Case Report: Anesthetic Management of Acute
Fatty Liver of Pregnancy in the Postpartum
Period
LCDR Dennis Spence, CRNA, PhD, NC, USN
Acute fatty liver of pregnancy (AFLP) is a potentially
fatal metabolic disorder that manifests during the third
trimester. Early diagnosis, termination of pregnancy,
and treatment of complications associated with AFLP
significantly reduce maternal morbidity and mortality.
While most cases of AFLP occur before delivery, some
may occur after vaginal delivery.
Anesthesia providers should have a high level of
suspicion for AFLP in a patient with altered mental sta-
tus and elevated liver function test results in the post-
partum period. Anesthetic implications include early
recognition of liver dysfunction and aggressive resus-
citation and treatment of hypoglycemia, disseminated
cute fatty liver of pregnancy (AFLP) is a
A potentially fatal metabolic disorder that
manifests during the third trimester. First
identified in 1934, the disorder was based
on the presence of accumulation of
microvesicular fat within hepatocytes.1 Acute fatty liver of
pregnancy is an obstetric emergency that requires prompt
delivery and aggressive treatment of complications associ-
ated with acute liver failure to minimize morbidity and
mortality. Most cases of AFLP involve patients with pro-
dromal symptoms of malaise, nausea, vomiting, abdomi-
nal pain, weight loss, jaundice, fever, and, in some cases,
hepatic encephalopathy and fetal distress, necessitating
emergency cesarean section.2-10 However, review of the
literature found limited reports of patients diagnosed with
AFLP after spontaneous vaginal delivery specifically
describing the use of epidural analgesia.5,9,11 This case
report describes the management of a woman given a
diagnosis of AFLP in whom acute liver failure rapidly
developed after a vaginal delivery with epidural analgesia
at a small overseas hospital.
Case Report
A healthy, ASA physical status II, 38-week pregnant, 25-
year-old woman, gravida 2, para 0, was admitted to a
small overseas hospital for onset of labor. Review of her
medical and surgical history was negative for systemic
disease and complications during pregnancy. The patient
did not specifically report any prodromal symptoms. At
90 minutes after admission, the patient was given 5 mg of
www.aana.com/aanajournalonline.aspx
intravascular coagulopathy, and other associated com-
plications and reduction or avoidance of medications
with substantial hepatic metabolism. This is a case
report describing the management of a woman with
AFLP in whom acute liver failure rapidly developed
after a vaginal delivery with epidural analgesia at a
small overseas hospital.
Keywords: Acute fatty liver of pregnancy, epidural
anesthesia for labor, long-chain hydroxyacyl-coen-
zyme-A dehydrogenase deficiency, morphine metabo-
lites, neuraxial anesthesia.
intramuscular morphine and 5 mg intravenously by the
obstetrician for latent labor pain. Five hours after admis-
sion, anesthesia personnel were consulted for labor anal-
gesia. The history and physical examination data were re-
viewed, and laboratory results showed a hemoglobin
level of 13.4 g/dL, a hematocrit value of 41.3%, and a
platelet count of 259 × 103/µL. A combined spinal-
epidural catheter was placed without complication, and
an intrathecal narcotic dose of 25 µg of fentanyl, 200 µg
of epinephrine, and 3 mg of tetracaine was administered.
After a negative test dose, an infusion of ropivacaine 0.2%
was started at 10 mL/h.
The patient required labor augmentation with oxytocin,
and 13 hours after admission, she vaginally delivered a
male infant. Uterine atony noted after delivery required 40
U of oxytocin and 2 doses of 0.2 mg of intramuscular
methylergonovine maleate, with an estimated blood loss of
500 mL. The epidural infusion was stopped, and later the
catheter was removed by the nursing staff. Fifteen hours
after admission, the patient became unresponsive. Vital
signs were as follows: blood pressure, 112/79 mm Hg;
heart rate, 107/min; respiratory rate, 18/min; and SaO2,
99%; her airway was patent. The patient could weakly
squeeze her hand to command but could not open her eyes
or move extremities. The patient was given oxygen at 10
L/min by nonrebreathing mask; complete blood cell count,
electrocardiogram, blood chemistry tests, and head com-
puted tomography were ordered immediately; and internal
medicine was consulted. After testing, the patient was
transferred to the intensive care unit.
AANA Journal ß June 2010 ß Vol. 78, No. 3 223
 Postoperative day (h after admission)
Test 28 wk EGA Admission 0 (15) 0 (22) 1 (30) 1 (36) 13
WBC count, /µL 10,400 14,900 21,700 20,300 16,600 15,900 6,400
Hemoglobin, g/dL 10.8 13.4 13.6 9.9 9.1 8.8 11.2
Hematocrit, % 31 41.3 39.8 30 28.4 27.2 33
Platelets, × 103/µL 354 259 160 117 77 79 420
PT/PTT, s 24/54.4 41.5 17.7/43.8 16.6/40.9
INR 4.31 2.09 2.25 1.96
Fibrinogen, mg/dL 152 253 259 290
BUN/creatinine, mg/dL 11/1.8 10/1.7 11/1.7 11/1.6
Glucose, mg/dL 62 79 70 129
Alkaline phosphatase, U/L 653 414 336 303 180
AST/ALT, U/L 367/400 203/240 128/172 101/149 24/42
LDH, U/L 306 265 242 243 130
Total bilirubin, mg/dL 5.48 5.49 5.43 5.5 0.9
Direct bilirubin, mg/dL 4.41 4.13 3.93 4.11
Arterial blood gases
pH 7.35
Oxygen, mm Hg 320
Carbon dioxide, mm Hg 35.9
Bicarbonate, mEq/L 20
Base excess, mEq/L –6
Ammonia, µmol/L* 15 22

Table 1. Patient Laboratory Results

ALT, indicates alanine aminotransferase; AST, aspartate aminotransferase; BUN, blood (serum) urea nitrogen; EGA, estimated gestational
age; INR, international normalized ratio; LDH, lactate dehydrogenase; PT, prothrombin time; PTT, partial thromboplastin time; WBC,
white blood cell.
* Values are given in Système International units; to convert to conventional units (µg/dL), divide by 0.714.

In the intensive care unit, a second large-bore intra-
venous and radial arterial lines were placed. Vital signs were
stable. The laboratory results are listed in Table 1. The com-
plete blood cell count showed a drop in platelet count from
259 × 103/µL before delivery to 160 × 103/µL after delivery
(15 hours after admission). Blood gas analysis revealed
compensated metabolic acidosis with a base deficit of –6
mEq/L; the glucose level was 62 mg/dL, and the liver func-
tion test results were extremely elevated, indicating acute
liver failure. Elevated serum urea nitrogen and creatinine
level indicated renal insufficiency. Coagulation studies re-
vealed a severe coagulopathy with an international normal-
ized ratio of 4.31. The computed tomography scan of the
head was negative. A neurological examination revealed no
clinical signs of an epidural hematoma.
The patient remained unresponsive, and a repeated
blood glucose level of 47 mg/dL (from a finger stick) was
treated with 1 ampule of 50% dextrose, with no improve-
ment in the level of consciousness. The patient then re-
ceived 0.2 mg of naloxone and within minutes became
more alert. Once the patient was alert, she described
symptoms of general malaise and nausea in the week
before delivery. A presumptive diagnosis of AFLP was
made, given laboratory results that indicated acute liver
failure, disseminated intravascular coagulopathy, renal
insufficiency, and hypoglycemia.
The coagulopathy was aggressively treated and began
to normalize after administration of 8 U of fresh frozen
plasma and 1 U of cryoprecipitate (see Table 1).
Hemoglobin and platelet counts continued to drop and
reached nadirs of 8.8 g/dL and 77 × 103/µL, respectively.
An abdominal ultrasound revealed no abdominal bleed-
ing or biliary obstruction. No other source of bleeding
was noted; the patient’s vital signs remained stable, and
she remained alert and orientated. Hourly neurological
examinations were performed and revealed no evidence
of an epidural hematoma.
Approximately 48 hours after admission, the patient
was medically evacuated to a tertiary care facility and en
route received 2 U of packed red blood cells and 1 six-
pack of platelets. The patient was discharged on post-
delivery day 7, and the results of follow-up liver function
tests, coagulation studies, and the complete blood cell
count normalized.

224 AANA Journal ß June 2010 ß Vol. 78, No. 3 www.aana.com/aanajournalonline.aspx

Discussion
Acute fatty liver of pregnancy is a potentially fatal meta-
bolic disorder of the liver. The incidence of AFLP ranges
from 1:1,00012 to 1:20,000,5 with mortality less than 10%
with aggressive treatment.5,9,12 The exact cause is
unknown, but some research suggests that AFLP results
from mitochondrial trifunctional protein dysfunction,
with a deficiency of long-chain 3-hydroxyacyl-coenzyme
A dehydrogenase (LCHAD) resulting in increased accu-
mulation of medium- and long-chain free fatty acids in
the liver.13 The LCHAD deficiency is a disorder that pre-
vents the body from converting long-chain fatty acids
into energy, which can result in lethargy; hypoglycemia;
hypotonia; liver, retinal, nervous system, and cardiac dys-
function; and death in the infant if the disorder is unrec-
ognized and untreated.14,15
Acute fatty liver of pregnancy may develop when a
mother who is heterozygous for LCHAD deficiency has a
fetus homozygous or compound heterozygous for a defi-
ciency in LCHAD. Unmetabolized free fatty acids theoret-
ically may accumulate in the mother because of 3 possible
sources: (1) heterozygous mother, (2) a homozygous
fetus, or (3) a homozygous placenta, which has the same
genetic makeup as the fetus.13 The stress of pregnancy and
delivery may overwhelm the ability of the mother’s liver to
metabolize the free fatty acids, resulting in the symptoms
of AFLP.16 Multiple gestation may increase the mother’s
risk for AFLP because of a combination of increased ma-
ternal and fetal fatty acid production and decreased free
fatty acid metabolism.17 These theories may also explain
why many mothers rapidly recover after delivery because
the major fatty acid load from the fetus is no longer
present.
Recent genetics research has found associations
between AFLP and genetic deficiencies in mitochondrial
trifunctional protein.13,15,18 Isaacs et al18 reported on the
molecular defects in a woman with AFLP and her infant,
who was diagnosed with mitochondrial trifunctional
protein deficiency and LCHAD. In this case, the infant
had a G1528C mutation in exon 15 of the α-subunit,
which alters amino acid 474 from glutamic acid to gluta-
mine (E474Q). Other researchers have confirmed the as-
sociation between a mutation in G1528C and AFLP19 and
other liver dysfunctions of pregnancy such as the HELLP
syndrome (hemolysis, elevated liver enzymes, and low
platelet count).20 The mutation has also been hypothe-
sized to be a cause of liver disease with hyperemesis
gravidarum.21 The implications of these findings are sig-
nificant because advances in genetic testing now allow
clinicians to screen infants for LCHAD deficiencies, al-
lowing for early detection and treatment. In addition,
screening helps to identify women who are heterozygous
for LCHAD deficiency because they may be at risk for
maternal complications and allows for genetic counseling
and molecular prenatal testing.14
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Acute fatty liver of pregnancy typically manifests in
the third trimester with nonspecific symptoms of malaise,
nausea, vomiting, headache, epigastric pain, and jaun-
dice.3,5,12 Common features of AFLP include evidence of
rapidly developing severe liver dysfunction, disseminated
intravascular coagulopathy, hypoglycemia, and hepatic
encephalopathy (Table 2).5,7,12,16,17 Fulminant liver
failure with renal insufficiency and sepsis can rapidly
develop. Other laboratory studies indicate elevated
bilirubin levels; low cholesterol, triglycerides, and fib-
rinogen levels; decreased antithrombin III levels; and
leukocytosis.5,12,15 The presence of hypoglycemia and hy-
perbilirubinemia in the presence of extremely elevated
liver enzyme levels is characteristic of AFLP and can be
used to differentiate it from liver disorders of pregnancy
such as the HELLP syndrome, obstetric cholestasis,
preeclamptic liver dysfunction, and hyperemesis gravi-
darum with liver dysfunction (see Table 2).5,12 Treatment
is prompt delivery and supportive care. Early diagnosis,
prompt delivery, aggressive treatment of hypoglycemia
and coagulopathy, and prevention of complications asso-
ciated with liver failure are key to survival.3,5,7,8,22,23 In
most cases, emergency cesarean section will be required,
with improved maternal outcomes if coagulopathy is rec-
ognized and treated before delivery.4,9,11 In rare cases,
auxiliary24 and orthotopic liver transplantation25,26 and
molecular absorbent recirculating system therapy27,28
have been used successfully to treat AFLP.
Knight et al5 conducted a prospective study of AFLP in
the United Kingdom. They found 55 cases of 1,132,964 de-
liveries, with only 26% diagnosed postnatally (median ges-
tation, 36 weeks; most diagnosed within 48 hours of de-
livery). Of the 55 cases, only 1 patient died (2%), and 1
patient required liver transplantation. Of the women diag-
nosed postnatally, 27% delivered vaginally. Characteristics
of the 55 patients included the following: primiparous,
61%; older than 35 years, 25%; twin pregnancy, 18%;
smoked during pregnancy, 16%; history of preeclampsia,
4%; current preeclampsia, 18%; and body mass index, less
than 20 kg/m2, 20%. Of significance to anesthesia
providers is that more than half of patients required
general anesthesia and half received regional anesthesia.
No patient who had regional anesthesia had complications,
including 5 patients who received regional anesthesia in
the presence of documented coagulopathy. Encephalo-
pathy did not worsen in patients who received general
anesthesia. More than 65% required admission to an in-
tensive care unit. The anesthetic implications of these find-
ings are that providers should keep AFLP in their differen-
tial diagnosis any time a patient has liver dysfunction late
in pregnancy, especially patients who are primiparous, are
of advanced maternal age, have concurrent preeclampsia,
have twin gestations, and are underweight.
Of significance to rural anesthesia providers is that
most of the women are critically ill and will require in-
AANA Journal ß June 2010 ß Vol. 78, No. 3 225
 Hyperemesis
Acute fatty liver Obstetric Preeclamptic liver gravidarum with
of pregnancy HELLP syndrome cholestasis dysfunction liver dysfunction
Vomiting Elevated aspartate Pruritus Elevated liver enzyme or Elevated liver enzyme
Abdominal pain aminotransferase level Elevated transaminase bilirubin level or bilirubin level
(> 70 U/L) and/or bile acid levels Hypertension Persistent vomiting, > 1
Polydipsia/polyuria
Low platelet count (< 100 in the second or third Proteinuria, after 20 wk wk during first or second
Encephalopathy × 109/L) trimester trimester
of gestation
Elevated bilirubin level Hemolysis (lactate
Hypoglycemia dehydrogenase level
Elevated urate level > 600 U/L)

Leukocytosis
Ascites or bright liver on
ultrasound scan
Elevated transaminase
levels
Elevated ammonia level
Renal impairment
Coagulopathy
Microvesicular steatosis
on liver biopsy
Table 2. Characteristics of Liver Disorders of Pregnancy
HELLP indicates hemolysis, elevated liver enzymes, and low platelet count.
(Adapted from Chᴵng et al.12 )

tensive care to minimize morbidity and mortality. The
care for patients may quickly overwhelm the resources of
a small community or overseas hospital; therefore, pa-
tients with AFLP should be transferred to a tertiary care
facility as soon as possible. Unfortunately, the condition
of patients with AFLP may be too unstable and trans-
portation not immediately available. Therefore, nurse
anesthetists may be asked to assist in the resuscitation
and management of patients with AFLP.
In the present case, signs and symptoms of AFLP were
first recognized 1 hour after delivery (15 hours after ad-
mission) when the patient became unresponsive. Only
later, after treatment of hypoglycemia and administration
of naloxone, did the patient report she had felt increasing
malaise and nausea the week before delivery. During her
preanesthetic interview, she had not reported any specif-
ic symptoms indicating liver dysfunction or coagulopa-
thy. The complete blood cell count was normal, and her
pregnancy was uncomplicated up until delivery. The
patient required double-strength oxytocin and 2 doses of
methylergonovine maleate for uterine atony, which in
hindsight was probably the first indication of coagulopa-
thy. However, the postpartum hemorrhage was con-
trolled, and good uterine tone was noted after treatment.
If the patient had required cesarean section, there would
have been the potential for massive blood loss and subse-
quent transfusion requirements, along with the associat-
ed complications. Resuscitation would have been chal-
lenging at a small overseas hospital owing to limited
blood bank and intensive care unit capabilities. Brooks et
al2 reported a case of AFLP in a 34-week, gravida 2, para
0 patient admitted to a tertiary care facility for severe
preeclampsia who required emergency cesarean section
for fetal distress. During that case, the patient required
massive resuscitation for hemorrhage during surgery and
was diagnosed 4 hours after delivery with AFLP.
Unfortunately, the patient died postoperatively of com-
plications of adult respiratory distress syndrome.
Nevertheless, when AFLP is diagnosed early and coagu-
lopathy is corrected before cesarean section, the morbid-
ity and mortality are significantly reduced.4,9,11
With AFLP, hypoglycemia is common, and in this
patient, it was treated with 1 ampule of 50% dextrose. This
measure was expected to improve the patient’s mental
status; however, no improvement in mental status was
noted. Despite the patient having a normal respiratory rate
and oxygen saturation, the decision was made to adminis-
ter naloxone because the patient had received morphine
sulfate, 5 mg intravenously and 5 mg intramuscularly, 12
hours earlier. After administration of naloxone, the patient
became more responsive. Morphine is metabolized to in-
active morphine-3-glucuronide and active morphine-6-
glucuronide in the liver and extrahepatic sites (ie,
kidneys).29 Elimination of morphine glucuronides is im-
paired in patients with renal dysfunction. It is hypothe-
sized that this patient’s unresponsiveness was related to a
synergistic effect of hypoglycemia and an inability to me-
tabolize and/or eliminate active morphine metabolites
because of acute liver failure and renal insufficiency.
The improvement in the patient’s mental status with

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naloxone highlights an important point to consider in the
management of a patient with AFLP. Once AFLP is diag-
nosed, it is important to review all medications the
patient has received given the role of the liver in bio-
transformation. Any medications that rely on biotrans-
formation may potentially worsen liver dysfunction. For
example, Gill et al26 reported a case of AFLP and aceta-
minophen toxicity leading to liver failure and postpartum
liver transplantation. In their case report, a 33-week,
gravida 1, para 0 woman had signs and symptoms of
AFLP and extremely elevated transaminase levels. Before
admission, the patient had been taking an unknown
amount of acetaminophen for malaise; she was not
known to be suicidal. The extremely elevated transami-
nase levels led clinicians to search for other causes, and
the patient was subsequently given a diagnosis of aceta-
minophen toxicity and AFLP based on a liver biopsy
demonstrating microvesicular steatosis consistent with
AFLP and superimposed centrilobular hepatocellular co-
agulative necrosis compatible with acetaminophen toxic-
ity. Gill et al26 speculated that the combination of a non-
toxic and possibly therapeutic level of acetaminophen
with an already severely injured liver from AFLP may
have resulted in fulminant liver failure and need for a
liver transplantation.
Due to the current patient’s significant coagulopathy
and thrombocytopenia, there was concern that she was at
risk for development of an epidural hematoma. Current
guidelines recommend leaving epidural catheters in place
until the coagulopathy is corrected.30 Unfortunately, per
protocol, the epidural catheter was removed by nursing
staff before laboratory results demonstrated a coagulopa-
thy. Because the patient was high risk for epidural
hematoma, hourly neurological examinations were per-
formed. The incidence of epidural hematoma ranges from
1:150,000 to 1:190,000, with signs and symptoms indi-
cating loss of recovered sensory and motor blockade
and/or loss of sphincter tone.30 Treatment is prompt sur-
gical evacuation. Inopportunely, our small overseas hospi-
tal did not have a neurosurgeon. In this case, an epidural
hematoma was prevented by atraumatic epidural catheter
placement and aggressive treatment of the coagulopathy.
Supportive care is the only treatment for AFLP, with
improved outcomes found with prompt delivery.5,9,12,22,31
Acute fatty liver of pregnancy should be considered in
any pregnant patient in the late second or third trimester
who has elevated liver enzyme levels, especially in the
presence of hypoglycemia. Anesthesia providers should
also have a high level of suspicion for AFLP in a patient
with altered mental status and elevated liver function test
results in the postpartum period. Anesthetic implications
include early recognition of liver dysfunction and aggres-
sive resuscitation and treatment of hypoglycemia, dis-
seminated intravascular coagulopathy, and other associat-
ed complications. Anesthesia providers should review all
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medications the patient has received at home and in the
hospital, especially if the patient has atypical signs or
symptoms or response to treatment. Reduction or avoid-
ance of medications with substantial hepatic metabolism
is important in preventing worsening encephalopathy or
fulminant liver failure.26 Consideration should be given
to administering reversal agents if the patient has re-
ceived narcotics (ie, morphine) during the admission or
at home. If cesarean section is required, coagulopathy
and thrombocytopenia should be corrected before
surgery when possible, and the anesthetist should be pre-
pared for massive blood loss (eg, 2 large-bore intravenous
catheters, blood products in room, fluid warmer and level
1 transfuser available, arterial line, and central line avail-
able). The anesthetic of choice is general anesthesia. If
neuraxial analgesia is used for vaginal delivery, the
epidural should be left in place until correction of coagu-
lopathy. Hourly neurological examinations should be
performed, and early surgical consultation should be
made if deficits are identified.
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AUTHOR
LCDR Dennis Spence, CRNA, PhD, NC, USN is the clinical research direc-
tor, Uniformed Services University of the Health Sciences, Nurse Anesthe-
sia Program, Naval Medical Center San Diego, California. This case
occurred while he was a staff nurse anesthetist at Naval Hospital Guam.
Email: dennis.spence@med.navy.mil.
DISCLAIMER
The views expressed in this article are those of the author and do not
reflect official policy or position of the Department of the Navy, Depart-
ment of Defense, Uniformed Services University of Health Sciences, or the
United States Government.
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