Pre-eclampsia is a syndrome of pregnancy-induced hypertension. proteinuria, and edema occurring arter the 20th week of gestation and resolving within 48 hours after delivery. [Morgan and Mikhail. Clinical Anesthesiology.
When seizures are associated with the syndrome of pregnancy-induced hypertension. the syndrome is termed eclampsia. [Morgan and Mikhail.
Clinical Anesthesiology. 1996. p717]
What does HELLP stand forI
HemolysiS. Elevated Liver enzymes. and Low Platelet count. [Morgan and Mikhail. Clinical Anesthesiology. 1996. p718]
When does the HELLP syndrome usually
occur? What should be done if this syndrome
The HELLP syndrome usually occurs before 36 weeks gestation. Its diagnosis calls for immediate delivery, regardless of gestation due to high maternal and fetal mortality. [Shnider and Levinson, Anes.for DB., 1993, pp32-34)
Severe pregnancy-induced hypertension (pre-eclampsia) is characterized by what seven signs and symptoms?
(1) Hypertension (arterial blood pressure greater than 1601110 mm Hg); (2) proteinuria (greater than 5 grams per day); (3) oliguria (urine flow less than 500 mLlday); (4) systemic and pulmonary edema; (5) eNS dysfunction (headaches, visual disturbances, seizures); (6) hepatic tenderness; and (7) presence ofHELLP syndrome. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p718; Shnider and Levinson, Anes. for DB., 1993,
List the diagnostic triad (most characteristic
signs and symptoms) of pre-eclampsia.
(1) Hypertension (2) proteinuria, and (3) generalized edema. [Stoelting, Co-Existing, 1993, p783)
The pregnant patient presents with maternal
hypertension, hyperreflexia, and convulsions.
Your immediate diagnosis is pregnancy-
induced hypertension (PIH). What other
diagnosis must be included in your differential
Cocaine abuse. Maternal hypertension, hyperreflexia, and convulsion due to cocaine abuse can mimic pregnancy-induced hypertension (PIH) and must be included in your differential diagnosis. [Hughes Shnider and Levinsons Anes. for DB., 2002, p60S]
The patient with pregnancy-induced hypertension (pre-eclampsia) is in danger of
developing what six very serious complications?
(1) Pulmonary edema, (2) cerebral hemorrhage, (3) renal failure, (4) cerebral edema, (5) disseminated intravascular coagulopathy, and (6) airway obstruction are serious complications of pregnancy-induced
hypertension. [Datta, Db. Anes. Handbook, 1995, p200]
In the pre-eclamptic patient, what are the
best tests to evaluate bleeding? Why?
PT and PTT might be best because prolongation ofPT and PTT indicates
consumption of coagulant factors. Platelets, fibrinogen, and fibrin split
products might also be assessed to check for disseminated intravascular
coagulation (DIe). [Yao and Artusio, Problem Oriented Patient Management,
1993, p50l; Stoelting, Co-Existing, 1993, pp562, 1281; Barash,
Clinical Anesthesia, 1997, pl070- 1074]
What is the number one cause of maternal
death in pregnancy-induced hypertension
(PIH = pre-eclampsia)? The second most
The number one cause of maternal death in pregnancy-induced hypertension is cerebral hemorrhage. The second leading cause of death is pulmonary
edema. [Yao, POPM, 5th ed. 2003, p81S; Stoelting & Dierdorf, CoExisting,
4th ed. 2002, p661J
How does pre-eclampsia affect the uteroplacental circulation?
Uterine vascular resistance increases in pre-eclampsia, so uterine blood flow decreases. The uteroplacental circulation is compromised in preeclampsia.
[Shnider and Levinson, Anes. for DB., 1993, pp306-314]
The mother has pre-eclampsia. What causes
the variations in fetal heart rate? What causes
the mother's increased blood pressure?
The placenta develops a vasculitis, and placental perfusion decreases. Decreased blood flow to the fetus with associated hypoxia causes variations in fetal heart
rate. Pregnancy-induced hypertension is thought to be due to decreased placental perfusion. Placental ischemia and placental dysfunction result in release into the
circulation of a variety of mediators including thromboxane, renin, angiotensin, aldos terone, catecholamines and thromboplastin. These mediators lead to generalized vasoconstriction and hypertension. [Morgan and Mikhail, Clinical AnestheSiology,
1996, p717; Davison, Eckhardt, and Perese, Mass General, 1993, pp466-
List 8 antihypertensive agents used prophylactically to prevent hypertension during
induction of general anesthesia or to treat
severe hypertension in the pre-eclamptic
All of the following antihypertensive drugs are used in the patient with pregnancy-induced hypertension (pre-eclampsia): (1) hydralazine (the "standard" agent for this condition); (2) labetalol; (3) sodium nitroprusside (briefly for hypertensive emergencies); (4) nifedipine (a calcium channel blocker); (5) trimethaphan Arfonad), which may be useful because it does not cause cerebral vasodilation and increased intracranial pressure; (6) alpha-methyldopa; (7) nitroglycerin; and (8) diazoxide. Note that all of these agents have vasodilating properties. [Hurford, Bailin, Davison, Hospel, Rosow, Mass General, 1998, pp535-536; Barash, Clinical Anesthesia, 1997, ppl073-1074; Longnecker et aI., PPA, 1998, p499;
Stoelting, Co-Existing, 1993, p563]
What are concerns with using sodium nitroprusside or nitroglycerin in the preeclamptic
Cyanide toxicity in fetal lambs occurs with high-dose nitroprusside. Toxicity in human fetuses, however, has not been demonstrated with shortterm use of recommended doses of nitroprusside. The actions of nitroglycerin are unpredictable. In pre-eclamptic patients with severe hypertension and low pulmonary capillary wedge pressure, either nitroprusside or nitroglycerin can precipitate profound hypotension. [Datta, Ob. Anes.Handbook, 1995, p211; Longnecker et al., PPA, 1998, p499]
What is the mainstay therapy for hypertension
in the pre-eclamptic patient? Why?
Hydralazine, which may be given 1M, PO, or IV, has been the intrapartum mainstay antihypertensive therapy. Hydralazine is popular because it lowers blood pressure and increases uteroplacental blood flow. [Datta, Ob. Anes. Handbook, 1995, p211; Longnecker et aI., PPA, 1998, p499]
Which drug on the following list would you
NOT give to treat severe hypertension in the
pre-eclamptic patient: hydralazine, sodium
nitroprusside, nitroglycerin, esmolol,
labetalol, or trimethaphan? Why?
Esmolol should be avoided in the treatment of hypertension in the preeclamptic patient. "Unlike labetalol, esmolol can have significant, potentially advcrse fetal cffects." [Morgan and Mikhail, Clinical Anesthesiology,
What drug(s) would you administer to a
pre-eclamptic patient with cerebral edema
prior to cesarean section?
Hydralazine or labctalol are the most popular drugs to reduce hypertension in the pre-eclamptic patient. Cerebral blood flow and intracranial pressure are maintained with both of these antihypertensives. Antihypertensive with reported adverse cffccts during pregnancy which may be avoided include esmolol, clonidine, nifedipine, and ACE inhibitors. [Norris,
Ob. Anes., 1999, pp509-51l; Hughes Shnider and Levinsons Anes. for OB., 2002, pp306- 307; Omoigui, Anesthesia Drug Handbook, 1999,
Why is the fetus at increased risk in the
patient with pregnancy-induced hyperten sion
The fetus is at increased risk because of marginal placental function.
[Stoelting, Co-Existing, 1993, p562]
List six complications during pregnancyinduced
hypertension (PIH, pre-eclampsia)
that necessitate immediate delivery of the
Six complications during pregnancy-induced hypertension (PIH, preeclampsia) that necessitate immediately delivery of the fetus are: (1) severe hypertension (systolic ~ 160 mmHg or diastolic ~ 110 mmHg), persisting for 24-48 hours, (2) progressive thrombocytopenia, (3) liver dysfunction, (4) progressive renal dysfunction, (5) premonitory signs of eclampsia, and (6) evidence of fetal jeopardy. [Chcstnut, Ob. Anes., yd ed.,
Should either a general or regional anesthetic
be used to lower blood pressure in the
No. [Stoelting and Miller, Basics, 1994, p370]
What is the most common cause of morbidity
and mortality in pregnancy?
Pre-eclampsia and eclampsia, often referred to as toxemia of pregnancy and now referred to as pregnancy-induced hypertension, are among the leading causes of maternal morbidity and mortality. [Miller, Anesthesia,
Your pregnant pre-eclamptic patient has
temporomandibular joint (TMj) rigidity. What would be safe anesthetics to consider?
Hyperreflexia and CNS irritability occur in pre-eclampsia, accounting for the TMJ rigidity. Anesthesia can be managed by epidural, spinal or general anesthesia. Continuous epidural lumbar anesthesia is a useful method
of analgesia for labor and vaginal delivery for the volume-depleted preeclamptic patient. [Yao and Artusio, POPM, 1993, pp499, 507- 513; Stoelting,
Co-Existing, 1993, p564]
What is the normal serum magnesium
concentration, and what is the therapeutic
anticonvulsant range in the treatment of
Normal serum magnesium is 1.4-2.0 mEq/liter, and the therapeutic range for the treatment of peeclampsia/eclampsia is 4-7 mEq/liter. [Longnecker
et aI., PPA, 1998, p973]
How can you convert a magnesium concentration reported in mEq/liter to mg/dL? If
serum magnesium is 4 mEq/lliter, what is the
concentration in mg/dL?
Divide mEq/liter by 0.8 to convert to mg/dL. 4 mEqlliter/0.8 = 5 mg/dL.
[Longnecker et aI., PPA, 1998, p973]
State the loading and maintenance doses
of magnesium sulfate administered for
seizure prophylaxis in pregnancy-induced
For seizure prophylaxis in pregnancy-induced hypertension (p reeclampsia),magnesium sulfate is administered at a loading dose of 4-6 g over 20-30 minutes, followed by a maintenance dose of 1-2 g/hr., continued for up to 24 hours postpartum. [Chestnut, OB Anes. 4th. 2009 pp986]
What is magnesium sulfate's anticonvulsive
mechanism of action in eclampsia and preeclampsia?
Magnesium depresses the CS and increases the threshold for seizure activity. Magnesium produces these effects by decreasing the presynaptic release of acetylcholine and reducing the sensitivity of postsynaptic membranes to acetylcholine. [Shnider and Levinson, Anes. for OB., 1993, p315; Stoelting, Co-Existing, 1993, p563]
List, in order of appearance, seven clinical
manifestations of progressive hypermagnesemia.
Signs of hypermagnescmia are: (1) diminished deep tendon reflexes (4-5 mEq/liter); (2) ECC changes including prolonged PR and ST intervals, widened QRS complexes, andlor elevated T waves (4-7 mEq/liter); (3) somnolence (5-7 mEq/liter); (4) loss of deep tendon reflexes, or myotonia (8-10 mEqlliter); (5) heart block (12 mEq/liter); (6) respiratory arrest (15 mEqlliter); and (7) cardiac arrest and cardiovascular collapse
(20 mEq/liter). [Longnecker et aI., PPA , 1998, p973]
What are cardiovascular signs and symptoms
ofhypermagnesemia? At what serum
magnesium levels are these cardiovascular
signs and symptoms manifested?
ECG changes are seen when serum magnesium is 4-7 mEq/.liter. Severe hypermagnesemia produces hypotension secondary to vasodilation, bradycardia, and myocardial depression. These signs and symptoms develop when serum magnesium exceeds 20 mEq/liter. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p540]
When the plasma concentration of magnesium
rises above the therapeutic range, as
suggested by the absence of the knee jerk
(patellar tap) reflex, what three things can
(1) Heart block, (2) ventilatory failure, and (3) cardiac arrest. [Stoelting, Co-Existing, 1993, pS63; Longnecker et al., PPA, 1998, p973]
What is the earliest sign of magnesium toxicity?
Clinically, the therapeutic effects of magnesium therapy are estimated by the response to deep tendon reflexes. Marked depression of deep tendon reflexes is an indication of impending magnesium toxicity. At therapeutic magnesium levels (4-6 mEq/L), lethargy, nausea & vomiting, and facial flushing may occur. At magnesium levels greater than 6 mEq/L, loss of deep tendon reflexes and hypotenSion ensue. [Miller & Stoelting, Basics. Se. 2007 pp494; Hines, Stoelting's Co-existing. Se. 2008 pp3S8]
What specific changes are often seen in
the ECG when magnesium levels reach 10
At magnesium levels of 10 mEq/L, prolonged P-Q intervals and widened QRS complexes may be observed. Asystole occurs at 20 mEq/L. [Yao, Yao & A rtusio's POPM. 6e. 2008 pp917J
The pre-eclamptic mother who has been
receiving IV magnesium and displays depression
of deep tendon reflexes delivers her infant by Caesarean section. What signs will the infant exhibit?
Magnesium crosses the placenta. Hypermagnesemia in the neonate results in drowsiness, decreased muscle tone (atonia), and hypoventilation requiring assisted ventilation. [Yao and Artusio, Problem Oriented Patient
Management, 1993, pS06]
What is the treatment for magnesium toxicity
in the pre-eclamptic/eclamptic patient if
supportive therapy is inadequate?
Magnesium toxicity is treated with IV calcium gluconate. [Shnider and Levi nson, Anes. for OB., 1993, pp349- 3S0; Stoelti ng, Co-Existing, 1993,
The parturient with pregnancy-induced
hypertension (p re-eclampsia) has been
treated with magnesium sulfate and has now
delivered the baby. Oxytocin has been given,
but uterine atony persists. What is your next
This is a "toughie." Magnesium sulfate is often given prophylactically to the patient with pregnancy-induced hypertension (PIH) to prevent seizures. Magne·
sium sulfate is often continued for up to 24 hours postpartum for seizure prophylaxis. Recall, though that MgSO, is also a tocolytic (relaxes the uterus). Tocolytics
(e.g., MgSO" beta-adrenergic agonists, and calcium channel blockers) given before or during labor have been implicated as causative agents of uterine atony.
A careful review of medications that the patient has received or is receiving should be made and the offending agent should be stopped immediately. You might have considered giving methylergonovine to treat the uterine atony. However, even the baby has been delivered-which is definitive treatment for PIH-ergot alkaloids are relatively contraindicated in PIH, due to their hypertensive effects (Chestnut). [Datta, Anesthetic and Obstetric Management of High-Risk Pregnancy, 3'" ed.,2004, p121; Chestnut, Ob. Anes., 3'd ed., 2004, p671 ; Authorsl
The pre-eclamptic patient should generally
not receive which general anesthetic? Why?
Ketamine should be avoided because it can aggravate the hypertension.
[Barash, Clinical Anesthesia, 1997, pl074j
What is the definitive treatment for pregnancy-
induced hypertension (preeclampsia)?
The definitive treatment of pregnancy·induced hypertension is delivery of the fetus and placenta. The pregnancy is allowed to continue as long as the intrauterine environment supports growth and maturation of the fetus without endangering the mother. Hospitalization and bedrest in thelateral decubitus position are begun. Adequate hydration and IV volume expansion with a balanced salt solution are also initiated. [Sh nider and Levinson, Anes. for OB., 1993, pp314-31S]