Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care

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CRITICAL CARE ISSUES IN PREGNANCY

807

the mother may improve with evacuation of the uterus, some

authorities, including the American Heart Association, sug-

gest that cesarean section should be started within 4–5 minutes

of initiation of CPR.

Several reports have described mothers who met elec-

troencephalographic criteria for death who were maintained

for prolonged periods on life support in order to allow

growth and maturation of the fetus. In a number of these

cases, apparently healthy infants have been delivered,

although the outcome of the infant in such cases cannot be

guaranteed.

Atta E, Gardner M. Cardiopulmonary resuscitation in pregnancy.

Obstet Gynecol Clin North Am 2007;34:585–97, xiii. [PMID:

17921016]

Mallampalli A, Guy E: Cardiac arrest in pregnancy and somatic

support after brain death. Crit Care Med 2005;33:S325–31.

[PMID: 16215355]

Soar J et al: European Resuscitation Council. European Resuscitation

Council guidelines for resuscitation 2005, Section 7: Cardiac

arrest in special circumstances. Resuscitation 2005;67:S135–70.

[PMID: 16321711]

MANAGEMENT OF CRITICAL COMPLICATIONS

OF PREGNANCY



Preeclampsia-Eclampsia

ESSENTIALS OF DIAGNOSIS



Hypertension.



Proteinuria.



Seizures (eclampsia).

General Considerations

Preeclampsia is a common disorder with an incidence of

14–20% in women undergoing their first pregnancy and

about 6% in multigravidas. It is one of the leading causes of

maternal death in the United States. Most preeclamptic

patients will be managed in the delivery suite and will not

require critical care. Patients with severe disease, however,

may have significant complications warranting ICU care.

Preeclampsia appears to be associated with defects in pla-

centation; it therefore originates in events early in pregnancy.

Although the mechanisms of preeclampsia are not com-

pletely understood, potential etiologies include abnormal

trophoblast invasion, immunologic intolerance between

mother and fetus, abnormalities of immune function, vita-

min deficiencies, and genetic abnormalities. Preeclamptic

women demonstrate an increased vascular smooth muscle

response to pressor agents, particularly angiotensin II, that

predates the development of overt hypertension. The resulting

vasospasm leads to hypertension and contraction of

intravascular volume. In more severe cases, this is accompa-

nied by endothelial cell injury with activation of the coagu-

lation system and multi-organ-system damage.

Preeclampsia may occur in previously normotensive

patients or in patients with preexisting chronic hypertension,

who are then said to have superimposed preeclampsia.

Indeed, preeclamptic patients with chronic hypertension or

with underlying renal or collagen-vascular disease may have

more severe disease and a more complicated course.

Preeclampsia generally occurs only after the twentieth week

of gestation but rarely may develop earlier in the woman

with multiple fetuses or with hydatidiform mole.

Clinical Features

A. Symptoms and Signs—Preeclampsia is classically

defined by the triad of hypertension, proteinuria, and

edema. However, because of the frequent occurrence of

edema in pregnancy without preeclampsia, edema has been

omitted as a diagnostic criterion for preeclampsia.

Nevertheless, a sudden and dramatic weight gain in late

pregnancy often presages the development of overt

preeclampsia. For this reason, all patients receiving prenatal

care have regular determinations made of their weight,

urine protein content, and blood pressure. According to the

National High Blood Pressure Education Working Group

Report on High Blood Pressure in Pregnancy, the minimum

criteria for the diagnosis of preeclampsia are (1) sustained

blood pressure elevation of 140 mm Hg systolic or 90 mm

Hg diastolic in a previously normotensive woman after 20

weeks of gestation and (2) proteinuria—at least 300 mg of

urinary protein in a 24-hour period or at least 30 mg/dL

(1+) in a random urine sample.

Preeclampsia is classified as mild or severe. Severe

preeclampsia is characterized by at least one of the following

additional criteria: (1) blood pressure of 160 mm Hg or

greater systolic or 110 mm Hg or greater diastolic, (2) pro-

teinuria of 5 g or more in 24 hours, (3) elevated serum crea-

tinine, (4) pulmonary edema, (5) oliguria (<500 mL/24 h),

(6) microangiopathic hemolytic anemia, (7) thrombocy-

topenia, (8) hepatocellular dysfunction (abnormally elevated

AST or ALT), (9) fetal growth restriction, (10) symptoms

suggestive of end-organ involvement (eg, headache, visual

disturbances, epigastric or right upper quadrant pain), or

(11) eclampsia, defined by the presence of seizures in a preg-

nant patient without other known cause.

B. Laboratory Findings—Preeclampsia is diagnosed prima-

rily by clinical criteria. The major role of the laboratory is

identifying and following the course of complications. These

include involvement of the renal, hepatic, or hematologic

systems. In the care of a severely preeclamptic patient, serial

determinations of platelet count, fibrinogen and fibrin

degradation products, hemoglobin, liver function tests, and

serum creatinine are essential.

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808

Differential Diagnosis

In addition to preeclampsia, the differential diagnosis of

hypertension in late gestation includes chronic hypertension,

gestational hypertension (ie, pregnancy-induced hyperten-

sion without proteinuria), and acute fatty liver of pregnancy.

Acute fatty liver, amniotic fluid embolism, and placental

abruption also may be associated with coagulopathy.

Proteinuria may result from urinary tract infection or from

chronic renal disease. Edema is common in pregnancy and

not necessarily a sign of preeclampsia, but nondependent

edema is more commonly associated with preeclampsia.

Management

A. Delivery—The only definitive treatment for preeclampsia

is delivery of the fetus. In the case of severe preeclampsia, this

should be undertaken without delay, except in rare cases

when the mother is stable and the fetus very immature. Such

a delay in delivery in the patient with severe preeclampsia—

while antihypertensive therapy is given—remains controver-

sial and should be permitted only when the anticipated

benefits to the fetus outweigh the potential risks to both

mother and the fetus.

B. Seizure Prophylaxis—Seizure prophylaxis should be

employed in all severely preeclamptic patients. This is

usually begun as soon as the diagnosis is made and is con-

tinued until the patient is either delivered or the patient is

deemed stable enough to be followed expectantly.

Treatment greatly reduces the likelihood of eclamptic

seizures that might occur during a patient’s initial hospital

evaluation. Once the decision is made to proceed with

delivery of the patient with preeclampsia, seizure prophy-

laxis should be initiated and continued throughout labor

and delivery and until 24 hours postpartum. The routine

use of magnesium sulfate prophylaxis in patients with mild

preeclampsia is controversial.

In the United States, magnesium sulfate is the most com-

monly employed seizure prophylaxis. It is usually adminis-

tered intravenously, although the intramuscular route also

can be employed. The usual regimen includes an intravenous

loading dose of 4–6 g given over 20–30 minutes, followed by

a continuous infusion of 2 g/h. The infusion rate should be

adjusted to achieve serum magnesium levels in the therapeu-

tic range of 4.8–8.4 mg/dL.

C. Control of Hypertension—In general, blood pressures

over 180 mm Hg systolic or 110 mm Hg diastolic should be

treated acutely with antihypertensives. Hydralazine, 5–20 mg

intravenously, according to patient response, is used com-

monly. An acceptable alternative is labetalol 20 mg, also given

by intravenous bolus. If an adequate response is not obtained,

the dose should be doubled and repeated at 10-minute intervals

up to a maximum single bolus dose of 80 mg and a total max-

imum dose of 220 mg. Oral or sublingual nifedipine also has

been suggested for this situation, but concurrent use of

nifedipine and magnesium sulfate may result in profound

hypotension. Nitroglycerin and sodium nitroprusside may

be used if severe hypertension is unresponsive to the preced-

ing agents, but intra-arterial pressure monitoring is recom-

mended. Owing to the potential for fetal cyanide toxicity,

the duration of nitroprusside treatment should be limited.

One should exercise caution in administering any vasodila-

tors to patients with preeclampsia because intravascular vol-

ume contraction is often present, making them susceptible to

dramatic falls in blood pressure. Excessive and rapid decreases

in blood pressure—even to above-normal levels—may be

associated with fetal distress secondary to decreased uteropla-

cental perfusion and therefore should be avoided.

D. Hemodynamic Monitoring—A pulmonary artery

catheter may be indicated in the presence of oliguria unre-

sponsive to initial fluid boluses, pulmonary edema that does

not respond to furosemide diuresis and positioning, or

severe hypertension unresponsive to hydralazine or labetalol.

Untreated preeclamptic patients without pulmonary edema

have been found to have greater systemic vascular resistance,

increased cardiac index, and hyperdynamic left ventricular

function when compared with normal controls. Treatment

may modify these findings. The pulmonary artery catheter is

essential in differentiating these mechanisms because central

venous pressures have been found not to reliably reflect pul-

monary artery pressures in preeclampsia.

E. Pulmonary Edema—Pulmonary edema may be due to

left ventricular dysfunction secondary to high systemic vas-

cular resistance, iatrogenic volume overload in the face of

contracted intravascular space, decreased plasma colloid

oncotic pressure (occurs in normal pregnancy and is exag-

gerated in preeclampsia), or pulmonary capillary membrane

injury. Colloid oncotic pressure may decrease further follow-

ing intravenous fluid replacement with crystalloids and as a

result of rapid intravascular mobilization of edema fluid

after delivery. Nevertheless, pulmonary edema remains an

uncommon complication of preeclampsia, with an incidence

of 2.9% in severe preeclampsia, usually occurring postpar-

tum. Management consists of diuretics and oxygen, with dig-

italis glycosides reserved for the rare patient with evidence of

left ventricular dysfunction.

F. Oliguria—Oliguria—defined as less than 30 mL of urine

output per hour for 2 hours—in severe preeclampsia seldom

progresses to frank renal failure. Oliguria associated with

preeclampsia can be due to (l) intravascular volume deple-

tion (most common), (2) oliguria accompanied by normal

cardiac function and systemic vascular resistance, probably

owing to isolated renal arteriolar spasm and perhaps respon-

sive to low-dose dopamine, l–5 μg/kg per minute, and (3) rel-

ative volume overload with depressed left ventricular

function secondary to high systemic vascular resistance,

managed with fluid restriction and afterload reduction.

Echocardiograpic assessment of cardiac function may assist

in differentiating these scenarios.

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CRITICAL CARE ISSUES IN PREGNANCY

809

G. HELLP Syndrome—Preeclampsia may be complicated by

the hemolysis, elevated liver enzymes, and low platelets

(HELLP) syndrome. There is controversy over whether the

HELLP syndrome represents a separate clinical entity or is part

of the spectrum of preeclampsia. Patients with the HELLP syn-

drome are older and more frequently multiparous than other

preeclamptic women. The hemolysis observed in these patients

is consistent with a microangiopathic hemolytic process and

seldom requires specific treatment (other than fetal delivery).

Severe thrombocytopenia (platelet count <30,000/μL) occurs

in fewer than 10% of patients. Treatment with platelet transfu-

sion is usually necessary only for cesarean section or other

major surgery. The elevated liver enzymes result from hepato-

cellular injury secondary to vasospasm and may be associated

with hepatic infarction, intrahepatic hemorrhage, and subcap-

sular hematomas. Rarely, a subcapsular hematoma may rup-

ture, precipitating hemodynamic instability. In the absence of

liver rupture, treatment of HELLP syndrome is usually sup-

portive, although the laboratory derangements associated with

the syndrome may be transiently reversed with steroid treat-

ment. Dexamethasone, 10 mg intravenously every 12 hours,

has been shown to result in clinical improvement and reversal

of laboratory abnormalities in HELLP syndrome. Treatment

may allow some delay in delivery in the extremely preterm

pregnancy. This regimen has the added advantage of promot-

ing fetal lung maturation. Abnormalities recur promptly if

steroids are discontinued. In addition, a meta-analysis of

steroid treatment confirmed an increase in platelet count but

failed to demonstrate any improvement in maternal or fetal

outcome. The maternal mortality rate associated with HELLP

syndrome has been estimated to be 1–2%.

H. Eclampsia—Eclampsia is defined as the occurrence of

grand mal seizures in a woman with preeclampsia in whom

the seizures cannot be attributed to some other cause.

Eclampsia carries a maternal mortality rate of 1–2% and a

fetal mortality rate of approximately 10%. Onset of seizures

is often preceded by a severe, unrelenting headache.

Management of eclampsia consists of control of seizures,

pharmacologic control of severe hypertension, and delivery.

Seizures can be controlled with a 4–6-g intravenous bolus of

magnesium sulfate (8 g in 50 mL of 0.9% NaCl) given at a

rate no more rapid than 1 g/min, followed by a continuous

infusion of 2 g/h, with monitoring as described earlier. A 2-g

bolus is employed if the patient is already receiving magne-

sium sulfate prophylaxis or if there is a recurrent seizure after

the initial bolus. Magnesium sulfate is the treatment of

choice because studies have demonstrated its superiority to

either phenytoin or diazepam and because it has less sedating

effect on the fetus. In addition, levels of magnesium are easy

to monitor, and magnesium sulfate has a long record of safe

use. Once seizures are controlled and the patient is consid-

ered stable, efforts should be directed toward accomplishing

delivery. In many cases, labor can be induced safely and vagi-

nal delivery achieved. Seizure prophylaxis with magnesium

sulfate should be continued until 24 hours postpartum.

I. Other Complications—Disseminated intravascular coag-

ulation, cerebral edema, cerebral bleeding, transient cortical

blindness, retinal detachments, placental abruption, fetal

growth restriction, and fetal distress rarely may complicate

preeclampsia and eclampsia.

ACOG Practice Bulletin Number 33: Diagnosis and management

of preeclampsia and eclampsia. Obstet Gynecol 2002;99:

159–67. [PMID: 16175681]

Chang J et al: Pregnancy-related mortality surveillance—United

States, 1991–1999. MMWR Surveill Summ 2003;52:1–8.

[PMID: 12825542]

Complications of preeclampsia. In Dildy G et al (eds), Critical Care

Obstetrics, 4th ed. Boston: Blackwell, 2003.

Heilmann L et al: Hemostatic abnormalities in patients with severe

preeclampsia. Clin Appl Thromb Hemost 2007;13:285–91.

[PMID 17636190]

Sibai BM: Imitators of severe preeclampsia. Obstet Gynecol

2007;109:956–66. [PMID 17400860]

Sibai BM: Diagnosis and management of gestational hypertension

and preeclampsia. Obstet Gynecol 2003;102:181–92. [PMID:

12850627]

Sibai BM: Diagnosis, controversies, and management of the syn-

drome of hemolysis, elevated liver enzymes, and low platelet

count. Obstet Gynecol 2004;103:981–91. [PMID: 15121574]



Acute Fatty Liver of Pregnancy

ESSENTIALS OF DIAGNOSIS



Hepatic dysfunction.



Microvesicular fatty infiltration of hepatocytes.

General Considerations

Acute fatty liver of pregnancy is a rare but potentially cata-

strophic complication of pregnancy with an incidence of

between 1:7,000 and 1:16,000 deliveries. It presents as hepatic

dysfunction associated with microvesicular fatty infiltration of

hepatocytes occurring during the last trimester of pregnancy

or immediately postpartum. Hypertension is commonly pres-

ent, and some consider the disorder to be a variant of

preeclampsia. Indeed, there is an increased incidence of both

conditions in first pregnancies and with twin gestations.

Although in the past fetal and maternal mortality rates exceed-

ing 70% were reported, data suggest that fetal and maternal

mortality is closer to 20%. This discrepancy is most likely the

result of earlier diagnosis and improved management as well

as recognition that milder forms of this disorder exist.

The etiology of acute fatty liver of pregnancy remains

unknown. In many, but not all, cases, mother or fetus has

been found to have a genetic defect of fatty acid beta oxida-

tion. This association is strong enough that infants of

affected mothers should be screened.

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810

Clinical Features

A. Symptoms and Signs—Typically, patients present with a

history of nausea, vomiting, anorexia, and malaise for 1–2

weeks. Epigastric or right upper quadrant pain also may be

present, as may jaundice of varying degrees. Hypertension

with or without proteinuria and edema is frequently present,

and transient diabetes insipidus is a common association. In

severe acute fatty liver of pregnancy, ascites and progressive

hepatic encephalopathy develop along with hypoglycemia,

consumptive coagulopathy, metabolic acidosis, and renal

failure. Pancreatitis and GI bleeding also may occur.

Improvement usually follows delivery of the fetus. If delivery

has not been performed, fetal death often results, presumably

from uteroplacental insufficiency or hypoglycemia.

B. Laboratory Findings—The white blood cell count is usu-

ally elevated, often to greater than 20,000/μL. There may be

normochromic, normocytic anemia with fragmented red

blood cells consistent with disseminated intravascular coag-

ulation (DIC) or microangiopathic hemolysis. Prothrombin

time and partial thromboplastin time are usually prolonged,

and there are decreased fibrinogen and platelets and elevated

fibrin degradation products, all indicative of consumptive

coagulopathy. Decreased coagulation factors also can result

from decreased hepatic synthesis.

AST and ALT are elevated, but seldom more than 2000

IU/L. Alkaline phosphatase and bilirubin are also elevated,

and serum albumin is decreased. Hypoglycemia is often pres-

ent and may be severe. Uric acid is usually high, and blood

urea nitrogen (BUN) and creatinine are elevated if renal

impairment is present. Hypernatremia may be present if

there is diabetes insipidus, and elevated serum lipase and

amylase indicate the presence of pancreatitis.

Diagnosis of acute fatty liver of pregnancy can be made

with reasonable certainty from the clinical presentation and

the laboratory findings, but confirmation requires the

demonstration of microvesicular fat within the hepatocytes

on liver biopsy. This is done with either staining a frozen tis-

sue section with oil red O stain or by electron microscopy.

Percutaneous liver biopsy should not be attempted if there

are significant coagulation abnormalities. Increased

echogenicity of the liver on ultrasound examination and

decreased attenuation over the liver on CT scan or MRI have

been described in patients with this disorder, but these find-

ings are not always present.

Treatment

Management of acute fatty liver of pregnancy can be divided

into four categories: monitoring, stabilization, delivery, and

support. Monitoring should apply to both the patient and

her fetus. Because the fetal condition can deteriorate rapidly,

continuous monitoring of the fetal heart rate should be per-

formed until delivery can be accomplished. Fetal biophysical

profiles sometimes can aid in the diagnosis of fetal compro-

mise. In severe acute fatty liver of pregnancy, the patient

should be managed in the ICU and may require invasive

hemodynamic monitoring. Laboratory parameters should be

followed at frequent intervals.

Stabilization involves maintenance of a patent airway and

adequate ventilation if mental obtundation exists, normaliza-

tion of intravascular volume, correction of electrolyte distur-

bances, treatment of hypoglycemia with intravenous glucose,

and correction of hematologic and coagulation abnormalities

with transfusions of red blood cells, platelets, and fresh-

frozen plasma. Intravenous magnesium sulfate and, less fre-

quently, hydralazine may be required if there is concomitant

preeclampsia. Maintenance magnesium sulfate dosage should

be decreased if there is significant renal impairment.

Once the patient has been stabilized, delivery should be

accomplished as soon as possible, for this is what will ulti-

mately lead to improvement. Delivery is often by cesarean

section because this is often the most expeditious method

and permits correction of coagulation defects just prior to

surgery. However, if the cervix is favorable for labor induc-

tion and there is no evidence of fetal compromise, vaginal

delivery can be attempted. This avoids the risks of abdominal

surgery in the face of coagulopathy and ascites and decreases

the need for anesthesia. The choice of anesthetic for cesarean

section is controversial. Conduction anesthesia can be used if

coagulation abnormalities are corrected. General anesthesia

is used otherwise, with care taken to avoid agents that are

hepatotoxic or that require metabolism in the liver.

Following delivery, the patient will require supportive

management until she recovers from her multiple-organ-

system failure. Protein intake should be limited, and nutri-

tional maintenance should be primarily in the form of

glucose to decrease the load of nitrogenous waste until

hepatic function improves. This can be administered intra-

venously or by nasogastric tube, and blood glucose should be

monitored every 1–2 hours to prevent hypoglycemia. To

decrease production of ammonia by intestinal bacteria, oral

lactulose, 20–30 g (30–45 mL) every 1–2 hours to induce diar-

rhea and then enough to produce two to four soft stools per

day, can be administered. Alternatively, oral neomycin, 0.5–1

g every 6 hours, can be used. Although poorly absorbed, small

amounts of neomycin may reach the bloodstream, and care

should be taken to avoid levels that might cause nephrotoxic-

ity. Magnesium citrate administered orally will decrease intes-

tinal transit time, further decreasing ammonia absorption.

Optimal fluid and electrolyte management is critical, par-

ticularly if there is significant renal impairment, diabetes

insipidus, or ascites. Diabetes insipidus can be managed with

desmopressin acetate until this phase of the disease resolves.

Vitamin K should be administered to aid restoration of coag-

ulation, and further transfusions of fresh-frozen plasma or

platelets should be necessary only in the face of clinical

bleeding or if a surgical procedure is anticipated. Care should

be taken to avoid nosocomial infection in this already com-

promised patient. Some patients have been treated success-

fully with liver transplantation after delivery for acute fatty

liver of pregnancy.

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CRITICAL CARE ISSUES IN PREGNANCY

811

Acute fatty liver. In Dildy G et al (eds), Critical Care Obstetrics, 4th

ed. Boston: Blackwell; 2003.

Browning MF et al: Fetal fatty acid oxidation defects and maternal

liver disease in pregnancy. Obstet Gynecol 2006;107:115–20.

[PMID: 16394048]

Guntupalli SR, Steingrub J: Hepatic disease and pregnancy: An

overview of diagnosis and management. Crit Care Med

2005;33:S332–9. [PMID: 16215356]

Ibdah JA: Acute fatty liver of pregnancy: An update on pathogene-

sis and clinical implications. World J Gastroenterol

2006;12:7397–404. [PMID: 17167825]

Rajasri AG et al: Acute fatty liver of pregnancy (AFLP): An

overview. J Obstet Gynaecol 2007;27:237–40. [PMID: 17464801]



Amniotic Fluid Embolism

ESSENTIALS OF DIAGNOSIS



Hypotension, hypoxia, coagulopathy.



Frequently seizures, pulmonary edema, cardiac arrest.

General Considerations

Amniotic fluid embolism is a rare but catastrophic complica-

tion of pregnancy. Its incidence is unknown but is thought to

be between 1:80,000 and 1:8000 pregnancies. It is classically

thought to be triggered by the release of amniotic fluid, con-

taining fetal squamous cells, into the maternal pulmonary

circulation, causing severe pulmonary vasoconstriction with

subsequent hemodynamic and cardiorespiratory collapse

and coagulopathy. Cardiac arrest is common, with 26–80%

of cases ending in maternal demise. There is significant con-

troversy about the pathophysiology of the condition, and

treatment therefore is empirical and supportive.

Amniotic fluid embolism has been reported as a compli-

cation of first- and second-trimester pregnancy termination

and during otherwise normal pregnancy and the puer-

perium. The time of greatest risk is during labor. Placental

abruption and fetal death are common antecedents to amni-

otic fluid embolism. Although links with hypertonic uterine

contractions, augmented labor, and meconium-stained

amniotic fluid also have been reported, a national registry of

amniotic fluid embolism did not confirm these associations.

Clinical Features

A. Symptoms and Signs—The patient with amniotic fluid

embolism presents with dyspnea and hypotension, which may

rapidly deteriorate to cardiac arrest. Half of all patients will die

within an hour of developing symptoms. An alternative pres-

entation is as a severe coagulopathy. Up to one-third of patients

have seizures, and nearly 75% exhibit pulmonary edema.

Although animal studies demonstrate a rise in pulmonary

artery pressure at the time of embolism, with resolution

within 30 minutes, no patient has had an amniotic fluid

embolism with a pulmonary artery catheter in place. Reports

of patients who have had a pulmonary artery catheter placed

hours to days after the acute event show no clear pattern of

pulmonary artery pressures. Patients surviving the initial

phase of the disorder may exhibit left-sided heart failure with

elevated pulmonary capillary wedge pressures and decreased

systemic vascular resistance. Acute respiratory distress syn-

drome is common, and 40–50% may have DIC with hemor-

rhage. The bleeding picture may be further complicated by

uterine atony, which appears also to be a result of the amni-

otic fluid embolism.

B. Laboratory Findings—The classic laboratory finding of

amniotic fluid embolism has been fetal squamous cells in the

maternal pulmonary circulation at autopsy. Some authors

have reported finding such cells in blood from a pulmonary

artery catheter in patients suspected of having the diagnosis,

but these appear to come from the maternal skin as an artifact

from insertion of the catheter. The presence of squamous cells

in the pulmonary circulation is of uncertain significance.

Treatment

Amniotic fluid embolism is a rare and unpredictable disor-

der. Few practitioners have seen more than a handful of

cases, and published data are subject to arguable interpreta-

tion. Treatment is supportive. The most common manifesta-

tion of the disorder in the ICU is acute respiratory distress

syndrome (ARDS), which should be managed in the same

way as for other patients. The severe uterine atony associated

with amniotic fluid embolism may necessitate hysterectomy

to control uterine bleeding.

Gilbert WM, Danielsen B: Amniotic fluid embolism: decreased

mortality in a population-based study. Obstet Gynecol

1999;93:973–7. [PMID: 10362165]

Moore J, Baldisseri MR: Amniotic fluid embolism. Crit Care Med

2005;33:S279–85. [PMID: 16215348]

Stafford I, Sheffield J. Amniotic fluid embolism. Obstet Gynecol

Clin North Am 2007;34:545–53, xii. [PMID: 17921014



Pyelonephritis in Pregnancy

ESSENTIALS OF DIAGNOSIS



Fever, flank pain.



Dysuria, pyuria.

General Considerations

Pyelonephritis occurs in 1–2% of pregnancies. In pregnancy,

progesterone mediates ureteral relaxation, predisposing to

urinary stasis. In addition, compression of the ureters by the

gravid uterus and engorged pelvic vessels is implicated. In

this context, bacteria from lower urinary tract infections can

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ascend more easily to the kidney. Obstetricians aggressively

treat even asymptomatic lower tract infections because,

untreated, 25% of such patients will progress to pyelonephri-

tis. The most frequent etiologic organism in pregnant

women is Escherichia coli. Pregnant women with

pyelonephritis usually are treated as inpatients because of the

greater incidence of severe complications of this disease in

pregnancy. In one series, 17% of pregnant women with

pyelonephritis developed septic shock, and 7% of these

patients developed respiratory insufficiency, which can occur

24–48 hours after starting antibiotic therapy and is presum-

ably due to release of bacterial endotoxin.

Clinical Features

A. Symptoms and Signs—The typical patient presents with

flank pain and fever of recent origin, often with rigors or

chills. There may be a history of lower urinary tract infec-

tion, and many patients complain of concurrent lower tract

symptoms such as dysuria and frequency. Some patients also

have nausea and vomiting and anorexia. On physical exami-

nation, flank tenderness is usually present, more frequently

on the right. There is usually fever, occasionally higher than

40°C. Tachycardia of both mother and fetus may be present

owing to fever and volume depletion. Uterine contractions

also may be present. The presence of hypotension, tachyp-

nea, extremely high fever, or marked tachycardia is ominous.

B. Laboratory Findings—The urine nearly always contains

white blood cells and bacteria, and red blood cells and casts are

also seen frequently. The urine should be sent for culture to

confirm the diagnosis and to check for antibiotic resistance.

Differential Diagnosis

In any febrile pregnant patient it is critical to exclude the

diagnosis of intraamniotic infection. If any doubt exists, con-

sideration should be given to performing amniocentesis to

exclude this possibility. Amniocentesis usually is performed

after the administration of antibiotics in order to avoid

injecting bacteria into a sterile uterus. Amniotic fluid should

be sent for cell count, glucose, Gram stain, and cultures. A

leukocyte count of more than 30/μL (especially polymor-

phonuclear cells [PMNs]) or a glucose concentration of less

than 18 mg/dL should be considered suspicious for infection.

Similarly, a Gram stain showing increased PMNs—even in

the absence of organisms—suggests bacterial infection. Any

organisms seen on Gram stain should be considered signifi-

cant and probably are an indication for delivery.

The pregnant patient also may have a renal stone, and one

should be sought, especially in patients in whom the febrile

course does not respond to antibiotics. This diagnosis can be

made by ultrasound in most cases, although an intravenous

urogram (single film to minimize radiation exposure) is

sometimes still necessary.

Also included in the differential are appendicitis, chole-

cystitis, and viral gastroenteritis. Appendicitis in the pregnant

patient often presents with tenderness higher in the

abdomen than at McBurney’s point, and in many cases there

are less remarkable peritoneal signs.

Treatment

The mainstay of treatment is intravenous antibiotics, with an

antimicrobial agent chosen empirically to cover the majority

of community-acquired urinary pathogens. Since nausea and

vomiting and anorexia frequently accompany pyelonephritis,

volume depletion and dehydration are common and should

be corrected promptly with intravenous crystalloid. The fever

and dehydration of pyelonephritis frequently lead to prema-

ture uterine contractions. In addition, high maternal fevers

have been shown to be associated with fetal neurologic harm.

For this reason, fever should be brought down below 38.3°C

with acetaminophen or a cooling blanket. Because of the high

risk of pulmonary damage in these patients, fluid overload

should be avoided, and tocolytic drugs should be reserved for

patients who demonstrate clear cervical changes.

Even with adequate treatment, the patient with

pyelonephritis may demonstrate a hectic fever course,

although uncomplicated patients become afebrile after 48 hours.

Effective treatment of pyelonephritis often results in the lib-

eration of bacterial endotoxins that may be associated with

hypotension, hypothermia, pulmonary infiltrates, and rarely,

ARDS. Patients who develop pulmonary edema or respira-

tory distress syndrome typically do so 24–48 hours after hos-

pital admission. Transient impairment of renal function is

also common. One group found that essentially all patients

with pyelonephritis demonstrated evidence of hemolysis,

sometimes leading to anemia and associated with bacterial

endotoxins. Finally, the number of uterine contractions

increases after the initiation of antibiotic therapy in some

patients; this effect also has been attributed to the release of

bacterial endotoxins. Treatment for endotoxin-mediated

complications is symptomatic and supportive while antibi-

otics are continued. Pyelonephritis-induced ARDS has been

treated with the fetus in utero with subsequent good fetal

outcome.

The possibility of endotoxin-mediated complications

mandates close observation of pregnant patients with

pyelonephritis even after antibiotics have been begun. This

routinely should include continuous fetal heart rate moni-

toring in all pregnancies beyond 22 weeks of gestation. Even

prior to this gestational age, maternal hypotension and

hypoxemia should be detected and corrected before fetal

injury results.

Pregnant patients with pyelonephritis typically are treated

for 10–14 days with antibiotics. These antibiotics can be

administered orally on an outpatient basis after the patient

becomes afebrile. After an episode of pyelonephritis, the preg-

nant patient is at increased risk for a recurrence. Often these

patients are given antibiotic prophylaxis for the duration of

the pregnancy and for 6 weeks postpartum. Serial urine cul-

tures are also an acceptable management scheme.



CRITICAL CARE ISSUES IN PREGNANCY

813

Hill JB et al: Acute pyelonephritis in pregnancy. Obstet Gynecol

2005;105:18–23. [PMID: 15625136]

Sheffield JS, Cunningham FG: Urinary tract infection in women.

Obstet Gynecol 2005;106:1085–92. [PMID: 16260529]



Septic Abortion

ESSENTIALS OF DIAGNOSIS



Fever.



Uterine or pelvic tenderness.



Recent history of uterine instrumentation with pregnancy.

General Considerations

Septic abortion is defined as sepsis in association with a

recent pregnancy termination (spontaneous or induced).

This complication was much more common when abortion

was illegal. Abortion-induced sepsis can progress rapidly to

septic shock with an incidence of 2–10%. Data from the

1960s suggests that 300 of 100,000 illegal abortion proce-

dures resulted in death of the mother. The current maternal

mortality related to legal abortion in the United States is 0.7

per 100,000 procedures, with infection and hemorrhage each

accounting for about one-quarter of those deaths. The likeli-

hood of complications increases in patients who have later

abortions and in those having dilatation and evacuation pro-

cedures. Clostridial infection was a feared complication of

illegal abortions and remains a factor in septic abortions

today. Several recent cases of fatal maternal sepsis following

medically induced abortion using mifepristone were due to

Clostridium sordellii.

Clinical Features

A. Symptoms and Signs—Patients will present with pelvic

pain and a serosanguineous to purulent discharge. Some

patients will complain more of vaginal bleeding, whereas

others will emphasize crampy pain. All describe a history of

recent (within a week) pregnancy termination, spontaneous

or induced, or other intrauterine instrumentation in preg-

nancy. Hematuria and shock may develop rapidly.

B. Laboratory Findings—Blood, urine, and cervical speci-

mens should be obtained for culture. Gram stain of poten-

tially infected material is useful for initial therapy. The

diagnosis of clostridial infection (C. perfringens) is sug-

gested by the presence of large gram-positive rods on Gram

stain of the cervical secretions or tissue obtained by curet-

ting. The white blood count is usually elevated but may be

low in patients with severe disease. Studies of renal and

coagulation function and blood gas analyses may be helpful

to predict the more severe complications of the infection.

Abdominal x-rays may be helpful in the diagnosis of uterine

or bowel perforation (which can be a complication of the

original procedure) or in the diagnosis of clostridial infec-

tion. The presence of gas in the myometrium is consistent

with clostridial infection and is a grave prognostic sign.

Finally, ultrasound may be helpful in assessing the presence

of retained products of conception and in detecting possible

pelvic abscesses.

Treatment

Sepsis after spontaneous or induced abortion is treated with

high-dose antibiotics followed promptly by uterine evacua-

tion. In clostridial infections, which are more than superfi-

cial, prompt hysterectomy may be lifesaving. Pelvic surgery

also may be required to drain hematomas or abscesses. These

also may be approached by guided needle aspiration. Other

aspects of septic shock, including hypotension, anemia, and

ARDS, are treated supportively.

Bartlett LA et al: Risk factors for legal induced abortion related

mortality in the United States. Obstet Gynecol

2004;103:729–37. [PMID: 15051566]

Finkielman JD et al: The clinical course of patients with septic

abortion admitted to an intensive care unit. Intensive Care Med

2004;30:1097–102. [PMID: 15007546]

Fischer M et al: Fatal toxic shock syndrome associated with

Clostridium sordellii after medical abortion. N Engl J Med

2005;353:2352–60. [PMID: 16319384]



Pulmonary Edema

ESSENTIALS OF DIAGNOSIS



Dyspnea, hypoxemia, cough.



Chest x-ray showing pulmonary edema with usually

bilateral diffuse interstitial and alveolar infiltrates and

perihilar congestion.

General Considerations

Women without known predisposing conditions may

develop pulmonary edema during the course of pregnancy,

especially at the time of delivery. Common obstetric condi-

tions responsible for this complication are (1) hypertensive

disorders of pregnancy, (2) undiagnosed underlying heart

disease, especially mitral stenosis, (3) use of tocolytic

drugs, especially β-adrenergic agonists, (4) iatrogenic fluid

overload, (5) systemic infection, especially pyelonephritis

or chorioamnionitis, and more rarely, (6) peripartum

cardiomyopathy.

Hypertensive disorders of pregnancy were discussed earlier.

These patients are particularly disposed to pulmonary edema

because of increased systemic vascular resistance and

decreased plasma oncotic pressure. Pulmonary edema also



CHAPTER 38

814

may supervene in these patients if left ventricular function is

compromised or in cases of pulmonary capillary or epithelial

injury. In other patients, the rapid mobilization of edema fluid

that follows delivery may result in transient pulmonary edema.

Patients with flow-restricting cardiac lesions (eg, mitral

stenosis) may be intolerant of the increased vascular volume

of pregnancy and especially of the autotransfusion that

accompanies delivery. In some women, the first symptom of

cardiac disease is pulmonary edema after delivery.

Pulmonary edema associated with the use of β-adrenergic

agonists appears to be unique to pregnancy. There is no asso-

ciation of pulmonary edema with these drugs in nonpregnant

patients despite considerable clinical experience. The inci-

dence of pulmonary edema as a complication of tocolytic

therapy with these drugs has been estimated to be between

0.15% and 4% in different studies. This risk may be increased

to more than 20% in the face of intraamniotic infection.

Intravenous β-adrenergic agonists are currently rarely used in

pregnancy owing to the number and severity of complica-

tions experienced with these agents. Pulmonary edema also

can complicate subcutaneous use of β-adrenergic agonists,

but the risk appears to be much less. Pulmonary edema also

has been described with other tocolytic agents, with an inci-

dence of 1:300 in one study of magnesium sulfate.

Patients in labor typically receive large volumes of intra-

venous crystalloid fluids. It is common practice to give labor-

ing women a 1000-mL bolus before administering epidural

anesthesia, and most women receive a maintenance rate of

crystalloid infusion at all other times. Most laboring patients

tolerate this regimen well. In some patients with pyelonephri-

tis or in those who are undergoing tocolysis, however, careful

fluid management can make the difference in developing

pulmonary edema.

Peripartum cardiomyopathy is a rare complication of preg-

nancy, occurring in about 1:2200 to 1:3200 pregnancies in the

United States, with one study showing an increase in recent

years. It is characterized by a dilated cardiomyopathy and fre-

quently is associated with systemic and pulmonary emboli.

About half of patients with peripartum cardiomyopathy have

complete resolution after delivery, with return of normal heart

size and cardiac function. The remainder have continued car-

diac dilatation. These patients tolerate future pregnancies

poorly, and some have required cardiac transplantation. The

cause of this condition is unknown, but at least some of the

affected patients have evidence of viral myocarditis.

The mechanism for the increased susceptibility to pul-

monary edema in pregnancy is not clear. Fluid overload has

been suggested as a cause because of the known increase in

extracellular fluid volume during pregnancy, decreased

excretion of sodium and water in pregnant patients when

supine, and concomitant administration of large amounts

of intravenous fluids in many cases. However, there is no

convincing evidence of increased pulmonary artery wedge

pressure to identify either fluid overload or left ventricular

failure as the cause of pulmonary edema in many cases.

The finding of a low pulmonary artery wedge pressure in

the face of pulmonary edema normally would be indicative

of increased capillary permeability pulmonary edema, but

evidence against this mechanism is the usually rapid resolu-

tion of edema with treatment in the case of tocolytic use or

in many cases of preeclampsia. Hypoalbuminemia and

decreased plasma oncotic pressure of pregnancy also may

play a role in the etiology of pulmonary edema.

Clinical Features

A. Symptoms and Signs—Patients present with dyspnea,

cough, chest discomfort, and frothy sputum. Findings

include bilateral rales, but most patients lack other signs of

heart failure, such as a third heart sound. Review of the hos-

pital records frequently documents administration of large

amounts of intravenous fluids, sometimes for treatment of

tachycardia or mild hypotension. Patients may have fever or

other symptoms of infection.

B. Laboratory Findings—The chest x-ray shows bilateral

interstitial or alveolar infiltrates consistent with pulmonary

edema. Occasionally, findings are unilateral. The cardiac size

may not be greatly enlarged, but it has been pointed out that

there is an apparent increase in heart size during normal

pregnancy. Pleural effusions are rare. Arterial blood gases

show hypoxemia with respiratory alkalosis in most patients.

Fetal heart monitoring may reveal late decelerations and loss

of variability of the fetal heart rate consistent with fetal

hypoxia and acidemia.

Ventilation-perfusion lung scans may be useful in exclud-

ing pulmonary thromboembolism in selected patients.

Echocardiography should be considered to exclude car-

diomyopathy or valvular heart disease.

Differential Diagnosis

Acute onset of dyspnea during late pregnancy may be due to

pulmonary embolism, amniotic fluid embolism, or asthma.

Patients with known underlying heart or lung disease also

should be suspected of having an exacerbation of these prob-

lems if symptoms occur.

Prevention

Patients who have severe underlying heart diseases should not

receive β-adrenergic agonists as tocolytic therapy because of

the risk of inducing pulmonary edema. Magnesium sulfate, if

necessary, may be considered. There is no place for tocolytic

therapy in preeclampsia. Any patient at increased risk of pul-

monary edema requires careful attention to fluid status. The

presence of an intraamniotic infection mandates delivery in

the great majority of cases, and patients with other infections

must be monitored closely while undergoing therapy.

Treatment

Discontinuation of tocolytic agents and administration of

intravenous furosemide (20–40 mg as needed) and oxygen are



CRITICAL CARE ISSUES IN PREGNANCY

815

generally associated with rapid reversal of symptoms and

resolution of pulmonary edema in the absence of structural

heart disease or sepsis. Patients with associated infection

should be treated with appropriate antibiotics. Continuous

fetal heart rate monitoring is essential until normal maternal

pulmonary function is restored and hypoxemia corrected.

In patients with slow resolution of pulmonary edema,

structural abnormalities should be considered. A pulmonary

artery catheter may be helpful in identifying the cause of pul-

monary edema and guiding therapy. A normal echocardio-

gram often predicts rapid resolution, but in patients with

abnormal findings, long-term treatment is usually needed.

Elkayam U, Bitar F. Valvular heart disease and pregnancy part I:

native valves. J Am Coll Cardiol 2005;46:223–30. [PMID:

16022946]

Lamont RF: The pathophysiology of pulmonary edema with the

use of beta agonists. Br J Obstet Gynaecol 2000;107:439–44.

[PMID: 10759259]

Mishra TK et al: Peripartum cardiomyopathy. Int J Gynaecol

Obstet 2006;95:104–9. [PMID: 16935289]

Murali S, Baldisseri MR: Peripartum cardiomyopathy. Crit Care

Med 2005;33:S340–6. [PMID: 16215357]

Mielniczuk LM et al: Frequency of peripartum cardiomyopathy.

Am J Cardiol 2006;97:1765–8. [PMID: 16765131]

Sciscione AC et al: Acute pulmonary edema in pregnancy. Obstet

Gynecol 2003;101:511–5. [PMID: 12636955]



Status Asthmaticus in Pregnancy

Asthma is the most common respiratory disease occurring in

conjunction with pregnancy. In general, the influence of

pregnancy on lung volumes, tidal volume, minute ventila-

tion, and arterial blood gases has little effect on asthma.

About 30–40% of asthmatics who become pregnant have

worsening of their asthma; 35–40% have no change in the

frequency and duration of symptoms; and 20–30% show an

improvement in symptoms. In most patients, the course of

asthma during pregnancy is similar in subsequent pregnan-

cies. This constancy of asthmatic outcome may be altered

with newer methods of asthma control.

Asthma can have adverse effects on pregnancy, especially

when maternal hypoxemia affects oxygenation of the fetus.

Premature labor and low birth weight are well-known com-

plications of maternal asthma, and patients with hypoxemia

owing to asthma are also at increased risk of fetal death. Thus

the central theme in managing the pregnant asthmatic is pre-

vention of maternal asthma exacerbation and hypoxemia.

There is no known association of pregnancy with status

asthmaticus (ie, asthma unresponsive to treatment and usu-

ally requiring hospitalization) or with severe asthma (ie,

daily wheezing and need for medication). On the other hand,

pregnant women with asthma may have worsening of

asthma or may be reluctant to use prescribed asthma medica-

tions, thus increasing the risk of these complications. Patients

with a history of asthma requiring hospitalization, mechani-

cal ventilation, and prolonged use of systemic corticosteroids

or of asthma complicated by pneumothorax should be mon-

itored carefully. These patients should be instructed to report

any asthmatic exacerbations, upper respiratory infections,

increased cough, or other respiratory symptoms. Anemia,

because it can adversely affect maternal oxygen transport,

should be assessed and treated.

Clinical Features

A. Symptoms and Signs—Pregnant asthmatics present no

differently than other patients with asthma. Patients with sta-

tus asthmaticus complain of dyspnea, wheezing, cough, and

failure of response to inhaled bronchodilator drugs. They

may note inability to sleep because of dyspnea or cough, and

they may report a frank upper airway infection. The time

from onset of the attack should be noted because a pro-

longed duration may be predictive of poor response to treat-

ment. Physical findings include wheezing, use of accessory

muscles of respiration, a prolonged expiratory phase, tachyp-

nea, tachycardia, and cyanosis. Patients presenting with acute

severe asthma usually have a history of asthma; rarely,

asthma will present initially during pregnancy.

B. Laboratory Findings—Arterial blood gases should be

interpreted in the light of changes seen in pregnancy. In nor-

mal pregnancy, serum bicarbonate is decreased, and Pa

approximately 30 mm Hg. Development of hypercapnia

therefore may be subtle, and only a slight elevation of Pa

above 40 mm Hg may be indicative of impending respira-

tory failure in the pregnant woman. Severe hypoxemia in

status asthmaticus is due to ventilation-perfusion mis-

matching resulting from bronchospasm and plugging of air-

ways with mucus. As in nonpregnant asthmatics, spirometry

is useful for assessing severity of asthma and following the

response to therapy, especially because the peak expiratory

flow rate does not change in pregnancy. Strong considera-

tion should be given to obtaining a chest x-ray in those with

unexplained fever, persistent bronchospasm, heavy sputum

production, asymmetry on chest examination, severe

hypoxemia, or suspicion of heart disease, pleural effusion, or

pneumothorax.

Differential Diagnosis

Dyspnea during pregnancy is common, with most patients

complaining of some subjective shortness of breath during

the last trimester. Patients with acute onset of shortness of

breath may have congestive heart failure, pulmonary edema,

pulmonary thromboembolism, amniotic fluid embolism,

pneumothorax, or sepsis. Valvular heart disease should be

considered—especially previously undiagnosed mitral

stenosis, mitral valve prolapse, aortic regurgitation, and aor-

tic stenosis. A rare but important problem that should be

considered in young women is primary pulmonary hyper-

tension; this disorder can present with new onset of dyspnea

and other symptoms in response to the increased cardiac

output that occurs with pregnancy.



CHAPTER 38

816

Treatment

Treatment of status asthmaticus in the pregnant asthmatic

should be aggressive and rapid. Fetal oxygenation is highly

dependent on adequate maternal arterial blood oxygen con-

tent, and delay in treatment is hazardous to the fetus. As with

all conditions adversely affecting maternal respiratory func-

tion, fetal heart rate should be monitored continuously in

potentially viable fetuses. Bronchodilator and anti-

inflammatory therapy are directed at reversing airway obstruc-

tion; oxygen is given to treat hypoxemia. Pharmacologic

therapy of asthma in pregnancy is based on administering

drugs with a long history of use with good outcome rather than

drugs that have been tested specifically during pregnancy.

A. Bronchodilators—β-Adrenergic agonists have been used

extensively in pregnancy, but there are no controlled experi-

mental studies in pregnant women for any of these agents.

Terbutaline, albuterol, and metaproterenol have been adminis-

tered to pregnant asthmatics with good results. Inhaled terbu-

taline is an FDA category B drug, whereas metaproterenol and

albuterol are category C drugs. Several clinical studies following

pregnant asthmatics have not found any differences in compli-

cations of pregnancy or fetal outcome among asthmatics

receiving bronchodilators and nonasthmatics who did not

receive these drugs. In general, the newer more selective β

adrenergic agonist drugs are used more commonly than other

agents. Administration of β-agonists by metered-dose inhalers,

as in nonpregnant asthmatics, is preferred to nebulizers. The

dose and frequency of inhaled bronchodilators should be

titrated to the clinical response (see Chapter 24).

B. Corticosteroids—These drugs play a major role in reversing

airway obstruction. Systemic corticosteroids—for example,

intravenous methylprednisolone and oral prednisone—are

well tolerated in pregnant women and are essential in the man-

agement of status asthmaticus. The optimal dose of corticos-

teroids in status asthmaticus is not known in the nonpregnant

patient, but 40–60 mg methylprednisolone every 6 hours is

usually given, and the dose in pregnancy should be similar. Use

of corticosteroids should be aimed at achieving control of

asthma, followed by rapid tapering and discontinuation over

approximately 2 weeks, if possible. In some patients, continued

administration of oral prednisone, 15–30 mg/day, is necessary

for prevention of asthma attacks. Inhaled corticosteroids also

may be used in the treatment of chronic asthma in the preg-

nant patient.

C. Cromolyn Sodium—Cromolyn sodium in inhaled or

nasal spray form has not been associated with any fetal effect

in observational studies. In chronic asthma, inhaled cro-

molyn may be a valuable agent, but cromolyn has no role in

status asthmaticus.

D. Oxygen and Other Therapy—Supplemental oxygen

should be provided to maintain Pa

at 85–100 mm Hg at all

times to ensure fetal oxygenation.

Antibiotics generally are not warranted in status asthmati-

cus because infection, when present as a triggering or exacer-

bating factor, is usually of viral origin. If there is evidence of

bacterial infection, broad-spectrum antibiotics can be given.

Ampicillin, cephalosporins, and erythromycin (but not eryth-

romycin estolate) generally are considered safe for use during

pregnancy. Sulfonamides should not be given—especially

during the third trimester—owing to a theoretical risk of ker-

nicterus in the newborn. Erythromycin estolate, tetracycline,

chloramphenicol, and quinolones should be avoided.

E. Intubation and Mechanical Ventilation—If the patient

fails to respond to the foregoing measures and exhibits a nor-

mal or increased Pa

, she should be admitted to an ICU. If

the fetus is potentially viable, fetal monitoring should be

instituted. Intubation and mechanical ventilation are indi-

cated for a Pa

of 70 mm Hg or less, significant mental sta-

tus changes, respiratory acidosis, cardiac arrhythmias, or

evidence of myocardial ischemia. If mechanical ventilation

does not correct the hypoxemia and the fetus is potentially

viable, delivery by cesarean section should be considered for

fetal reasons.

American College of Obstetricians and Gynecologists (ACOG)

and American College of Allergy, Asthma and Immunology

(ACAAI): The use of newer asthma and allergy medications

during pregnancy. Ann Allergy Asthma Immunol

2000;84:475–80. [PMID: 10830999]

Bracken MB et al: Asthma symptoms, severity, and drug therapy: A

prospective study of effects on 2205 pregnancies. Obstet

Gynecol 2003;102:739–52. [PMID: 14551004]

Clifton V: Maternal asthma during pregnancy and fetal outcomes:

Potential mechanisms and possible solutions. Curr Opin

Allergy Clin Immunol 2006;6:307–11. [PMID 16954781]

Dombrowski MP. Asthma and pregnancy. Obstet Gynecol

2006;108:667–81. [PMID: 16946229]

Leaderer BP: Asthma symptoms, severity, and drug therapy: A

prospective study of effects on 2205 pregnancies. Obstet

Gynecol 2003;102:739–52. [PMID: 14551004]

Namazy JA, Schatz M: Current guidelines for the management of

asthma during pregnancy. Immunol Allergy Clin North Am

2006;26:93–102. [PMID: 16443145]



Postpartum Hemorrhage

ESSENTIALS OF DIAGNOSIS



Rapid loss of 500–1000 mL or more of blood after

delivery.

General Considerations

Postpartum hemorrhage has been defined classically as an

estimated blood loss of more than 500 mL after delivery.