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Fetal Growth Restriction (FGR), formerly called Intrauterine Growth Restriction, refers to a condition in which an unborn baby is smaller than it should be because it is not growing at a normal rate inside the womb.
Delayed growth puts the baby at risk of certain health problems during pregnancy, delivery, and after birth. They include:
Low birth weight
Difficulty handling the stresses of vaginal delivery
Decreased oxygen levels
Hypoglycemia (low blood sugar)
Low resistance to infection
Low Apgar scores (a test given immediately after birth to evaluate the newborn’s physical condition and determine need for special medical care)
Meconium aspiration (inhalation of stools passed while in the uterus), which can lead to breathing problems
Trouble maintaining body temperature
Abnormally high red blood cell count
In the most severe cases, FGR can lead to stillbirth. It can also cause long-term growth problems
Intrauterine growth restriction (IUGR) is a common complication of pregnancy in developing countries, and carries an increased risk of perinatal mortality and morbidity. IUGR refers to a condition in which foetus (an unborn baby) is smaller or less developed than normal for the baby’s gender and gestational age. Gestational age is the age of a foetus or baby that starts on the first day of the mother’s last menstrual period.
In IUGR foetal weight is below the 10th percentile for gestational age as estimated by an ultrasound. At term, the birth weight less than 2,500 g (5lb, or 8oz) is considered as IUGR. Small for gestational age or fetal growth restriction are the other terms used for IUGR. The term intrauterine growth restriction has largely replaced the term intrauterine growth retardation.
IUGR is classified into two types-
Symmetric or primary IUGR: In this condition all internal organs are reduced in size. It is found in 20%-30% of all cases of IUGR.
Asymmetric or secondary IUGR: In this condition the head and brain are normal in size, but the abdomen is smaller. It is evident mostly in the 3rd trimester. It is more common and found in 70% to 80% of total IUGR cases.
Intrauterine growth restriction is observed in about 24% of newborns. In Asia IUGR accounts for nearly 75% of all affected infants. After prematurity IUGR is the second leading cause of perinatal morbidity and mortality.
Growth-restricted pregnancies are often complicated by a high rate of antepartum and intrapartum fetal distress and the need for cesarean delivery. These infants have many acute neonatal problems that include perinatal asphyxia, hypothermia (low body temperature), hypoglycemia (low blood sugar), and polycythemia (increased red blood cells), jaundice, feeding difficulties, feed intolerance, necrotizing enterocolitis, late-onset sepsis, and pulmonary hemorrhage.
When IUGR infants grow up long-term complications include growth retardation, neurodevelopment defects may occur. These infants are more likely to develop adult onset diseases because of fetal epigenetic changes.
Timely diagnosis (by assessment of fetal growth at each prenatal visit) and management of IUGR are the major activities in reducing perinatal morbidity and mortality.
Causes
IUGR has many causes related to mother, foetus and placenta (part that joins the mother and foetus). Various risk factors for IUGR can be summarized as-
A. Maternal causes –
Before pregnancy:
Low pre-pregnancy weight and small maternal size
Poor periconceptual nutritional status such as anemia, folate deficiency
Low socioeconomic status
Parity- none and more than 5 births
Recent pregnancy
During pregnancy:
Poor weight gain during pregnancy, especially in latter half
Moderate to heavy physical work
Chronic illness – such as malabsorption, diabetes, renal disease
Use of certain drugs, smoking, and alcohol
Pregnancy induced hypertension
Decreased oxygen availability such as in high altitude, severe maternal anemia
B. Uterine and placental factors:
Inadequate placental growth
Uterine malformations
Decreased utero-placental blood flow (such as in toxemias of pregnancy, diabetic vasculopathy)
Multiple gestations
C. Fetal causes include familial genetic and chromosomal abnormalities and intrauterine infections such as TORCH- which includes toxoplasmosis, other infections (syphilis, varicella-zoster, parvovirus B19), rubella, cytomegalovirus (CMV), and herpes infections.
Symmetric or primary IUGR is due to genetic or chromosomal causes, early gestational intrauterine infections (TORCH) and maternal alcohol use.
Asymmetric IUGR is more commonly due to extrinsic influences that affect the foetus later in gestation, such as preeclampsia, chronic hypertension, and uterine anomalies.
Symptoms
The main symptom of IUGR is a small for gestational age baby. During the antenatal checkup, a doctor measures the height of the uterus from the pubic bone to estimate the size of the fetus. After about the 20th week, uterine fundal height in centimeters is usually equal to the number of weeks of the pregnancy. A lag in fundal height of 4 cm or more with weeks of pregnancy suggests IUGR, and additional tests are required to confirm diagnosis.
During ultrasound, the baby’s estimated weight with IUGR is below the 10th percentile or less than that of 90% of babies of the same gestational age. At term, the birth weight less than 2,500 g (5 lb, 8 oz) is considered as IUGR. Not all babies that are born small have IUGR. In most severe cases IUGR can lead to stillbirth.
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At term birth, symptoms of IUGR are:
Baby is small all over or malnourished.
Thin, pale, loose and dry skin
Umbilical cord is thin and often stained with meconium
Diagnosis
One of the most important things when diagnosing IUGR is to know accurate gestational age of baby. Gestational age can be calculated by using the first day of last menstrual period (LMP) and also by early ultrasound calculations. Once the gestational age is known the following methods can be used to diagnose IUGR.
Fundal height: It is the simplest and most common method to diagnose IUGR. Fundal height is size of uterus measured as the distance from the pubic bone to the top of the uterus in centimeters. After the 20th week of pregnancy, the measure in centimeters usually corresponds with the number of weeks of pregnancy. A lag in fundal height of 4 cm or more suggests IUGR.
Weight checkups: Doctors routinely check and record the mother’s weight at every prenatal checkup. If a mother is not gaining weight properly, it could indicate a growth problem in her baby.
Ultrasound: It is used to measure the baby’s head and abdomen and compared with growth charts to estimate the baby’s weight. Ultrasound can also be used to determine amniotic fluid.
Doppler assessment: It is a technique that uses sound waves to measure the amount and speed of blood flow through the blood vessels. Doctors may use this test to check the flow of blood in the umbilical cord and vessels in the baby’s brain. Abnormal Doppler tests are diagnostic of IUGR
Complications
IUGR causes many health problems during pregnancy, delivery, and after birth. These include:
Difficulty during vaginal delivery
Low Apgar scores (a test done immediately after birth to evaluate the newborn’s physical condition to determine need for special medical care)
Meconium aspiration (inhalation of stools passed while in the uterus), which can lead to breathing problems
low birth weight
Hypoglycemia (low blood sugar)
High red blood cell count
Low resistance to infection
Difficulty in maintaining body temperature
Prevention
Although IUGR can occur even when a mother is perfectly healthy, still there are some measures to reduce the risk of IUGR and increase the chances of a healthy pregnancy and baby.
Care before pregnancy:
Providing care to women before and between pregnancies (inter-conception care) improves the chances of mothers and babies being healthy.
Advocating healthy eating and physical activity to women in their daily routine to improve weight and cardiovascular status before pregnancy.
Diagnosis and management of chronic diseases such as hypertension, diabetes before pregnancy.
Correction of anaemia/folic acid supplementation before pregnancy.
Care during pregnancy:
Pregnant mothers should take only those medicines which are prescribed by doctors.
Healthy diet should be advised to pregnant women with behavior change to encourage healthier eating patterns during pregnancy. Foods fortified with nutrients can be provided to pregnant women.
Pregnant women are advised to take enough rest with proper duration of sleep during night and an hour or two of rest in the afternoon.
Expectant mothers should follow healthy lifestyle habits. Tobacco use, smoking and alcohol intake should be avoided during pregnancy.
Care during delivery-
Delivery should be planned in health facilities having emergency obstetric care and neonatal care facilities.
Management
General management measures: These include treatment of maternal disease, good nutrition and advice for bed rest.
Preterm delivery is indicated if the fetus shows evidence of abnormal function on biophysical profile testing. Antenatal administration of steroids in preterm pregnancies and delivery at an institution with an emergency obstetric care and neonatal care unit is advised.
The foetus should be monitored continuously during labor to minimize fetal hypoxia.
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An antepartum haemorrhage (APH) is bleeding from the vagina that occurs after the 20th week of pregnancy and before the birth of your baby. The common causes of bleeding during pregnancy are cervical ectropion, vaginal infection, placental edge bleed, placenta praevia or placental abruption.
Cervical ectropion
The cells on the surface of the cervix often change in pregnancy and make the tissue more likely to bleed, particularly after sex. This is called cervical ectropion. This condition does not affect the pregnancy at all. If there is bleeding from the cervix it is important to ensure you are up to date with your PAP smear and it is normal.
Infection
Cervical and vaginal infections can also cause a small amount of vaginal bleeding (eg severe Thrush or Chlamydia) and you may be very uncomfortable. It is important to seek treatment from your doctor for these conditions.
Placental edge bleed
In the second half of your pregnancy, the lower-half of the uterus begins to stretch and grow. This can lead to the edge of the placenta separating from the wall of the uterus. In most cases bleeding will stop after a few hours, and your baby will not be adversely affected. However it is important that you contact the hospital immediately if you notice any bleeding.
Placenta praevia
Placenta praevia is diagnosed when the placenta grows in the lower part of the uterus and is located near to or actually covering the cervix. Placenta praevia is classified into four types:
Type I: the placenta is located in the lower part of the uterus but does not come close to the cervix. You can usually expect to birth vaginally with this type
Type II (or marginal) – the placenta touches but does not cover the cervix
Type III (or partial) – the placenta partially covers the cervix
Type IV (or complete) – the placenta completely covers the cervix
Types II, III and IV are associated with a risk of heavy bleeding in labour as the cervix dilates and, therefore caesarean birth is usually recommended.
Causes of placenta praevia
The cause of placenta praevia is often unknown but these are some of the factors that put women more at risk. :
previous caesarean birth or uterine surgery
previous placenta praevia
age above 35 years
multiple pregnancy twins or triplets etc.
multiple previous pregnancies
endometriosis
closely spaced pregnancies
placental abnormalities
abnormalities in the baby
smoking.
Diagnosis
As part of the 18–20 weeks ultrasound scan (USS) the site of the placenta is identified. Approximately one in five women will have a low-lying placenta at this time. A repeat USS will be recommended between 32 and 36 weeks of pregnancy depending on where the placenta is positioned at the earlier scan. By this time only 2 per cent of women will still have a low-lying placenta. Your doctor will discuss ongoing management and care. Most women with Type II, III & IV placenta praevia will need to give birth by caesarean section.
Placental abruption
Placental abruption occurs when part of the placenta separates from the wall of the uterus prior to term. A large amount of vaginal blood loss usually occurs. Some of the blood may however remain in the uterus and this can lead to a blood clot forming behind the placenta. The amount of vaginal blood loss seen is therefore, not an accurate measurement of the total amount of blood loss which has occurred.
If you have any blood loss or abdominal pain it is important to contact your midwife/obstetrician immediately. Some causes of vaginal bleeding are more serious than others so it is important to find out the reason as soon as possible.
Management
You may be admitted to hospital for observation and assessment of the cause of your bleeding. You will have an ultrasound scan and your baby may have a cardiotocograph (CTG) which checks your baby’s heart beat. Depending on how much bleeding has occurred, you may need to have an intravenous (IV) drip inserted and may require IV fluids. In severe circumstances you may require a blood transfusion or your baby may need to be born early. Initially you will be encouraged to rest in bed.
At this point in time, we recommend that you:
change sanitary pads at least every four hours while you have any blood loss (personal hygiene is very important to reduce the risk of infection)
do not use tampons
wipe from front to back after going to the toilet
do not go swimming
do not have baths or use a spa—please shower
do not have sexual intercourse
do not use any vaginal medications/creams.
If you experience an increase in vaginal bleeding, or abdominal pain or contractions it is important to notify the midwives or doctors as soon as it occurs.
If you have any bleeding in pregnancy there is an increased risk of your baby’s blood crossing into your blood stream. If you have a rhesus negative blood group you will be offered an injection of Anti-D immunoglobulin. THis should be discussed with your doctor.
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Aetiology
No definite cause is diagnosed in about 50% of all women who present with APH; however, placenta praevia and placental abruption are the major identifiable causes:
Placenta praevia: insertion of the placenta, partially or fully, in the lower segment of the uterus. See the separate Placenta Praevia article.
Placental abruption: premature separation of a normally placed placenta. See the separate Placenta and Placental Problems article.
Local causes – eg, vulval or cervical infection, trauma or tumours.
Partner violence is common in pregnancy, occurring in 2.8% of pregnant women in a Canadian population-based study. It may result in APH. Women should be asked about this, particularly if there are repeated episodes. See the separate Domestic Violence article.
Vasa praevia: bleeding from fetal vessels in the fetal membranes, leading to high risk of fetal haemorrhage and death at rupture of the membranes. See the separate Placenta and Placental Problems article
Uterine rupture: rare but very dangerous for both mother and baby. See separate Uterine Rupture article
Inherited bleeding problems are very rare, occurring in 1 in 10,000 women[5].
Whilst risk factors for APH, in particular for placenta praevia and placental abruption, have been identified, APH cannot be predicted; 70% of cases of placental abruption occur in low-risk pregnancies.
There is limited evidence that APH can be prevented but women should be encouraged to change modifiable risk factors such as smoking and cocaine and amfetamine abuse.
Antenatal anaemia should be investigated and treated. Iron-deficiency anaemia not only reduces a woman’s tolerance to bleeding but may also contribute to uterine atony.
Presentation
Bleeding, which may be accompanied by pain (suggestive of abruption) or be painless (suggesting praevia).
Uterine contractions may be provoked.
There may be malpresentation or failure of the fetal head to engage, with placenta praevia.
There may be associated signs of fetal distress.
If the bleeding is severe, the mother may show signs of hypovolaemic shock; however, young, fit, pregnant women can compensate very well until sudden and catastrophic decompensation occurs.
Management
Always admit the patient to hospital for assessment and management, even if bleeding is only a very small amount; there may be a large amount of concealed bleeding with only a small amount of revealed vaginal bleeding. Phone 999/112/911 if there are any major concerns regarding maternal or fetal well-being.
Estimate amount of blood loss. This is often underestimated and needs to combined with an assessment of signs of clinical shock:
Minor haemorrhage = blood loss <50 ml and has stopped.
Major haemorrhage = blood loss 50-1000 ml with no signs of shock.
Massive haemorrhage = blood loss >1000 ml and/or signs of shock.
The mainstays of management of massive haemorrhage are effective communication between clinical staff, resuscitation, monitoring and accurate diagnosis of the underlying cause. The bleeding will be arrested by delivery of the fetus.
Severe bleeding: the mother’s life should take priority. Any decision regarding the delivery of the baby should wait until the mother’s condition is stable.
Fetal distress: urgent delivery of the baby, irrespective of gestational age. Fetal compromise is an important indicator of reduced circulating blood volume.
No vaginal examination should be attempted, at least until a placenta praevia is excluded by ultrasound. It may initiate torrential bleeding from a placenta praevia.
Resuscitation can be inadequate because of underestimation of blood loss and misleading maternal response, especially in small women. For example, a woman who weighs 55 kg will have lost almost 30% of her blood volume if she loses 1500 ml of blood, whereas for a woman of 70 kg, this represents about 20% of her blood volume[2].
Blood tests:
FBC and ‘group and save’. NB: initial Hb may not reflect degree of blood loss. Low platelet count may suggest significant abruption.
Clotting studies, if platelet count is abnormal, as coagulopathy is common and should be anticipated.
Crossmatch four units and check U&Es and LFTs, if there is major or massive haemorrhage.
Gentle palpation of the abdomen to determine the gestational age of the fetus, presentation and position.
Fetal monitoring.
Arrange urgent ultrasound to exclude placenta praevia; ultrasound cannot exclude placental abruption, which is a clinical diagnosis.
With every episode of bleeding, a rhesus-negative woman should have a Kleihauer test and be given prophylactic anti-D immunoglobulin.
Maternal corticosteroids should be offered to any woman at risk of preterm birth, who is between 24+0 and 35+6 weeks of gestation.
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Further management
Further management will depend on fetal distress, the cause of the APH, the extent of bleeding and gestation.
All women need to be assessed individually, taking into account not only the amount of blood loss but also any relevant current or past medical and obstetric history.
Placenta praevia: see the separate Placenta Praevia article.
Moderate or severe placental abruption: see the separate Placenta and Placental Problems article.
Complications
Premature labour.
Disseminated intravascular coagulopathy.
Acute kidney injury.
Postpartum haemorrhage.
Placenta accreta: this may complicate cases of placenta praevia but is rare in the absence of placenta praevia or previous caesarean section. See the separate Placenta and Placental Problems article.
Anaemia.
Infection.
Prolonged hospital stay.
Psychological sequelae.
Fetal complications:
Fetal hypoxia.
Fetal growth restriction.
Prematurity, both iatrogenic and spontaneous.
Fetal death.
Prognosis
One population-based study found that bleeding in the second half of pregnancy is an independent risk factor for perinatal mortality.
Maternal mortality is low if managed by an experienced obstetrician and if no vaginal examination is performed before admission to hospital.
Perinatal mortality is 119 per 1,000 births complicated by abruption.
In pregnancies when the cause of APH is not known, there is still a greater risk of preterm delivery and induced labour but no increase in perinatal mortality after adjusting for gestational age
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Pregnancy stresses your heart and circulatory system. During pregnancy, your blood volume increases by 30 to 50 percent to nourish your growing baby, your heart pumps more blood each minute and your heart rate increases.
Labor and delivery add to your heart’s workload, too. During labor — particularly when you push — you’ll have abrupt changes in blood flow and pressure. It takes several weeks after delivery for the stresses on the heart to return to the levels they were before you became pregnant.
Heart disorders account for about 10% of maternal obstetric deaths. In the US, because incidence of rheumatic heart disease has markedly declined, most heart problems during pregnancy result from congenital heart disease. However, in Southeast Asia, Africa, India, the Middle East, and parts of Australia and New Zealand, rheumatic heart disease is still common.
Despite dramatic improvements in survival and quality of life for patients with severe congenital heart defects and other heart disorders, pregnancy remains inadvisable for women with certain high-risk disorders such as the following:
Pulmonary hypertension (pulmonary artery systolic pressure > 25 mm Hg) caused by any condition, including Eisenmenger syndrome
Coarctation of the aorta if uncorrected or if accompanied by an aneurysm
Marfan syndrome with aortic root diameter of > 4.5 cm
Severe symptomatic aortic stenosis or severe mitral stenosis
Bicuspid aortic valve with ascending aorta diameter > 50 mm
A single ventricle and impaired systolic function (whether treated with the Fontan procedure or not)
Cardiomyopathy with ejection fraction < 30% or New York Heart Association (NYHA) class III or IV heart failure
What are the risks?
The risks depend on the nature and severity of your heart condition. For example:
Heart rhythm issues. Minor abnormalities in heart rhythm are common during pregnancy. They’re not usually cause for concern. If you need treatment for an arrhythmia, you’ll likely be given medication, the same as you would if you weren’t pregnant.
Heart valve issues. Having an artificial heart valve or scarring or malformation of your heart or valves can increase your risk of complications during pregnancy. If your valves aren’t working properly, you might have trouble tolerating the increased blood flow that occurs during pregnancy. In addition, artificial or abnormal valves carry an increased risk of a potentially life-threatening infection of the lining of the heart (endocarditis) and heart valves. Mechanical artificial heart valves also pose serious risks during pregnancy due to the need to adjust use of blood thinners, the potential for life-threatening clotting (thrombosis) of heart valves. Taking blood thinners can also put your developing baby at risk.
Congestive heart failure. As blood volume increases, congestive heart failure can worsen.
Congenital heart defect If you were born with a heart problem, your baby has a greater risk of developing some type of heart defect, too. You might also be at risk for heart problems occurring during pregnancy and of premature birth.
Pre-existing cardiovascular conditions and pregnancy
Congenital heart conditions and pregnancy
Congenital heart defects are the most common heart problems that affect women of childbearing age. These include shunt lesions, obstructive lesions, complex lesions and cyanotic heart disease.
Shunt lesions
Shunt lesions are the simplest and most common congenital heart defects. Shunts include atrial septal defect (ASD), which is a hole between the upper chambers of the heart; ventricular septal defect (VSD), which is a hole between the lower chambers of the heart; and patent ductus arteriosus (PDA), which means there is abnormal blood flow between the aorta and pulmonary artery. If the hole is large, a fair amount of blood from the left side of the heart will flow back into the right side of the heart. The blood gets pumped back to the lungs again and causes strain on the heart. This can lead to an enlarged heart, abnormal heart rhythms and increased pressure in the lungs (pulmonary hypertension). Pulmonary hypertension, when severe, can cause the blood flow across the shunt to move in reverse. This can cause low levels of oxygen in the blood (cyanosis). In such cases, pregnancy is not recommended due to the high risk of the mother dying.
Obstructive Lesions
Obstructive lesions reduce the amount of blood flow to the heart and the body’s major blood vessels. One such lesion, aortic coarctation is a narrowing in the descending aorta, which is the largest artery in the body. Aortic coarctation can cause a pregnant woman to have high blood pressure. The condition can also keep the placenta (the collection of blood vessels that supplies the baby with blood) from getting enough blood. Depending on how severe the narrowing is, you may need a procedure before or during pregnancy to keep you and the baby safe during pregnancy.
Complex lesions
Complex lesions include transposition of the great arteries. This means the aorta and pulmonary arteries are attached to the wrong ventricles (bottom chambers of the heart). Surgery to repair the problem can cause problems with the heart chambers, especially if the right ventricle pumps blood out to the body (this is usually the job of the left ventricle). In this case, the problem can cause heart failure and leaky heart valves, and the conditions can become worse during pregnancy. If you have this condition, you will need to be closely followed during pregnancy.
Cyanotic heart disease includes tetralogy of Fallot. This is a condition that includes a VSD, narrowing of the pulmonary valve and abnormal configuration of the aorta. Treatment usually keeps cyanosis from recurring. However, the repair can cause a leaky pulmonary valve, and that problem can lead to heart failure and heart rhythm disturbances. If you have a leaky pulmonary valve, you may need to have it corrected before you become pregnant.
In general, most women with congenital heart defects, especially those who have had corrective surgeries, can safely become pregnant. However, the outcome of the pregnancy and risk of complications depends on the type of heart defect you have, how severe your symptoms are, and whether you have heart muscle dysfunction, heart rhythm disturbances or pulmonary hypertension with related lung disease. Your pregnancy can also be affected if you have had particular types of heart surgery.
Valve disease and pregnancy
Aortic valve stenosis means the aortic valve (the valve between the left ventricle and the aorta) is narrowed or stiff. If the narrowing is severe, the heart has to work harder to pump the increased blood volume out of the narrowed valve. This, in turn, can cause the left ventricle (the major pumping chamber of the heart to enlarge – a condition called hypertrophy). Over time, symptoms of heart failure can occur or become worse and increase the risk of long-term complications for the mother.
One common cause of aortic valve stenosis is bicuspid aortic valve disease. This is a congenital heart condition in which there are only two leaflets (also called cusps), instead of the normal three leaflets inside the valve. The leaflets open and close to keep blood flowing in the right direction and prevent backflow. Without the third leaflet, the valve can become narrowed or stiff.
Women with bicuspid aortic valve disease or any type of aortic valve stenosis need to be evaluated by a cardiologist before planning a pregnancy. In some cases, surgery is recommended to correct the valve before pregnancy.
Mitral valve stenosis means the mitral valve (the valve between the left atrium and left ventricle) is narrowed. This condition is often caused by rheumatic fever.
The increased blood volume and increased heart rate that occur during pregnancy can make symptoms of mitral stenosis get worse. The left atrium can become bigger and cause a rapid, irregular heart rhythm called atrial fibrillation. In addition, the problem can cause heart failure symptoms (shortness of breath, irregular heart beat, fatigue and swelling/edema). This can increase the risk to the mother. If you have mitral valve stenosis, you may need to take medications while you are pregnant. Your doctor may also recommend an catheter-based procedure, called percutaneous valvuloplasty, to correct the narrowed valve while you are pregnant. It is important to have mitral stenosis evaluated before you become pregnant. In some cases, surgery or valvuloplasty to correct the valve will be recommended before pregnancy.
Mitral valve prolapse is a common condition that usually doesn’t cause symptoms or require treatment. Most patients with mitral valve prolapse tolerate pregnancy well. If the prolapse causes a severe leak, you may need treatment before you become pregnant. Be sure to talk to your doctor if you plan to become pregnant and follow any recommendations.
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Pregnancy in women with prosthetic (artificial) valves
Women who have artificial heart valves may experience complications during pregnancy because:
Women who have an artificial heart valve need to take lifelong anticoagulant medication, and certain anticoagulant medications can be harmful to the baby. There is controversy about which anticoagulant medication regimen is best during pregnancy.*
During pregnancy, there is an increased risk of blood clots.
*Use of warfarin, heparin, aspirin, and combinations of these anticoagulant medications have been suggested and compared. The most recent recommendations from the European Heart Association are to use heparin during the first trimester, followed by warfarin up to the 36th week of pregnancy, and subsequent replacement with heparin until delivery OR to use oral anticoagulation medication throughout pregnancy, until the 36th week, followed by heparin until delivery.
The use of warfarin is less harmful if the dose is kept to less than 5 mg. In addition, other specialists have recommended the addition of low-dose aspirin to treat women who are at high risk.
If you have a prosthetic valve and are taking an anticoagulant medication, it is very important to be evaluated by a cardiologist before planning a pregnancy. The cardiologist will talk to you about your potential risks and determine the best anticoagulant therapy routine for you.
In addition, ask your doctor what precautions you should continue to follow to prevent endocarditis.
Aorta Disease and pregnancy
Women who have conditions that affect the aorta, such as aortic aneurysm, dilated aorta, or connective tissue disorders such as Marfan syndrome, are at increased risk during pregnancy.
Pressure in the aorta increases during pregnancy and when bearing down during labor and delivery. This extra pressure increases the risk of an aortic dissection or rupture, which can be life-threatening.
It is very important for women who have aorta disease to be evaluated by a cardiologist before planning a pregnancy. A thorough evaluation of your condition will provide the physician with information about the potential risks of pregnancy. It is also important to note that some conditions, such as Marfan syndrome, are genetic and can be passed down to children, so genetic counseling may be recommended.
Cardiovascular disorders that may develop during pregnancy
Peripartum cardiomyopathy
Peripartum cardiomyopathy is a rare condition. It is when heart failure develops in the last month of pregnancy or within five months after delivery. The cause of peripartum cardiomyopathy remains unknown. Certain patients, including those with multiple pregnancies and those of African descent, are at greatest risk. Women with peripartum cardiomyopathy have symptoms of heart failure. After pregnancy, the heart usually returns to its normal size and function. But, some women continue to have poor left ventricular function and symptoms. Women with peripartum cardiomyopathy have an increased risk of complications during future pregnancies, especially if the heart dysfunction continues.
Hypertension (high blood pressure)
About 6% to 8% of women develop high blood pressure, also called hypertension, during pregnancy. This is called pregnancy-induced hypertension (PIH) and is related to preeclampsia, toxemia, or toxemia of pregnancy. Symptoms of PIH include high blood pressure, swelling due to fluid retention, and protein in the urine. Pregnancy-induced hypertension can be harmful to the mother and the baby. To learn more about who is at risk for PIH, symptoms of PIH, and how PIH is diagnosed and treated, click on the following links:
Cleveland Clinic – Pregnancy-Induced Hypertension
Cleveland Clinic – Preeclampsia and Eclampsia
American Heart Association – Pregnancy and High Blood Pressure
Myocardial infarction
Heart attack (myocardial infarction) is fortunately a very rare but potentially deadly complication that can occur during pregnancy or during the first few weeks afterwards. A heart attack can be caused by many things. Patients with coronary artery disease (“hardening of the arteries”) can have a myocardial infarction if the plaque inside their arteries ruptures. This problem is becoming more common, since many women wait until later in life to become pregnant. Other causes of a heart attack include a spontaneous blood clot inside a coronary vessel (because pregnancy increases the risk of blood clots) and coronary dissection (a weakening of the vessel wall that leads to a spontaneous tear and clotting). If you have a heart attack, it is critical to get emergency help. Treatment will be focused on ensuring your survival.
Heart Murmur
Sometimes, the increase in blood volume during pregnancy can cause a heart murmur(an abnormal “swishing” sound). In most cases, the murmur is harmless. But in rare cases, it could mean there’s a problem with a heart valve. Your doctor can evaluate your condition and determine the cause of the murmur.
Arrhythmias and pregnancy
Abnormal heartbeats (arrhythmias) during pregnancy are common. Women who have never had an arrhythmia or heart problem may first develop an arrhythmia during pregnancy. When an arrhythmia develops during pregnancy, it can be a sign of a heart condition you didn’t know you had. Most of the time, the arrhythmia causes little in the way of symptoms and does not require treatment. If you have symptoms, your doctor may order tests to determine the type arrhythmia you have and attempt to determine its cause.
Special considerations before and during pregnancy
Congenital heart defects (in either the mother or father) increase the baby’s risk of having a heart problem. Your cardiologist may refer you to a geneticist for further evaluation. A fetal echocardiogram may be recommended to check the baby’s heart for possible defects. This test is usually done in the 18th week of pregnancy.
If you have been diagnosed with a congenital heart defect, a cardiologist should evaluate your heart condition before you plan a pregnancy. The cardiologist will talk to you about the possible risks of pregnancy and can work with your healthcare team to monitor your health and your baby’s health while you are pregnant.
How can I prevent complications?
Taking good care of yourself is the best way to take care of your baby. For example:
Keep your prenatal appointments. Visit your health care provider regularly throughout your pregnancy.
Take your medication as prescribed. Your health care provider will prescribe the safest medication at the most appropriate dose.
Get plenty of rest. Take a daily nap, if you can, and avoid strenuous physical activities.
Monitor your weight gain. Gaining the right amount of weight supports your baby’s growth and development. Gaining too much weight places additional stress on your heart.
Manage anxiety. Ask questions about your progress. Find out what to expect during labor and delivery. Knowing what’s happening can help you feel more at ease.
Know what’s off-limits. Avoid smoking, alcohol, caffeine and illegal drugs.
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When you’re pregnant, you may develop anemia. When you have anemia, your blood doesn’t have enough healthy red blood cells to carry oxygen to your tissues and to your baby.
During pregnancy, your body produces more blood to support the growth of your baby. If you’re not getting enough iron or certain other nutrients, your body might not be able to produce the amount of red blood cells it needs to make this additional blood.
It’s normal to have mild anemia when you are pregnant. But you may have more severe anemia from low iron or vitamin levels or from other reasons.
Anemia can leave you feeling tired and weak. If it is severe but goes untreated, it can increase your risk of serious complications like preterm delivery.
Normally during pregnancy, erythroid hyperplasia of the marrow occurs, and red blood cell (RBC) mass increases. However, a disproportionate increase in plasma volume results in hemodilution (hydremia of pregnancy): hematocrit (Hct) decreases from between 38% and 45% in healthy women who are not pregnant to about 34% during late single pregnancy and to 30% during late multifetal pregnancy. Thus during pregnancy, anemia is defined as hemoglobin (Hb) < 10 g/dL (Hct < 30%). If Hb is < 11.5 g/dL at the onset of pregnancy, women may be treated prophylactically because subsequent hemodilution usually reduces Hb to < 10 g/dL. Despite hemodilution, oxygen-carrying capacity remains normal throughout pregnancy. Hct normally increases immediately after birth.
Anemia occurs in up to one third of women during the 3rd trimester. The most common causes are
Iron deficiency
Folate deficiency
Obstetricians, in consultation with a perinatologist, should evaluate anemia in pregnant Jehovah’s Witness patients (who are likely to refuse blood transfusions) as soon as possible.
Types of Anemia During Pregnancy
Several types of anemia can develop during pregnancy. These include:
Iron-deficiency anemia
Folate-deficiency anemia
Vitamin B12 deficiency
Here’s why these types of anemia may develop:
Iron-deficiency anemia. This type of anemia occurs when the body doesn’t have enough iron to produce adequate amounts of hemoglobin. That’s a protein in red blood cells. It carries oxygen from the lungs to the rest of the body.
In iron-deficiency anemia, the blood cannot carry enough oxygen to tissues throughout the body.
Iron deficiency is the most common cause of anemia in pregnancy.
Folate-deficiency anemia. Folate is the vitamin found naturally in certain foods like green leafy vegetables A type of B vitamin, the body needs folate to produce new cells, including healthy red blood cells.
During pregnancy, women need extra folate. But sometimes they don’t get enough from their diet. When that happens, the body can’t make enough normal red blood cells to transport oxygen to tissues throughout the body. Man made supplements of folate are called folic acid.
Folate deficiency can directly contribute to certain types of birth defects, such as neural tube abnormalities (spina bifida) and low birth weight.
Vitamin B12 deficiency. The body needs vitamin B12 to form healthy red blood cells. When a pregnant woman doesn’t get enough vitamin B12 from their diet, their body can’t produce enough healthy red blood cells. Women who don’t eat meat, poultry, dairy products, and eggs have a greater risk of developing vitamin B12 deficiency, which may contribute to birth defects, such as neural tube abnormalities, and could lead to preterm labor.
Blood loss during and after delivery can also cause anemia.
Symptoms and Signs
Early symptoms of anemia are usually nonexistent or nonspecific (eg, fatigue, weakness, light-headedness, mild dyspnea during exertion). Other symptoms and signs may include pallor and, if anemia is severe, tachycardia or hypotension.
Anemia increases risk of
Preterm delivery
Postpartum maternal infections
Diagnosis
Complete blood count (CBC), followed by testing based on mean corpuscular value (MCV) value
Diagnosis of anemia begins with CBC; usually, if women have anemia, subsequent testing is based on whether the MCV is low (< 79 fL) or high (> 100 fL): Lab Test Ferritin
For microcytic anemias: Evaluation includes testing for iron deficiency (measuring serum ferritin) and hemoglobinopathies (using hemoglobin electrophoresis). If these tests are nondiagnostic and there is no response to empiric treatment, consultation with a hematologist is usually warranted.
For macrocytic anemias: Evaluation includes serum folate and vitamin B12 levels.
For anemia with mixed causes: Evaluation for both types is required.
Risk Factors for Anemia in Pregnancy
All pregnant women are at risk for becoming anemic. That’s because they need more iron and folic acid than usual. But the risk is higher if you:
Are pregnant with multiples (more than one child)
Have had two pregnancies close together
Vomit a lot because of morning sickness
Are a pregnant teenager
Don’t eat enough foods that are rich in iron
Had anemia before you became pregnant
Symptoms of Anemia During Pregnancy
The most common symptoms of anemia during pregnancy are:
Pale skin, lips, and nails
Feeling tired or weak
Dizziness
Shortness of breath
Rapid heartbeat
Trouble concentrating
In the early stages of anemia, you may not have obvious symptoms. And many of the symptoms are ones that you might have while pregnant even if you’re not anemic. So be sure to get routine blood tests to check for anemia at your prenatal appointments.
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Risks of Anemia in Pregnancy
Severe or untreated iron-deficiency anemia during pregnancy can increase your risk of having:
A preterm or low-birth-weight baby
A blood transfusion (if you lose a significant amount of blood during delivery)
Postpartum depression
A baby with anemia
A child with developmental delays
Untreated folate deficiency can increase your risk of having a:
Preterm or low-birth-weight baby
Baby with a serious birth defect of the spine or brain (neural tube defects)
Untreated vitamin B12 deficiency can also raise your risk of having a baby with neural tube defects.
Tests for Anemia
During your first prenatal appointment, you’ll get a blood test so your doctor can check whether you have anemia. Blood tests typically include;
Hemoglobin test. It measures the amount of hemoglobin — an iron-rich protein in red blood cells that carries oxygen from the lungs to tissues in the body.
Hematocrit test. It measures the percentage of red blood cells in a sample of blood.
If you have lower than normal levels of hemoglobin or hematocrit, you may have iron-deficiency anemia. Your doctor may check other blood tests to determine if you have iron deficiency or another cause for your anemia.
Even if you don’t have anemia at the beginning of your pregnancy, your doctor will most likely recommend that you get another blood test to check for anemia in your second or third trimester.
Treatment for Anemia
If you are anemic during your pregnancy, you may need to start taking an iron supplement and/or folic acid supplement in addition to your prenatal vitamins. Your doctor may also suggest that you add more foods that are high in iron and folic acid to your diet.
In addition, you’ll be asked to return for another blood test after a specific period of time so your doctor can check that your hemoglobin and hematocrit levels are improving.
To treat vitamin B12 deficiency, your doctor may recommend that you take a vitamin B12 supplement.
The doctor may also recommend that you include more animal foods in your diet, such as:
meat
eggs
dairy products
Your OB may refer you to a hematologist, a doctor who specializes in anemia/ blood issues. The specialist may see you throughout the pregnancy and help your OB manage the anemia.
Preventing Anemia
To prevent anemia during pregnancy, make sure you get enough iron. Eat well-balanced meals and add more foods that are high in iron to your diet.
Aim for at least three servings a day of iron-rich foods, such as:
lean red meat, poultry, and fish
leafy, dark green vegetables (such as spinach, broccoli, and kale)
iron-enriched cereals and grains
beans, lentils, and tofu
nuts and seeds
eggs
Foods that are high in vitamin C can help your body absorb more iron. These include:
citrus fruits and juices
strawberries
kiwis
tomatoes
bell peppers
Try eating those foods at the same time that you eat iron-rich foods. For example, you could drink a glass of orange juice and eat an iron-fortified cereal for breakfast.
Also, choose foods that are high in folate to help prevent folate deficiency. These include:
leafy green vegetables
citrus fruits and juices
dried beans
breads and cereals fortified with folic acid
Follow your doctor’s instructions for taking a prenatal vitamin that contains a sufficient amount of iron and folic acid.
Vegetarians and vegans should talk with their doctor about whether they should take a vitamin B12 supplement when they’re pregnant and breastfeeding.
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Iron Deficiency Anemia in Pregnancy
About 95% of anemia cases during pregnancy are iron deficiency anemia. The cause is usually
Inadequate dietary intake (especially in adolescent girls)
A previous pregnancy
The normal recurrent loss of iron in menstrual blood (which approximates the amount normally ingested each month and thus prevents iron stores from building up) before the woman became pregnant
Diagnosis
Measurement of serum iron, ferritin, and transferrin
Typically, Hct is ≤ 30%, and MCV is < 79 fL. Decreased serum iron and ferritin and increased serum transferrin levels confirm the diagnosis of iron deficiency anemia.
Treatment
Usually ferrous sulfate 325 mg po once/day
One 325-mg ferrous sulfate tablet taken midmorning is usually effective. Higher or more frequent doses increase GI adverse effects, especially constipation, and one dose blocks absorption of the next dose, thereby reducing percentage intake.
About 20% of pregnant women do not absorb enough supplemental oral iron; a few of them require parenteral therapy, usually iron dextran 100 mg IM every other day for a total of ≥ 1000 mg over 3 weeks. Hct or Hb is measured weekly to determine response. If iron supplements are ineffective, concomitant folate deficiency should be suspected.
Neonates of mothers with iron deficiency anemia usually have a normal Hct but decreased total iron stores and a need for early dietary iron supplements.
Prevention
Although the practice is controversial, iron supplements (usually ferrous sulfate 325 mg po once/day) are usually given routinely to pregnant women to prevent depletion of body iron stores and prevent the anemia that may result from abnormal bleeding or a subsequent pregnancy.
Folate Deficiency Anemia in Pregnancy
Folate deficiency increases risk of neural tube defects and possibly fetal alcohol syndrome. Deficiency occurs in 0.5 to 1.5% of pregnant women; megaloblastic macrocytic anemia is present if deficiency is moderate or severe.
Rarely, severe anemia and glossitis occur.
Diagnosis
Measurement of serum folate
Folate deficiency is suspected if CBC shows anemia with macrocytic indices or high RBC distribution width (RDW). Low serum folate levels confirm the diagnosis.
Treatment
Folic acid 1 mg po bid
Treatment is folic acid 1 mg po bid.
Severe megaloblastic anemia may warrant bone marrow examination and further treatment in a hospital.
Prevention
For prevention, all pregnant women and women who are trying to conceive are given folic acid 0.4 to 0.8 mg po once/day. Women who have had a fetus with spina bifida should take 4 mg once/day, starting before conception.
Hemoglobinopathies in Pregnancy
During pregnancy, hemoglobinopathies, particularly sickle cell disease, Hb S-C disease, and beta- and alpha-thalassemia, can worsen maternal and perinatal outcomes. Genetic screening genetic screening for some of these disorders is available.
Preexisting sickle cell disease, particularly if severe, increases risk of the following:
Anemia almost always becomes more severe as pregnancy progresses. Sickle cell trait increases the risk of UTIs but is not associated with severe pregnancy-related complications.
Treatment of sickle cell disease during pregnancy is complex. Painful crises should be treated aggressively. Prophylactic exchange transfusions to keep Hb A at ≥ 60% reduce risk of hemolytic crises and pulmonary complications, but they are not routinely recommended because they increase risk of transfusion reactions, hepatitis, HIV transmission, and blood group isoimmunization. Prophylactic transfusion does not appear to decrease perinatal risk. Therapeutic transfusion is indicated for the following:
Symptomatic anemia
Heart failure
Severe bacterial infection
Severe complications of labor and delivery (eg, bleeding, sepsis)
Hb S-C disease may first cause symptoms during pregnancy. The disease increases risk of pulmonary infarction by occasionally causing bony spicule embolization. Effects on the fetus are uncommon but, if they occur, often include fetal growth restriction.
Sickle cell–beta-thalassemia is similar to Hb S-C disease but is less common and more benign.
Alpha-thalassemia does not cause maternal morbidity, but if the fetus is homozygous, hydrops and fetal death occur during the 2nd or early 3rd trimester.
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Women who develop hypertension after 20 weeks’ gestation and who do not have proteinuria or other criteria for preeclampsia are diagnosed with gestational hypertension. This is a provisional diagnosis that includes women who eventually develop preeclampsia, those with unrecognized chronic hypertension (diagnosed by persistently elevated BP beyond 12 weeks postpartum), and women with transient hypertension of pregnancy. Approximately 50% of women diagnosed with gestational hypertension between 24 and 35 weeks’ gestation ultimately develop preeclampsia. Management of gestational hypertension is similar to that of preeclampsia, with expectant monitoring and labor induction at 37 weeks’ gestation
Worldwide there is disagreement about many aspects of the classification, diagnosis, and management of the hypertensive disorders of pregnancy. This lack of consensus hampers our ability to study not only the immediate rates of adverse maternal and fetal outcomes for the various hypertensive disorders in pregnancy, particularly preeclampsia, but also the long-term health outcomes of women and babies who survive this condition. It also impacts on research into the pathophysiology of this condition and has almost certainly delayed the development of effective screening tests and treatments, leading to poorer pregnancy outcomes.
One scholarly review of available guidelines has shown broad agreement in the following areas:
Definitions of hypertension, proteinuria, chronic hypertension, and gestational hypertension;
Prevention of preeclampsia with low-dose aspirin and supplemental calcium (if low calcium intake);
Treatment of severe hypertension;
Use of MgSO4 for eclampsia and severe preeclampsia;
Use of antenatal corticosteroids to enhance fetal lung maturity at <34 weeks’ gestation if delivery is likely within the next 7 days;
Delivery for preeclampsia at term; and
Oxytocin in the third stage of labor.
However, in this analysis, there was little or no agreement on
The definition of preeclampsia;
Target BP when hypertension is not severe;
Timing of delivery for women with chronic hypertension, gestational hypertension, or preterm preeclampsia;
Use of MgSO4 for preeclampsia that is not severe; and
Postpartum maternal monitoring.
Classification
1.Hypertension in pregnancy may be chronic (predat-ing pregnancy or diagnosed before 20 weeks of preg-nancy) or de novo (either preeclampsia or gestational hypertension).
2.Chronic hypertension is associated with adverse mater-nal and fetal outcomes and is best managed by tightly controlling maternal blood pressure (BP, 110–140/85 mmHg), monitoring fetal growth, and repeatedly as-sessing for the development of preeclampsia and ma-ternal complications. This can be done in an outpatient setting.
3.White-coat hypertension refers to elevated office/clin-ic (≥140/90 mmHg) BP, but normal BP measured at home or work (<135/85 mmHg); it is not an entirely benign condition and conveys an increased risk for preeclampsia.
4.Masked hypertension is another form of hypertension, more difficult to diagnose, characterized by BP that is normal at a clinic or office visit but elevated at other times, most typically diagnosed by 24-hour ambula-tory BP monitoring (ABPM) or automated home BP monitoring.
5.Gestational hypertension is hypertension arising de novo after 20 weeks’ gestation in the absence of protein-uria and without biochemical or hematological abnor-malities. It is usually not accompanied by fetal growth restriction. Outcomes in pregnancies complicated by gestational hypertension are normally good, but about a quarter of women with gestational hypertension (par-ticularly those who present at <34 weeks) will progress to preeclampsia and have poorer outcomes.
6.Preeclampsia is a complex medical disorder; worldwide, each year, it is responsible for >500000 fetal and neo-natal deaths and >70000 maternal deaths. Preeclampsia can deteriorate rapidly and without warning; we do not recommend classifying it as mild or severe
7. Proteinuria is not mandatory for a diagnosis of pre-eclampsia. Rather, this is diagnosed by the presence of de novo hypertension after 20 weeks’ gestation accom-panied by proteinuria and/or evidence of maternal acute kidney injury (AKI), liver dysfunction, neurological fea-tures, hemolysis or thrombocytopenia, or fetal growth restriction. Preeclampsia may develop or be recognized for the first time intrapartum or early postpartum in some cases.
8.The hemolysis, elevated liver enzymes, low platelets syndrome is a (serious) manifestation of preeclampsia and not a separate disorder.
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Diagnosis of Hypertension and Proteinuria
1.Home BP monitoring is a useful adjunct in the manage-ment of chronic hypertension and is mandatory in the management of white-coat hypertension.
2.Proteinuria is optimally assessed by screening with au-tomated dipstick urinalysis and then if positive quantify-ing with a urine protein/creatinine ratio. A ratio ≥30 mg/mmol (0.3 mg/mg) is abnormal.
Pathophysiology of Preeclampsia
Abnormal placental implantation (defects in trophoblasts and spiral arterioles)
Angiogenic factors (low level of placental growth factor)
Preeclampsia in a previous pregnancy (particularly if severe or before 32 weeks’ gestation)
7
Diabetes mellitus (preexisting)
3
Family history of preeclampsia (first-generation relative)
3
Multiple gestation
3
Nulliparity
3
Elevated body mass index
2
Maternal age > 40 years
1.6
Chronic hypertension or renal disease
Management
Regardless of the hypertensive disorder of pregnancy, BP requires urgent treatment in a monitored setting when severe (>160/110 mm Hg); acceptable agents for this include oral nifedipine or intravenous labetalol or hydralazine. Oral labetalol may be used if these treatments are unavailable.
Regardless of the hypertensive disorder of pregnancy, BPs consistently at or >140/90 mm Hg in clinic or office (or ≥135/85 mm Hg at home) should be treated, aiming for a target diastolic BP of 85 mm Hg in the office (and systolic BP of 110–140 mm Hg) to reduce the likelihood of developing severe maternal hypertension and other complications, such as low platelets and elevated liver enzymes with symptoms. Antihypertensive drugs should be reduced or ceased if diastolic BP falls <80 mm Hg. Acceptable agents include oral methyldopa, labetalol, oxprenolol, and nifedipine, and second or third line agents include hydralazine and prazosin.
Women with preeclampsia should be assessed in hospital when first diagnosed; thereafter, some may be managed as outpatients once it is established that their condition is stable and they can be relied on to report problems and monitor their BP.
Women with preeclampsia who have proteinuria and severe hypertension, or hypertension with neurological signs or symptoms, should receive magnesium sulfate (MgSO4) for convulsion prophylaxis.
Fetal monitoring in preeclampsia should include an initial assessment to confirm fetal well-being. In the presence of fetal growth restriction, a recommended schedule for serial fetal surveillance with ultrasound is detailed within these recommendations.
Maternal monitoring in preeclampsia should include BP monitoring, repeated assessments for proteinuria if it is not already present, clinical assessment including clonus, and a minimum of twice weekly blood tests for hemoglobin, platelet count, and tests of liver and renal function, including uric acid, the latter being associated with worse maternal and fetal outcomes.
Women with preeclampsia should be delivered if they have reached 37 weeks’ (and zero days) gestation or if they develop any of the following:
Repeated episodes of severe hypertension despite maintenance treatment with 3 classes of antihypertensive agents;
Progressive thrombocytopenia;
Progressively abnormal renal or liver enzyme tests;
Pulmonary edema;
Abnormal neurological features, such as severe intractable headache, repeated visual scotomata, or convulsions;
Nonreassuring fetal status.
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Postpartum Care
In the early postpartum period, women with preeclampsia should be considered at high risk for preeclamptic complications for at least 3 days and should have their BP and clinical condition monitored at least every 4 hours while awake. Antihypertensives administered antenatally should be continued, and consideration should be given to treating any hypertension before day 6 post-partum with antihypertensive therapy. Thereafter, antihypertensive therapy may be withdrawn slowly over days but not ceased abruptly. It is important to note that eclamptic seizures may develop for the first time in the early postpartum period.
Nonsteroidal anti-inflammatory drugs (NSAIDs) for postpartum analgesia should be avoided in women with preeclampsia unless other analgesics are not working; this is especially important if they have known renal disease, or preeclampsia is associated with placental abruption, AKI, or other known risk factors for AKI (eg, sepsis, postpartum hemorrhage).
All women should be reviewed at 3 months postpartum to ensure that BP, urinalysis, and any laboratory abnormalities have normalized. If proteinuria or hypertension persists, then appropriate referral for further investigations should be initiated.
There are significant long-term cardiovascular risks for women with chronic hypertension and those who have had gestational hypertension or preeclampsia. One initial recommendation may be to aim to achieve prepregnancy weight by 12 months and to limit interpregnancy weight gain through healthy lifestyle.
Annual medical review is advised life-long, and all such women should adopt a healthy lifestyle that includes exercise, eating well, and aiming for ideal body weight.
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Legg-Calvé-Perthes disease (LCPD) is an idiopathic juvenile avascular necrosis of the femoral head in a skeletally immature patient, i.e. children. Legg-Calvé and Perthes discovered this disease approximately 100 years ago. The disease affects children from ages of two to fourteen. The disease can lead to permanent deformity and premature osteoarthritis
Perthes disease is a rare childhood condition that affects the hip. It occurs when the blood supply to the rounded head of the femur (thighbone) is temporarily disrupted. Without an adequate blood supply, the bone cells die, a process called avascular necrosis.
Although the term “disease” is still used, Perthes is really a complex process of stages that can last several years. As the condition progresses, the weakened bone of the head of the femur (the “ball” of the “ball-and-socket” joint of the hip) gradually begins to collapse. Over time, the blood supply to the head of the femur returns and the bone begins to grow back.
Treatment for Perthes focuses on helping the bone grow back into a more rounded shape that still fits into the socket of the hip joint. This will help the hip joint move normally and prevent hip problems in adulthood.
The long-term prognosis for children with Perthes is good in most cases. After 18 to 24 months of treatment, most children return to daily activities without major limitations.
Description
Perthes disease — also known as Legg-Calve-Perthes, named for the three individual doctors who first described the condition — typically occurs in children who are between 4 and 10 years old. It is five times more common in boys than in girls, however, it is likely to cause more extensive damage to the bone in girls. In 10% to 15% of all cases, both hips are affected.
Epidemiology /Etiology
LCPD is an idiopathic disease, but a variety of theories about the underlying cause have been proposed since its discovery over a century ago, ranging from congenital to environmental and from traumatic to socio-economic causes. LCPD has been associated with thrombosis, fibrinolysis, and abnormal growth patterns of the bone. It has also been associated with an abnormality in the Insulin-like Growth Factor-1 Pathway, repeated mircotrauma or mechanical overloading related to hyperactivity of the child or a very low birth weight or short body length at birth.
Some studies suggest a genetic factor, i.e. a type II collagen mutation, and other studies report maternal smoking during pregnancy as well as other prenatal and perinatal risk factors.
It may be be that LCPD requires a set or subset of the aforementioned causes. As of yet it is hard to discern which are determining or merely contributing factors to the onset of the disease.
Pathogenesis
The pathogenesis of osteonecrosis is becoming better understood. Most research suggests either a single infarction event with subsequent mechanical loading that further injures and/or compresses the vessels during the repair process or multiple episodes of infarction are required to produce LCPD.
The key pathological event associated with the initiation of the development of LCPD is disruption of the blood supply to the capital femoral epiphysis. Subsequently ischaemic necrosis occurs in the bone, marrow and cartilage of the femoral head which results in a cessation of endochondral ossification and decreased mechanical strength (fig.2). When mechanical loading surpasses the weakened head’s capacity, deformity is initiated and progresses due to resorption of the necrotic bone and asymmetric restoration of endochondral ossification.
There are four stages in Perthes disease:
Initial / necrosis. In this stage of the disease, the blood supply to the femoral head is disrupted and bone cells die. The area becomes intensely inflamed and irritated and your child may begin to show signs of the disease, such as a limp or different way of walking. This initial stage may last for several months.
Fragmentation. Over a period of 1 to 2 years, the body removes the dead bone beneath the articular cartilage and quickly replaces it with an initial, softer bone (“woven bone”). It is during this phase that the bone is in a weaker state and the head of the femur is more likely to collapse into a flatter position.
Reossification. New, stronger bone develops and begins to take shape in the head of the femur. The reossification stage is often the longest stage of the disease and can last a few years.
Healed. In this stage, the bone regrowth is complete and the femoral head has reached its final shape. How close the shape is to round will depend on several factors, including the extent of damage that took place during the fragmentation phase, as well as the child’s age at the onset of disease, which affects the potential for bone regrowth.
Cause
The cause of Perthes disease is not known. Some recent studies indicate that there may be a genetic link to the development of Perthes, but more research needs to be conducted.
Symptoms
One of the earliest signs of Perthes is a change in the way your child walks and runs. This is often most apparent during sports activities. Your child may limp, have limited motion, or develop a peculiar running style, all due to irritability within the hip joint. Other common symptoms include:
Pain in the hip or groin, or in other parts of the leg, such as the thigh or knee (called “referred pain.”).
Pain that worsens with activity and is relieved with rest.
Painful muscle spasms that may be caused by irritation around the hip.
Depending upon your child’s activity level, symptoms may come and go over a period of weeks or even months before a doctor visit is considered.
Doctor Examination
After discussing your child’s symptoms and medical history, your doctor will conduct a thorough physical examination.
Physical examination tests. Your doctor will assess your child’s range of motion in the hip. Perthes typically limits the ability to move the leg away from the body (abduction), and twist the leg toward the inside of the body (internal rotation).
X-rays. These scans provide pictures of dense structures like bone, and are required to confirm a diagnosis of Perthes. X-rays will show the condition of the bone in the femoral head and help your doctor determine the stage of the disease.
A child with Perthes can expect to have several x-rays taken over the course of treatment, which may be 2 years or longer. As the condition progresses, x-rays often look worse before gradual improvement is seen.
Treatment
The goal of treatment is to relieve painful symptoms, protect the shape of the femoral head, and restore normal hip movement. If left untreated, the femoral head can deform and not fit well within the acetabulum, which can lead to further hip problems in adulthood, such as early onset of arthritis.
There are many treatment options for Perthes disease. Your doctor will consider several factors when developing a treatment plan for your child, including:
Your child’s age. Younger children (age 6 and below) have a greater potential for developing new, healthy bone.
The degree of damage to the femoral head. If more than 50% of the femoral head has been affected by necrosis, the potential for regrowth without deformity is lower.
The stage of disease at the time your child is diagnosed. How far along your child is in the disease process affects which treatment options your doctor will recommend.
Nonsurgical Treatment
Observation. For very young children (those 2 to 6 years old) who show few changes in the femoral head on their initial x-rays, the recommended treatment is usually simple observation. Your doctor will regularly monitor your child using x-rays to make sure the regrowth of the femoral head is on track as the disease runs its course.
Anti-inflammatory medications. Painful symptoms are caused by inflammation of the hip joint. Anti-inflammatory medicines, such as ibuprofen, are used to reduce inflammation, and your doctor may recommend them for several months. As your child progresses through the disease stages, your doctor will adjust the dosage or discontinue the medication.
Limiting activity. Avoiding high-impact activities, such as running and jumping, will help relieve pain and protect the femoral head. On occasion, your doctor may also recommend crutches or a walker to prevent your child from putting too much weight on the joint.
Physical therapy exercises. Hip stiffness is common in children with Perthes disease and physical therapy exercises are recommended to help restore hip joint range of motion. These exercises often focus on hip abduction and internal rotation. Parents or other caregivers are often needed to help the child complete the exercises.
Hip abduction. The child lies on his or her back, keeping knees bent and feet flat. He or she will push the knees out and then squeeze the knees together. Parents should place their hands on the child’s knees to assist with reaching a greater range of motion.
Hip rotation. With the child on his or her back and legs extended out straight, parents should roll the entire leg inward and outward.
Casting and bracing. If range of motion becomes limited or if x-rays or other image scans indicate that a deformity is developing, a cast or brace may be used to keep the head of the femur in its normal position within the acetabulum.
Petrie casts are two long-leg casts with a bar that hold the legs spread apart in a position similar to the letter “A.” Your doctor will most likely apply the initial Petrie cast in an operating room in order to have access to specific equipment.
Arthrogram. During the procedure, your doctor will take a series of special x-ray images called arthrograms to see the degree of deformity of the femoral head and to make sure he or she positions the head accurately. In an arthrogram, a small amount of dye is injected into the hip joint to make the shape of the femoral head even easier to see.
Tenotomy. In some cases, the adductor longus muscle in the groin is very tight and prevents the hip from rotating into the proper position. Your doctor will perform a minor procedure to release this tightness — called a tenotomy — before applying the Petrie casts. During this quick procedure, your doctor uses a thin instrument to make a small incision in the muscle.
After the cast is removed, usually after 4 to 6 weeks, physical therapy exercises are resumed to restore motion in the hips and knees. Your doctor may recommend continued intermittent casting until the hip enters the final stage of the healing process.
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Surgical Treatment
Your doctor may recommend surgery to re-establish the proper alignment of the bones of the hip and to keep the head of the femur deep within the acetabulum until healing is complete. Surgery is most often recommended when:
Your child is older than age 8 at the time of diagnosis. Because the potential for deformity during the reossification stage is greater in older children, preventing damage to femoral head is even more critical.
More than 50% of the femoral head is damaged. Keeping the femoral head within the rounded acetabulum may help the bone grow into a functional shape.
Nonsurgical treatment has not kept the hip in correct position for healing.
The most common surgical procedure for treating Perthes disease is an osteotomy. In this type of procedure, the bone is cut and repositioned to keep the femoral head snug within the acetabulum. This alignment is kept in place with screws and plates, which will be removed after the healed stage of the disease.
In many cases, the femur bone is cut to realign the joint. Sometimes, the socket must also be made deeper because the head of the femur has actually enlarged during the healing process and no longer fits snugly within it. After either procedure, the child is usually placed in a cast for several weeks to protect the alignment.
After the cast is removed, physical therapy will be needed to restore muscle strength and range of motion. Crutches or a walker will be necessary to reduce weightbearing on the affected hip. Your doctor will continue to monitor the hip with x-rays through the final stages of healing.
Outcomes
In most cases, the long-term prognosis for children with Perthes is good and they grow into adulthood without further hip problems.
If there is deformity remaining in the shape of the femoral head, there is more potential for future problems; however, if the deformed head still fits into the acetabulum, problems may be avoided. In cases where the deformed head does not fit well into the acetabulum, hip pain or early onset of arthritis is likely in adulthood.
Differential Diagnosis
Listed are some other disorders that should be included in the differential diagnosis for LCPD: All diseases which induce necrosis of the head or those resembling them are questioned in a differential diagnosis[27] :
Septic arthritis or infectious arthritis: this is an infection of the joint.
Sickle cell-Osteonecrosis of the hip can be a result of this disease
Spondyloepiphyseal Dysplasia Tarda: this disease typically affects the spine and the larger more proximal joints
Gaucher Disease: An autosomal recessive inherited genetic disorder of metabolism in which a dangerous level of a fatty substance called glucocerebroside collects in the liver, spleen, bone marrow, lungs, and at times in the brain
Transient Synovitis of the hip is a self-limiting condition in which there is an inflammation of the inner lining (the synovium) of the capsule of the hip joint.
Hip Labral Disorders: The hip labrum is a dense fibrocartilagenous structure, mostly composed of type 1 collagen that is typically between 2-3mm thick that outlines the acetabular socket and attaches to the bony rim of the acetabulum. Hip labral disorders are pathologies of this structure.
Chondroblastoma: Chondroblastoma refers to a benign bony tumour that is caused by the rapid division of chondroblast cells which are found in the epiphysis of long bones. They have been described as calcified chondromatous giant cell tumours.
Juvenile Rheumatoid Arthritis : a chronic inflammatory disorder that occurs before the age 16 and can occur in all races.
Multiple epiphyseal dysplasia – This is a disorder of cartilage and bone development primarily affecting the ends of the long bones in the arms and legs.
Diagnostic Procedures
A MRI is usually obtained to confirm the diagnosis; however x-rays can also be of use to determine femoral head positioning.
Since LCPD has a variable end result, an imaging modality that can predict outcome at the initial stage of the disease before significant deformity has occurred is ideal.
The extent of femoral head involvement depicted by non-contrast and contrast MRI showed no correlation at the initial stage of LCPD, indicating that they are assessing two different components of the disease process. In the initial stage of LCPD, contrast MRI provided a clearer depiction of the area of involvement.
To quantify femoral head deformity in patients with LCPD novel three dimensional (3D) magnetic resonance imaging (MRI) reconstruction and volume based analysis can be used. The 3D MRI volume ratio method allows accurate quantification and demonstrated small changes (less than 10 percent) of the femoral head deformity in LCPD. This method may serve as a useful tool to evaluate the effects of treatment on femoral head shape.
Outcome Measures
The questionnaires below can be used to assess the initial function of a person and progress and outcome of operative as well as non-operative treatments. The surveys test the patient on a functional level are useful to provide a baseline and monitor functional progress in the patient’s activities.
Lower Extremity Functional Scale.
Harris Hip ScoreThe total score reliability was excellent for physicians (r = 0.94) and physiotherapists (r = 0.95). The physiotherapist and the orthopaedic surgeon showed excellent test–retest reliability in the domains of pain (r = 0.93 and r = 0.98, respectively) and function (r = 0.95 and r = 0.93, respectively). The calculations were done with Pearson’s and Spearman’s correlation coefficients. The inter-rater correlations were good to excellent (0.74–1.0)
Hip Disability and Osteoarthritis Outcome Score (HOOS). The HOOS is suggested to be valuable for younger and more active people due to the subscales.
As for the difference in outcome for non-operative and operative treatments, a meta-analysis performed in 2012 suggests that operative treatment is more likely to yield a spherical congruent femoral head than non-operative methods among six-year-olds or older. For patients who are younger than the age of six, operative and non-operative methods have the same likelihood to yield a good outcome. Children who were six years or older who were treated operatively had the same likelihood of a good radiographic outcome regardless of surgical intervention with a femoral or pelvic procedure. Patients younger than six had a greater benefit from pelvic procedures than femoral procedures.
Examination
Gait
Is usually antalgic. It is possible that the child has a Trendelenburg gait (a positive Trendelenburg sign on the affected side)
The child can also have a Duchenne gait, which is marked by a trunk lean toward the stance limb with the pelvis level or elevated on the unloaded side.
There is insufficient evidence and lack of reliability and validity to support use of the observational gait assessment tools with this population.
Range of movement
The restriction of hip motion is variable in the early stages of the disease. Many patients, may only have a minimal loss of motion at the extremes of internal rotation and abduction. At this stage there usually is no flexion contracture. Loss of hip ROM in patients with early LCPD without intra-articular incongruity is due to pain and muscle spasm. This is why, if the child is examined for instance after a night of bed rest, the range will be much better then later in the day.
Further into the disease process, children with mild disease may maintain a minimal loss of motion at the extremes only and there after regain full mobility. Those with more severe disease will progressively lose motion, in particular abduction and internal rotation. Late cases may have adduction contractures and very limited rotation, but the range of flexion and extension is only seldom compromised.
Pain
Pain occurs during the acute disease. The pain may be located in the groin, anterior hip area, or around the greater trochanter. Referral of pain to the knee is common.
It’s recommended that pain is assessed using the Numerical Rating Scale (NRS).
Atrophy
In most cases there is atrophy of the gluteus, quadriceps and hamstring muscles, depending upon the severity and duration of the disorder.
Medical Management
The approach to treatment is controversial. Prior to evaluating if a surgical intervention is necessary, there has to be a clear understanding of the disease prognosis.
Approaches to treatment can be divided in conservative or operative treatments.
Medications include non-steroidal anti-inflammatories (NSAIDs) for pain and/or inflammation.
Psychological factors are also considered. Persons with a history of LCPD are 1.5 times more likely to develop attention deficit disorders compared to their peers. They also have a higher risk of developing depression.
Physical Therapy Management
There is no consensus concerning the possible benefits of physiotherapy in LCPD, or in which phase of the development of the health problem it should be used.
Some studies mention physiotherapy as a pre- and/or postoperative intervention, while others consider it a form of conservative treatment associated with other treatments, such as skeletal traction, orthesis, and plaster cast.
In studies comparing different treatments, physiotherapy was applied in children with a mild course of the disease. The characteristics of the patients were:
Children with less than 50% femoral head necrosis (Catterall groups 1 or 2)
Children with more than 50% femoral head necrosis, under six years, whose femoral head cover is good (>80%)
Herring type A or B
Salter Thompson type A
For patients with a mild course, physiotherapy can produce improvement in articular range of motion, muscular strength and articular dysfunction. The physiotherapeutic treatment included:
Passive mobilisations for musculature stretching of the involved hip.
Straight leg raise exercises, to strengthen the musculature of the hip involved for the flexion, extension, abduction, and adduction of muscles of the hip.
They started with isometric exercises and after eight session, isotonic exercises.
A balance training initially on stable terrain, and later on unstable terrain.
For children over 6 years at diagnosis with more than 50% of femoral head necrosis, proximal femoral varus osteotomy gave a significantly better outcome than orthosis and physiotherapy.
There is an evidence-based care guideline concerning post-operative management of LCPD in children for age 3 to 12 and an evidence-based care guideline for conservative management of LCPD in children age 3 to 12. These studies are mostly based on ‘local consensus’ of the members of the LCPD team from Cincinnati Children’s Hospital Medical Center. These guidelines express the evidence regarding physical therapy (PT) treatment pathways, post-operatively and conservative management (see appendix 3 about evidence levels) . The following recommendations are made:
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Conservative management
Physical therapy interventions have been shown to improve ROM and strength in this patient population (3).
Individuals who participate in supervised clinic visits demonstrate greater improvement in muscle strength, functional mobility, gait speed, and quality of exercise performance than those who receive a home exercise program alone or no instruction at all (2).
Individuals who receive regular positive feedback from a physical therapist are more likely to be compliant with a supplemental home exercise program. (4)
It is recommended that supervised physical therapy is supplemented with a customized written home exercise program in all phases of rehabilitation. (2)
Improve ROM: (see appendix 1 for exercise prescription)
Static stretch for lower extremity musculature (2)
Dynamic ROM (2)
Perform AROM and AAROM (active assistive range of motion) following passive stretching to maintain newly gained ROM (2)
Improve strength:
Begin with isometric exercise and progress to isotonic exercises in a gravity lessened position with further progression to isotonic exercises against gravity. It is appropriate to include concentric and eccentric contractions (3).
Begin with 2 sets of 10 to 15 repetitions of each exercise (2), with progression to 3 sets of each exercise to be used (2)
Local consensus would also do exercises to improve balance and gait and interventions to reduce pain.
The hip overloading pattern should be avoided in children with LCPD. Gait training to unload the hip might become an integral component of conservative treatment in children with LCPD.
Non-surgical treatment with a brace is a reliable alternative to surgical treatment in LCPD between 6 and 8 years of age at onset with Herring B involvement. However, they could not know whether the good results were influenced by the brace or stemmed from having good prognosis of these patients.
Post-operative management
The rehabilitation is described with reference to the various stages of rehabilitation.
Initial Phase (0-2 weeks post-cast removal)
Goals of the Initial Phase
Minimize pain
Hot pack for relaxation and pain management with stretching (2)
Cryotherapy (5)
Medication for pain (5)
Optimize ROM of hip, knee and ankle (see appendix 1 for exercises)
Passive static stretch (2) (A hot pack may be used, based on patient preference and comfort (2))
Dynamic ROM (2)
Perform AROM and AAROM following passive stretching to maintain newly gained ROM (2)
Increase strength for hip flexion, abduction, and extension and knee and ankle (see appendix 2 for exercises)
Begin with isometric exercises at the hip and progress to isotonic exercises in a gravity lessened position (3)
Begin with isometric exercises at the knee and ankle, progressing to isotonic exercises in a gravity lessened position with further progression to isotonic exercises against gravity (3)
Begin with 2 sets of 10 to 15 repetitions of each exercise with progression to 3 sets of each exercise to be used (2)
Improve gait and functional mobility
Follow the referring physician’s guidelines for WB status (5)
Transfer training and bed mobility to maximize independence with ADL’s (5)
Gait training with the appropriate assistive device, focusing on safety and independence (5).
Improving skin integrity
Scar massage and desensitization to minimize adhesions (5)
Warm bath to improve skin integrity following cast removal, if feasible in the home environment (5)
Warm whirlpool may be utilized if the patient is unable to safely utilize a warm bath for skin integrity management (5)
PT is supervised at a frequency of 2-3 time per week (weekly) (5)
Intermediate Phase (2-6 weeks post-cast removal)
Goals of the Intermediate Phase
Minimize pain (see ‘initial phase’)
Normalize ROM of the knee and ankle and optimize ROM of hip in all directions
See ‘initial phase’ and see appendix 1 for exercises
Increase strength of the knee and hip (see appendix 2 for exercises)
Isotonic exercises of the hip in gravity lessened positions and advancing to against gravity positions (3)
Isotonic exercises of the knee and ankle in gravity lessened and against gravity positions (3)
Maintain independence with functional mobility maintaining WB status and use of appropriate assistive devices (5)
Improving gait and functional mobility (5)
Follow the referring physician’s guidelines for WB status (5)
Continue gait training with the appropriate assistive device focusing on safety and independence (5)
Begin slow walking in chest deep pool water with arms submerged (5)
Improving Skin Integrity
Continue with scar massage and desensitization (5)
PT is supervised at a frequency of 2-3 time per week (weekly) (5)
It is recommended that activities outside of PT are restricted at this time due to WB status. If the referring physician allows, swimming is permitted (5)
Advanced Phase (6-12 weeks post-cast removal)
Goals
Minimize pain (see ‘initial phase’)
optimize ROM and flexibility of the hip, knee, and ankle
see ‘initial phase’ and see appendix 1 for exercises
Increase strength of the knee and hip, except for hip abductors, to at least 70% of the uninvolved lower extremity and increase strength of the hip abductors to at least 60% of the uninvolved lower extremity due to mechanical disadvantage (4 + 5) (see appendix 2 for exercises)
Isotonic exercises of the hip, knee, and ankle in gravity lessened and against gravity positions, including concentric and eccentric contractions (3)
WB and non-weight bearing (NWB) activities can be used in combination based on the patient’s ability (4) and goals of the treatment session (5)
Begin upper extremity supported functional dynamic single limb activities (e.g. step ups, side steps) (5)
Continue with double limb closed chain exercises with resistance, progressing to single limb closed chain exercises with light resistance if WB status allows (5)
Use of a stationary bike in an upright or recumbent position keeping the hip in less than 90 degrees of flexion (5)
Ambulation without use of an assistive device or pain (5)
Negotiate stairs independently using step to pattern with upper extremity (UE) support (5)
Improve balance to greater than 69% of the maximum Pediatric Balance Score (39/56) or single limb stance of the uninvolved side (5)
Improving gait and functional mobility (5)
PT is supervised at a frequency of 1-2 time per week (weekly) (5)
It is recommended that activities outside of PT are limited to swimming if the referring physician allows (5).
Note: Running and jumping activities are restricted at this time (5).
Pre-Functional Phase (12 weeks to 1+ year post-cast removal)
Goals
Minimize pain (see ‘initial phase’)
Optimize ROM and flexibility of the hip, knee, and ankle
Static stretch (2)
Increase strength of the knee and hip, except for hip abductors, to at least 80% of the uninvolved lower extremity and increase strength of the hip abductors to at least 75% of the uninvolved lower extremity due to mechanical disadvantage (4 + 5)
see ‘advanced phase’ and see appendix 1 for exercises
Negotiate stairs independently with reciprocal pattern an upper extremity support (5)
Improve balance to 80% or greater of the maximum Pediatric Balance Score (at least 45/56) or single limb stance of the uninvolved side (5)
Non-painful gait pattern with minimal deficits and normal efficiency (5)
PT is supervised at a frequency of 1-2 time per week (weekly) (5)
It is recommended that activities outside of PT include swimming and bike riding as guided by the referring physician (5).
Note: Running and jumping activities are restricted at this time (5).
Functional phase
Goals
Reduce pain to 1/10 or less (see ‘initial phase’)
Normalizing ROM: Increase ROM to 90% or greater of the uninvolved side for the hip, knee, and ankle, except for hip abduction (5) and Increase hip abduction ROM to 80% or greater due to potential bony block (4)
Static stretch (2)
Normalizing strength: Increase strength of the knee and hip, except for hip abductors, to 90% or greater of the uninvolved lower extremity (5) and Increase strength of the hip abductors to at least 85% of the uninvolved lower extremity due to mechanical disadvantage (4+5)
Progress isotonic exercises of the hip, knee, and ankle and include concentric and eccentric contractions (3).
WB and NWB activities used in combination based on the patient’s ability (4) and goals of the treatment session.
Functional dynamic single limb activities (e.g. step ups, side steps) with upper extremity support as needed for patient safety (5)
Progress single leg closed chain exercises with resistance (4)
Use of a stationary bike in an upright or recumbent position keeping the hip in less than 90 degrees of flexion
Ambulation with a non-painful limp and normal efficiency (5)
Negotiation of stairs independently using a reciprocal pattern without UE support (5)
Improve balance to 90% or greater of the maximum score on the Pediatric Balance Scale (at least 51/56) or single limb stance of the uninvolved side (5) It is recommended that progression to the Functional Phase occur when the physician has determined there is sufficient re-ossification of the femoral head based on radiographs (5). Note: Jumping and other impact activities are still limited and only progressed per instruction from the physician based on healing and progression of the disease process
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Definition/Description
Coxa valga is defined as the femoral neck shaft angle being greater than 139 °
Coxa vara is as a varus deformity of the femoral neck. It is defined as the angle between the neck and shaft of the femur being less than 110 – 120 ° (which is normally between 135 ° – 145 °) in children.
Coxa vara is classified into several subtypes:
Congenital coxa vara, which is present at birth and is caused by an embryonic limb bud abnormality.
Developmental coxa vara occurs as an isolated deformity of the proximal femur. It tends to go unnoticed until walking age is reached, when the deformity results in a leg length difference or abnormal gait pattern.
Acquired coxa vara is caused by an underlying condition such as fibrous dysplasia, rickets, or traumatic proximal femoral epiphyseal plate closure.
Clinically Relevant Anatomy
Congenital coxa vara results in a decrease in metaphyseal bone as a result of abnormal maturation and ossification of proximal femoral chondrocyte. As a result of congenital coxa vara, the inferior medial area of the femoral neck may be fragmented. A progressive varus deformity might also occur in congenital coxa vara as well as excessive growth of the trochanter and shortening of the femoral neck.
A review on the development of coxa vara by Currarino et al showed an association with spondylometaphyseal dysplasia, demonstrating that stimulated corner fractures were present in most instances.
Ashish Ranade et al also showed that a varus position of the neck is believed to prevent hip subluxation associated with femoral lengthening. An associated dysplastic acetabulum can lead to a hip subluxation. In this case study, the acetabulum is abnormal in coxa vara. Acetabular index (AI) and sourcil slope (SS) are significantly different than in the normal acetabulum.
Epidemiology /Etiology
Femoral neck fractures, less than 1 % of all pediatric fractures in children, are associated with a high incidence of complications. The most serious ones with high and long term morbidity being osteonecrosis and coxa vara.
A retrospective study of femoral neck fractures in children show the following complications: 1) avascular necrosis (14.5%) 2) limb shortening in seven (11.3%) 3) coxa vara (8%) and premature epiphysis fusion (8%) 4) coxa valga (3.2%), arthritic changes (3.2%). 5) non-union in one (1.6%)
Premature epiphyseal closure is described as one of the ethiological factors of coxa vara. Incidences of premature physeal closure reported in the literature range from 6 % to 62 %. Another possible explanation for the high occurrence of coxa vara is the loss of reduction after initial fracture reduction of implant failure in unstable fractures. Developmental coxa vara is a rare condition with an incidence of 1 in 25 000 live births. Incidence of coxa vara can be decreased by using internal fixation such as pins or screws.
Characteristics/Clinical Presentation
Clinically, the condition presents itself as an abnormal, but painless gait pattern. A Trendelenburg limp is sometimes associated with unilateral coxa vara and a waddling gait is often seen when bilateral coxa vara is present. Patients with coxa vara often show:
Limb length discrepancy
Prominent greater trochanter
Limitation of abduction and internal rotation of the hip.
Patients may also show femoral retroversion or decreased anteversion.
Diagnostic Procedures
Radiography (AP view of the pelvis) can be utilised to determine the HEA (Hilgenreiner Epiphyseal Angle). Signs to look out for are as follows:
The neck; shaft angle is less than 110 – 120°.
The greater trochanter may be elevated above the femoral head.
A growth plate with an overly vertical orientation.
MRI can be used to visualise the epiphyseal plate, which may be widened in coxa vara. CT can be used to determine the degree of femoral anteversion or retroversion.
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Examination
AP radiographs in standing are taken, usually of both hips in a neutral position. Measuremenst are then taken: the Acetabular Index and the Sourcil Slope (the angle formed by a line joining the 2 ends of the sourcil with the horizontal line). Subluxation in children is measured by the Migration Index and the Centre edge Angle.
Medical Management
The objective of medical interventions is to restore the neck-shaft angle and realigning the epiphysial plate to decrease shear forces and promote ossification of the femoral neck defect. This is achieved by performing a valgus osteotomy, with the valgus position of the femoral neck improving the action of the gluteus muscles, normalising the femoral neck angle, increasing total limb length and improving the joint congruence.
The following are indications for surgical intervention:
Neck: shaft angle less than 90 °.
Progressive development of deformity.
Vertical physis and a significant limb.
Other indications are based on the HE angle;
HE angle > 60 ° is an indication for surgery.
HE angle 45 – 60 ° warrants close follow up.
HE angle < 45 ° warrants spontaneous resolution
Except when the neck/shaft angle is less than 110°, progression of the varus angulation takes place, gait pattern abnormalties or degenerative changes take place.
Physical Therapy Management
Literature is lacking, but surgical management appears to be the accepted treatment protocol for this condition.
Clinical Bottom Line
Due to the low incidence of coxa vara and even lower for coxa valga, there is little literature currently available. There are 3 types Coxa Vara, acquired, congenital and developmental, usually displaying greater acetabular dysplasia and an abnormal acetabulum. Surgery is the most effective treatment protocol. In the case of acquired coxa vara from a fracture, the proximal femur and femoral neck need accurate reduction and rigid fixation to avoid potential serious complications.
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When viewed from the side, a normal spine stands upright and curves slightly inward near the top, then outward, then inward again near the bottom. This “S” shape enables the spine to provide excellent support and balance to the body while also offering shock absorption to distribute the force of everyday activities like walking.
Spinal deformity is an abnormal alignment or curve of the bony vertebral column. Adult scoliosis and kyphosis can be caused by age-related wear and tear on the back or complications from past surgeries. Moderate deformity occurs when the facet joints and discs deteriorate over time and are no longer able to support the spine’s normal posture. Pain results from stressed joints and pinched nerves, not the abnormal curve. Treatment can include medications, physical therapy, injections, or surgery.
Anatomy of the spine
The spine is a column of 24 moveable bones called vertebrae that are connected to one another by ligaments. The bones are separated by discs, which act as shock absorbers and give the spine flexibility. Each vertebra has a three-joint complex with a large disc in the front and two facet (pronounced fah-CETTE) joints in the back. This strong, tripod design keeps the bones connected and aligned, one on top of the other, while allowing our spine to bend and twist.
Figure 1. Front and side views of the body show normal alignment of the spine bones and the natural curves.
When viewed from the front the spine is perfectly straight, but from the side it has three curves (Fig. 1). This curvature absorbs the shock of footsteps and positions our head naturally over the pelvis and hip. At the neck, or cervical level, the normal spine arches slightly inward toward the jaw in a curvature called lordosis. The spine arches out slightly at the chest level (kyphosis), and it curves inward again (lordosis) at lumbar level, or lower back.
What is spinal deformity?
Spinal alignment and curvature can be altered in many ways. They can occur as a result of a birth defect, a child’s growth, aging, injury, or previous spine surgery. The most common type of spinal deformity in adults is degenerative scoliosis.
Figure 2. Types of spinal deformities: a side-to-side curve is called scoliosis; a forward curve (kyphosis) shifts the center of balance in front of the hip; a concave lower back (lordosis) thrusts the hips forward.
Scoliosis
Scoliosis is a side-to-side curvature of the spine that can develop in adults when their facet joints and discs begin to deteriorate (Fig. 2). The facet joints give the spine flexibility, enabling us to twist, stretch, or curl up on the couch. When these joints deteriorate, the spine bones can tilt and begin to shift to one side.
Kyphosis
Kyphosis is an abnormal forward rounding (more than 50 degrees of curvature) of the spine. In the upper (thoracic) back, kyphosis is commonly due to osteoporotic compression fractures. It can also occur in the lower (lumbar) spine. It limits function and results in a common complaint among older people: “I can’t stand up straight.” Another common scenario is a patient who has previously had one or more spine surgeries. These patients can develop what is called “flat back syndrome,” which means they have lost some of the natural lordosis (inward curvature) of their lower spine. A patient who has had a previous lumbar fusion may develop a junctional kyphosis. In this situation, the spine has weakened right above the fusion, causing the patient’s posture to bend forward.
Lordosis
Also called swayback, lordosis is a condition in which the spine curves significantly inward at the lower back, giving a backward leaning appearance.
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causes
As you get older, your bones undergo degenerative changes that are part of the natural aging process. When joints deteriorate, arthritis can develop and the spinal column can shift sideways. Other conditions that might cause degeneration include:
Arthritis from degenerative discs and facet joint syndrome, resulting in the loss of normal vertebral alignment (Fig. 3).
Osteoporosis (loss of bone mass) and vertebral compression fractures.
Previous spine surgery (adjacent level disease). The passage of time after a spine surgery is a leading cause of spinal deformity.
The aging of joints, combined with a fracture at a level above a previous fusion, can also cause a significant deformity. Simply removing material from the spine can cause a problem down the road. It may reduce or eliminate pain in the near term, but symptoms can return later because of instability of the spine. Think of the game, Jenga. When you remove a block from the tower, other blocks can be affected. Like the Jenga tower, what goes on globally in the spinal balance and pathology is important.
The spine can become deformed for many reasons, including damage to the vertebrae or intervertebral discs and disease processes like osteoporosis. A person also can be born with an abnormally curved spine (called a congenital spinal deformity) due to a malfunction of the genes that regulate spinal development in the embryo. In some cases, spine abnormalities show up later as the child grows and develops. Despite this genetic link, researchers have not established a single inherited trait that makes a person more susceptible to being born with a deformed spine.
Both males and females may be born with a spinal deformity, and older adults are at higher risk of developing a deformed spine due to medical conditions or wear-and-tear.
In some cases, a spinal deformity is deemed “idiopathic,” which means no cause can be identified.
Some of the more common causes of spinal deformity are:
Accidents, such as falls, that result in spinal fracture (one or more vertebrae)
Genetic defects that lead to abnormal spine development such as fused vertebral segments
Infectious diseases like spinal tuberculosis that destroy the bones and other structures of the spine
Inflammatory diseases, such as arthritis, which can cause bone spurs to develop and push the vertebrae out of alignment
Neuromuscular diseases like muscular dystrophy that lead to weakness in the muscles that support the spine
Osteoporosis, which can cause the vertebrae to collapse and result in a hunched back
Poor posture including poor body mechanics when lifting, which can displace vertebrae or spinal discs
symptoms
Scoliosis is not a single disease. It falls along a spectrum, from mild to moderate to severe. Symptoms include pain or stiffness in the mid-to-lower back, and numbness or weakness in the legs or feet. Not all adults with degenerative scoliosis experience pain. When pain does occur, a pinched nerve is typically the cause, not the curvature.
In more severe cases, scoliosis can cause shooting pain down the leg (sciatica), an inability to stand up straight, and an inability to walk more than a short distance. Symptoms of severe, progressive scoliosis are similar to those of stenosis, but with visible spinal imbalance. This imbalance can result in strain on the hips and knees, the inability to walk a straight line, and falls.
Patients with kyphosis have lost their ability to stand up straight. Hunched over while standing, they may become quickly fatigued and have difficulty talking to others or maintaining eye contact. They also may have difficulty lying flat.
The signs and symptoms of a spinal deformity depend on the severity and location of the abnormal spine segment. Many types of spinal deformity do not cause any symptoms beyond a visible abnormality of the spine’s alignment.
Common symptoms of spinal deformity
The most common possible symptoms of any type of spinal deformity are:
Loss of sensation in the extremities
Pain to any degree
Visible misalignment of the spine, either when viewed with the naked eye or on an X-ray film
Weakness of the legs or arms
Because some types of spinal deformity can occur due to a coexisting condition like muscular dystrophy, you should seek prompt medical attention for any type of spine symptoms. Early diagnosis and treatment offers the best hope for correcting spinal misalignment because the misalignment is easier to correct in the initial stages.
diagnosis
Diagnostic tests include a physician examination, x-rays, CT scan, MRI, or myelogram.
X-rays create images of the bones in your spine and show whether any of them are too close together or whether you have arthritic changes, bone spurs, fractures, or slippage of the vertebrae. Special flexion and extension x-rays will be taken to measure misalignment of the bones and curve progression (Fig. 4).
Computed Tomography (CT) scan is a noninvasive test that uses an x-ray beam and a computer to make 2-dimensional images of your spine. It may or may not be performed with a dye (contrast agent) injected into your bloodstream. It is useful for viewing changes in bony structures.
Magnetic resonance imaging (MRI) scan is a noninvasive test that uses a magnetic field and radiofrequency waves to give a detailed view of the soft tissues of your spine. Unlike an x-ray, nerves and discs are clearly visible. It may or may not be performed with a dye (contrast agent) injected into your bloodstream. MRI is useful in evaluating soft-tissue damage to the ligaments and discs, and assessing spinal cord injury.
Myelogram is a specialized X-ray where contrast dye is injected into the spinal canal. A fluoroscope then records the images formed by the dye. Myelograms can show a nerve being pinched by a disc, bony overgrowth or stenosis. The dye gives a picture of the spinal canal, spinal cord, and nerves in detail. A CT scan follows the test.
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risk factors
The most common risk factors include:
Activities or occupations with a higher-than-average exposure to spinal injury
Younger and older age. Young children may be more susceptible to such diseases as spinal tuberculosis that can lead to a spinal deformity, while older adults are at higher risk for spinal deformity due to such conditions as osteoporosis.
Female gender for some types of spinal deformity such as spondylolisthesis
Inadequate calcium or vitamin D levels leading to bone loss
Personal history of neuromuscular or inflammatory disease processes
Poor body mechanics when lifting
Sedentary lifestyle
Reducing your risk of spinal deformity
You may be able to lower your risk of developing a spinal deformity by:
Avoiding contact sports or other activities that expose you to a risk of back injury
Exercising regularly including strength training to maintain good bone health and muscle mass
Taking calcium or Vitamin D, if your doctor advises it to avoid osteoporosis
Using good body mechanics when sitting, lifting or standing
If you suspect a spinal misalignment in your child, your pediatrician can perform a spinal screening and refer you to an orthopedic spine specialist if necessary. Many spinal deformities respond well to early treatment in children. Adults with multiple risk factors for spinal deformity should discuss with their doctor how to reduce their risk or treat any symptoms that arise.
potential complications of a spinal deformity
A mild spinal deformity may cause no complications at all, while a serious deformity could lead to paralysis. A deformed spine can also press on other organs, such as the lungs. The types and degrees of complications depend greatly on the cause, severity and location of the spinal deformity.
Potential complications of spinal deformity include:
Difficulty breathing due to severe curvature of the mid-back (kyphosis)
Inability to perform activities of daily living, such as walking or dressing, due to postural problems from a curved spine
Loss of sensation in the legs, incontinence, or reduced sexual function due to nerve compression in the lower back
Pain due to compressed spinal nerves or muscle spasms
All types of spinal deformity should be monitored by a doctor in order to slow or avoid progression of the abnormal curvature and retain motor functions in the limbs.
treatments
Treatment for mild to moderate spine deformity in adults is determined by the severity of the symptoms, not the size of the curve. It begins with a trial period of pain management, physical therapy, and nonsurgical options. If pain is caused by inflammation of the facet joints, treatment involves facet joint therapy. If the curvature is mild, the deformity is not treated. If the curvature is severe, complex spinal surgery may be recommended. Barring serious “red flags,” such as a neurologic impairment, conservative care is used for 3 to 6 months before surgery is considered.
Self care: Using correct posture and keeping your spine in alignment are the most important things you can do for your back. The lower back (lumbar curve) bears most of your weight, so proper alignment of this section can prevent injury to your vertebrae and discs. You may need to make adjustments to your daily standing, sitting, and sleeping habits. You may also need to learn proper ways to lift and bend. If you smoke or are overweight, you may be able to reduce your symptoms by quitting smoking and/or achieving a healthy weight appropriate for your body frame.
Bone density: Because good bone density reduces the risk of fractures in aging adults, you may be asked to undergo a bone-density scan to determine the strength of your bones. If osteoporosis is detected, your risk of a fracture to your spine is increased because your bones have weakened and become more brittle. Your doctor may prescribe a medication that slows bone loss.
Physical therapy
Exercise and strengthening exercises are key elements to your treatment and should become part of your life-long fitness. Physical therapists can instruct you on proper lifting and walking techniques, and they will work with you to strengthen your back, leg, and stomach muscles. They will also encourage you to stretch and increase the flexibility of your spine and legs. Check with your doctor before you begin any new exercise program and be sure to see a physical therapist who specializes in spine rehabilitation.
Medication: Over-the-counter and prescription medications can help you cope with back pain.
Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, naproxen (Aleve, Naprosyn), and ibuprofen (Motrin, Nuprin, Advil) are used to reduce inflammation and relieve pain.
Analgesics, such as acetaminophen (Tylenol), can relieve pain but do not have the anti-inflammatory effects of NSAIDs. Long-term use of analgesics and NSAIDs may cause stomach ulcers as well as kidney and liver problems.
Steroids reduce the swelling and inflammation of the nerves. They are taken orally (as a Medrol dose pack) in a tapering dosage over a 5-day period. They have the advantage of providing pain relief within a 24-hour period.
Epidural steroid injection (ESI): This minimally invasive procedure involves an injection of corticosteroid and an analgesic-numbing agent into the epidural space of the spine to reduce the swelling of the spinal nerves. Many patients have some relief after an ESI, although the results tend to be temporary. If injections are helpful, they can be repeated.
Facet injection: This minimally invasive procedure involves an injection of corticosteroid and an analgesic-numbing agent into the painful facet joint.
Bracing: Wearing a brace is often used for childhood scoliosis, but it will not straighten the adult spine. A brace may help reduce pain in the short-term, but it also will allow the muscles to get weaker, eventually leading to more back pain.
Chiropractic care: Chiropractors apply pressure to an area to align bones and return joints to a more normal motion. Patients with spinal deformity might benefit from tissue massage for a muscle spasm, traction for a pinched nerve, or ultrasound for tight muscles. Dry needling or acupuncture might also prove helpful. But most patients with spinal deformity are not candidates for a high-velocity spinal adjustment (a back crack). Such adjustments (by x-ray criteria) do not result in a measureable change of spinal alignment. Anyone with a major spinal deformity who is considering chiropractic treatment should consult with a neurosurgeon first to determine whether it is safe.
Surgery: Surgical options vary depending on the severity of the symptoms, the number of levels affected, and the type of deformity. A combination of different fusion and instrumentation techniques are used to treat the patient’s specific condition.
Decompression: If the scoliosis is mild and is causing a pinched nerve at one level, only that level is treated with a laminectomy.
Fusion: A patient suffering from foraminal stenosis and scoliosis usually requires a fusion to restore disc height when a vertebra has collapsed on a nerve. Fusion makes the vertebrae square in relation to each other and restores proper alignment. It involves joining two vertebrae with a bone graft (Fig. 5), which is held together with hardware that could include plates, rods, hooks, pedicle screws, or cages. The goal of the bone graft is to join the vertebrae above and below to form one solid piece of bone. Creating a solid fusion may take several months or longer.
Minimally invasive fusion: A lateral lumbar interbody fusion (LLIF) surgery is an option for some patients with scoliosis (Fig. 6). The surgeon operates through a tube incision at the waist and avoids cutting the back muscles.
Spinal reconstruction: Complex deformities and kyphosis often require the cutting of bone (osteotomy) and stabilization with long rods and screws in staged operations.
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The term ‘floating’ has been used quite vaguely in the literature to describe various injury patterns /surgical procedures and even congenital anomalies. When the term is used to describe an injury pattern, it commonly implies that a joint/bone has lost its continuity at adjacent ends either as a result of fractures, fracture dislocations or pure dislocations and hence has become ‘floating’
Blake and McBryde initially described this injury. Floating knee is a flail knee joint resulting from fractures of the shafts or adjacent metaphyses of the femur and ipsilateral tibia. Floating knee injuries may include a combination of diaphyseal, metaphyseal, and intra-articular fractures.
The fractures range from simple diaphyseal to complex articular types. This complex injury has increased in proportion to population growth, number of motor vehicles on the road, and high speed traffic. Although the exact incidence of the floating knee is not known, it is an uncommon injury.
Epidemiology
Most of the patients are in their third decade
Preponderance of males.
Etiology
Road traffic accident (RTA) accounts for majority of the cases and this is followed by fall from height (FFH)
Presentation
The ‘floating knee’ is a serious injury.
Floating knee injuries must be included in assessment and treatment protocols for patients with polytrauma.
Damage to the vessels (mainly the popliteal and posterior tibial arteries) and lesions of the nerves (eg, peroneal nerve) are common. Vascular injury is common and may be limb threatening if not recognized and addressed. Often, the vascular injury is to the anterior tibial artery and does not result in ischemia and is not treated with vascular repair or reconstruction. However, vascular status needs to be assessed and addressed as appropriate. Traction usually causes neurapraxia, which often resolves, but complete resolution cannot always be anticipated.
The incidence of open fractures is high, approaching 50-70%, at 1 or both fracture sites. The most common combination is a closed femoral fracture with an open tibial fracture.
Simultaneous skeletal disruption of two strong bones of the body almost always occurs following high-velocity impact. The ipsilateral femoral and tibial shaft fractures and knee ligament injury appear to be part of a continuum of combined injuries resulting from complex, high-energy forces. The most common pattern is an open tibia and closed femur fracture.
This injury may be associated with multiple remote organ damage that may range from head injury to foot fractures.
The soft tissue trauma is usually immense and most of the patients are hemodynamically compromised.
A well-documented finding is injury to the knee ligaments that occur in association with ipsilateral femoral and tibial fractures. Anterolateral rotatory instability is the most common pattern of instability. Knee ligament injury is not always suspected, and joint swelling due to hemarthrosis should not be mistaken for a sympathetic effusion.
In skeletally immature patients, floating knee is uncommon. Few studies of this injury have been conducted in children. Data from available studies show that findings observed in children are comparable to those in adults in terms of the mechanism of fracture, the incidence of associated major injuries, and the complexity of treatment.
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Complications
Epiphyseal injury can adversely affect open growth plates, predisposing a child to limb-length discrepancy and angular deformities.
Rates of infection, nonunion, malunion, and stiffness of the knee are relatively high. These complications can lead to functional impairment and frequently cause unsatisfactory results.
Management
Early reports favored a non-operative regime. Floating knee is a complex multisystem injury and soft tissue damage to the affected limb is extensive. The need for early mobilization was recognized, but the fixation techniques did not provide the desired stability to do so predictably. The surgeons preferred life over limb.
The current recommendation for floating knee is surgical stabilization of both the fractures. There are a number of methods to do this and there is no single ideal technique.The surgical sequence should be individualized for each patient and each fracture should be addressed according to its personality.The chosen method depends on the fracture pattern, location of the fractures, the soft tissue injury, available resources, surgical capability and preference. The impact of the osteosynthesis technique on the overall physiology of the patient should be kept in mind.
Rehabilitation
After surgical stabilization of the fractures, the knee should be examined for range of motion and stability.
Collateral ligament laxity is best managed by bracing for 6 weeks.
Reconstruction of the injured ligaments is usually delayed until adequate rehabilitation of the skeletal injury.
The patient should have regained a good range of knee movement.
Adequate pain control in the early postoperative phase by an epidural catheter or systemic opioid infusion is mandatory.
Weight bearing is delayed in Type I pattern till callus is visible on the radiograph.
In Type II variants, weight bearing is permitted only after 10 weeks to guard against subsidence of the articular fragments. Regardless of the injury pattern, the probability of optimum outcome is dependent on early mobilization of the knee. This is even more imperative with an intra-articular fracture.
The benefit of early motion on cartilage and periarticular tissues health is well documented in the literature. Salter’s work was pioneering in this field
Conclusion
Floating knee injury is an indicator of severe trauma. Damage to remote organs should be suspected and systematically sought for. Following standardized resuscitation protocols, early stabilization of the fractures and aggressive postoperative rehabilitation offer the best chance of an optimum outcome.
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Femoral neck fractures and peritrochanteric fractures are equally prevalent and make up over 90 percent of proximal femur fractures.
The femoral neck is the most common location for a hip fracture. Your hip is a ball and socket joint where your upper leg meets your pelvis. At the top of your femur (which is your thigh bone) is the femoral head. This is the “ball” that sits in the socket. Just below the femoral head is the femoral neck.
Femoral neck fractures are intracapsular fractures. The capsule is the area that contains the fluid that lubricates and nourishes the hip joint. Fractures in this area are categorized based on the location of the fracture along the femoral neck:
subcapital is the femoral head and neck junction
transcervical is the mid portion of femoral neck
basicervical is the base of femoral neck
Though anyone can fracture their femoral neck, it’s considerably more common in elderly adults who have poor bone density. More than 90 percent Trusted Source of these fractures occur in people older than 50. They are more common in women.
A femoral neck fracture can tear the blood vessels and cut off the blood supply to the femoral head. If the blood supply to the femoral head is lost, the bone tissue will die (a process called avascular necrosis), leading to the eventual collapse of the bone. Fractures that occur in places where the blood supply is not disrupted have a better chance of healing.
For these reasons, treatment for an elderly patient with displaced femoral fractures will depend upon the location of the break and the quality of the blood supply.
The standard of care for a displaced fracture where the blood supply is disrupted involves replacing the femoral head (hemiarthroplasty or a total hip arthroplasty). If there’s no displacement, then surgically stabilizing the fracture with screws or other hardware may be done. However, there’s still the risk that the blood supply may be disrupted.
fractured neck of femur (broken hip) is a serious injury, especially in older people. It is likely to be life changing and for some people life threatening. It occurs when the top part of the femur (leg bone) is broken, just below the ball and socket joint.
types
There are two main types of hip fracture, intracapsular and extracapsular.
Intracapsular Fracture
In this injury the ball on the top of the femur has broken off at its junction with the neck of the upper thigh bone, within the hip joint.
Occasionally, it is possible to re-attach the ball, but it is usually removed and replaced with half a hip replacement (called a hip hemiarthroplasty) or a total hip replacement, if appropriate.
Extracapsular Fracture
This break is further down the femur, outside the hip joint and is fixed using metal work. The surgeon will explain which type of fracture you have.
causes
Trauma is the most common cause of femoral neck fractures. Being over the age of 50 or having a medical condition that weakens your bones, such as osteoporosis, increases your risk of a fracture in the femoral neck. Having bone cancer is also a risk factor.
Falls are the most common cause of femoral neck fractures in older adults. In younger people, these fractures most often result from high-energy trauma, such as a vehicle collision or fall from a great height.
Femoral neck fractures are rare in children. Along with high-energy trauma, they can also be caused by low bone mineral density, such as osteopenia or osteoporosis, or by other conditions like cerebral palsy or muscular dystrophy.
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Femoral neck fracture symptoms
The most common symptom of a femoral neck fracture is pain in the groin that gets worse when you put weight on the hip or try to rotate the hip. If your bone is weakened by osteoporosis, cancer, or another medical condition, you might experience groin pain leading up to the time of the fracture.
With a femoral neck fracture, your leg may appear shorter than your uninjured leg, or your leg may be externally rotated with your foot and knee turned outward.
Diagnosing a hip fracture
Often your doctor can determine that you have a hip fracture based on your symptoms and the abnormal position of your hip and leg. An X-ray usually will confirm that you have a fracture and show where the fracture is.
If your X-ray doesn’t show a fracture but you still have hip pain, your doctor might order an MRI or bone scan to look for a hairline fracture.
Most hip fractures occur in one of two locations on the long bone that extends from your pelvis to your knee (femur):
The femoral neck. This area is situated in the upper portion of your femur, just below the ball part (femoral head) of the ball-and-socket joint.
The intertrochanteric region. This region is a little farther down from the hip joint, in the portion of your upper femur that juts outward.
A doctor can usually determine if you have a hip fracture based on the position of your hip and leg, along with your symptoms. After a physical examination, your doctor will use an X-ray to confirm you have a fracture and determine which part of the hip is affected.
Small hairline fractures or incomplete fractures may not show up on an X-ray. If your fracture can’t be seen in the images and you still have symptoms, your doctor may recommend a CT scan, or an MRI or bone scan for a more detailed look.
Treatment
Treatment for hip fracture usually involves a combination of surgery, rehabilitation and medication.
Surgery
The type of surgery you have generally depends on the where and how severe the fracture is, whether the broken bones aren’t properly aligned (displaced), and your age and underlying health conditions. The options include:
Internal repair using screws. Metal screws are inserted into the bone to hold it together while the fracture heals. Sometimes screws are attached to a metal plate that runs down the femur.
Total hip replacement. Your upper femur and the socket in your pelvic bone are replaced with artificial parts (prostheses). Increasingly, studies show total hip replacement to be more cost-effective and associated with better long-term outcomes in otherwise healthy adults who live independently.
Partial hip replacement. If the ends of the broken bone are displaced or damaged, your surgeon might remove the head and neck of the femur and install a metal replacement. Partial hip replacement might be recommended for adults who have other health conditions or cognitive impairment or who no longer live independently.
Your doctor might recommend partial or total hip replacement if the blood supply to the ball part of your hip joint was damaged during the fracture. That type of injury, which occurs most often in older people with femoral neck fractures, means the bone is less likely to heal properly.
Rehabilitation
Your care team will likely get you out of bed and moving on the first day after surgery. Physical therapy will initially focus on range-of-motion and strengthening exercises. Depending on the type of surgery you had and whether you have help at home, you might need to go from the hospital to an extended care facility.
In extended care and at home, you might work with an occupational therapist to learn techniques for independence in daily life, such as using the toilet, bathing, dressing and cooking. Your occupational therapist will determine if a walker or wheelchair might help you regain mobility and independence
Treating a femoral neck fracture
Treatment of femoral neck fractures usually involves surgery, medication, and rehabilitation.
Pain medication provides short-term relief from pain. This may include over-the-counter (OTC) pain medication, such as nonsteroidal anti-inflammatory drugs (NSAIDs), or prescription drugs, such as opioids.
Your doctor may prescribe bisphosphonates and other osteoporosis medications to help reduce your risk of another hip fracture, depending on your age. These medications help strengthen your bones by increasing your bone density.
Emergency surgery is usually recommended for hip fractures to relieve pain and restore mobility as soon as possible. There are different types of surgery used to treat femoral neck fractures. The type of surgery required will depend on the severity of your fracture, your age, and underlying medical conditions.
Whether your fracture has caused damage to the blood supply to your femoral head will also help determine which type of surgery will be needed.
Internal fixation
Internal fixation uses metal pins or screws to hold your bone together so the fracture can heal. The pins or screws are inserted into your bone, or the screws may be attached to a metal plate that runs along your femur.
Partial hip replacement
This procedure is used if the end of the bones is damaged or displaced. It involves removing the head and neck of the femur and replacing it with a metal prosthesis.
Partial hip replacement may also be recommended for adults with other serious medical conditions, rather than a total hip replacement.
Total hip replacement
Total hip replacement involves replacing your upper femur and socket with a prosthesis. Based on research, this type of surgery has the best long-term outcomes in otherwise healthy people who live independently. It’s also the most cost-effective because it often eliminates the need for more surgery later on.
Femoral neck fracture recovery time
How long it takes you to recover from a femoral neck fracture will depend on the severity of your fracture, your overall state of health, and the type of surgery used. Recovery varies from person to person.
Rehabilitation will be required once you’re discharged from the hospital. Depending on your age and condition, you may be sent home or to a rehabilitation facility.
You’ll need physical therapy to help you regain your strength and ability to walk. This can take up to three months. Most people who have hip surgery to repair a fracture regain most, if not all of their mobility following treatment.
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