Pregnancy-induced-hypertension (PIH) is a potentially life-threatening disorder that usually develops after the 20th week of pregnancy. It typically occurs in nulliparous women and may be nonconvulsive or convulsive. Preeclampsia, the nonconvulsive form of the disorder, is marked by the onset of hypertension after 20 weeks of gestation. It develops in about 7% of pregnancies and may be mild or severe. The incidence is significantly higher in low socioeconomic groups.
Eclampsia, the convulsive form, occurs between 24 weeks' gestation and the end of the first postpartum week. The incidence increases among women who are pregnant for the first time, have multiple fetuses, and have a history of vascular disease. About 5% of women with preeclampsia develop eclampsia; of these, about 15% die of eclampsia or its complications. Fetal mortality is high because of the increased incidence of premature delivery PIH and its complications are the most common cause of maternal death in developed countries.
Cause of Preeclampsia
The cause of preeclampsia is unknown, it is often called the “DISEASE OF THEORIES” because many causes have been proposed, yet none has been well established. than how does preeclampsia occur Experts believe that decreased levels of prostaglandins and a decreased resistance to angiotensin II lead to a generalized arterial vasospasm that then causes endothelial damage. The brain, liver, kidney, and blood are particularly susceptible to multiple dysfunctions. Several risk factors have been identified that may predispose a woman to developing preeclampsia: nulliparity; familial history; multiple gestation; patient history of diabetes mellitus, chronic hypertension, renal disease, trophoblastic disease, and malnutrition.
Complications
Generalized arteriolar vasoconstriction is thought to produce decreased blood flow through the placenta and maternal organs. This decrease can result in intrauterine growth retardation, placental infarcts, and abruptio placentae. Hemolysis, elevated liver enzyme levels, and a low platelet count characterize severe eclampsia. A unique form of coagulopathy is also associated with this disorder. Other possible complications include stillbirth of the neonate, seizures, coma, premature labor, renal failure, and hepatic damage in the mother.
Disseminated Intravascular Coagulation (DIC) can occur in virtually all persons without distinction of race, sex, and age. The symptoms of DIC, generally strongly associated with the underlying disease, plus additional symptoms due to thrombosis, embolism, organ dysfunction, and bleeding. Disseminated Intravascular Coagulation (DIC) is a complex diagnosis that involves a component of blood clots as a result of other diseases that precede.
Definition of Disseminated Intravascular Coagulation
Disseminated Intravascular Coagulation is a syndrome characterized by bleeding / clotting disorders are caused by the formation of plasmin which is a specific plasma protein that is active as a fibrinolytic in getting the circulation (Healthy Cau's)
In general, disseminated intravascular coagulation (DIC) is defined as a complex disorder or blood clotting disorder due to excessive stimulation of procoagulant and anticoagulant mechanisms in response to injury (Yan Euphrates Sembiring, Paul Tahalele)
Etiology of Disseminated Intravascular Coagulation
Bleeding occurs due to the following matters:
-Hypofibrinogenemia.
-Thrombocytopenia (a common cause of abnormal bleeding, can occur due to insufficient -production of platelets by the bone marrow, or due to increased destruction of platelets).
-Circulating anticoagulant in blood circulation.
-Excessive fibrinolysis.
Diseases that predispose to DIC is as follows:
•Infections (dengue hemorrhagic fever, sepsis, meningitis, severe pneumonia, tropical malaria, •rickettsial infection by some types). Where bacteria release endotoxins (a substance that causes clotting activation).
•Pregnancy complications (placental abruption, intrauterine fetal death, amniotic fluid embolism).
•After surgery (lung surgery, bypass cardiopulmonal, lobectomy, gastrectomy, splenectomy).
•malignancies (prostate carcinoma, lung carcinoma, acute leukemia).
•Acute liver disease (acute liver failure, obstructive jaundice).
•Palepasan severe trauma occurs to the network with a large number of blood vessels. The release coincides with hemolysis and endothelial damage that would release blood clotting factors in large numbers then activates blood coagulation systemically.
•Changes in the level of consciousness.
•Cyanosis and tachypnea (increased respiratory rate) due to poor tissue perfusion and oxygenation are common. Splotches on the skin indicates tissue ischemia.
•Hematuria (blood in the urine) due to bleeding or oliguria (decreased urine output) due to poor perfusion.
Hypoglycemia occurs due to an excess of insulin in the blood resulting in low blood sugar levels. Blood sugar levels can cause symptoms of hypoglycemia, varies between one another.
At first the body responds to low blood sugar levels by releasing epinephrine (adrenaline) from the adrenal glands and certain nerve endings. Epinephrine stimulates the release of sugar from body reserves but also causes symptoms that resemble anxiety attacks (sweating, restlessness, trembling, fainting, palpitations, and sometimes hunger). More severe hypoglycemia cause a reduction of glucose to the brain and cause dizziness, confusion, fatigue, weakness, headache, unusual behavior, inability to concentrate, impaired vision, convulsions and coma. Prolonged hypoglycemia can cause permanent brain damage. Symptoms that resemble anxiety and disruption of brain function can begin slowly or suddenly. It most often occurs in people who take insulin or oral hypoglycemic drugs. In patients with insulin-producing pancreatic tumor, symptoms occurred on the morning after an overnight fast, especially if the blood sugar stores are depleted by exercise before breakfast. At first only occasional episodes of hypoglycemia-time, but after a long time the attacks become more frequent and more severe.
Signs and symptoms of hypoglycemia consists of two phases include:
The first phase of the symptoms that arise as a result of activation of the autonomic centers in the hypothalamus so that the release of the hormone epinephrine. Symptoms include palpitations, out a lot of sweat, tremors, fear, hunger and nausea (glucose by 50 mg%).
The second phase is the symptoms that occur as a result of the start of the disruption of brain function, symptoms such as dizziness, blurred vision, decreased mental acuity, loss of fine motor skills, loss of consciousness, seizures and coma (blood glucose of 20 mg%).
The symptoms of hypoglycemia are not typical is the following:
•Changes in behavior.
•Syncope sudden attack.
•Headache in the morning, which will disappear with the morning meal.
Excessive sweating bedtime.
•Waking from sleep at night to eat.
•Hemiplegia / aphasia passing.
•Angina pectoris without coronary artery abnormalities.
Research on people who are not diabetic indicate a disturbance in brain function that is ahead of phase I and in the call subliminal brain dysfunction, in addition to symptoms that are not typical.
Sometimes symptoms do not appear adrenergic phase and direct patients away in the phase disruption of brain function, there are two types of loss of alertness, namely acute and chronic.
Acute example: in patients with type 1 diabetes mellitus with blood glucose control is very tight near normal, the neuropathy autonomic in a patient who had been suffering from diabetes, and use of beta-blockers are nonselective, loss of alertness that chronicles usually irreversible and is considered a complication of diabetes serious.
As a basic diagnosis of Whipple's triad can be used, hypoglycaemia with symptoms of central nervous, glucose levels less than 50 mg% and the symptoms will disappear with the administration of glucose.
