Delayed postpartum hemorrhage: A rare presentation of carbon
monoxide poisoning
Patrick S. Ramsey, MD, Lane M. Meyer, MD, Kirk D. Ramin, MD, and Robert H. Heise, MD
Rochester, Minnesota
A 41-year-old woman presented with postpartum hemorrhage and altered mentation. A markedly elevated
serum carboxyhemoglobin level was noted. Oxygen therapy was initiated with resolution of the patient’s
bleeding and improved mental status. Carbon monoxide poisoning is a rare and previously unreported cause
of postpartum hemorrhage resulting from a unique pathophysiologic mechanism. (Am J Obstet Gynecol
2001;184:243-4.)
Key words: Carbon monoxide poisoning, postpartum hemorrhage, pregnancy, uterine atony,
hypoxia
Carbon monoxide is a leading cause of poisoning
deaths in the United States.1 It rapidly diffuses across the
alveolar-capillary interface, strongly binding to hemoglobin (200-250 times greater than oxygen) to form carboxyhemoglobin, which results in a left shift in the oxygen dissociation curve.1, 2 This shift, along with carbon
monoxide inhibition of cytochrome P-450–mediated cellular respiration, leads to tissue hypoxia, anaerobic metabolism, and lactic acidosis.1 Clinical manifestations of
carbon monoxide poisoning are variable, vague, and
nonspecific. Symptoms include headache, lightheadedness, nausea, visual disturbances, palpitations, and confusion.1 Whereas retinal hemorrhages and “cherry red” mucous membranes are classically associated with carbon
monoxide poisoning, these findings are rare.1 Postpartum hemorrhage has not previously been reported as a
finding associated with carbon monoxide poisoning. We
report a case of delayed postpartum hemorrhage associated with carbon monoxide poisoning and discuss the
unique pathophysiologic characteristics related to the
case.
Case report
A 41-year-old white woman, gravida 16, para 10-0-6-10
(8 normal spontaneous vaginal deliveries, 1 cesarean deFrom the Division of Maternal-Fetal Medicine, Department of Obstetrics
and Gynecology, Mayo Medical Center.
Presented by Lane M. Meyer at the Stump the Professor Session during
the Annual Meeting of The American College of Obstetricians and Gynecologists, New Orleans, Louisiana, May 9-13, 1998.
Received for publication March 23, 2000; revised June 12, 2000;
accepted July 21, 2000.
Reprint requests: Patrick S. Ramsey, MD, Division of Maternal-Fetal
Medicine, Department of Obstetrics/Gynecology, 446 Old Hillman Bldg,
619 19th St S, Birmingham, AL 35249-7333. E-mail: ramsey_patrick@
hotmail.com.
Copyright © 2001 by Mosby, Inc.
0002-9378/2001 $35.00 + 0 6/1/110297
doi:10.1067/mob.2001.110297
livery, 1 vaginal delivery after cesarean, and 7 spontaneous abortions) presented with profuse vaginal bleeding 2 weeks after an uncomplicated indicated low-forceps
assisted vaginal delivery. The perineum was intact. Her
postpartum convalescence was uncomplicated until 2 to 3
hours before presentation, when she began to have
soaked pads every 10 minutes by the passage of large
clots. She also reported lightheadedness, nausea, blurred
vision, headache, and shaking chills. Her medical history
was significant for tobacco use and mild asthma.
She was afebrile with stable vital signs (blood pressure,
110/60 mm Hg; pulse, 71 beats/min; respiratory rate, 25
breaths/min) and no orthostatic blood pressure changes.
The results of cardiac and abdominal examinations were
unremarkable. Chest auscultation revealed mild scattered bilateral inspiratory wheezing. Pelvic examination
revealed large clots in the vagina; however, no active
bleeding was noted. Bimanual examination revealed a
well-contracted, nontender uterus.
During examination the patient appeared confused.
She was disoriented to time and place and was unable to
perform concentration or short memory tasks. Neurologic examination revealed intact cranial nerves II to XII.
A slight lateral gaze nystagmus was noted. Strength, coordination, and sensory and fine motor function were intact throughout. Deep tendon reflexes were normal.
Ophthalmologic examination revealed no evidence of
papilledema.
Laboratory investigations included the following:
hematocrit value, 41%; leukocyte count, 6800/mm3;
platelet count, 207,000/mm3; sodium level, 137
mEq/dL; potassium level, 3.5 mEq/dL; glucose level, 79
mg/dL; prothrombin time, 12.5 seconds; activated partial thromboplastin time, 25 seconds; drug screen, negative. Electrocardiogram and chest x-ray film were normal.
Ultrasonography revealed a normal-appearing uterine
stripe. Pulse oximetry was 93% on room air. Arterial
blood gas values were as follows: PO2, 68 torr; PCO2, 38
torr; pH, 7.36; base deficit, –3 mEq/L; oxygen saturation,
80%. The serum carboxyhemoglobin level was markedly
243
244 Ramsey et al
elevated at 17% (normal values, <3% for nonsmokers and
<5% for smokers), which was consistent with carbon
monoxide poisoning.
Immediate treatment with 100% oxygen by nonrebreather mask was initiated. Over the subsequent 4 hours
the oxygen saturation normalized, the bleeding completely resolved, and the mental status of the patient returned to baseline. The local emergency medical service
was dispatched to the patient’s home. High carbon
monoxide levels were noted within the home as a result
of a faulty gas heater. All family members received
prompt evaluation, with 2 of the patient’s children having
high carboxyhemoglobin levels. All family members responded well to treatment and were discharged without
complications.
Comment
Postpartum hemorrhage is a serious and potentially
catastrophic obstetric complication. Whereas early (<24
hours) postpartum hemorrhage is often the result of
uterine atony or occult genital tract lacerations, delayed
hemorrhage (>24 hours through 6 weeks post partum) is
more commonly associated with retained placental tissue,
placental site subinvolution, or infection.3 Review of the
literature (MEDLINE, 1966-2000, with the key words carbon monoxide poisoning, hemorrhage, pregnancy) revealed no
previously reported cases of postpartum hemorrhage
caused by acute carbon monoxide poisoning. We have reported a unique case of delayed postpartum hemorrhage
as a secondary effect of acute carbon monoxide poisoning. Recent evidence has shown that carbon monoxide,
similar to nitric oxide, is a potent vasodilator.4 Vedernikov et al4 demonstrated that carbon monoxide,
January 2001
Am J Obstet Gynecol
through activation of guanylate cyclase, results in arterial
vascular smooth muscle relaxation with subsequent vasodilation. In addition, studies have shown that carbon
monoxide inhibits platelet aggregation through a similar
mechanism.4 These effects set the stage for tissue and vascular smooth muscle relaxation, which in the case presented resulted in postpartum hemorrhage.
Standard treatment for carbon monoxide poisoning is
administration of 100% oxygen.1 Elimination of carbon
monoxide is highly dependent on the concentration of
inspired oxygen (half life with room air, 4-6 hours; half
life with 100% normobaric oxygen, 40-80 minutes; half
life with 100% hyperbaric oxygen, 15-30 minutes).1, 2
Whereas delayed neuropsychiatric complications occur
in 10% to 30% of patients, the majority of patients recover completely with oxygen therapy.1 Our patient
responded well to oxygen therapy. As the carboxyhemoglobin level normalized with administration of normobaric oxygen, the uterine bleeding resolved completely,
concurrent with improvement in mental status. This observation further supports the role of carbon monoxide
in the development of postpartum hemorrhage in our
patient.
REFERENCES
1. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med
1998;339:1603-7.
2. Longo LD. The biological effects of carbon monoxide on the
pregnant woman, fetus, and newborn infant. Am J Obstet Gynecol 1977;129:69-103.
3. Khong TY, Khong TK. Delayed postpartum hemorrhage: a morphologic study of cause and their relation to other pregnancy
disorders. Obstet Gynecol 1993;82:17-22.
4. Vedernikov YP, Graser T, Vanin AF. Similar endothelium-independent arterial relaxation by carbon monoxide and nitric
oxide. Biomed Biochim Acta 1989;48:601-3.