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Case presentation: Eclampsia By R2 王鎮華
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Brief history A 30y/o female G1P0, GA:33+ weeks Hypertension and proteinuria since AP 11 w Prenatal examination at a local clinic
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Brief history Dyspnea occurred 2 days ago Dyspnea recurred with conscious change BT:36.1,HR:110,BP:221/173,RR:44, SpO2:78,BW:>90Kg Breath sound:coarse and crackle over bilateral lungs
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Brief history Seizure attack at our ER On endotracheal tube Impression:Eclampsia ASA:4
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Brief history HR:112, BP:165/120, SpO 2 :98 when arrived at OR On A-line, CVP before induction CVP:12 Induction agent:Fentanyl,Nimbex Tidal volume:500ml, PEEP:6cmH 2 O, airway pressure:30cmH 2 O after induction
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Brief history Frothy secretion flowed through endotracheal tube SpO 2 dropped slowly from 98% to 92% Suction+Lasix 1 amp Everything went well until birth of the baby BP dropped quickly from 142/80mmHg to 68/48mmHg
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Brief history IV fluid fully ran Intermittent bolus of levophed Dopamine ran 12mic g/Kg/min Operation duration:75min. Intake:1200ml, urine output:300ml The patient was transferred to ICU after operation(HR:100, BP:110/78, SpO 2 :97)
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Eclampsia Preeclampsia+seizure Preeclampsia may present as a syndrome of multiorgan failrue including neurologic, renal, liver, hematologic, cardiorespiratory, and fetoplacental abnormalities Definition of preeclampsia:hypertension, proteinuria>300mg/24hr,oliguria, elevated liver enzymes,headache,visual disturbances, hematologic disturbances, intrauterine growth retardation
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Classification of preeclampsia: Mild and Severe Systolic pressure <160mmHg Diastolic pressure <110mmHg Urinary protein <5g/24hr,dipstick+or2+ Urine output >500ml/24hr No headache No visual disturbance
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Classification of preeclampsia: Mild and Severe No cyanosis No HELLP syndrome Platelet count>100,000/mm 3 No pulmonary edema
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Pathophysiology of preeclampsia The pathogenesis of preeclampsia is incompletely understood. Anatomic changes in blood vessels of placental bed Acute atherosis:partial luminal obstruction by lipid-laden cells Endothelial perturbation and altered vascular reactivity
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Pathophysiology of preeclampsia Augmented release of a host of vasoconstrictors (platelet-derived thromboxane, endothelin, catecholamines) The expression of cell adhesion molecules Postmortem studies reveal evidence of vascular injury ( interstitial edema, intravascular dehydration, intensified peripheral vasospasm,diminished perfusion )
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Clinical presentation of preeclampsia A non-life-threatening disease for most women that resolves on delivery Leading causes of maternal mortality: eclampsia,pulmonary complications, HELLP syndrome and renal failure
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Principles of management for eclampsia Prevent recurrent seizures Control airway Plasma volume expansion Control hypertension Termination of the pregnancy always secures remission of the disease
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