The prevalence of obstetric patients in critical care is 1 to 9 in 1000 pregnancies, with a 12% to 20% mortality.^1-4 The majority of puerperium cases are related to hemorrhage or hypertension, while the majority of postpartum cases are due to hemorrhage and postsurgical complications.⁵ Physiologic changes associated with pregnancy affect diagnostics and treatment.

Maternal cardiovascular changes occur in the first trimester, may manifest as early as 5 weeks, peak by the end of the second trimester, plateau up to term, and normalize 2 to 12 weeks postpartum.⁶ This is primarily mediated by estrogen effecting uterine blood flow and progesterone and prostaglandin E2 causing vasodilation of uteroplacental vessels.¹ Cardiac output (CO) increases by 30% to 50% from 8 to 28 weeks.^3,6 Central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) are unchanged secondary to reduced systemic vascular resistance (SVR; 20–30%) and pulmonary vascular resistance (PVR; 20–30%).⁷ After 24 weeks, supine hypotension syndrome is characterized by hypotension, 5 to 10 mmHg below normal, and bradycardia secondary to decrease in cardiac output from compression of the inferior vena cava (IVC) by the gravid uterus. This can be alleviated by a left lateral tilt positioning.^3,6,7 During labor, there is an increase of 10% to 20% in CO due to a return of 300 to 500 mL of blood to the maternal circulation with each uterine contraction.^3,7

Prothrombogenic effects include changes with coagulation factors such as increased fibrinogen, factor VII, and factor X and decreased factor XI, factor XIII, and platelets.¹ The patient’s ability to tolerate up to 1 liter of blood loss during labor counteracts the effects of physiologic anemia (ie, increased plasma volume by up to 50% by term with a much lower increase in red blood cells) and decrease in colloid oncotic pressure (by 14%).^3,6,7 There is an increased lower extremity venous pressure from compression of the uterus on the inferior vena cava, causing varicose veins and hemorrhoids.

Pulmonary changes are progesterone mediated, causing an increase in tidal volume (30–35%), minute ventilation (20–40%), and respiratory alkalosis (Paco₂ of 28–32 mmHg) with compensatory renal excretion of bicarbonate (CO₂ of 18–21 mEq/L) by term.^3,6 The gravid uterus causes a 10% to 25% decrease in functional residual capacity with a 4-cm elevation of diaphragm, and much less decrease in total lung capacity secondary to compensation of the thoracic cage.^3,6,7 Chest wall and total respiratory compliance decrease with no effect on total lung compliance.³ Maternal-to-fetal oxygen exchange is enhanced by the ability of the fetus to extract oxygen better at higher hemoglobin (Hgb) concentrations, a higher oxygen saturation of fetal hemoglobin (HgbF) (80–90%) compared to that of HgbA (50–55%) at a Po₂ of 30 to 35 mmHg, and the presence of a patent ductus arteriosus.^1,3

Renal changes include a 45% to 50% increase in glomerular filtration rate (GFR) and creatinine clearance resulting in a decrease in the following: serum creatinine (< 0.8–0.9 mg/dL), blood urea nitrogen (< 15 mg/dL), and uric acid levels (< 6 mg/dL).^1,6 Decreased blood pressure and wide pulse pressure in the late second and early third trimester are partly due to the decreased serum osmolarity and reduced sensitivity to increasing levels of aldosterone, estrogen, and plasma renin. Acute kidney injury is defined in a pregnant patient as having a serum creatinine of greater than 1 mg/dL.¹ Beginning in the sixth week, the right ureter is compressed secondary to the growing uterus, which increases urinary stasis and therefore infection.

Gastrointestinal changes are linked to progesterone-related smooth muscle relaxation and the displacement of organs. Nutrient adsorption may be increased, but at the same time, the patient may experience increased constipation, obstipation, or exacerbated gastroesophageal reflux disease (GERD). There will also be decreased utility of diagnostic physical signs such as Murphy sign and McBurney point.¹ Decreased gallbladder tone and emptying, biliary stasis secondary to progesterone, and increased cholesterol and lithogenicity of bile secondary to estrogen increase ­cholelithiasis. Alkaline phosphate maybe increased from 2 to 15 times normal.

Rheumatologic Diseases

Pregnant patients with systemic lupus erythematosus (SLE) have a higher incidence of spontaneous abortions, intrauterine growth restriction, preterm labor, premature rupture of membranes, and preeclampsia. There is also an additional challenge in differentiating between SLE nephritis and preeclampsia, although elevated anti–double stranded DNA (anti-dsDNA) could suggest active SLE and normal or slightly elevated complement C3 and C4 could suggest preeclampsia. Other autoimmune diseases may show improvement, such as rheumatoid arthritis, especially in the second and third trimester, although the reason has not been definitively established.⁸

Neurologic Diseases

Headaches are common during pregnancy and in the postpartum period. Headache frequency and characteristics should prompt the clinician to investigate for secondary causes. Thunderclap headache, described as having an abrupt onset of severe unusual headaches, may be due to preeclampsia, posterior reversible encephalopathy syndrome (PRES), or cerebral vein thrombosis. Multiple episodes of migraine headaches (5 or more) or tension headaches (10 or more) should be considered in diagnosing primary headache disorders. Migraines with auras can manifest with transient positive or negative neurologic deficits that typically resolve after 30 minutes. Prompt evaluation for other causes such as cerebrovascular accident (CVA), preeclampsia, HELLP (hemolysis, elevated liver enzymes, low platelet count), cervicoarterial dissection, orbital hemorrhage, and pituitary apoplexy should be considered. Bilateral throbbing headaches that may be accompanied by blurred vision and scotomata are typical in preeclamptics. Postdural headaches secondary to low cerebrospinal fluid (CSF) pressure from the administration of spinal anesthesia can occur up to 1 week postpartum. These headaches, typically nuchal and occipital, that are exacerbated by standing up and relieved by sitting down, may be accompanied by tinnitus, diplopia, and hyperacusis, and can resolve in 48 hours after a blood patch.⁹

Patients with multiple sclerosis have reduced exacerbations during the third trimester but increased risk of exacerbations up to 3 months postpartum.^8,10 The cause of this is unclear but may be due to decreased cell-mediated immunity, increased production of tolerance promoting signals, and interferon γ.¹⁰ Forty percent of patients with myasthenia gravis will experience an exacerbation.¹¹

The incidence of cardiovascular disease is as follows: Ischemic CVA occurs more frequently than intracerebral hemorrhage (ICH), which occurs more frequently than subarachnoid hemorrhage (SAH), which occurs more frequently than cerebral venous thrombosis.^12,13 Diagnosis is via computed tomography (CT) of the head with abdominal shield or magnetic resonance imaging (MRI) with iodine, but avoiding gadolinium.^12,13 Thrombolysis with recombinant tissue plasminogen activator can be given to patients with ischemic CVA within 3 to 4.5 hours of onset, since it does not cross the placenta.^14-21 Aspirin can be used as thromboprophylaxis, although there is an association with gastroschisis in the first trimester.²²

Patients with epilepsy do not have an increased frequency of seizures during pregnancy.²³ Antiepileptic medications are associated with fetal complications. Phenytoin is associated with cleft palate and lip, and nail and distal phalangeal hypoplasia. Phenobarbital is associated with congenital heart defects and facial defects. Valproic acid is associated with spina bifida and cardiovascular and urogenital malformations.

Pulmonary Diseases

In acute respiratory distress syndrome (ARDS) and other pulmonary diseases, a plateau pressure of greater than 30 cm H₂O may not be applicable in pregnant patients where normal intra-abdominal pressures increase to 14 mmHg; therefore monitoring of transpulmonary pressures is required. Maintenance of a maternal Pao₂ greater than 70 mmHg is required to ensure adequate fetal oxygenation. The normal Paco₂ is 28 to 32 mmHg, but hypocapnia and hypercapnia must be avoided in pregnancy. Hypocapnia causes decreased uteroplacental blood flow and fetal alkalosis. Hypercapnia, Pao₂ greater than 60 to 70 mmHg, can lead to elevated intracranial pressure. Termination of pregnancy is recommended if ARDS is secondary to specific obstetric causes.¹²

For patients with thromboembolic disease, deep vein thrombosis (DVT) is more common than pulmonary edema (PE). Eighty-five percent of DVT cases occur in the left lower extremity due to compression of the left iliac vein by the uterus. The initial test for DVT is ultrasound, although there is a high false-negative rate in pelvic vein thrombosis; if the initial test is negative, it may be repeated in 1 week. A chest radiograph should be used to rule out other cases of hypoxia with abdominal shielding. Computed tomography angiography (CTA) is indicated if the patient presents with severe hypoxia, hemodynamic compromise, or ventilation/perfusion (V/Q) scan with negative results but high suspicion. A V/Q scan is preferred if the patient is hemodynamically stable so as to expose breast milk to less carcinogenic radiation. Treatment with low-molecular-weight heparin (LMWH) is preferred over unfractionated heparin (UFH), except in the cases of obesity, renal dysfunction, and high risk of bleeding. If patient is on long term LMWH, after 36 to 37 weeks, it is recommended that the patient be switched to UFH for massive DVT, massive PE, or thrombolysis.¹²

Cardiac Diseases

Pregnancy is contraindicated in the following cases: pulmonary hypertension, systolic ejection fraction less than 30%, New York Heart Association (NYHA) class III/IV, previous peripartum cardiomyopathy with residual deficit, severe mitral or aortic stenosis, severe coarctation of aorta, aortic dilation greater than 45 mm in Marfan syndrome, or aortic dilation greater than 50 mmHg with bicuspid aortic valve. Balloon valvotomy for severe mitral or aortic stenosis is tolerated after 20 weeks age of gestation (AOG). If the patient presents with resistant heart failure for aortic stenosis, delivery via cesarean section and then valvotomy are recommended.¹²

If cardiac arrest occurs after 20 weeks AOG, delivery via cesarean section is recommended if return of spontaneous circulation (ROSC) is not achieved within 4 minutes. Neurological fetal outcome is better if delivery is within 5 minutes of cardiac arrest.¹²

Endocrinologic Diseases

Diabetic ketoacidosis can occur in glucose as low as 180 mg/dL.¹²

Gastrointestinal Diseases

For acute abdomen, ultrasound is preferred, but MRI is preferred if the patient is greater than 35 weeks AOG or the ultrasound is nonconclusive.^24-26 Laparoscopy is safe at any trimester, although fetal demise has been reported.^27-29

Infectious Diseases