absence of a
uterus. A karyotype can confirm or exclude forms of dysgenetic primary hypogonadism, such as
Klinefelter syndrome or mixed gonadal dysgenesis. Hormone levels (especially gonadotropins and
AMH) can help confirm that there are hormonally functional testes worth attempting to rescue, as
can stimulation with a few injections of human chorionic gonadotropin to elicit a rise of the
testosterone level. Occasionally these tests reveal an unsuspected and more complicated intersex
condition.
In the even smaller minority of cryptorchid infants who have other obvious birth defects of the
genitalia, further testing is crucial and has a high likelihood of detecting an intersex condition or
other anatomic anomalies. Ambiguity can indicate either impaired androgen synthesis or reduced
sensitivity. The presence of a uterus by pelvic ultrasound suggests either persistent mllerian duct
syndrome (AMH deficiency or insensitivity) or a severely virilized genetic female with congenital
adrenal hyperplasia. An unambiguous micropenis, especially accompanied by hypoglycemia or
jaundice, suggests congenital hypopituitarism.
VI.
INHERITANCE AND RECURRENCE RISK

A small percentage of cases of isolated cryptorchidism are familial. It has been reported that about
4% of fathers and 6-10% of brothers of affected boys have also had cryptorchidism. Few specific
genes associated with isolated cryptorchidism have been identified.
In contrast, many of the genes causing some of the intersex conditions associated with androgen or
AMH deficiency or insensitivity have been identified, and genetic counseling to explain recurrence
risk to families is appropriate.
A new study shows that pregnant women who drink caffeine (at least 3drinks per day*) will increase
the risk of cryptorchidism.
VII.
ASSOCIATIONS
Cryptorchidism occurs at a much higher rate in a large number of congenital malformation
syndromes. Among the more common are Prader-Willi syndrome, Noonan syndrome, and cloacal
exstrophy.
VIII. MANAGEMENT
The primary management of cryptorchidism is surgery, called orchiopexy. It is usually performed in
infancy, if inguinal testes have not descended after 4-6 months, often by a pediatric urologist or
pediatric surgeon, but in many communities still by a general urologist or surgeon.
When the undescended testis is in the inguinal canal, hormonal therapy is sometimes attempted and
occasionally successful. The most commonly used hormone therapy is human chorionic
gonadotropin. A series of hCG injections (10 injections over 5 weeks is common) is given and the
status of the testis/testes is reassessed at the end. Although many trials have been published, the
reported success rates range widely, from roughly 5 to 50%, probably reflecting the varying criteria
for distinguishing retractile testes from low inguinal testes. Hormone treatment does have the
occasional incidental benefits of allowing confirmation of Leydig cell responsiveness (proven by a

rise of the testosterone by the end of the injections) or inducing additional growth of a small penis
(via the testosterone rise). Some surgeons have reported facilitation of surgery, perhaps by enhancing
the size, vascularity, or healing of the tissue. A newer hormonal intervention used in Europe is use of
GnRH analogs such as nafarelin or buserelin; the success rates and putative mechanism of action are
similar to hCG, but some surgeons have combined the two treatments and reported higher descent
rates. Limited evidence suggests that germ cell count is slightly better after hormone treatment;
whether this translates into better sperm counts and fertility rates at maturity has not been
established. The cost of either type of hormone treatment is less than that of surgery and the chance
of complications at appropriate doses is minimal. Nevertheless, despite the potential advantages of a
trial of hormonal therapy, many surgeons do not consider the success rates high enough to be worth
the trouble since the surgery itself is usually simple and uncomplicated.
In cases where the testes are identified preoperatively in the inguinal canal, orchiopexy is often
performed as an outpatient and has a very low complication rate. An incision is made over the
inguinal canal. The testis with accompanying cord structure and blood supply is exposed, partially
separated from the surrounding tissues ("mobilized"), and brought into the scrotum. It is sutured to
the scrotal tissue or enclosed in a "subdartos pouch." The associated passage back into the inguinal
canal, an inguinal hernia, is closed to prevent re-ascent.
Surgery becomes more complicated if the blood supply is not ample and elastic enough to be
stretched into the scrotum. In these cases, the supply may be divided, some vessels sacrificed with
expectation of adequate collateral circulation. In the worst case, the testis must be "autotransplanted" into the scrotum, with all connecting blood vessels cut and reconnected
("anastomosed").
When the testis is in the abdomen, the first stage of surgery is exploration to locate it, assess its
viability, and determine the safest way to maintain or establish the blood supply. Multi-stage
surgeries, or auto-transplantation and anastomosis, are more often necessary in these situations. Just
as often, intra-abdominal exploration discovers that the testis is non-existent ("vanished"), or
dysplastic and not salvageable.
The principal major complication of all types of orchiopexy is loss of the blood supply to the testis,
resulting in loss of the testis due to ischemic atrophy or fibrosis.
There have been cases where the condition has resolved itself during contact sports, following blunt
force to the abdomen. However, this technique is not recommended because the impact sufficient to
'pop' the testicle into place may cause trauma to the abdomen.
IX.
COMPLICATIONS
Infertility Prevalence
Many men who were born with undescended testes have reduced fertility, even after orchiopexy in
infancy. The reduction with unilateral cryptorchidism is subtle, with a reported infertility rate of
about 10%, compared with about 6% reported by the same study for the general population of adult
men.
The fertility reduction after orchiopexy for bilateral cryptorchidism is more marked, about 38%, or 6
times that of the general population. The basis for the universal recommendation for early surgery is
research showing degeneration of spermatogenic tissue and reduced spermatogonia counts after the
second year of life in undescended testes. The degree to which this is prevented or improved by early
orchiopexy is still uncertain.
Pathophysiology
At least one contributing mechanism for reduced spermatogenesis in cryptorchid testes is
temperature. The temperature of testes in the scrotum is at least a couple of degrees cooler than in the
abdomen. Animal experiments in the middle of the 20th century suggested that raising the
temperature could damage fertility. Some circumstantial evidence suggests tight underwear and other
practices that raise testicular temperature for prolonged periods can be associated with lower sperm
counts. Nevertheless, research in recent decades suggests that the issue of fertility is more complex
than a simple matter of temperature. It seems likely that subtle or transient hormone deficiencies or
other factors that lead to lack of descent also impair the development of spermatogenic tissue.
The inhibition of spermatogenesis by ordinary intra-abdominal temperature is so potent that
continual suspension of normal testes tightly against the inguinal ring at the top of the scrotum by
means of special "suspensory briefs" has been researched as a method of male contraception, and
was referred to as "artificial cryptorchidism" by one report.
An additional factor contributing to infertility is the high rate of anomalies of the epididymis in boys
with cryptorchidism (over 90% in some studies). Even after orchiopexy, these may also affect sperm
maturation and motility at an older age.
Later cancer risk

One of the strongest arguments for early orchiopexy is prevention of testicular cancer. About 1 in
500 men born with one or both testes undescended develops testicular cancer, roughly a 4- to 40-fold
increased risk. The peak incidence occurs in the 3rd and 4th decades of life. The risk is higher for
intra-abdominal testes and somewhat lower for inguinal testes, but even the normally descended
testis of a man whose other testis was undescended has about a 20% higher cancer risk than those of
other men.
The most common type of testicular cancer occurring in undescended testes is seminoma. It is
usually treatable if caught early, so urologists often recommend that boys who had orchiopexy as
infants be taught testicular self-examination, to recognize testicular masses and seek early medical
care for them. Cancer developing in an intra-abdominal testis would be unlikely to be recognized
before considerable growth and spread, and one of the advantages of orchiopexy is that a mass
developing in a scrotal testis is simply far easier to recognize than an intra-abdominal mass.
Although orchiopexy makes cancer more easily recognizable at an early stage, whether early
orchiopexy actually reduces the chance of developing cancer remains a subject of controversy. As
with infertility, the causes of cancer associated with cryptorchidism are not known. Most evidence
suggests the cancer risk is due to an inherent abnormality of the undescended testis rather than to the
ability of an abdominal location to cause cancer in an otherwise normal testis.
The risk of malignancy in the undescended testis is 4 to 10 times higher than that in the general
population and is approximately 1 in 80 with a unilateral undescended testis and 1 in 40 to 1 in 50 for
bilateral undescended testes. The peak age for this tumor is 1545 yr. The most common tumor
developing in an undescended testis is a seminoma (65%); in contrast, after orchiopexy, seminomas

represent only 30% of testis tumors.
REFERENCE
1. Docimo SG (1995). "The results of surgical therapy for cryptorchidism: a literature review and
analysis". J. Urol. 154 (3): 114852. PMID 7637073.
http://linkinghub.elsevier.com/retrieve/pii/S0022-5347(01)67015-0.
2. Kolon TF, Patel RP, Huff DS (2004). "Cryptorchidism: diagnosis, treatment, and long-term
prognosis". Urol. Clin. North Am. 31 (3): 46980, viiiix. doi:10.1016/j.ucl.2004.04.009. PMID
15313056.
3. Mller H, Cortes D, Engholm G, Thorup J (1998). "Risk of testicular cancer with cryptorchidism
and with testicular biopsy: cohort study". BMJ 317 (7160): 729. PMID 9732342. PMC: 28664.
http://bmj.com/cgi/pmidlookup?view=long&pmid=9732342.
FAKULTAS KEDOKTERAN
373438,
Skenario G Blok 23 Tahun 2014
Learning outcome:
20. Have the ability for anamnesis, general and gynecology physical examination and to plan supporting
examination as indicated, such as routine blood, urine and ultrasound examination.
e. External examination (inspection, palpation, percussion and auscultations)
f. Internal examination (speculum & bimanual)
18. Etiology, symptoms, clinical signs, physical examination and management of bleeding in early
pregnancy and gynecologic disease
19. Term in pregnancy
20. Differential diagnosis of bleeding in early pregnancy
21. Interpretation of laboratory findings (blood and urine)
Mrs. Anita, a 39-year-old woman in her first pregnancy delivered twin sons 2 h ago. There were no
significant antenatal complications. She had been prescribed ferrous sulphate and folic acid during the
pregnancy as anemia prophylaxis, and her last haemoglobin was 10.9 g/dL at 38 weeks.
The fetuses were within normal range for growth and liquor volume on serial scan estimations. A vaginal
delivery was planned and she went into spontaneous labor at
38 weeks and 4 days. The labor had been unremarkable and the midwife recorded both placenta as appearing
complete.
As this was a twin pregnancy, an intravenous cannula had been inserted when labor was established.
The lochia has been heavy since delivery but the woman is now bleeding very heavily and passing large
clots of blood.
On arrival in the room you find that the sheets are soaked with blood and there is also approximately
500 mL of blood clot in a kidney dish on the bed.
The woman is conscious but drowsy and pale.
Height = 155 cm; Weight 50 kg
The temperature is 35.9C, blood pressure 120/70 mmHg and heart rate 112/min. The peripheral extremities
are cold. The uterus is palpable to the umbilicus and felt soft. The abdomen is otherwise soft and non-tender.
On vaginal inspection there is a second-degree tear which has been sutured but you are unable to assess
further due to the presence of profuse bleeding.
The midwife sent blood tests 30 min ago because she was concerned about the blood loss at the time.
Haemoglobin
7.2 g/dL
Mean cell volume
99.0 fL
White cell count
3.200/mm3
Platelets
131.000/mm3
International normalized ratio (INR)
1.3
Activated partial thromboplastin time (APTT)
39 s
Sodium
138 mmol/L
Potassium
3.5 mmol/L
Urea
5.2 mmol/L
Creatinine
64 mol/L
OBJECTIVES
Term Clarification
First pregnancy
Twin delivery
Ferrous sulphate
Folic acid
Anemia prophylaxis
Vaginal bleeding
Heavy lochia
Drowsy and pale
Intravenous cannula
A second-degree tear
Mrs. Anita, a 39-year-old woman in her first pregnancy
Twin delivery
Ferrous sulphate and folic acid during the pregnancy as anemia prophylaxis
The lochia has been heavy since delivery
Approximately 500 mL of blood clot in a kidney dish on the bed.
Drowsy and pale
The peripheries feel cool.
The uterus is palpable to the umbilicus and feels soft.
A second-degree tear which has been sutured
Haemoglobin 7.2 g/dL
Mean cell volume 99.0 fL
White cell count 3.200/mm3
Platelets 131.000/mm3
International normalized ratio (INR) 1.3
Activated partial thromboplastin time (APTT) 39 s
Problem Analysis
Mrs. Anita, a 39-year-old woman in her first pregnancy
o What is the risk of pregnancy in the age 39 year old?
o What is the connection of age in first pregnancy and postpartum bleeding?
Twin delivery
o What is twin delivery?
o What are the cause of twin delivery?
o How is the management of twin delivery?
o What is the connection of twin delivery and postpartum bleeding?
Ferrous sulphate and folic acid during the pregnancy as anaemia prophylaxis
o What is ferrous sulphate?
o What is folic acid?
o What is the mechanism of ferrous sulphate as anaemia prophylaxis?
o What is the mechanism of folic acid as anaemia prophylaxis?
The lochia has been heavy since delivery
o What is lochia?
o How is the lochia after delivery?
Approximately 500 mL of blood clot in a kidney dish on the bed.
o How much blood is considered as normal bleeding?
o What are the risk of heavy bleeding?
o How is the management of postpartum bleeding?
Drowsy and pale
o What is the meaning of drowsy and pale?
o What is the connection of drowsy and pale with heavy bleeding?
The peripheries feel cool.
o What is the meaning of the condition of cool peripheries?
The uterus is palpable to the umbilicus and feels soft.
o How is the uterus after delivery?
o What is the meaning of soft contraction?

o What is the connection of soft uterus and vaginal bleeding ?
A second-degree tear which has been sutured
o How is the degree of perineal tear ?
o How is the management of perineal tear according to the degree?
Haemoglobin 7.2 g/dL
o How is normal hemoglobin count?
o What is the meaning of haemoglobin 7.2 g/dL?
o What is the management of hemoglobin 7.2 g/dL?
Mean cell volume 99.0 fL
o How is normal mean cell volume?
o What is the meaning of mean cell volume 99.0 fL ?
o What is the management of mean cell volume 99.0 fL?
Platelets 131.000/mm3
o How is normal platelets?
o What is the meaning of platelets 131.000/mm3?
o What is the management of platelets 131.000/mm3?
International normalized ratio (INR) 1.3
o How is normal international normalized ratio (INR)?
o What is the meaning of international normalized ratio (INR) 1.3?
o What is the management of international normalized ratio (INR) 1.3?
Activated partial thromboplastin time (APTT) 39 s
o How is normal Activated partial thromboplastin time (APTT) ?
o What is the meaning of Activated partial thromboplastin time (APTT) 39 s
o What is the management of Activated partial thromboplastin time (APTT) 39 s?
Hypothesis:
Mrs. Anita has a postpartum bleeding due to twin delivery and advance maternal age.
Learning Issues:
17. Anatomy of reproduction system
18. Obstetric physical examination, which include:
19. Etiology, symptoms, clinical signs, physical examination and management of postpartum bleeding
20. Determine the risk factors of postpartum bleeding
23. Interpretation of laboratory findings (blood, urine)
Concepts Framework:
Risk factors, etiology, predisposition postpartum bleeding outcome, management,
complication, prevention.
Theory Review.
POSTPARTUM HAEMORRHAGE
XVIII. DEFINITION
The diagnosis is primary postpartum haemorrhage (PPH), defined as the loss of more than 500 mL of blood
in the first 24 h following delivery. This classification applies even if the blood is lost at Caesarean section
or while awaiting placental delivery.
XIX. INCIDENCE
15-25% of all pregnancy
XX. CAUSES AND RISK FACTORS
1. Uterine atony (multiple pregnancy, grand multiparity, polyhydramnios, prolonged labour)
2. Antepartum haemorrhage
3. Uterine sepsis (chorioamnionitis)
4. Retained placenta
5. Lower genital tract trauma (perineal or cervical tears)
6. Coagulopathy (heparin treatment, inherited bleeding disorders)
7. Previous PPH
This womans major risk factor is multiple pregnancy and with the high uterus, the cause is likely to be
uterine atony (inability of the uterus to contract adequately). Blood loss is often underestimated, the high
uterus may contain a large volume of concealed blood, and the blood pressure in young fit women remains
relatively normal until decompensation occurs. Therefore this woman is in fact extremely sick and at risk of
cardiac arrest if immediate management is not employed.
XXI. MANAGEMENT
rub up a contraction by placing the dominant hand over the uterus and rubbing and
squeezing firmly until the uterus becomes firm
ensure two large-bore cannulae are inserted with cross-matched blood requested
recheck full blood count and coagulation
commence intravenous fluids for volume expansion
give 500 g ergometrine intramuscularly or intravenously to enhance uterine contraction
start a syntocinon infusion to maintain uterine contraction
consider other uterotonics such as misoprostol or carboprost
transfer to theatre for examination under anaesthetic to assess for vaginal trauma, cervical
laceration or retained placental tissue
the doctor or midwife should continue bimanual compression until the clinical situation is under
control
if the bleeding does not settle with the above measures then further options are uterine artery
embolization or laparotomy with B-Lynch haemostatic suture, uterine artery ligation or
hysterectomy.

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