Overview

• Severe preeclampsia – pathophysiology, Dx, maternal/fetal issues, Treatment

• Case - Ante partum flash Pulmonary edema

• Discussion

PREECLAMPSIA

A syndrome characterized by the new onset of hypertension and

proteinuria after 20 weeks gestation. Additional signs and

symptoms that can occur include edema, visual disturbances,

headache, epigastric pain, thrombocytopenia, and abnormal liver

function. These clinical manifestations are the results of

mild to severe microangiopathy of target organs such as brain,

liver, kidney, and placenta.

PATHOPHYSIOLOGY OF PREECLAMPSIA

A state of endothelial dysfunction secondary to excessive amounts of circulating factors released from the diseased placenta. These factors effect the establishment of a suitable vascular network of the placenta needed to supply oxygen and nutrients to the fetus.

• Molecular/Cellular level

– Abnormal expression of VEGF and sFlt-1 (Vascular endothelial growth factor –proangiogenic and soluble fms-like tyrosine kinase 1- anti-angiogenic factors respectively) appear to play a central role.

– Increased expression of cytokines, angiotensin, catecholamines, and pro-coagulant factors.

• Anatomic level– Increased vascular tone– Increased vascular permeability– Coagulopathy– Ischemia of target organs (brain, liver, kidney, placenta)

Multisystemic Disease

• CNS – Cortical blindness, cerebral edema, cerebral hemorrhage, and seizures

• Cardiovascular – Hypovolemia, increased SVR, LVH, increase sensitivity to catecholamines, sympathomimetics, and oxytocin

• Respiratory – pulmonary edema, V/Q mistmatch, airway edema

• Renal – Decreased renal blood flow, increased GFR, proteinuria, increased BUN and creatinine

• Hepatic – subscabular hemorrhage, abnormal LFTs, decreased plasma cholinesterase levels

• Hematologic – Prolonged bleeding time, platelet dysfunction, thrombocytopenia, DIC

• Placenta – Uteroplacental insufficiency, placental abruption, chronic fetal hypoxia, IUGR, premature labor, premature birth.

Diagnosis of Severe Preeclampsia

If one or more of the following criteria are present:

• Systolic blood pressure > 160 mmHg

• Diastolic blood pressure greater than 110 mmHg

• Proteinuria greater than 5 g/24 hrs

• Evidence of end organ damage

–Oliguria (<500ml/24hr)

–Cerebral or visual disturbances

–Pulmonary edema or cyanosis

–Epigastric pain or right upper-quadrant pain

–Impaired liver function

–Fetal growth restriction

–Thrombocytopenia

*ACOG Compendium of Selected Publications

Goals

• Control CNS irritability

– Magnesium sulfate – anti-convulsant; reduces irritability of the neuromuscular jxn.

• Restore intravasuclar fluid volume

– Strictly monitor urine output

– CVP monitor with goal 4-6 cm H20

• Normalize blood pressure

– Magnesium sulfate – direct vasodilating action on smooth muscles of arterioles and uterus.

– Labetolol, Hydralazine, nifedipine, SNP (in extreme circumstances due to fetus susceptability to cyanide toxicity)

• Correct coagulation abnormalities – Platelets, FFP, Cryoprecipitate

Effects of Increasing Plasma Magnesium Levels

• MgSO4 in excess of therapeutic range– Skeletal muscle weakness– Respiratory depression– Cardiac arrest (Ca++ can counter-act this)– MgSO4 potentiates NMB and sedative effects of opiods

Observed Condition mEq/LNormal Plasma level 1.5-2.0Therapeutic Range 4.0-8.0ECG Changes (Prolonged P-Q, widened QRS) 5.0-10Loss of deep tendon reflexes 10SA and AV node block 15Respiratory Paralysis 15Cardiac Arrest 25

Functional effects

Anatomical Effects Functional Effects

Airway edema friability

Widened AP andTransverse diameter

Elevated Diaphragm

Widened Subcostalangle

Enlarging uterus

Increased respiratory drive

Minimal change in TLCIncreased Minute ventilationReduced FRC

Normal diaphramatic Fxn

Increased O2 consumptionand CO2 production

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Increased cardiac output

ManagementDefinitive treatment for Preeclampsia is delivery of the fetus and placenta.

• Vaginal Delivery – Lumbar epidural– No fetal distress– Before catheter placement, r/o coagulopathy and insure adequate volume replacement.

• Cesarean Delivery – Regional or GA– Maternal/and or fetal status dictates the urgency for delivery– Use epidural if in place. Maintain volume status. Typically, drops in BP improve

placental blood flow.– Spinal anesthesia, in the past, has been controversial due to possibility of severe

hypotension. However, it has been shown to be a safe technique for cesarean delivery in severe preeclampsia.

– General anesthesia is an acceptable way to manage preeclamptic pts, however, there are associated risks.• Apiration• Airway compromise• Cerebral hemmorrhage• Pulmnary Edema

Case ReportPersonal Hx

• Mrs N. Safi

• 38 yrs .

• Married for 16 yrs.

• G6P5L4

• Pregnant at full term.

• Was brought to our Emergancy Department on 25.9.2011 at 1:45 am .

Chief complain:• Sudden coughing, dyspnea and choking. Hx of present illness :• Pt complained of sudden onset coughing,

dyspnea and choking • She had suffered from persisted headache for

four days.Obstetric Hx• She had 4 living baby product of 4 uncomplicated

normal vaginal deliveries.• No previous miscarriage .• Her previous pregnancies was smooth except for

mild PIH in the first pregnancy. • She was unbooked (Only one visit to P.H.C at 4

month of gestation).

Gynecologic Hx: Normal menarche & menses.

Past Hx : Uneventful

Drug Hx: None

Family Hx : Mother and father are hypertensive

on AdmissionPHYSICAL EXAMINATIONUnconscious , extreme dyspnea, marked cyanosis and blood-stained frothy mucus streamed from her nose and mouth.

Vital Signs:• T= 37.1oC BP= 270/150 mmHg• RR= 25 bpm HR=120 bpm R bil• SpO2 = 74%• There is moderate bilateral biting LL edema extending up to

Knees.

on Admission

• Chest: Large bubbling rales were heard on both sides

• Abdomen: extended with gravid uterus .FL± 34 Wk• Cardiac: RRR, no murmur appreciated, no JVD.• Fetal heart heart by Doppler

• Vaginal examination: Closed unfavorable cervix

In summary,,,

• Mrs N. Safi is 38 yrs , P4+oL4,Preg. At FT admitted as case of severe hypertension associated with extreme dyspnea, marked cyanosis and blood-stained frothy mucus streamed from her nose and mouth.

The Impression

• Pulmonary edema complicating severe preeclampsia.

• Pulmonary edema likely secondary to malignant hypertension

PROGRESS IN HOSPITAL

• 2 IV Line.

• Oxygen support

• Control of BP

• Urgent Intubation.

• Lasix administered to resolve pulmonary edema.

• Urgent CS.

Control of BP

• Hydralazine: 10 mg IV bolus (repeated twice) followed with IV infusion.

• Lasix: 20mg IV

Urgent CS At 02:00amAt 02:00am• Started at 2:30 am … finish 3:05pm.

• Strait forward surgery

• Female baby, 3 Kg with apgar score: 8-10

• Ascetic

• 2 cytotec tab rectally.

• 20 mg Lasix.

• Heparin 5000u IV.

BP Pulse SPO2

Preoperative 190/125 141 94%

At the end of Op. 126/86 115 100%

Postoperative Progress

• Pt remained intubated. Transferred to the ICU for care/post-op mgmt.

• Antihypertensive treatment (hyrdalazine infusion)

• MgSO4

• IV antibiotic.

• Heparin 5000u 1*2.

• Sedation.• Cardiology Consultation.

INVESTIGATIONS

• BG:BG: A+ve A+ve• CBC :CBC :

• Chemistry :Chemistry :

WBC HB PLT

14.3 12.5 154000

AST ALT RBS urea Uric dcid

creat

48 41 130 14 5.9 0.7

INVESTIGATIONS

• chemistry:chemistry:

• Urine analysisUrine analysis

• TSH: 2.6 T4: 8.4

WBC RBC Protien

13-15 0-2 +++

Na K Ca cl

140 4.3 8.2 109

Post op events (Day 1)

• Pt was extubated POD#1.

• BP 140-180/90-95

• Urine output: normal

• MgSO4 continue for 24hr.

• Atenolol 100mg 1*1

• Nifedipine 20mg 1*2

Cardiology Consultation

• ECG: Sinus tachycardia

• Echocardiogram: Good left ventricle contraction, normal dimension and function. Valves were normal .LVEF -60% and no pericardial effusion

Post op events

• Pt transferred to postnatal ward in POD2.

• Remained stable

• Discharged on postoperative D5 in good general condition on Atenolol 100mg 1*1 +Nifedipine 20mg 1*2 and advised to bee followed in medical out patient clinic for treatment of hypertension.

Acute Pulmonary Edema

• Pulmonary edema is defined as the accumulation of fluid in the pulmonary interstitial spaces and alveoli,

• Which prevents the adequate diffusion of both oxygen and carbon dioxide.

The pathogenesis of pulmonary edema complicating pre-eclampsia-• Generalised arterial vasospasm resulting in an increased

systemic vascular resistance (increased after load).

• Reduced plasma volume (decreased pre-load), and increased left ventricular stroke work index (hyper dynamic heart).

• Impaired renal function.

• Serum albumin is reduced and capillary permeability is increased due to endothelial damage.

All these changes predispose to an increased risk of pulmonary edema.

Acute Pulmonary Edema in Pregnancy• Cohort study(Anthony C. Sciscione et al) – 62,917 consecutive

pregnancies from 1989-1999, to describe the incidence, predisposing factors contributing to pulmonary edema in the pregnant patient.

– Fifty-one women (0.08%) were diagnosed with acute pulmonary edema during ante partum - post partum period.

– 24 patients (47%) antepartum

– 7 patients (14%) intrapartum

– 20 patients (39%) post partum

• Most common causes:

– Tocolytics (25.5%) most commonly MgSO4 and SC terbutaline

– Cardiac disease (25.5%)

– Fluid overload (21.5%)

– Preeclampsia (18%)

Acute Pulmonary Edema in PregnancyIn a study of 37 cases of pre-eclampsia, Sibai et al reported an • incidence of pulmonary edema in 2.9% patients• 30% of these cases developed pulmonary edema antenatally,

whilst 70% developed it after delivery, within an average time of 71 hours.

• The mechanisms responsible for this increased incidence in the post-partum period are recently reviewed by Benedetti et all and Hankins et al, and are related to delayed post-partum mobilisation of extracellular fluids.

• The incidence of pulmonary edema is influenced by pre-existing chronic hypertension, maternal age and parity

→ 7.1% in patients with chronic hypertension as compared to l .7% in those with pure pre-eclampsia.

→patients with maternal age of 26. 8 years have higher incidence than those with mean age of 20.7 years.

Acute Pulmonary Edema in Pregnancy

• A report by Donnelly and Lock, on 533 patients who died of toxaemia showed that pulmonary edema was a cause of death in 25% cases.

• However, though it is a major cause of obstetric mortality, its incidence is infrequent in well managed cases of pre-eclampsia

Risk Factors

• Preeclampsia/eclampsia

• Tocolytic therapy

• Sever infection

• Cardiac disease

• Iatrogenic fluid overload

• Multiple gestation

EBM Discussion on Anesthetic Technique for Cesarean Section for Severe Preeclampsia

• Randomized comparison of general and regional anesthesia for cesarean delivery in pregnancies complicated by severe preeclampsia (1995)

– Eighty women who required C/S

– Randomized - epidural/CSE/General

– Intra-operative BP compared in all groups

– No statistical or clinical difference in maternal or fetal outcome

– Aside from logistical implications, general as well as regional were shown to be equally acceptable if steps are taken to ensure careful approach to either method.

EBM Discussion on Anesthetic Technique for Cesarean Section for Severe Preeclampsia

• Prospective cohort study; Patients with severe preeclampsia experience less hypotension during spinal anesthesia for elective cesarean delivery than healthy parturients (2003).

• Compared incidence and severity of spinal anesthesia associated hypotension in severe preeclamptic (n=30) vs. healthy parturient (n=30).– Under spinal, mean BP decreased by 32-39% in severe

preeclamptics and 33-60% in the healthy parturient.– Healthy patients were given more ephedrine than the

preeclamptics for hypotension. Possible explained by increased sensitivity of pressor drugs in the preeclamptic.

• Findings suggest that the incidenc of severity of spinal hypotension in preeclamptic patients with severe hypertension may be less than previously believed.

Discussion

• Most likely cause of pulmonary edema is multifactorial. No specific etiology was assigned.

• Unsuspected cardiac findings were common, and there was a high incidence of valvular disease.

• Most pts had severe systolic dysfunction and LVH and not cardiac disease.

• Underlying cardiac disease is most likely under-diagnosed and under-reported due to under-use of echocardiography.

Discussion

• Although an uncommon event in pregnancy,

• it is associated with an increased risk of maternal and fetal morbidity and mortality.

• Several risk factors have been identified: preeclampsia or eclampsia, use of tocolytic therapy, severe infection, cardiac disease, iatrogenic fluid overload,and multiple gestation.

• The physiologic changes associated with pregnancy may predispose the pregnant patient to pulmonary edema.

• Despite the multiple causes of pulmonary edema, there is no clear consensus on the role that each of these risk factors plays in the pregnant population.

Conclusion

• Early diagnosis and management of pulmonary edema in pregnancy is critically important to improve maternal and neonatal out come.

• Termination of pregnancy for patients with pulmonary edema complicating severe pre-eclampsia is mandatory.

• Echocardiography should be performed early to evaluate the patient for possible underlying cardiac disease.

Thank You