Induced Hypertension complicates approximately 7% of pregnancies in the
US annually and is normally found in the second half of pregnancy. PIH
is the occurrence of hypertension, proteinuria, and edema, and eclampsia.
PIH can range from mild to severe. Complications of pregnancy that
likely increase the chances of PIH include diabetes, multiple gestation
and persistent hypertension.
The short of what happens is
For some reason Vasospasms start
in your body. The blood vessels start to act like a muscle relaxing
and contracting. Like opening and closing your fist. As blood
is passed through these relaxing and contracting veins it causes damage
to a special lining that is found in the veins. As this damage occurs
to your red blood cells your platelets come to the rescue to try
and heal the damage. In the process they create clots over the damage.
Those clots get bigger and bigger and begin to stress your body as it try's
to push the blood past this damage.
Your body tries to make up for
the damage red blood cells, which causes your veins to become 'leaky' by
increasing your body's water volume. Your kidneys start to hold on
to more water resulting in low urine output. Swelling come from those
leaky veins. The decreased blood flow only adds further strain to your
heart, lungs, brain, kidneys and liver.
In HELLP the liver is mainly affected.
It is deprived of Oxygen because the the clots. It begins to die. This
begins the rise in Liver Enzymes or the pain that is often misdiagnosed
as Heartburn or feeling "Flu-y".
Of course these Vasospasm that
cause damage also cause damage to the vessels in and out of the Placenta.
The stress causes IUGR.
Now for the longer version:
is a variant of Pre-eclampsia. HELLP
stands for Hemolysis, Elevated liver, Low platelet. HELLP occurs
in approximately 0.2 to 0.6 of all pregnancies. It occurs in 4 to
12% of all women with pre-eclampsia, eclampsia or PIH. In 11% of
patients it occurs before 27 weeks gestation. It presents in 69%
of patients antepartume and 31% of patients postpartum occuring within
48 hours but can occur up to 7 days. The mortality rate on HELLP
is 1.1 - 2% percent. In some case studies it has been noted to be
as high as 33%*. *http://www.imbiomed.com.mx/Medcrit/Tiv11n1/english/Zti71-1.html
Infant Mortality rates range from
20%-25% depending on the severity of HELLP in the mother. Some case
studies have noted to be as high as 60% - http://www.ahima.org/journal/coding/coding.9709.2.html
The main causes are abruption of
the placenta, intrauterine asphyxia, and prematurity.
is not an entity separate from PIH but a group of sign diagnostic of the
disease. HELLP syndrome may also involve Disseminated
Intravascular Coagulation. It is theorized that all patients
who develope HELLP have an underlying coagulopathy that is usually undetectable.
In some reported cases of HELLP
pre-eclampsia was absent or mild. Women with HELLP
are often critically ill. Their infants are frequently premature with compromised
conditions. Maternal mortality related to the disease is prevalent around
the world. Higher incidences of still birth and fetal growth retardation
(IUGR) are apparent. Some have estimated that the maternal mortality has
been estimated to be as high as 24% in cases of HELLP
where there are other complications. Women with HELLP
are also at greater risk of pulmonary edema, adult Respitory Distress Syndrome,
abruptio placenta, disseminated intravascular coagulation, ruptured liver
hematomas, and acute renal failure.
The reason why PIH/HELLP
occurs isn’t fully understood yet. New research suggests that it starts
with a failure in the placenta not being as well developed as it should
be, with thinning of the blood vessels from mother’s side that invade the
placenta as it grows. These changes begin as early as 18-20 weeks, even
in the (usual) women who don't develop pre-eclampsia until toward the end
of pregnancy. There are also blood clots blocking off the arteries in the
placenta, reducing the amount of blood getting across to the baby. This
explains the common finding of a smaller than expected baby in women who
Gestational thrombocytopenia is
expierenced by some women during and after pregnancy. The platelet
lifespan is theorized to be shorter during pregnancy. Some of the
other maternal blood disorders that can come up are or are confused with
The difference between TTP (thrombotic
thrombocytopenic purpura), ITP (Idiopathic Thrombocytopenic Purpura), HUS
(hemolytic uremic syndrome) and HELLP.
systemic lupus erythematosus (SLE)
antiphospholipid antibody syndrome
thrombotic thrombocytopenic purpura
idiopathic thrombocytopenic purpura
hemolytic uremic syndrome (HUS)
acute fatty liver of pregnancy
In my non medical opinion the main
difference is in how the platelets are destroyed that leads to what the
disorder is. When the Dr. looks under a microscope at your blood
and runs the liver tests they will be able to determine the problem.
It's how the platelets are damaged, destroyed and consumed that guide them
in the diagnosis.
ITP, TTP & HUS can affect a women
at any time, mainly during her childbearing years. HELLP only affects
those pregnant or just post partum.
HELLP is also usually the only one
of these blood disorders that affects the liver.
The effects on the kidneys is usually
minimal in HELLP but mild to sever in TTP & HUS. Renal failure
is often associated with HUS.
HUS usually affects infants and children
and may occur following delivery in a woman.
All three have in common thrombocytopenia
and features of microangiopathic hemolysis, including anemia & increased
Most HELLP patients present with some
of the following symptoms - epigastric or right upper quadrant pain, malaise,
nausea and/or vomiting, headache, flu-like symptoms, abdominal tenderness,
elevated blood pressure & edema.
Getting to the more
Medical side of HELLP
Hemolysis: significantly decreased
erythrocyte life span
The hemolysis in HELLP syndrome
is a microangiopathic hemolytic anemia (Consequence of disseminated
intravascular coagulation (DIC): fragments of red blood cells, damaged
by being forced through a fibrin meshwork, are found in the circulation).
The red blood cells are unable to live for their normal 120 day span.
Hemolytic anemias are usually due to defects in the red blood cells structure/function
or a hostile external enviornment which they are forced to live.
When red blood cell production is unable to keep up with the red blood
cell destruction anemia results.
FYI - There is extravascular hemolysis
(in tissues and organs) and intravascular hemoysis (in the blood)
Endothelial damage is what
results from the arteriolar (The smallest divisions of the arteries located
between the muscular arteries and the capillaries) spasm that accompanies
Development of hemolytic anemia
accompanied by unusual erythrocyte (red blood cell) morphology and consumption
of platelets and other coagulation factors occurs more commonly.
Red blood cells become fragmented
as they pass through small blood vessels with endothelial damage
(The layer of epithelial cells that lines the cavities of the heart and
of the blood and lymph vessels and the serous cavities of the body, originating
from the mesoderm-It is permeable to water- It transports a little bit
of blood protein- It can contract to regulate flow -Damage is measured
in how a vessel relaxs in response to a shear stress) and fibrin
(insoluble protein formed from fibrinogen by the proteolytic action of
thrombin during normal clotting of blood. Fibrin forms the essential
portion of the blood clot) deposits.
The peripheral smear (view of your
blood under a microscope) may reveal spherocytes, schistocytes, triangular
cells and burr cells when HELLP is diagnosed. This is a way for your
Dr. to diagnose whether microangiopathic hemolytic anemia
is present. For
more information on your red blood cells click here.
The body will generally react to
the loss of RBC (red blood cells). It reacts by adding more water
to the circulation of blood. The body causes the kidneys to hold
more water that is ingested by you. That is why during HELLP you
see the decreased urine output. As the blood continues to thin out it carrys
less oxygen then normal.
At the bottom of this page you
will read how PIH affects the cardiac output. With HELLP the body
progresses into increased cardiac output. The heart pumps harder
and hard to push those damaged red blood cells past the damaged firbrin.
Simply put it's like trying to push mud through a small diameter straw.
The heart has to increase it's pressure to do this. In most situations
the body can react by adapting the blood vessels. In HELLP patients
it is unable to, therefore blood pressure rises. In this high pressure
environment fluid seeps into the tissues resulting in Edema. This
swelling is normally seen in the ankles and lower back.
The body now is forced to redistribute
it's blood flow. Areas such as the skin are last to recieve oxygenated
blood. In HELLP patients the results are damage to the capillaries
under the skin resulting in bruises.
Some of the symptoms of HELLP are
because of what is discussed above. Some complaints are:
Those symptoms are not unique only
to the Hemolysis side of HELLP. For example High Blood Pressure can
be a result of Kidney problems
Shortness of breathe
Dizziness & Fainting
HELLP vs. DIC: Hematologic changes
are more severe with DIC and
are more extensive than thrombocytopenia
and hemolysis of RBC’s
Inappropriate activation of coagulation
process in which thrombin
formation and hemorrhage occur
There must be a large wounded area
eg. Many microlesions throughout
the cardiovascular system (PIH)
or a massive burn or trauma site or an
abruptio placenta or fetal demise
(septicemia) in utero or an amniotic
Fibrinogen is released and causes
large quantities of fibrin to be release.
Pregnancy is a time where there
is an abundance of fibrin. Fibrin goes to
the massive trauma area and in
the process of clot building clotting
factors are used up . Excess fibrin
begins to degrade. In so doing anti
coag. factors are released from
FDP’s or FSP. Hemorrhage ensues
reflected in thrombocytopenia plus
prolonged PTT & PT
Platelets are the first line of defense against bleeding, plugging up little
holes in capillaries (primary hemostasis).
Of course, they also help initiate
coagulation (to solidify the blood before it gets through the bigger holes),
and eventually become an important component of most clots. Thrombocytopenia
is the increased consumption or destruction of platelets.
Platelets, fibrin, or both accumulate
wherever the endothelial cells are damaged or lost. Again Fibrin
is what makes endothelial cells migrate (rendering the surface permeable),
causing vascular smooth muscle to proliferate
Vasospastic HTN associated with
PIH causes breakdown in vascular
endothelium. Microlacerations cause
platelet adherence and fibrin
deposits. Increased responsiveness
to presser effects of Angiotensin II
and deficiency of Prostacyclin
in PIH are associated with vasospastic
HTN. Platelet counts usually improve
in 4 to 5 days.
Elevated Liver Enzyme Levels
HELLP syndrome impairs liver function:
Epigastric (right upper quadrant)
pain resulting from obstruction of
blood flow in the hepatic sinusoids
by intravascular fibrin deposition
Obstruction of hepatic (liver) blood
flow by fibrin deposits (Fibrin being what keeps the vessel smooth and
water permeable, Red Blood Cells can get caught on large deposits of Fribrin
and become damaged). It is this obstuction that results in blocked
hepatic blood flow which lead to elevated liver enzymes and liver distension.
Other noticeable factors in PIH/HELLP:
Cardiac output is increased 30-50%
in normal pregnant women and is
not altered significantly in patients
with PIH. The control of peripheral resistance in normal and PIH-complicated
pregnancies is critical to understanding bloodpressure control because
blood pressure is the product of cardiac output times peripheral resistance,
and peripheral resistance is increased in women with PIH. This likely occurs
as the consequence of an increased sensitivity of the maternal vasculature
to a variety of naturally occurring vasopressors (contraction of the muscular
tissue of the capillaries and arteries), such as angiotensin II (An octapeptide
found in blood, it is synthesised from angiotensin I and quickly destroyed.
Angiotensin II causes profound vasoconstriction with resulting increase
in blood pressure).
Some of the information on the above
paragraphs came from :
This page is constantly changing
as I learn more about the medical aspects of HELLP. I try to present
the information in the most accurate and comprehensive way that I can.
Not being a Dr. the accuracy of some of the information is only as valid
as the pages I find them on. I do most of my searching for information
via the web.
Still looking for more HELLP
will take you to the next page.
Also if you have a HELLP story to share please stop by the HELLP
Syndrome Birth Stories Page and leave or read a story. Here you
will also find up to date HELLP/Pre-E net articles and books. You
wil also find WebRing information at the above listed url.