Eclmpsia

Anesthesia for the Preeclamptic Patient Shane Yates, M.D. MAJ, MC

Origin • From the Greek meaning “to shine forth” implying a ‘sudden development’. • “Fits” occurring during pregnancy recorded as early as 4th century BC by Hippocrates.

Definition of Preeclampsia • Remains nebulous since exact etiology is still unknown • Onset of systemic hypertension and proteinuria with or without edema occurring after the 20th wk of gestation. • Preeclampsia + seizures = eclampsia. • Disease can occur before the 20th week in the presence of trophoblastic disease.

Criteria • ISSHP (International Society for the Study of Hypertension in Pregnancy) 1988 • Single DBP >110 mmHg or two readings >90 mmHg 4 hrs apart. • SBP >140 or DBP >90 mmHg on two readings 6 hrs apart. (ACOG, 1996). • Proteinuria either 1+ or greater on dipstick or >300 mg in a 24hr urine.

Severe Preeclampsia • SBP >160 mmHg, DBP >110 mmHg on more than one reading (ACOG). • Proteinuria >5g in 24 hrs. or 3+/4+ on dipstick. • Oliguria with UOP <400cc in 24 hrs. • Neurologic sxs- HA, blurred vision, altered LOC. • Pulmonary edema or cyanosis. • Epigastric or RUQ pain. • Hepatic insufficiency or rupture • Thrombocytopenia • HELLP syndrome

Incidence • • • •

Hypertensive d/o’s complicate 10% pregnancies Preeclampsia - 5% of pregnant women. Eclampsia complicates about 1:2000 pregnancies. Incidence is significantly higher in developing countries presumably due to lack of prenatal care. • 1/3 of seizures occur before diagnosis of preeclampsia is made. • 30% of all seizures post-partum.

Risk Factors • • • •

Nulliparity Family History High body mass Multiple gestation (or any condition where there is an incr’d placental tissue) • Chronic HTN • There is no test to predict pre-eclampsia

Pathophysiology • Exact pathophysiology is not known • 20th wk- failure of the trophoblastic cells to invade the spiral arteries supplying the placenta. • Spiral arteries maintain their adrenergic innervation. • Leads to placental insufficiency and ischemia • Injured placenta releases toxins which damage the vascular endothelium. • results in a systemic microvascular disease

Pathophysiology Cont’ • Capillaries become leaky with movement of protein to the interstitial space. • Injured endothelial cells produce decreased amounts of PGI2 • Activates platelets and procoagulants (VIIIc, VonWillebrands) • Activated platelets produce TXA2 and 5HT which promote vasospasm. • Autoimmune theory vs. PGI2/TXA2 imbalance theory

Pathology by System

Cardiovascular • HTN is an early sign • Responses to catecholamines are exaggerated. • Increased sensitivity to angiotensin II • No consistency among CO, MAP, SVR(?) • May be signif disparity btwn PAOP and CVP • Plasma vol reduced in concert with severity • COP (colloid oncotic pressure) reduced

Pulmonary • Predisposed to pulmonary edema due to alterations in Starling forces. • Pulmonary edema complicates about 3% of pre-eclampsia cases. • About 70% of pulm edema episodes occur in the post-partum period.

Central Nervous System • • • • •

Mechanism of seizures is unknown. Vasospasm, edema and microinfarct. EEGs incr theta and delta wave activity. No correlation between HTN and onset of seizures. CNS Sx- HA (retroorbital), photophobia, diplopia, scotomata, blurry vision. • Signs- clonus, hyperreflexia, altered LOC • CNS signs signify increased cerebral irritation • Seizures can develop without CNS Sxs.

Renal • Non-selective proteinuria • Decr’d RBF and GFR, increase in serum Cr. • Decr urate clearance. Nl uric acid is inconsistent with severe disease. • Glomerular swelling, narrowing of glomerular capillary and fibrin deposition. • Oliguria common • Overt renal failure rare (ATN) • Cortical necrosis cause of irreversible ARF (rare)

Hematologic System • • • • • •

Thrombocytopenia is common; <100K in 15% Antiplatelet IgG(support for autoimmune theory). Incr’d factor VIIIc, Von Willebrand factor Reduced AT3 Hypercoagulable state HELLP (hemolysis, inc LFTs, low plts) – hemolysis dx by peripheral blood smear, inc bili – AST >70 U/L, LDH >600 U/L – platelet count <100K/mm3

• DIC in a small subset etiology unclear

Hepatic • Elevation of liver enzymes – periportal endothelial damage – can lead to dec clearance of drugs

• Spontaneous liver rupture – rare, but lethal – preceded by subcapsular edema or hemorrhage

• Abnormal LFTs may signify HELLP • Ascites

Fetus • Placental insufficiency • Higher incidence of emergent Csection for fetal distress. • Higher incidence perinatal mortality • Often forced to deliver fetus prematurely • Placental abruption more common

Treatment • Treatment is symptomatic • The only cure for preeclampsia is delivery of the fetus AND the placenta.

Blood Pressure Control • Chronic control- methyldopa, nifedipine. • Acute control- hydralazine, nifedipine, nitrates, labetolol. • ACE inhibitors are contraindicated • Goals- SBP 130-170 mmHg, DBP 90-110 mmHg • Invasive monitoring if BP is difficult to control or if nitrates are being used

Fluid Therapy • Goal: organ perfusion w/o pulmonary edema. • Prehydrate before anesthesia? • Repeated fluid boluses should not be given without invasive monitoring • No proven benefit of colloid over crystalloid.

Treatment of Oliguria • Rule out postrenal • Treat initially with fluid bolus • Invasive monitoring if fluid bolus unsuccessful • Loop diuretics can be used after prerenal causes are eliminated • DA shown to be safe and effective for increasing UOP.

Seizure prophylaxis and Tx • Mg++ mainstay for seizure prophylaxis – not an anticonvulsant – inhibition of cerebral vasoconstriction – toxicity - hyporeflexia, resp depression, hypotension – toxicity treated with calcium – Ca++ tx can reverse anticonvulsant effects – predisposes pt to neuromuscular blocker sensitivity

Seizure management • If a seizure occurs. 1. ABCs 2. benzodiazepine, barbituates 3. rule out other causes -LA toxicity -preexisting seizure disorder

Delivery of Fetus • Only “cure” for pre-eclampsia • Mother at risk for seizures for 48 hrs after delivery, rarely after this. • Must weigh maternal risks with fetal risks (prematurity)

Anesthesia and Analgesia Management in the Preeclamptic Patient

Epidural • Preferred for labor and operative delivery • Analgesia, BP control, gradual onset of sympathectomy, conversion to surg anesthesia. • Smaller HD and neuroendocrine responses compared to GA for C-section. • Larger fall in BP compared to normal pt. • Prehydrate? • ephedrine safe if titrated in small doses • avoid epinepherine • lidocaine, bupivicaine, ropivicaine, 2CP all safe

Spinal Anesthesia • Speed and degree of sympathectomy may be greater compared to epidural. • Accepted form of anesthesia for C-section • Evidence of coagulopathy (thrombocytopenia) is a contraindication • Must weigh risks of epidural hematoma with risk of GA. • Prehydration?

“Randomized Comparison of General and Regional Anesthesia for C-section in pregnancy complicated by severe pre-eclampsia”, Wallace et al., Ob&Gyn, Aug 1995 • Prospective, ramdomized trial comparing HD and outcomes of GA vs. Epid vs. SAB • Inclusion: severe pre-E by BP • Exclusion: no fetal probs, no plt<100K, no signif comorbid problems. • More fluid & ephed w/regional. Lower BP with reg. No diff btwn SAB and Epid • No severe maternal or fetal complications • Conc: SAB is safe reg anesth for C-sec in severe pre-E

“Spinal vs. Epidural Anesth for C-section in Severely Preeclamptic Patients”, Hood et.al., Anesthesiology, May 1999 • Retrospective review of 138 women w/severe pre-e undergoing c/s under either SAB or Epid. • Did not include women in labor • Indication worsening pre-e in all cases • No diff in HD btwn groups • No diff in ephedrine use • More Cx in SAB group • No diff in incidence of pulm edema or ICU admits • No diff in fetal outcome

General Anesthesia • emergent C-sections • absolute contraindication for regional.

Airway management • increased pharyngeal and laryngeal edema • observe for stridor or hoarseness • difficult airway equipment should be available • Na Citrate • RSI with cricoid pressure

Extubation • laryngeal edema may worsen during surgery • see if patient can breath around cuff • hypertensive response to extubation • If signs of pulm edema, consider postoperative mechanical ventilation

Hemodynamic Control • exaggerated andrenergic response to intubation, incision, extubation • CVAs, uteroplacental insufficiency, pulmonary edema • labetolol and hydralazine -> NTP • Lidocaine pretreatment

Induction Agents • Ketamine should be avoided • Pentothal may be agent of choice – documented safety in parturient – anticonvulsant properties – vasodilating properties

• Etomidate and propofol may also be used

Neuromuscular Blockade • Sux safe to use; may not see fasciculations with Mg++ • All neuromuscular blockers are potentiated by Mg++

Remember… to avoid trouble • Evaluate and examine the patient as soon as possible • Have a preformulated plan (and backup plan) for – fetal complications – maternal complication – emergent C-section

? Questions ?