Define and describe the overview, risk factors, etiological factors, clinical manifestations and special implications for the physical therapist assistant. Eclampsia is the onset of seizures in a woman with pre-eclampsia. Onset may be before, during, or after delivery. Exercise during pregnancy may also be useful. This is true in both the developed and developing world. In the devel

Define and describe the overview, risk factors, etiological factors, clinical manifestations and special implications for the physical therapist assistant.

Eclampsia is the onset of seizures in a woman with pre-eclampsia. Onset may be before, during, or after delivery. Exercise during pregnancy
may also be useful. This is true in both the developed and developing world. In the developed world rates are about 1 in 2,000 deliveries due to
improved medical care. They resulted in 46,900 deaths in 2015. Around one percent of women with eclampsia die.

Signs and symptoms
Eclampsia is a disorder of pregnancy characterized by seizures in the setting of pre-eclampsia. Pre-eclampsia is diagnosed when repeated blood
pressure measurements are greater or equal to 140/90mmHg, in addition to any signs of organ dysfunction, including: proteinuria, thrombocytopenia,
renal insufficiency, impaired liver function, pulmonary edema, cerebral symptoms, or abdominal pain.
Typically the pregnant woman develops hypertension and proteinuria before the onset of a convulsion.
Long-lasting headaches
Blurred vision
Photophobia
Abdominal pain
Either in the epigastric region
And/or in the right upper quadrant of the abdomen
Altered mental status
Any of these symptoms may present before or after a seizure occurs. If postpartum seizures develop, it is most likely to occur within the first 48 hours
after delivery. However, late postpartum seizures of eclampsia may occur as late as 4 weeks after delivery. Eclampsia may cause problems with the
placenta to occur. The placenta may bleed or it may begin to separate from the wall of the uterus. It is normal for the placenta to separate from the
uterine wall during delivery, but it is abnormal for it to separate prior to delivery; this condition is called placental abruption and can be dangerous for
the fetus. Placental insufficiency may also occur, a state in which the placenta fails to support appropriate fetal development because it cannot deliver
the necessary amount of oxygen or nutrients to the fetus. It may be safer to deliver the infant preterm than to wait for the full 40 weeks of fetal
development to finish, and as a result prematurity is also a potential complication of eclampsia.
In the mother, changes in vision may occur as a result of eclampsia, and these changes may include blurry vision, one-sided blindness, or cortical
blindness, which affects the vision from both eyes. There are also potential complications in the lungs. The woman may have fluid slowly collecting in
the lungs in a process known as pulmonary edema. It is also possible that during a seizure breathing will stop temporarily or become inefficient, and
the amount of oxygen reaching the woman’s body and brain will be decreased. If it becomes difficult for the woman to breathe, she may need to have
her breathing temporarily supported by an assistive device in a process called mechanical ventilation. In some severe eclampsia cases, the mother may
become weak and sluggish or even comatose. Women who have long term high blood pressure before becoming pregnant have a greater risk of preeclampsia. In addition, there is a genetic component: a woman whose mother or sister had the condition is at higher risk than otherwise. Women who
have experienced eclampsia are at increased risk for pre-eclampsia/eclampsia in a later pregnancy.
Mechanism
The presence of a placenta is required, and eclampsia resolves if it is removed. Also, an activation of the coagulation cascade may lead to
microthrombi formation, which can further impair blood flow. Thirdly, increased vascular permeability results in the shift of extracellular fluid from
the blood to the interstitial space, with further reduction in blood flow, and edema. These events lead to hypertension; renal, pulmonary, and hepatic
dysfunction; and cerebral edema with cerebral dysfunction and convulsions. Before symptoms appear, increased platelet and endothelial activation may
be detected. Other vasodilators are also reduced, including prostacyclin, thromboxane A2, nitric oxide, and endothelins, also leading to
vasoconstriction. An eclamptic convulsion usually does not cause chronic brain damage unless intracranial haemorrhage occurs.
Diagnosis
If a pregnant woman has already been diagnosed with pre-eclampsia during the current pregnancy and then develops a seizure, she may be assigned a
‘clinical diagnosis’ of eclampsia without further workup. While seizures are most common in the third trimester, they may occur any time from 20
weeks of pregnancy until 6 weeks after birth. A diagnosis of eclampsia is most likely given the symptoms and medical history, and eclampsia can be
assumed to be the correct diagnosis until proven otherwise. However, if a woman has a seizure and it is unknown whether or not she has pre-eclampsia,
testing can help make the diagnosis clear.
Vital signs
One of the core features of pre-eclampsia is high blood pressure. Blood pressure is a measurement of two numbers. If either the top number is greater
than 140 mmHg or the bottom number is greater than 90 mmHg, then the blood pressure is higher than the normal range and the person has high blood
pressure. If the systolic blood pressure is greater than 160 or the diastolic pressure is greater than 110, the hypertension is considered to be severe.
Appropriate management of women with pre-eclampsia generally involves the use of magnesium sulfate to prevent eclamptic seizures. In some cases,
low-dose aspirin has been shown to decrease the risk of pre-eclampsia in pregnant women, especially when taken in the late first trimester. The study
demonstrating the effectiveness of magnesium sulfate for the management of eclampsia was first published in 1955. Effective anticonvulsant serum
levels range from 2.5 to 7.5 mEq/L.
With intravenous administration, the onset of anticonvulsant action is fast and lasts about 30 minutes. Following intramuscular administration the onset
of action is about one hour and lasts for three to four hours. Magnesium is excreted solely by the kidneys at a rate proportional to the plasma
concentration and glomerular filtration.
Even with therapeutic serum magnesium concentrations, recurrent convulsions may occur, and additional magnesium may be needed, but with close
it i f i t di d l i l d i If i d i i t ti ith lt t hi h t ti f il t t l
monitoring for respiratory, cardiac, and neurological depression. If magnesium administration with resultant high serum concentrations fail to control
convulsions, the addition of other intravenous anticonvulsants may be used, facilitate intubation and mechanical ventilation, and to avoid magnesium
toxicity including maternal thoracic muscle paralysis

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