Case presentation: Eclampsia By R2 王鎮華

Brief history A 30y/o female G1P0, GA:33+ weeks Hypertension and proteinuria since AP 11 w Prenatal examination at a local clinic

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

Brief history Seizure attack at our ER On endotracheal tube Impression:Eclampsia ASA:4

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

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

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)

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

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

Classification of preeclampsia: Mild and Severe No cyanosis No HELLP syndrome Platelet count>100,000/mm 3 No pulmonary edema

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

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 )

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

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