AZCEP Posted July 27, 2006 Share Posted July 27, 2006 The Poiseuille's law (or the Hagen-Poiseuille law also named after Gotthilf Heinrich Ludwig Hagen (1797-1884) for his experiments in 1839) is the physical law concerning the voluminal laminar stationary flow Φ of incompressible uniform viscous liquid (so called Newtonian fluid) through a cylindrical tube with the constant circular cross-section, experimentally derived in 1838, formulated and published in 1840 and 1846 by Jean Louis Marie Poiseuille (1797-1869), and defined by: where V is a volume of the liquid, poured in the time unit t, v the median fluid velocity along the length of the tube, x the direction of flow, R the internal radius of the tube, P the pressure difference between the two ends, η dynamic fluid viscosity and L the total length of the tube in the x direction. The law can be derived from the Darcy-Weisbach equation, developed in the field of hydraulics and which is otherwise valid for all types of flow, and also expressed in the form: where Re is the Reynolds number and ρ fluid density. In this form the law approximates the Darcy friction factor, the energy (head) loss factor, friction loss factor or Darcy (friction) factor Λ in the laminar flow at very low velocities in cylindrical tube. The theoretical derivation of a slightly different form of the law was made independently by Wiedman in 1856 and Neumann and E. Hagenbach in 1858 (1859, 1860). Hagenbach was the first who called this law the Poiseuille's law. The law is also very important specially in hemorheology and hemodynamics, both fields of physiology. The Poiseuilles' law was later in 1891 extended to turbulent flow by L. R. Wilberforce, based on Hagenbach's work. Viscosity Two fluids moving past each other in the x direction. The liquid on top is moving faster and will be pulled in the negative direction by the bottom liquid while the bottom liquid will be pulled in the positive direction by the top liquid.The derivation of Poiseuille's Law is surprisingly simple, but it requires an understanding of Viscosity. When two layers of liquid in contact with each other move at different speeds, there will be a force between them. This force is proportional to the area of contact A, the velocity difference in the direction of flow Δvx/Δy, and a proportionality constant η and is given by The negative sign is in there because we are concerned with the faster moving liquid (top in figure), which is being slowed by the slower liquid (bottom in figure). By Newton's third law of motion, the force on the slower liquid is equal and opposite (no negative sign) to the force on the faster liquid. This equation assumes that the area of contact is so large that we can ignore any effects from the edges and that the fluids behave as Newtonian fluids. [edit] Liquid flow through a pipe In a tube we make a basic assumption: the liquid in the center is moving fastest while the liquid touching the walls of the tube is stationary (due to friction). A cross section of a hypothetical tube shows the lamina moving at different speeds. Those closest to the edge of the tube are moving slow while those near the center are moving fastTo simplify the situation, let's assume that there are a bunch of circular layers (lamina) of liquid, each having a velocity determined only by their radial distance from the center of the tube. To figure out the motion of the liquid, we need to know all forces acting on each lamina: The force pushing the liquid through the tube is the change in pressure multiplied by the area: F = -ΔPA. This force is in the direction of the motion of the liquid - the negative sign comes from the conventional way we define ΔP. The pull from the faster lamina immediately closer to the center of the tube The drag from the slower lamina immediately closer to the walls of the tube The first of these forces comes from the definition of pressure. The other two forces require us to modify the equations above that we have for viscocity. In fact, we are not modifying the equations, instead merely plugging in values specific to our problem. Let's focus on the drag from the faster lamina (#2) first. [edit] Faster lamina Assume that we are figuring out the force on the lamina with radius s. From the equation above, we need to know the area of contact and the velocity gradient. Think of the lamina as a cylinder of radius s and thickness ds. The area of contact between the lamina and the faster one is simply the area of the inside of the cylinder: A = 2πsΔx. We don't know the exact form for the velocity of the liquid within the tube yet, but we do know (from our assumption above) that it is dependent on the radius. Therefore, the velocity gradient is the change of the velocity with respect to the change in the radius at the intersection of these two laminae. That intersection is at a radius of s. So, considering that this force will be positive with respect to the movement of the liquid, the final form of the equation becomes where the vertical bar and subscript s following the derivative indicates that it should be taken at a radius of s. [edit] Slower lamina Next let's find the force of drag from the slower lamina. We need to calculate the same values that we did for the force from the faster lamina. In this case, the area of contact is at s+ds instead of s. Also, we need to remember that this force opposes the direction of movement of the liquid and will therefore be negative. [edit] Putting it all together To find the solution for the flow of liquid through a tube, we need to make one last assumption. There is no acceleration of liquid in the pipe, and by Newton's first law, there is no net force. If there is no net force then we can add all of the forces together to get zero 0 = Fpressure + Fviscosity,fast − Fviscosity,slow or Before we move further, we need to simplify this ugly equation. First, to get everything happening at the same point, we need to do a Taylor series expansion of the velocity gradient, keeping only the linear and quadratic terms (a standard mathematical trick). Let's use this relation in our equation. Also, let's use r instead of s since the lamina we chose was arbitrary and we want our expression to be valid for all laminae. Grouping like terms and dropping the vertical bar since all derivatives are assummed to be at radius r, Finally, let's get this in the form of a differential equation, moving some terms around to make it easier to solve later, and neglecting the term quadratic in dr since this will be really small compared to the rest (another standard mathematical trick) This type of differential equation has solutions of the form v = A+Br2. To solve, we will substitute this into our equation and solve for A and B. this means that to solve for A we'll use the assumption we made at the beginning that at the wall of the tube (r = R) the velocity must be 0. or Now we have a formula for the velocity of liquid moving through the tube as a function of the distance from the center of the tube or, at the center of the tube where the liquid is moving fastest (r = 0) with R being the radius of the tube, [edit] Poiseuille's Law To get the total volume that flows through the tube, we need to add up the contributions from each lamina. To calculate the flow through each lamina, we multiply the velocity (from above) and the area of the lamina. Finally, we integrate over all lamina via the radius variable r. There are a lot of diagrams that help to explain some of this at: http://en.wikipedia.org/wiki/Poiseuille's_law Basically: Fluid flows faster through a large, short, smooth tube than it does through a small, long, rough one PIH, PreEclampsia, Eclampsia Link to comment Share on other sites More sharing options...
AZCEP Posted July 29, 2006 Share Posted July 29, 2006 Come on now. There is too much good information here to let this thread die. Someone out there knows the differences between them, and how they will present So I re-submit: PIH, PreEclampsia, Eclampsia Link to comment Share on other sites More sharing options...
Ace844 Posted July 29, 2006 Share Posted July 29, 2006 “AZCEP,” Wanted to let some of the newbie’s take a shot at this, but I guess they are uninterested. Here’s the data you were looking for and PIH- or Pregnancy Induced Hypertension is an older term which is actually ‘Preeclampsia’. Preeclampsia-Eclampsia Background: Hypertensive disease in pregnancy is a major cause of maternal and fetal morbidity and mortality. Pregnancy-related hypertension is divided into 4 categories. The first category consists of normotensive, pregnant patients who have sustained hypertension, proteinuria, and edema after the 20th week of gestation, with preeclampsia or pregnancy-induced hypertension. Preeclampsia causes 50-70% of cases of hypertension in pregnancy. Mild preeclampsia is characterized by an increase in systolic BP of 30 mm Hg, an increase in diastolic BP of 15 mm Hg, or an absolute reading of 140 mm Hg/90 mm Hg in a pregnant patient with minimal proteinuria and pathologic edema. A systolic BP greater than 160 mm Hg or a diastolic BP greater than 110 mm Hg with significant proteinuria (>5.0 g/d) and evidence of end-organ damage indicate severe preeclampsia. In the second category, chronic hypertension begins prior to pregnancy. A BP greater than 140 mm Hg/90 mm Hg occurs prior to the 20th week of gestation, is not associated with significant proteinuria or end-organ damage, and continues well after delivery. The third category consists of patients with chronic hypertension with superimposed preeclampsia; this condition is responsible for 15-30% of cases of pregnancy-related hypertensive disease. Pregnant patients with documented hypertension before pregnancy may have preeclampsia. In the fourth category, transient hypertension results in a BP greater than 140 mm Hg/90 mm Hg without proteinuria or end-organ damage. Initially normotensive women may become hypertensive late in pregnancy, during labor, or within 24 hours postpartum, and their BPs return to normal within 10 days postpartum. Pathophysiology: The cause of preeclampsia remains unknown; however, placental dysfunction may initiate the systemic vasospasm, ischemia, and thrombosis that eventually damages maternal organs. Females with pregnancy-induced hypertension have been noted to have an increased responsiveness to a variety of endogenous substances (prostaglandins, thromboxane) that can cause vasospasm and platelet aggregation. Thrombus formation or hemorrhage causes the central nervous system findings of headache, local neurological deficits, and seizure. Renal necrosis leads to a decreased glomerular filtration rate and proteinuria. Liver injury from hepatocellular necrosis causes right upper quadrant pain and elevated liver function tests. Cardiovascular manifestations include a lower than normal intravascular volume, increased cardiac output, and an abnormally elevated peripheral vascular resistance. Microangiopathic hemolysis leads to anemia and thrombocytopenia. Placental infarction and abruptio placentae lead to intrauterine growth retardation and fetal death. Preeclampsia typically develops after the 20th week of gestation and involves a wide spectrum of clinical signs and symptoms. Mild preeclampsia is characterized by mild hypertension with no evidence of end-organ pathology aside from minimal proteinuria (<2.0 g/d). Severe preeclampsia is at the other end of the spectrum and is characterized by significant hypertension, more pronounced proteinuria (>5.0 g/d), and evidence of end-organ damage due to systemic vasoconstriction. The following signs and symptoms can indicate severe preeclampsia: (1) headache, (2) visual disturbances, (3) confusion, (4) abdominal pain, (5) impaired liver function with hyperbilirubinemia, (6) proteinuria, (7) oliguria, (8) pulmonary edema, (9) microangiopathic hemolytic anemia, (10) thrombocytopenia, and (11) fetal growth retardation. Risk factors for preeclampsia include extremes of maternal age, primigravida, multiple gestations, molar pregnancy, preexisting HTN, diabetes mellitus (DM), renal disease, preexisting connective tissue disease, vascular disease, prior history of preeclampsia or eclampsia, and family history of preeclampsia or eclampsia. Frequency: • In the US: Preeclampsia is a complication in approximately 5% of all pregnancies. Mortality/Morbidity: Preeclampsia is one of the most common causes of perinatal morbidity and mortality, resulting in an estimated 35-300 deaths per 1000 births, depending on neonatal support capabilities of the hospital delivering care. This mortality rate is almost double that of normotensive pregnancies. • If unrecognized, preeclampsia can progress to the syndrome of hemolysis (microangiopathic hemolytic anemia), elevated liver-enzyme levels (hepatocellular damage), and low platelet count (HELLP) and eclampsia. HELLP syndrome is noted in 5-10% of patients with preeclamptic symptoms. In addition to the signs and symptoms of preeclampsia, most patients have right upper quadrant (RUQ) abdominal pain, nausea, and vomiting. Unless the ED physician maintains a high index of suspicion, gastritis, cholecystitis, or hepatitis may be misdiagnosed. • The most serious complication of pregnancy-induced hypertension is eclampsia, which is severe preeclampsia complicated by seizures or coma. Eclampsia occurs in approximately 0.2% of pregnancies and causes the termination of 1 in 1000 pregnancies. Seizures and mental status changes in eclampsia are thought to be secondary to hypertensive encephalopathy. Intracranial hemorrhage is the major cause of maternal death. The maternal mortality rate is 8-36%. • The definitive treatment for eclampsia is delivery of the fetus. Premature delivery and its complications often contribute to the fetal mortality rate of 13-30%. Placental infarcts, abruptio placentae, and intrauterine growth retardation also contribute to fetal demise. Age: Preeclampsia usually occurs in women at both extremes of reproductive age; however, the risk of preeclampsia is greatest in women younger than 20 years. History: Mild preeclampsia does not involve clinical evidence of end-organ pathology, except for minimal proteinuria. Severe preeclampsia is characterized by end-organ damage due to systemic vasoconstriction. Features of the history may include the following: • Headache • RUQ abdominal pain • Decreased urine output • Shortness of breath or dyspnea on exertion • Hand and facial edema • Visual disturbances • Confusion and apprehension • Nausea and vomiting Physical: Findings at physical examination may include the following: • Sustained systolic BP increases by 30 mm Hg, and diastolic BP increases by 15 mm Hg, or absolute BP higher than 140 mm Hg/90 mm Hg. • Severe preeclampsia (sustained systolic BP >160 mm Hg or diastolic BP >110 mm Hg with end-organ damage) • Tachycardia • Tachypnea • Rales • Pulmonary edema • Mental status changes • Hypertensive encephalopathy • Hyperreflexia, clonus • Localizing neurologic deficits • Intracranial hemorrhage • Cerebrovascular accident • Hepatocellular injury • Generalized edema • Small fundal height for estimated gestational age • Intrauterine growth retardation Causes: The cause of preeclampsia is not fully understood; however, dysfunction of the uteroplacental bed is thought to cause the generalized vasoconstriction, platelet aggregation, and hypercoagulable state seen in preeclampsia. Aneurysms, Abdominal] Angioedema Encephalitis Hypertensive Emergencies [Hyperthyroidism, Thyroid Storm and Graves Disease] Meningitis Pregnancy, Eclampsia Renal Failure, Acute Shock, Septic Stroke, Hemorrhagic Stroke, Ischemic Systemic Lupus Erythematosus Withdrawal Syndromes Other Problems to be Considered: Cocaine poisoning Phencyclidine poisoning Pheochromocytoma Lab Studies: The CBC may reveal the following: o Anemia due to the microangiopathic hemolytic anemia and dilution of pregnancy o Thrombocytopenia (platelet count <100,000) due to HELLP syndrome • The serum creatinine is elevated due to decreased intravascular volume and a decreased glomerular filtration rate (GFR). • Liver function test (LFT) results may reveal the following: o Aspartate aminotransferase (SGOT) level higher than 72IU/L, total bilirubin levels higher than 1.2 mg/dL, lactate dehydrogenase (LDH) levels higher than 600 IU/L o Elevated levels due to HELLP syndrome • The coagulation profile may reveal a normal prothrombin time (PT) and a normal activated partial thromboplastin time (aPTT), fibrin split products, and fibrinogen levels o Rule out associated disseminated intravascular coagulopathy (DIC). • Urinalysis may reveal the following findings: o Proteinuria o Positive human chorionic gonadotropin (HCG) result Imaging Studies: • CT scan of the head o Obtain a head CT scan in patients with severe preeclampsia and associated neurologic deficits. o This is used to assess intracranial hemorrhage or cerebrovascular accident. • Transabdominal sonogram o This is used to estimate gestational age. o It also is used to rule out abruptio placentae, which can complicate severe preeclampsia. Procedures: • Perform a 24-hour urine test for protein. Prehospital Care: EMS personnel should secure an intravenous line, begin cardiac monitoring, administer oxygen, and transport the patient in the left lateral decubitus position. Emergency Department Care: The goal of management is to limit maternal and fetal morbidity pending delivery of the fetus, the only definitive treatment for preeclampsia. The severity of symptoms and the gestational age of the fetus ultimately determine the course of treatment in the ED. • The mildest form of hypertension in a pregnant patient without proteinuria, edema, or evidence of end-organ damage may be managed on an outpatient basis, because these do not meet the diagnostic criteria for true preeclampsia. Prior to discharging the patient, discuss the case in detail with the patient's obstetrician, and ensure reassessment within 48 hours. Each patient must be counseled regarding the reasons for immediate return to the hospital. • Hypertension and proteinuria indicate preeclampsia. Patients with these conditions should be admitted to the hospital for an immediate obstetric evaluation. Hypertension and proteinuria could be due to chronic primary hypertension; however, chronic primary hypertension is a diagnosis of exclusion and may be considered once preeclampsia has been ruled out. • Severe preeclampsia is managed in an intensive care setting as if the patient had eclampsia. o Magnesium sulfate is administered for seizure prophylaxis, and hydralazine or certain other antihypertensive drugs are administered for BP control. o Be careful not to decrease the BP too drastically; a drastic reduction can cause inadequate uteroplacental perfusion and fetal distress. o Maintaining a diastolic BP of 90 mm Hg is the goal of antihypertensive therapy. o If the gestational age is greater than 30 weeks, delivery is indicated. Drug treatment consists of seizure prophylaxis and antihypertensives. Drug Category: Electrolytes -- Magnesium sulfate has anticonvulsant properties and can be used for seizure prophylaxis. Drug Name Magnesium sulfate -- Used to treat and prevent seizures. For clinically significant hypermagnesemia, calcium gluconate (10% solution) 10-20 mL IV can be given. Adult Dose Initial: 2-6 g (20% solution) IV over 5-10 min Maintenance: 1-3 g/h IV Alternative: 5 g IM in each buttock (10 g total) initially; 5 g IM q4h maintenance Pediatric Dose 25-50 mg/kg/dose IV q4-6h for 3-4 doses; not to exceed 2 g; repeat if hypomagnesemia persists Contraindications Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis Interactions Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone; may increase cardiotoxicity of ritodrine Pregnancy A - Safe in pregnancy Precautions May alter cardiac conduction, leading to heart block in patients receiving digitalis; respiratory rate, deep tendon reflex, and renal function should be monitored when electrolyte is administered parenterally; caution in administration (may produce significant hypertension or asystole); in overdose, calcium gluconate, 10-20 mL IV of 10% solution, is antidote for clinically significant hypermagnesemia Drug Category: Antihypertensives -- Hydralazine is the DOC for BP control in preeclamptic patients. However, parenteral hydralazine is provided only to pharmacists upon special emergency request. Therefore, the physician must be comfortable using other antihypertensive agents. Labetalol has alpha-adrenergic and beta-adrenergic blocking effects and can be used to provide rapid control of severe hypertension. Other antihypertensive agents have significant adverse effects and should not be used as primary agents. Diazoxide may cause hyperglycemia and inhibit labor, and nitroprusside may cause fetal cyanide toxicity. Diuretics should be avoided because of the relative intravascular volume depletion already present in patients with preeclampsia. Drug Name Hydralazine (Apresoline) -- Decreases systemic resistance by means of direct vasodilation of arterioles Adult Dose Initial: 5 mg IV Maintenance: 5-10 mg IV q20-30min Pediatric Dose 0.1-0.2 mg/kg/dose IV q4-6h prn; not to exceed 20 mg or 1.7-3.5 mg/kg/d divided in 4-6 doses Contraindications Documented hypersensitivity; mitral valve rheumatic heart disease Interactions MAOIs and beta-blockers may increase toxicity; indomethacin may decrease pharmacologic effects Pregnancy B - Usually safe but benefits must outweigh the risks. Precautions Implicated in MI; caution in suspected coronary artery disease Drug Name Labetalol (Normodyne) -- Used as an alternative to hydralazine in eclampsia. It blocks beta1-adrenergic, alpha-adrenergic, and beta2-adrenergic receptor sites, decreasing BP. It is used as an alternative to hydralazine. Adult Dose 20-30 mg IV initially; 40-60 mg IV q10-20 min; not to exceed 300 mg Pediatric Dose Not established Suggested dose: 0.4-1 mg/kg/h IV; not to exceed 3 mg/kg/h Contraindications Documented hypersensitivity; cardiogenic shock; pulmonary edema; bradycardia; atrioventricular block; uncompensated congestive heart failure; reactive airway disease; severe bradycardia Interactions Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia resulting from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase labetalol blood levels; glutethimide may decrease effects by inducing microsomal enzymes Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in impaired hepatic function; discontinue therapy with signs of liver dysfunction; in elderly patients, a lower response rate and higher incidence of toxicity may be observed Further Inpatient Care: • Patients with preeclampsia require admission to the hospital for immediate obstetric consultation. Patients with severe preeclampsia need supportive care and treatment in an intensive care setting. • Hospitalization with bedrest in the left lateral decubitus position may be required. • Seizure prophylaxis (magnesium sulfate) and antihypertensive agent (hydralazine) are required for severe preeclampsia. • Delivery is the definitive treatment. Further Outpatient Care: • An obstetrician may evaluate pregnant patients with hypertension and no proteinuria, edema, or evidence of end-organ pathology may be evaluated on an outpatient basis within 48 hours of presentation. Transfer: • Patients with severe preeclampsia or eclampsia must be treated in a high-risk obstetric facility. • Once the patient with preeclampsia or eclampsia is stabilized, arrange for immediate transfer to the nearest high-risk obstetric facility that can deliver neonatal and maternal intensive care. Complications: • Abruptio placentae with disseminated intravascular coagulopathy • Renal insufficiency or failure • Hemolysis, elevated liver-enzyme levels, and low platelet count (or HELLP) syndrome • Eclampsia • Cerebral hemorrhage • Death Prognosis: • Generally good with appropriate treatment and delivery of fetus Medical/Legal Pitfalls: • Aspirin blocks platelet aggregation and vasospasm in preeclampsia, and it may be effective in preventing preeclampsia. Recent studies have shown that low dose aspirin in females at risk for preeclampsia can contribute to a decreased risk of developing preeclampsia, a reduction in preterm delivery rates, and a reduction in fetal death rates without increasing the risk for placental abruption. An obstetrician should directly supervise aspirin therapy, if it is to be used in high risk patients. • Maintain a high index of suspicion for preeclampsia when evaluating any complaint in a pregnant patient with abnormally elevated BP. • Any pregnant patient, regardless of age, is at risk for preeclampsia. • Immediate obstetric consultation is required for all preeclamptic patients. Eclampsia Background: Eclampsia is defined as seizure activity or coma unrelated to other cerebral conditions in an obstetrical patient with preeclampsia. While most cases present in the third trimester of pregnancy or within the first 48 hours following delivery, rare cases have been reported prior to 20 weeks' gestation or as late as 23 days postpartum. Eclampsia has also been described without prior development of preeclampsia. Pathophysiology: Many investigators have proposed genetic, immunologic, endocrinologic, nutritional, and even infectious agents as the cause for preeclampsia/eclampsia. Despite extensive research, no definitive cause has been identified. Presumably, the placenta and fetal membranes play a role in the development of preeclampsia because of the prompt resolution of the disease following delivery. A common pathway thought to be associated with the development of preeclampsia is utero-placental ischemia. Uteroplacental ischemia is postulated to predispose to the production and release of biochemical mediators that enter the maternal circulation, causing widespread endothelial dysfunction and generalized arteriolar constriction and vasospasm. Preeclampsia/eclampsia creates a functional derangement of multiple organ systems, such as the central nervous system and the hematologic, hepatic, renal, and cardiovascular systems. The severity depends on medical or obstetric factors. Systemic derangements in eclampsia include the following: • Cardiovascular o Generalized vasospasm o Increased peripheral vascular resistance o Increased left ventricular stroke work index o Decreased central venous pressure o Decreased pulmonary wedge pressure • Hematologic o Decreased plasma volume o Increased blood viscosity o Hemoconcentration o Coagulopathy • Renal o Decreased glomerular filtration rate o Decreased renal plasma flow o Decreased uric acid clearance • Hepatic o Periportal necrosis o Hepatocellular damage o Subcapsular hematoma • Central nervous system o Cerebral edema o Cerebral hemorrhage Frequency: • In the US: Approximately 5% of pregnancies are complicated by preeclampsia. Of these patients, 0.5-2% progress to eclampsia. The incidence is increased in women of low socioeconomic status, extremes of age, and primigravid state. Both preeclampsia and eclampsia account for significant maternal and fetal morbidity and mortality. Mortality/Morbidity: Eclampsia accounts for approximately 50,000 maternal deaths worldwide annually. In the United States, the maternal mortality rate from eclampsia has been reduced with early diagnosis and aggressive management and is currently less than 1%. The fetal mortality rate from eclampsia has also decreased but still remains at approximately 12%. • Maternal complications of eclampsia may include permanent CNS damage from recurrent seizures or intracranial bleeds, renal insufficiency, and death. • Causes of neonatal death include prematurity, placental infarcts, intrauterine growth retardation, abruptio placentae, and fetal hypoxia. Race: Racial predilection is unclear. A higher incidence of this condition may exist in African Americans. Sex: Only females are affected. Age: Preeclampsia/eclampsia affects women of all ages, but the frequency is increased in nulliparous women younger than 20 years. Women older than 40 years with preeclampsia have 4 times the incidence of seizures compared to women in their third decade of life. Other risk factors include the following: • Nulliparity and age older than 35 years • Preexisting hypertension or renal disease • Poor prenatal care • Strong family history of preeclampsia/eclampsia • Systemic lupus erythematous • Obstetric conditions associated with an abundance of chorionic villi (eg, twin gestations, molar pregnancies, triploidy, nonimmune hydrops fetalis) History: • Signs include tonic-clonic seizure activity (focal or generalized). • Symptoms include the following: o Headache (82.5%) o Hyperactive reflexes (80%) o Marked proteinuria (52%) o Generalized edema (49%) o Visual disturbances (44.4%) o Right upper quadrant pain or epigastric pain (19%) • Prior to a seizure, some patients may present with the following: o Lack of edema (39%) o Absence of proteinuria (21%) o Normal reflexes (20%) o Presentation: Approximately 70% of eclamptic seizures occur prior to delivery. • Twenty-five percent of eclampsia cases occur before labor (ie, antepartum). • Fifty percent of eclampsia cases occur during labor (ie, intrapartum). • Twenty-five percent of eclampsia cases occur after delivery (ie, postpartum). • Patients with severe preeclampsia are at greater risk to develop seizures. • Twenty-five percent of patients with eclampsia have only mild preeclampsia prior to the seizures. Physical: • Eclamptic seizure o The patient may have 1 or more seizures. o Seizures generally last 60-75 seconds. o The patient's face initially may become distorted, with protrusion of the eyes. o The patient may begin foaming at the mouth. o Respiration ceases for the duration of the seizure. • The seizure may be divided into 2 phases: o Phase 1 lasts 15-20 seconds and begins with facial twitching. The body becomes rigid, leading to generalized muscular contractions. o Phase 2 lasts approximately 60 seconds. It starts in the jaw, moves to the muscles of the face and eyelids, and then spreads throughout the body. The muscles begin alternating between contracting and relaxing in rapid sequence. • A coma or a period of unconsciousness follows phase 2. o Unconsciousness lasts for a variable period. o Following the coma phase, the patient may regain some consciousness. o The patient may become combative and very agitated. o The patient has no recollection of the seizure. • A period of hyperventilation occurs after the tonic-clonic seizure. This compensates for the respiratory and lactic acidosis that develops during the apneic phase. • Seizure-induced complications may include tongue biting, head trauma, broken bones, or aspiration. Causes: • The cause of the seizures is not clear, although several processes have been implicated in their development. o Areas of cerebral vasospasm may be severe enough to cause focal ischemia, which may in turn lead to seizures. o Pathologic alterations in cerebral blood flow and tissue edema induced by vasospasm may result in headaches, visual disturbances, and hypertensive encephalopathy, resulting in a seizure. Other Problems to be Considered: Cerebral tumors Cerebral venous thrombosis Drug overdoses Epilepsy Intracranial hemorrhage Head trauma Stroke (ischemic or nonischemic) Electrolyte imbalance Lab Studies: • No single laboratory test or set of laboratory determinations is useful in predicting maternal or neonatal outcome in women with eclampsia. • Laboratory studies that should be ordered include the following: o Complete blood cell count o Platelet count o Twenty-four–hour urine for protein/creatinine o Electrolytes o Liver function tests (ie, lactate dehydrogenase [LDH], aspartate aminotransferase [AST]) o Uric acid o Serum glucose • The most common hematologic abnormality in obstetric disorders is thrombocytopenia, occurring in 17% of patients with eclampsia. • Disseminated intravascular coagulation (DIC) appears to be uncommon in patients with eclampsia. Imaging Studies: • A CT scan of the head, with or without contrast, may be indicated in certain patients to exclude cerebral venous thrombosis, intracranial hemorrhage, and central nervous system lesions, all of which can occur in pregnancy. o CT scan is a technique that is considered safe in pregnancy when performed after the first trimester. o Consider obtaining a CT scan of the head in patients (1) who have been involved in a trauma, (2) who are refractory to magnesium sulfate therapy, and (3) who have atypical presentations (such as seizures >24 h after delivery). o Although obtaining a CT scan in eclampsia is not routine, abnormalities can be observed in as many as one half of patients. o Characteristic cortical hypodense areas, particularly in the occipital lobes, and diffuse cerebral edema are thought to correspond to the petechial hemorrhages and diffuse edema noted in postmortem studies. o Reported CT scan findings - Cerebral edema Diffuse white matter low-density areas Patchy area of low density Occipital white matter edema Loss of normal cortical sulci Reduced ventricular size o Reported CT scan findings - Cerebral hemorrhage Intraventricular hemorrhage Parenchymal hemorrhage (high density) o Reported CT scan findings - Cerebral infarction Low attenuation areas Basal ganglia infarctions • Magnetic resonance imaging and eclampsia o MRI is a recently developed noninvasive technique that appears to be superior to other processes for defining intracranial anatomy and pathophysiology. o Abnormal findings have been reported in as many as 90% of women with eclampsia. o Findings with MRI may be increased signal at the grey-white matter junction on T2-weighted images or cortical edema and hemorrhage. • Angiography o The use of cerebral angiography is limited in eclampsia. o The principle finding observed with eclampsia on angiography is widespread arterial vasoconstriction of the intracranial vessels. Other Tests: • EEG and cerebral spinal fluid studies rarely are useful in management; however, they may be indicated if epilepsy or meningitis is considered in the diagnosis. Medical Care: Eclamptic convulsions are life-threatening emergencies and require the proper treatment to decrease maternal morbidity and mortality. • Presentation: If the patient develops convulsions at home, she usually is brought to the hospital in a comatose (ie, postictal) condition. These patients should be cared for by a team of qualified physicians (preferably obstetricians) and nurses. Patients should undergo continuous intensive monitoring. They should be placed in a monitored labor room with minimal noise and external stimuli. • Initial management: As with any seizure, the initial management is to clear the airway and administer adequate oxygenation. The patient should be positioned in the left lateral position to help improve uterine blood flow and obstruction of the vena cava by the gravid uterus. The patient should be protected against maternal injury during the seizure, ie, the guardrails should be up on the bed, a padded tongue blade is placed between the teeth, and secretions are suctioned from the patient's mouth. • Intravenous access: After the seizure has ended, a 16- to 18-gauge intravenous line should be obtained for drawing specimens for laboratory studies and administering fluids. Intravenous fluids should be limited to isotonic solutions to replace urine output and about 700 mL/d to replace insensible losses. • Control of the seizure: Do not attempt to shorten or abolish the initial seizure. A syringe containing 2-4 g of magnesium sulfate should be the only anticonvulsant at the bedside. Magnesium sulfate is administered intramuscularly or intravenously to decrease and prevent further convulsions. • Laboratory workup: A complete blood count, chemistry panel, and liver function tests should be conducted. A urinalysis should be sent to evaluate for proteinuria, and a 24-hour urine collection for protein should be initiated. • Hypertension control: Record blood pressure every 10 minutes. Control blood pressure (diastolic 90-100 mm Hg) with administration of antihypertensive medications (ie, hydralazine, labetalol). • Monitoring: Carefully monitor the neurologic status, urine output, respirations, and fetal status for all patients. An indwelling Foley catheter should be placed in the bladder to help collect and record urine output. • Invasive monitoring: Pulmonary artery pressure monitoring may be necessary for accurate fluid management in eclamptic patients. This is particularly important in patients who have evidence of pulmonary edema or oliguria/anuria. • Assessment of medical condition: Once the seizure is controlled and the patient has regained consciousness, the general medical condition is assessed. Induction of labor may be initiated when the patient is stable. • Delivery o Delivery is the treatment for eclampsia after proper stabilization. If the patient is undelivered, no attempt should be made to deliver the infant either vaginally or by cesarean delivery until the acute phase of the seizure or coma has passed. The mode of delivery should be based on obstetric indications but should be chosen with an awareness of the fact that vaginal delivery is preferable from a maternal standpoint. o In the absence of fetal malpresentation or fetal distress, oxytocin should be initiated to induce labor in the following situations: At 30 weeks' gestation or greater, irrespective of the cervical dilation or effacement Prior to 30 weeks' gestation with a favorable cervix o Patients with an unfavorable cervix with a gestational age of 30 weeks or less, once stabilized, should be delivered electively by cesarean delivery. This approach is preferred because pregnancies prior to 30 weeks' gestation with eclampsia have a higher risk of complications intrapartum. Intrapartum complications include the following: Fetal growth retardation (30%) Fetal distress (30%) Abruption (23%) • Fetal monitoring o Fetal heart rate and intensity of the contractions should be monitored closely. Fetal bradycardia is a common finding following the eclamptic seizure and has been reported to last from 30 seconds to 9 minutes. The interval from the onset of the seizure to the fall in the fetal heart rate is typically 5 minutes. Transitory fetal tachycardia may occur following the bradycardia. o During the recovery phase, the fetal heart rate tracing may reveal a loss of beat-to-beat variability and late decelerations. The mechanism for the fetal tracing abnormalities is most likely due to a decrease in uterine blood flow caused by the intense vasospasm and uterine hyperactivity during the convulsion. If the fetal heart tracing does not improve following a seizure, other conditions should be considered. Growth restricted and preterm fetuses may take longer to recover following a seizure. Consider placental abruption if uterine hyperactivity remains and fetal bradycardia persists. Surgical Care: • Patients with eclampsia may need to be delivered immediately by cesarean delivery, depending on the maternal and fetal condition. • Stabilize the patient before initiating cesarean delivery during the acute phase because delivery may aggravate oliguria and other manifestations of the disease. • The anesthesiologist should be informed of the maternal condition and may be helpful if endotracheal intubation or an operative delivery is necessary. • For nonemergent cesarean delivery, epidural anesthesia is preferred and can be induced in a steplike fashion, being careful not to cause maternal hypotension. • The use of spinal anesthesia is controversial because of the possibility of extreme sympathetectomy, resulting in maternal hypotension and uteroplacental insufficiency. Consultations: • An experienced obstetrician should be consulted immediately. • Consider consultation with a maternal-fetal medicine specialist, with transport to a tertiary care site after stabilization if it is in the fetal or maternal best interest. • In the event of prematurity or fetal compromise, a pediatrician or neonatologist should be consulted. Diet: • Patients with eclampsia should have nothing by mouth until medically stabilized. • During a seizure, maintaining the patient's airway and being careful to help avoid aspiration of stomach contents is important. Activity: • Strict bedrest • Left lateral hip roll to help improve uterine blood flow to the fetus The goals of pharmacotherapy are to reduce morbidity, prevent complications, and correct eclampsia. Drugs of choice include magnesium sulfate, phenytoin, diazepam, hydralazine, labetalol, and nifedipine. Drug Category: Anticonvulsants -- Prevent seizure recurrence and terminate clinical and electrical seizure activity. Drug Name Magnesium sulfate -- Several studies have revealed that magnesium sulfate is the drug of choice for treating eclamptic seizures. Magnesium sulfate is successful in controlling seizures in >95% of cases. Agent has physiologic advantages to the fetus by increasing uterine blood flow. Mechanism of action of magnesium sulfate therapy is that it inhibits the release of acetylcholine at the motor endplate. In addition, magnesium has a direct effect on skeletal muscle by virtue of its competitive antagonistic effects with calcium. Magnesium sulfate is excreted exclusively by the kidneys and has little antihypertensive effect. It is an effective anticonvulsant and helps prevent recurrent seizures and maintain uterine and fetal blood flow. Can be administered both IV and IM. Intravenous route is preferred over IM route because administration is controlled more easily and time to therapeutic levels is shorter. Intramuscular administration of magnesium sulfate tends to be more painful and less convenient. If IV access or close patient monitoring is unavailable, this is an effective therapy. The goals of magnesium therapy are to terminate ongoing seizures and prevent further seizures. Patient should be evaluated qh to assure that deep tendon reflexes are present, respirations are at least 12 breaths per min, and urine output is at least 100 mL during the preceding 4 h. When using magnesium sulfate IV, close monitoring of patient and fetus is necessary. Magnesium therapy usually is continued for 12-24 h following delivery and may be stopped when the hypertension resolves and the patient has shown adequate diuresis. Renally compromised patients should be monitored with magnesium levels, with aggressive adjustments made to facilitate levels at 6-8 mg/dL. Patients with increased urine output may need maintenance dose increased to 3 g/h to maintain therapeutic levels. Monitor patient for signs of worsening condition and magnesium toxicity. The Parkland IM protocol is as follows: Magnesium sulfate 4 g IV over 5 min, plus magnesium sulfate 10 g deep IM (3-in needle) divided in both buttocks and mixed with 1 mL 2% lidocaine. If a seizure persists more than 15 min after above dose, administer an additional 2 g of magnesium sulfate IV over 3-5 min. Magnesium sulfate 5 g IM q4h, starting 4 h later unless patellar reflexes are absent, respiratory depression occurs, or urine output is <100 mL in the prior 4 h. Therapeutic levels are 4.8-8.4 mg/dL. With the above protocol, serum magnesium levels usually are 4-7 mg/dL in a patient with an average volume of distribution and normal renal function. Actual serum magnesium levels are monitored only in patients with symptomatic magnesium toxicity or renal compromise. Patients may have seizures while receiving magnesium sulfate. If seizure occurs in first 20 min after loading dose, the convulsion usually is short, and no additional treatment is indicated. If seizure occurs >20 min after the loading dose, an additional 2-4 g of magnesium may be administered. Adult Dose Initial: 4-6 g bolus IV over 15-20 min; if convulsion occurs after initial bolus, an additional 2 g IV over 3-5 min may be administered Approximately 10-15% of patients will have another convulsion after the loading dose Maintenance: 2-4 g/h IV maintenance drip If magnesium level is >10 mg/dL at 4 h after initial bolus, decrease the maintenance dose Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis; or myasthenia gravis Interactions Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine Pregnancy A - Safe in pregnancy Precautions Always monitor for loss of reflexes, respiratory depression, and decreased urine output; magnesium infusion should be stopped for evidence of hypermagnesemia, and patient may require assisted ventilation; maternal dose-related adverse effects at various serum levels include CNS depression at 6-8 mg/dL, loss of deep tendon reflexes at 8-10 mg/dL, respiratory depression at 12-17 mg/dL, coma at 13-17 mg/dL, and cardiac arrest 19-20 mg/dL; calcium gluconate 1 g IV may be administered slowly for evidence of magnesium toxicity Drug Name Phenytoin (Dilantin) -- Phenytoin has been used successfully in eclamptic seizures, but cardiac monitoring is required secondary to associated bradycardia and hypotension. The central anticonvulsant effect of phenytoin is by stabilizing neuronal activity by decreasing the ion flux across depolarizing membranes. Some benefits to using phenytoin are that it can be continued orally for several days until the risk of eclamptic seizures has subsided, it has established therapeutic levels that are easily tested, and no known neonatal adverse effects are associated with short-term usage. Adult Dose 10 mg/kg loading dose IV infused no faster than 50 mg/min, followed by maintenance dose started 2 h later at 5 mg/kg Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome Interactions Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase phenytoin toxicity; phenytoin effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate; phenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid Pregnancy D - Unsafe in pregnancy Precautions Perform blood counts and urinalyses when therapy is begun and at monthly intervals for several mo thereafter to monitor for blood dyscrasias; discontinue use if a skin rash appears and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugars); discontinue use if hepatic dysfunction occurs Drug Name Diazepam (Valium) -- Has also been used in emergencies to control eclamptic seizures but has a short CNS half-life and significant fetal CNS depressant effects. Diazepam should not be administered to stop or shorten the initial seizure, especially if IV access or the ability to rapidly intubate the patient is not readily available. Adult Dose Up to 5 mg IV over a 60-s period Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity; narrow-angle glaucoma Interactions Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohols, and MAOIs Pregnancy D - Unsafe in pregnancy Precautions May cause phlebitis and venous thrombosis and should not be administered if IV line is not secured; may cause maternal apnea and cardiac arrest if infused too quickly; neonatal adverse effects include respiratory depression, hypotonia, and poor feeding; sodium benzoate preservative competes with bilirubin for albumin binding, thus predisposing the infant to kernicterus Drug Category: Antihypertensives -- Hypertension associated with eclampsia often is controlled adequately by stopping the seizure. Antihypertensive medications are used for diastolic blood pressures >110 mm Hg. The goal of therapy is to maintain diastolic blood pressure in the range of 90-100 mm Hg. Antihypertensive therapy has 2 main goals: (1) reducing maternal morbidity and mortality associated with seizures, strokes, and pulmonary embolism and (2) reducing fetal morbidity and mortality secondary to intrauterine growth restriction, placental abruption, and infarcts. Uterine hypoperfusion may result if blood pressure is lowered too quickly. Uterine vasculature always is maximally vasodilated, and a decrease in maternal blood pressure tends to decrease uteroplacental perfusion. Although total body water in patients with eclampsia is excessive, intravascular volume is contracted and women with eclampsia are very sensitive to further volume changes. Hypovolemia results in decreased uterine perfusion. Therefore, diuretics and hyperosmotic agents should be avoided in eclampsia without prior assessment of intravascular volume. Drugs used most commonly for hypertension in pregnancy are hydralazine and labetalol. Nifedipine has been used as well to control hypertension, but it is less accepted. Drug Name Hydralazine (Apresoline) -- Drug is a direct arteriolar vasodilator that causes a secondary baroreceptor-mediated sympathetic discharge resulting in tachycardia and increased cardiac output. Hydralazine helps to increase uterine blood flow and blunts the hypotensive response. Hydralazine is metabolized in the liver. Controls hypertension in 95% of patients with eclampsia. Adult Dose 5 mg IV q15-20min as needed to keep the diastolic blood pressure <110 mm Hg Onset of action 15 min; peak effect 30-60 min; duration of action 4-6 h Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity; mitral valve rheumatic heart disease Interactions MAOIs and beta-blockers may increase hydralazine toxicity; pharmacologic effects of hydralazine may be decreased by indomethacin Pregnancy C - Safety for use during pregnancy has not been established. Precautions Implicated in myocardial infarction; caution in suspected coronary artery disease; adverse effects include flushing, headache, dizziness, palpitations, angina, and an idiosyncratic lupuslike syndrome (dose-related as well as chronic use) Drug Name Labetalol (Normodyne, Trandate) -- Nonselective beta-blocker. Available in IV and PO preparations. Used as an alternative to hydralazine in eclampsia. Uteroplacental blood flow appears to be unaffected by IV labetalol. Adult Dose IV dosing q10min in a step-wise fashion 20 mg initial dose; second dose is increased to 40 mg; subsequent doses are administered at 80 mg to a max cumulative dose of 300 mg; may be administered as a constant infusion; onset of action 5 min; peak effect 10-20 min; duration of action 45 min to 6 h Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity; cardiogenic shock; pulmonary edema; bradycardia; atrioventricular block; uncompensated congestive heart failure; reactive airway disease; severe bradycardia Interactions Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia resulting from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase labetalol blood levels; glutethimide may decrease labetalol effects by inducing microsomal enzymes Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in impaired hepatic function; discontinue therapy if signs of liver dysfunction are present; in elderly patients, a lower response rate and higher incidence of toxicity may be observed Drug Name Nifedipine (Adalat, Procardia) -- Produces calcium channel blockade, causing powerful arteriolar vasodilation. Only available in PO form. Adult Dose 10 mg PO tid; may increase to maximum dose of 120 mg/d Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity Interactions Caution with coadministration of any agent that can lower BP, including beta-blockers and opioids; H2 blockers (cimetidine) may increase toxicity Pregnancy C - Safety for use during pregnancy has not been established. Precautions May cause lower extremity edema; allergic hepatitis has occurred but is rare; the main problem with nifedipine is profound hypotension; hypotension usually responds to the administration of calcium; best to avoid in growth restricted pregnancies or in patients with abnormal fetal heart rate tracings; not well used in the setting of eclampsia Further Inpatient Care: • Blood pressure, neurologic status, and urine output should be monitored closely. Further Outpatient Care: • Patients with eclampsia should be followed up postpartum to evaluate for evidence of essential hypertension, residual deficits from the eclamptic seizure, and patient education. In/Out Patient Meds: • This disease is treated on an inpatient basis, as described above. Outpatient care plays no role in management. Transfer: • Eclampsia clearly poses a risk of considerable maternal and neonatal morbidity and mortality. All patients with eclampsia should be managed at a tertiary care center. Deterrence/Prevention: • Routine prenatal care • Early diagnosis and aggressive management Complications: • As many as 56% of patients with eclampsia may have transient deficits, including cortical blindness. • Most women do not develop long-term sequelae from eclamptic seizures, but their cases should be followed closely for resolution of symptoms. • Maternal, as well as fetal, death can be a consequence of eclampsia and its complications. Prognosis: • Approximately 25% of women with eclampsia have hypertension in subsequent pregnancies. • Only 5% of patients with hypertension develop severe preeclampsia. • Approximately 2% of women with eclampsia develop eclampsia with future pregnancies. • Multiparous women with eclampsia may be at higher risk for development of essential hypertension. • Multiparous women with eclampsia have a higher mortality rate in subsequent pregnancies than primiparous women. Patient Education: • The patient should be advised and educated on the course of the disease and any residual problems. • The patient should be educated on prevention and avoidance of eclampsia in future pregnancies by obtaining adequate prenatal care. • If the patient has preexisting hypertension, she should have good control prior to conception and throughout pregnancy. Her case should be followed closely for recognition and treatment of early preeclampsia. Medical/Legal Pitfalls: • The mode of delivery should be based on obstetric indications, with the understanding that vaginal delivery is preferable from a maternal standpoint. • When emergent cesarean delivery is indicated, substantiating the absence of DIC prior to the procedure is important. • Fetal bradycardia is extremely common following an eclamptic seizure and usually resolves within 10 minutes. Consider placental abruption if uterine hyperactivity remains and fetal bradycardia persists. • Cervical examination should not be overlooked. The delivery mode may be largely dependent on the cervical status. • Fluid management is critical in patients with eclampsia. • Avoid the use of multiple agents to abate eclamptic seizures. • Ruling out eclampsia in an obstetrical patient who has been involved in an unexplained trauma is important. Special Concerns: • Do not overlook other neurologic causes, particularly if the seizure occurs more than 24 hours after delivery. • When preeclampsia occurs in the early second trimester (ie, 14-20 weeks' gestation), the diagnosis of hydatiform mole or choriocarcinoma should be considered. • Eclampsia always should be considered in a visibly pregnant patient with a seizure episode. A pregnant patient who has been involved in an unexplained trauma (such as a single-vehicle auto accident) without obvious cause for seizure should be evaluated for eclampsia. ACE HELLP syndrome? Link to comment Share on other sites More sharing options...
ncmedic309 Posted July 29, 2006 Share Posted July 29, 2006 HELLP Syndrome H – Hemolytic Anemia (abnormal breakdown of red blood cells) EL – Elevated Liver Enzymes LP – Low Platelet Count HELLP Syndrome occurs during pregnancy with patients who have pre-eclampsia and eclampsia. The syndrome is typically an early warning sign of pre-eclampsia. Common signs and symptoms of the syndrome include abdominal pain (usually in upper quadrants), headache, and worsening nausea and vomiting. Lab work will reveal elevated liver enzymes along with low red blood cell and platelet counts. The most significant complication of HELLP syndrome is liver damage. Care is mainly supportive in the pre-hospital environment and treating the signs and symptoms of eclampsia should they present. Definitive treatment in the hospital setting is delivery of the child in the most severe cases. Differences between Fetal Circulation and Newborn/Neonatal Circulation Link to comment Share on other sites More sharing options...
FL_Medic Posted July 30, 2006 Share Posted July 30, 2006 HELLP Syndrome H – Hemolytic Anemia (abnormal breakdown of red blood cells) EL – Elevated Liver Enzymes LP – Low Platelet Count HELLP Syndrome occurs during pregnancy with patients who have pre-eclampsia and eclampsia. The syndrome is typically an early warning sign of pre-eclampsia. Common signs and symptoms of the syndrome include abdominal pain (usually in upper quadrants), headache, and worsening nausea and vomiting. Lab work will reveal elevated liver enzymes along with low red blood cell and platelet counts. The most significant complication of HELLP syndrome is liver damage. Care is mainly supportive in the pre-hospital environment and treating the signs and symptoms of eclampsia should they present. Definitive treatment in the hospital setting is delivery of the child in the most severe cases. Differences between Fetal Circulation and Newborn/Neonatal Circulation Foramen Ovale, Ductus Arteriosus, Ductus venosus, And umbilical cord. What is the strap sequence for a KED. Link to comment Share on other sites More sharing options...
Cookie Posted July 30, 2006 Share Posted July 30, 2006 A. KENDRICK EXTRICATION DEVICE (KED) First EMT 1. Stabilize and support the head in a neutral position 2. Maintain stabilization until patient’s head is secured to KED Second EMT 1. Assist in repositioning the patient’s body to a neutral position, as necessary 2. Assess and record circulation, movement and sensation in all four extremities 3. Select and apply an appropriately sized cervical collar 4. Prepare and position KED behind patient (Request additional help in positioning patient if necessary) 5. Secure KED with center and bottom chest straps. Assure firm contact of device with lower back and armpits 6. Pad any void between patient’s head and the device to preserve neutral alignment as is necessary 7. Secure head to device; first strap over forehead, second strap over chin NOTE: The chin strap may be omitted or removed if airway compromise exists 8. First EMT may now release manual stabilization Both EMTs 1. Secure groin and top chest straps 2. Secure hands and lower extremities 3. Position long immobilization device adjacent to patient 4. Slide and pivot patient; support patient at thighs and with device handles 5. Lower patient to long immobilization device; maintain legs in flexed position 6. Move patient to head of long immobilization device 7. Release groin straps and lower the patient’s legs to the long immobilization device. Loosen top chest strap as necessary to facilitate breathing and patient comfort 8. Secure patient to long immobilization device at chest, pelvis, thighs, and below knees, padding as necessary 9. Reassess and record circulation, movement and sensation in all four extremities What are Cheyne-Stokes respirations Link to comment Share on other sites More sharing options...
FL_Medic Posted July 31, 2006 Share Posted July 31, 2006 A. KENDRICK EXTRICATION DEVICE (KED) First EMT 1. Stabilize and support the head in a neutral position 2. Maintain stabilization until patient’s head is secured to KED Second EMT 1. Assist in repositioning the patient’s body to a neutral position, as necessary 2. Assess and record circulation, movement and sensation in all four extremities 3. Select and apply an appropriately sized cervical collar 4. Prepare and position KED behind patient (Request additional help in positioning patient if necessary) 5. Secure KED with center and bottom chest straps. Assure firm contact of device with lower back and armpits 6. Pad any void between patient’s head and the device to preserve neutral alignment as is necessary 7. Secure head to device; first strap over forehead, second strap over chin NOTE: The chin strap may be omitted or removed if airway compromise exists 8. First EMT may now release manual stabilization Both EMTs 1. Secure groin and top chest straps 2. Secure hands and lower extremities 3. Position long immobilization device adjacent to patient 4. Slide and pivot patient; support patient at thighs and with device handles 5. Lower patient to long immobilization device; maintain legs in flexed position 6. Move patient to head of long immobilization device 7. Release groin straps and lower the patient’s legs to the long immobilization device. Loosen top chest strap as necessary to facilitate breathing and patient comfort 8. Secure patient to long immobilization device at chest, pelvis, thighs, and below knees, padding as necessary 9. Reassess and record circulation, movement and sensation in all four extremities What are Cheyne-Stokes respirations Cheyne-Stokes respirations are a form of periodic breathing. Typically, over a period of 1 minute, a 10-20 second episode of apnea or hypopnea is observed followed by respirations of increasing depth and frequency. The cycle then repeats itself. Despite periods of apnea, significant hypoxia rarely occurs. Cheyne-Stokes respirations are not unique to congestive heart failure although they are perhaps more common in older patients with CHF. common resp. in a Head trauma or stroke. What endogneous neclueotide do we use in the field that may put a pt. in Asystole for a period of time? Link to comment Share on other sites More sharing options...
ncmedic309 Posted July 31, 2006 Share Posted July 31, 2006 What endogneous neclueotide do we use in the field that may put a pt. in Asystole for a period of time? That would be Adenosine (Adenocard)... Stevens-Johnson Syndrome Link to comment Share on other sites More sharing options...
FL_Medic Posted July 31, 2006 Share Posted July 31, 2006 That would be Adenosine (Adenocard)... Stevens-Johnson Syndrome Stevens Johnson Syndrome Stevens Johnson syndrome, also known as SJS, is a severe disorder of mucous membranes. It can have signs and symptoms similar to those of severe erythema multiforme, a skin condition that causes blistering and erosion of the skin and mucous membranes, especially in the mouth. Doctors believe this disorder is an allergic or hypersensitivity reaction. Known causes include: Certain medications, including sulfonamide, penicillin, antibiotics, Dilantin (phenytoin) and Bextra (valdecoxib) Bacterial and viral infection, such as the herpes simplex virus and mycoplasma Radiation therapy What medication and dosage would you concider for eclampsia? Link to comment Share on other sites More sharing options...
Ace844 Posted July 31, 2006 Share Posted July 31, 2006 What medication and dosage would you concider for eclampsia? Anticonvulsants -- Prevent seizure recurrence and terminate clinical and electrical seizure activity. Drug Name Magnesium sulfate -- Several studies have revealed that magnesium sulfate is the drug of choice for treating eclamptic seizures. Magnesium sulfate is successful in controlling seizures in >95% of cases. Agent has physiologic advantages to the fetus by increasing uterine blood flow. Mechanism of action of magnesium sulfate therapy is that it inhibits the release of acetylcholine at the motor endplate. In addition, magnesium has a direct effect on skeletal muscle by virtue of its competitive antagonistic effects with calcium. Magnesium sulfate is excreted exclusively by the kidneys and has little antihypertensive effect. It is an effective anticonvulsant and helps prevent recurrent seizures and maintain uterine and fetal blood flow. Can be administered both IV and IM. Intravenous route is preferred over IM route because administration is controlled more easily and time to therapeutic levels is shorter. Intramuscular administration of magnesium sulfate tends to be more painful and less convenient. If IV access or close patient monitoring is unavailable, this is an effective therapy. The goals of magnesium therapy are to terminate ongoing seizures and prevent further seizures. Patient should be evaluated qh to assure that deep tendon reflexes are present, respirations are at least 12 breaths per min, and urine output is at least 100 mL during the preceding 4 h. When using magnesium sulfate IV, close monitoring of patient and fetus is necessary. Magnesium therapy usually is continued for 12-24 h following delivery and may be stopped when the hypertension resolves and the patient has shown adequate diuresis. Renally compromised patients should be monitored with magnesium levels, with aggressive adjustments made to facilitate levels at 6-8 mg/dL. Patients with increased urine output may need maintenance dose increased to 3 g/h to maintain therapeutic levels. Monitor patient for signs of worsening condition and magnesium toxicity. The Parkland IM protocol is as follows: Magnesium sulfate 4 g IV over 5 min, plus magnesium sulfate 10 g deep IM (3-in needle) divided in both buttocks and mixed with 1 mL 2% lidocaine. If a seizure persists more than 15 min after above dose, administer an additional 2 g of magnesium sulfate IV over 3-5 min. Magnesium sulfate 5 g IM q4h, starting 4 h later unless patellar reflexes are absent, respiratory depression occurs, or urine output is <100 mL in the prior 4 h. Therapeutic levels are 4.8-8.4 mg/dL. With the above protocol, serum magnesium levels usually are 4-7 mg/dL in a patient with an average volume of distribution and normal renal function. Actual serum magnesium levels are monitored only in patients with symptomatic magnesium toxicity or renal compromise. Patients may have seizures while receiving magnesium sulfate. If seizure occurs in first 20 min after loading dose, the convulsion usually is short, and no additional treatment is indicated. If seizure occurs >20 min after the loading dose, an additional 2-4 g of magnesium may be administered. Adult Dose Initial: 4-6 g bolus IV over 15-20 min; if convulsion occurs after initial bolus, an additional 2 g IV over 3-5 min may be administered Approximately 10-15% of patients will have another convulsion after the loading dose Maintenance: 2-4 g/h IV maintenance drip If magnesium level is >10 mg/dL at 4 h after initial bolus, decrease the maintenance dose Pediatric Dose Administer as in adults Contraindications Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis; or myasthenia gravis Interactions Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine Pregnancy A - Safe in pregnancy Precautions Always monitor for loss of reflexes, respiratory depression, and decreased urine output; magnesium infusion should be stopped for evidence of hypermagnesemia, and patient may require assisted ventilation; maternal dose-related adverse effects at various serum levels include CNS depression at 6-8 mg/dL, loss of deep tendon reflexes at 8-10 mg/dL, respiratory depression at 12-17 mg/dL, coma at 13-17 mg/dL, and cardiac arrest 19-20 mg/dL; calcium gluconate 1 g IV may be administered slowly for evidence of magnesium toxicity How about, ATN? Link to comment Share on other sites More sharing options...
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