INTRODUCTION — Although fewer than 2 percent of patients require admission to an intensive care unit (ICU) during pregnancy or the peripartum period, defined as the last month of gestation and the first few weeks after delivery, both maternal and fetal mortality are high when such care is required [1-8].
The disorders that are most common among patients admitted to the ICU during pregnancy or the peripartum period are reviewed here. Issues related to acute respiratory failure during pregnancy and the peripartum period are discussed separately. (See "Acute respiratory failure during pregnancy and the peripartum period".)
INCIDENCE AND MORTALITY — The incidence of intensive care unit (ICU) admission for pregnant and postpartum patients ranges from 0.7 to 13.5 per 1000 deliveries [2,9,10]. The most common indications for ICU admission are postpartum hemorrhage and the hypertensive disorders (severe preeclampsia or eclampsia) . However, all medical conditions that can complicate pregnancy can be encountered in the ICU.
The overall pregnancy-related mortality ratio in the United States is 17.3 deaths per 100,000 live births . In the United States, the leading cause of maternal mortality is death due to cardiovascular disease and cardiomyopathy, which may relate to rising maternal age and high incidence of obesity, diabetes, and hypertension [8,11]. Other common causes of pregnancy-related mortality include venous thromboembolic disease, hemorrhage, infection, and amniotic fluid embolism. According to some studies, more than 60 percent of maternal deaths are preventable . Causes of preventable maternal death included postpartum hemorrhage, preeclampsia, medication errors, and some infections. (See "Overview of maternal mortality".)
Fetal mortality is also high when critical care is required [2,13-15]. Early gestational age, severe maternal illness, maternal shock, the need for maternal blood transfusions, and the absence of prenatal care are associated with fetal mortality.
MANAGEMENT OF SPECIFIC DISEASES — Management of critical illness in pregnant and postpartum patients is best done collaboratively with subspecialities including intensivists and obstetric gynecologists .
Cardiovascular disease — Maternal cardiac disease and peripartum cardiomyopathy is a major cause of maternal morbidity and mortality that can be encountered in the intensive care unit (ICU). The management of acquired heart disease and peripartum cardiomyopathy are discussed in detail separately. (See "Acquired heart disease and pregnancy" and "Peripartum cardiomyopathy: Etiology, clinical manifestations, and diagnosis" and "Management of heart failure during pregnancy".)
Venous thromboembolism — Venous thromboembolism (VTE) is the fifth leading cause of maternal death in the United States [1,8]. VTE can result in, or complicate, an ICU admission. The diagnosis and management of VTE during pregnancy is discussed in detail separately. (See "Deep vein thrombosis in pregnancy: Epidemiology, pathogenesis, and diagnosis" and "Diagnosis of pulmonary embolism in pregnancy" and "Deep vein thrombosis and pulmonary embolism in pregnancy and postpartum: Treatment".)
Hemorrhage — Severe postpartum hemorrhage is a major cause of maternal ICU admission, accounting for 6.9 to 49 percent of admissions [1,3-8,17,18] and approximately 11 percent of maternal deaths [1,8,18]. The most common causes of postpartum hemorrhage are uterine atony due to poor myometrial contraction after delivery and abnormal placentation, including placenta accreta, placental abruption, and placenta previa.
The incidence, diagnosis, etiologies, risk factors, management, and complications of postpartum hemorrhage are reviewed in detail separately. (See "Overview of postpartum hemorrhage".)
Preeclampsia or eclampsia — Preeclampsia and eclampsia are multisystem diseases that develop during pregnancy:
●Preeclampsia is the new onset of hypertension and proteinuria or the new onset of hypertension and end-organ dysfunction with or without proteinuria occurring after 20 weeks of gestation in a previously normotensive patient . Proteinuria is characterized as >0.3 g per day and hypertension is defined as a systolic blood pressure >140 or diastolic blood pressure >90 mmHg. Peripheral edema may be present, but this is not essential for diagnosis. (See "Preeclampsia: Clinical features and diagnosis".)
●Eclampsia exists if the features of preeclampsia are accompanied by new-onset seizures. (See "Eclampsia".)
Complications of the disease are the usual indications for admitting patients with severe preeclampsia or eclampsia to the ICU. Examples include refractory hypertension, neurological dysfunction (eg, seizures, intracranial hemorrhage, elevated intracranial pressure), renal failure, liver rupture, liver failure, pulmonary edema, the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets), and/or disseminated intravascular coagulation (DIC) .
ICU care involves managing complications including:
●Severe hypertension (ie, systolic BP ≥150 mmHg or diastolic BP ≥100 mmHg and persisting ≥15 minutes) is typically treated with labetalol, hydralazine, or nicardipine [20-24]. Angiotensin-converting enzyme (ACE) inhibitors should be avoided due to their toxic effects on the embryonic kidney. Nitroprusside is contraindicated in the later stages of pregnancy due to possible fetal cyanide poisoning if used for more than four hours. The use of antihypertensive agents in pregnancy is discussed in detail separately. (See "Chronic hypertension in pregnancy: Prenatal and postpartum care".)
●Seizures should be treated promptly with a bolus of intravenous magnesium, followed by the continuous infusion of magnesium sulfate [25,26]. In addition, supportive care (eg, recovery position, bite protection, supplemental oxygen) is indicated. (See "Eclampsia", section on 'Prevention of recurrent seizures'.)
●Intracerebral hemorrhage requires immediate reversal of any coagulopathy, as well as the discontinuation of any anticoagulant or antiplatelet therapy. Antihypertensive therapy, seizure prophylaxis, and neurosurgical consultation may also be indicated. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Triage'.)
●Intracranial hypertension can occur in any patient with severe preeclampsia or eclampsia, but patients who have had an intracerebral hemorrhage are at particularly high risk. Suspected elevated intracranial pressure should prompt elevation of the head of the bed to 30 to 45 degrees, positioning of the head in a midline position to promote venous outflow through the jugular veins, avoidance of hypotonic intravenous fluids, and neurosurgical consultation for potential intracranial pressure monitoring. Sedation and treatment of fever should be optimized. Some patients require osmotic diuresis using hypertonic saline, mannitol, and/or hyperventilation [27,28]. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'ICP monitoring' and "Evaluation and management of elevated intracranial pressure in adults", section on 'General management'.)
●Pulmonary edema may present with dyspnea or acute respiratory failure. Supportive management includes supplemental oxygen and fluid restriction. Diuresis is indicated if there is fluid overload, although this is rare because most patients with severe preeclampsia are volume depleted. (See "Acute respiratory failure during pregnancy and the peripartum period", section on 'Pulmonary edema'.)
●Management of DIC consists of treating the underlying cause, which is frequently placental abruption (abruptio placentae). Aggressive blood component replacement may be necessary when there is severe placental abruption. However, blood products can usually be administered more selectively in the absence of placental abruption. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults" and "Acute placental abruption: Management and long-term prognosis", section on 'Initial approach for all patients'.)
All of these complications are indications for prompt delivery of the fetus, which remains the primary therapy for both preeclampsia and eclampsia.
Acute respiratory failure — Acute respiratory failure is a rare complication of pregnancy. It may be due to a conventional respiratory insult or a pregnancy-specific disorder. Examples include pulmonary edema, community-acquired pneumonia, aspiration, pulmonary embolism, asthma exacerbation, amniotic fluid embolism, and venous air embolism .
The clinical presentation, differential diagnosis, diagnosis, and management of acute respiratory failure during pregnancy and the peripartum period are reviewed separately. (See "Acute respiratory failure during pregnancy and the peripartum period".)
Infection/sepsis — Obstetrical infections may require ICU admission, particularly if they are complicated by severe sepsis or septic shock, which has been reported to occur in 0.002 to 0.04 percent of all deliveries [30-32]. Such infections are a significant cause of maternal morbidity and mortality [31,33,34]. The reported maternal mortality rate ranges from 12 to 28 percent in pregnant patients with septic shock and multiple organ failure [32,34,35]. Black females, those who smoke cigarettes, and those older than 35 years may be more likely to develop maternal sepsis .
The etiologies of infection during pregnancy are different in the antenatal and postnatal period:
●Antenatal infections – The most common severe infections that occur before delivery are septic abortion, intraamniotic infection (chorioamnionitis), complicated pyelonephritis, and pneumonias caused by Streptococcus pneumoniae and influenza [34-36]. (See "Intraamniotic infection (clinical chorioamnionitis)" and "Urinary tract infections and asymptomatic bacteriuria in pregnancy", section on 'Acute pyelonephritis' and "Approach to the pregnant patient with a respiratory infection" and "Seasonal influenza and pregnancy".)
●Postnatal infections – The most common postpartum infection is endometritis. It is usually due to mixed flora, including anaerobic, gram negative, and gram positive organisms. (See "Postpartum endometritis".)
Other postpartum infections include wound infections, necrotizing fasciitis, toxic shock syndrome, pelvic abscess, gas gangrene of the myometrium (usually due to clostridial species that colonize the GI tract and vagina), septic pelvic thrombophlebitis, pyogenic sacroiliitis [37-40], and Clostridioides difficile colitis . (See "Postpartum endometritis" and "Clostridioides difficile infection in adults: Treatment and prevention" and "Pelvic osteomyelitis and other infections of the bony pelvis in adults" and "Cesarean birth: Postoperative care, complications, and long-term sequelae", section on 'Complications'.)
Although there are no prospective studies of early goal-directed therapy during pregnancy, the management of sepsis should be similar to that of the nonpregnant patient and use the same targets . However, the SvO2 decreases in the later stages of the third trimester of pregnancy, so utilizing this target in late pregnancy may be less reliable [34,43,44]. Delivery of the fetus is determined by obstetric indications. Delay in administering antibiotics is associated with an increased mortality, similar to that seen in nonpregnant females with sepsis. One study reported an increase in death from 8.3 percent in females who received antibiotics within one hour of diagnosis to 20 percent in females who received antibiotics later than one hour from the time of diagnosis . The use of vasopressors and management of severe sepsis and septic shock are described separately. (See "Evaluation and management of suspected sepsis and septic shock in adults" and 'Vasopressors' below.)
The performance characteristics of commonly used sepsis scores are not well studied in pregnant patients but appear to have similar limitations as adults with suspected sepsis who are not pregnant. The systemic inflammatory response system, quick Sequential [Sepsis-related] Organ Failure Assessment (qSOFA) and modified early warning (MEW) criteria were evaluated in one retrospective study of 82 mothers with sepsis and compared with 328 pregnant patients who did not have sepsis . Among the scores evaluated, SIRS was the most sensitive (0.93) and qSOFA was the most specific (0.95) for the diagnosis of sepsis. However, SIRS was poorly specific (0.63) and qSOFA was poorly sensitive (0.5). The sensitivity and specificity of MEW was 0.82 and 0.87, respectively. The sepsis in obstetrics score (SOS) incorporates clinical criteria that have been modified for expected changes in pregnancy, with a score of >6 predicting the risk of admission to the intensive care unit . This scoring system needs further validation before routine use. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Early sepsis'.)
Liver disease — A variety of diseases may lead to liver failure during pregnancy or the immediate postpartum period [46,47] (see "Approach to evaluating pregnant patients with elevated liver biochemical and function tests"):
●Acute fatty liver of pregnancy is a third-trimester disease that occurs in approximately 1 in 13,000 pregnancies [46,47]. Inherited genetic mutations in the intramitochondrial fatty acid oxidation pathway leads to microvesicular fat accumulation within hepatocytes. Patients present with nausea, vomiting, right upper quadrant pain, jaundice, and increased serum aminotransferase (AST) levels (although usually not above 1000 IU/L). Treatment is delivery of the fetus, as well as supportive measures such as mechanical ventilation for coma, dialysis for renal failure, and blood products for coagulopathy. The maternal mortality rate is approximately 7 to 18 percent; however, most survivors have minimal sequelae [46-48]. Fetal mortality is 9 to 23 percent [47,48]. (See "Acute fatty liver of pregnancy".)
●A variety of liver diseases may occur in individuals with preeclampsia or eclampsia. These include the HELLP syndrome (hemolysis, elevated liver enzymes, low platelets), hepatic hematoma, and hepatic failure. Therapy for the preeclampsia-related liver diseases consists of supportive care and delivery of the fetus. Rupture of a hepatic hematoma is likely to require surgical intervention, preferably by a team experienced in liver trauma surgery. (See "HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets)" and "Acute liver failure in adults: Management and prognosis".)
●Viral hepatitis may occur during pregnancy and lead to fulminant hepatic failure. Findings usually include fever, nausea, right upper quadrant pain, and markedly elevated transaminases (usually above 1000 IU/L). In addition to the hepatitis viruses, herpes simplex virus (HSV) can cause severe hepatitis and should be suspected in the presence of vesicular lesions of the skin. The diagnosis of HSV hepatitis is important because treatment with antiviral agents may be beneficial, though the mortality of this disorder remains very high [49-52]. Treatment for hepatitis caused by other viruses is supportive (see "Overview of coincident acute hepatobiliary disease in pregnant women" and "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection"). The treatment of hepatitis C during pregnancy with direct-acting antivirals is not recommended because there are no large trials studying the safety and efficacy of these medications in pregnancy .
Thrombotic microangiopathy — Thrombotic microangiopathies (TMAs) are a group of systemic diseases characterized by microangiopathic hemolysis, thrombocytopenia, acute renal failure, neurological abnormalities (eg, coma, seizures), and fever. There are three major TMAs: thrombotic thrombocytopenic purpura (TTP), complement-mediated TMA (CM-TMA), and Shiga toxin-mediated hemolytic uremic syndrome (ST-HUS).
●TTP is defined by a severe deficiency of ADAMTS13 (defined as activity <10 percent), but the initial diagnosis of TTP generally is based on clinical judgment since ADAMTS13 measures are often not available for several days and different methodologies may yield different results. Acquired, autoimmune TTP caused by antibodies to ADAMTS13 is more common than hereditary TTP due to ADAMTS13 mutation, but individuals with hereditary TTP often have the first presentation of disease during pregnancy. (See "Diagnostic approach to suspected TTP, HUS, or other thrombotic microangiopathy (TMA)", section on 'Terminology' and "Diagnosis of immune TTP" and "Hereditary thrombotic thrombocytopenic purpura (hTTP)".)
●CM-TMA, also known as complement-mediated HUS, is a condition characterized by enhanced activation of complement on endothelial cells, resulting in the formation of microthrombi in small vessels. The kidney is often severely affected. The dysregulation of the complement may be due to a neutralizing autoantibody or an inherited mutation in a complement regulatory gene. (See "Complement-mediated hemolytic uremic syndrome in children".)
●ST-HUS is a disorder in which TMA arises from an intestinal infection with a toxin-producing bacterium. Similar to CM-TMA, the kidneys are frequently impacted. (See "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome (HUS) in children".)
TTP, CM-TMA, and ST-HUS are rare and potentially lethal diseases. The presentation usually occurs during the second trimester, third trimester, or early postpartum period. The clinical course is unaffected by the delivery of the fetus [53,54]. (See "Thrombocytopenia in pregnancy", section on 'Thrombotic microangiopathy (TMA)'.)
TMA can be difficult to differentiate from preeclampsia because the clinical findings overlap and the diseases may occur simultaneously . An onset of illness prior to a gestation age of 20 weeks, the presence of significant hemolysis, and/or a large elevation of lactate dehydrogenase favors TMA. In contrast, significant hypertension, severe liver dysfunction, and/or a large elevation of AST favors preeclampsia [53,54]. Other diseases that should be considered whenever the diagnosis of TMA is entertained include sepsis, malignant hyperthermia, systemic lupus erythematous, and disseminated intravascular coagulation. (See "Diagnostic approach to suspected TTP, HUS, or other thrombotic microangiopathy (TMA)", section on 'Terminology'.)
Recognition and diagnosis of TMA is important because aggressive treatment with plasma exchange improves outcome for TTP and anti-complement therapy may rescue renal function in CM-TMA [53,55]. Management of TMA in pregnancy is discussed separately. (See "Thrombocytopenia in pregnancy", section on 'Thrombotic microangiopathy (TMA)' and "Immune TTP: Initial treatment", section on 'Immune TTP during pregnancy' and "Hereditary thrombotic thrombocytopenic purpura (hTTP)", section on 'Management of pregnancy' and "Complement-mediated hemolytic uremic syndrome in children", section on 'Treatment'.)
Posterior reversible encephalopathy syndrome — Posterior reversible encephalopathy syndrome (PRES), also referred to as reversible posterior leukoencephalopathy syndrome, is a radiographic clinical syndrome with reversible subcortical vasogenic edema that can occur during pregnancy, most often in association with eclampsia. It presents with an acute increase in the blood pressure accompanied by headache, seizures, visual deficits, and/or an altered sensorium [13,56-59]. (See "Reversible posterior leukoencephalopathy syndrome", section on 'Clinical manifestations'.)
Magnetic resonance imaging (MRI) of the brain is the gold standard for diagnosing PRES. The T2-weighted images typically reveal punctate or confluent symmetric bilateral hyperintensity in the parieto-occipital lobes [60,61]. Computed tomography (CT) demonstrates symmetric hypodensities that usually involve the occipitoparietal regions of the brain [61,62]. (See "Reversible posterior leukoencephalopathy syndrome", section on 'Neuroimaging'.)
PRES is associated with severe preeclampsia, renal failure, hypertensive encephalopathy, chemotherapy, and/or immunosuppressive medications . (See "Reversible posterior leukoencephalopathy syndrome", section on 'Related conditions'.)
The management of PRES during pregnancy or the peripartum period is similar to the management of PRES when it is associated with another condition. Initial priorities include discontinuing offending medications, lowering the elevated blood pressure, and treating any seizures. (See "Reversible posterior leukoencephalopathy syndrome", section on 'Management'.)
There are several aspects of treating PRES that are unique to pregnant patients:
●The fetus should be delivered as soon as possible.
●Intravenous labetalol, hydralazine, and nicardipine are the preferred antihypertensive agents during pregnancy. ACE inhibitors should be avoided due to their toxic effects on the fetal kidney. Nitroprusside should be avoided due to its potential to cause fetal cyanide toxicity .
●Status epilepticus should be initially treated with magnesium sulfate at a dose that is similar to that used to treat preeclampsia or eclampsia (4 to 5 gram bolus intravenously, followed by an infusion of 1 to 2 grams per hour) .
The neurological and radiographic abnormalities of PRES usually resolve within days to weeks if appropriate treatment is quickly instituted. Neurological deficits may become permanent or fatal if treatment is insufficient or delayed.
Diabetic ketoacidosis — Diabetic ketoacidosis (DKA) occurs in approximately 1 to 3 percent of diabetic females who become pregnant, probably because pregnancy predisposes diabetic females to poor glycemic control [65-67]. Maternal mortality related to DKA is <1 percent, however the perinatal mortality of a single episode of DKA is 9 to 35 percent [65,66]. (See "Pregestational (preexisting) diabetes mellitus: Antenatal glycemic control" and "Gestational diabetes mellitus: Glucose management and maternal prognosis" and "Pregestational (preexisting) diabetes: Preconception counseling, evaluation, and management" and "Diabetic ketoacidosis in pregnancy".)
The presentation of DKA is similar in pregnant and nonpregnant females, with symptoms of nausea, vomiting, thirst, polyuria, polydipsia, and a change in mental status. Typical laboratory findings include acidemia, an elevated anion gap, renal dysfunction, and hyperglycemia (although as many as 36 percent of pregnant individuals may have blood glucose levels less than 200 mg/dL) [66,68]. Maternal hyperglycemia results in fetal hyperglycemia and fetal osmotic diuresis. Maternal acidemia decreases uterine blood flow with a resultant decrease in placental perfusion leading to decreased oxygen delivery to the fetus. Fetal oxygen delivery is further compromised by the rightward shift of the maternal oxyhemoglobin dissociation curve caused by acidemia. Fetal acidosis and fetal volume depletion may occur, which jeopardizes the viability of the fetus [66,68]. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".)
Other than fetal heart rate monitoring, which is used to assess and monitor the fetus, DKA is treated similarly in pregnant and nonpregnant patients. This includes administration of insulin, replacement of intravascular volume, and repleting electrolytes (including calcium, phosphate, potassium, and magnesium). The cause of the DKA should also be sought. Common etiologies include infection and insulin non-compliance. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment" and "Nonstress test and contraction stress test".)
COVID-19 — Content that discusses the care of critically ill patients with coronavirus disease 2019 (COVID-19) in nonpregnant and pregnant adults is found elsewhere. (See "COVID-19: Epidemiology, clinical features, and prognosis of the critically ill adult" and "COVID-19: Respiratory care of the nonintubated hypoxemic adult (supplemental oxygen, noninvasive ventilation, and intubation)" and "COVID-19: Management of the intubated adult" and "COVID-19: Overview of pregnancy issues" and "COVID-19: Antepartum care of pregnant patients with symptomatic infection".)
Limited data are available in pregnant females who were critically ill with COVID-19. One study of 91 pregnant females with critical illness from COVID-19 found similar lung mechanics and ventilatory parameters to those in the nonpregnant population with COVID-19 . Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score was the only risk factor for invasive mechanical ventilation. Fetal delivery was induced mainly for maternal reasons. Risk factors for maternal mortality were body mass index (odds ratio [OR] 1.10, 95% CI 1.00-1.20) and comorbidities (OR 4.15, 95% CI 1.21-14.20). Risk factors for fetal or neonatal mortality were gestational age at delivery and SOFA score. Delivery did not improve ventilatory parameters other than the arterial oxygen tension to fraction of inspired oxygen ratio.
SUPPORTIVE CARE — Supportive care refers to interventions that sustain life and prevent complications, but do not treat the underlying cause of the critical illness. This includes oxygenation and ventilation (ie, supplemental oxygen or mechanical ventilation), sedation, pain control, hemodynamic support (ie, vasopressors), monitoring, volume management (ie, intravenous fluids or diuretics), nutritional support, stress ulcer prophylaxis, and venous thromboembolism prophylaxis.
Mechanical ventilation, sedation, hemodynamic support, and monitoring are discussed in this section. The other interventions that constitute supportive care are discussed separately. (See "Nutrition support in critically ill patients: An overview" and "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention" and "Deep vein thrombosis and pulmonary embolism in pregnancy: Prevention".)
Mechanical ventilation — Most aspects of mechanical ventilation are identical for pregnant and nonpregnant females. An exception is the target arterial carbon dioxide tension (PaCO2):
●Minute ventilation should be adjusted to maintain the PaCO2 between 30 to 32 mmHg. This replicates normal physiology during pregnancy since pregnant females maintain a respiratory alkalosis (PaCO2 is approximately 32 mmHg and arterial pH is 7.4 to 7.47) due to respiratory stimulation by progesterone . (See "Maternal adaptations to pregnancy: Dyspnea and other physiologic respiratory changes", section on 'Physiologic pulmonary changes in pregnancy'.)
●A PaCO2 lower than 30 mmHg should be avoided because significant respiratory alkalosis may decrease uterine blood flow .
●Maternal hypercapnia (PaCO2 >40 mmHg) causes fetal respiratory acidosis. Thus, it seems prudent to avoid maternal hypercapnia even though studies have not identified any adverse sequelae in fetuses that were exposed to PaCO2 levels as high as 60 mmHg during permissive hypercapnia . The use of intravenous maternal bicarbonate therapy during permissive hypercapnia is controversial due to conflicting data from animal and human studies [72,73]. (See "Permissive hypercapnia during mechanical ventilation in adults".)
●A reasonable goal is a maternal arterial oxygen tension above 70 mmHg, although the optimal oxygen tension and peripheral saturation are unknown.
Mechanical ventilation is reviewed in detail elsewhere. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit".)
Sedation — Most drugs used for analgesia, sedation, and neuromuscular blockade are capable of getting into the umbilical venous blood and fetal circulation [74-77]. Thus, the potential adverse effects of an agent on the fetus (including teratogenic potential) must be considered when selecting a medication. As a general rule of thumb:
●Analgesia – Any opioid is acceptable. However, nonsteroidal antiinflammatory drugs should be avoided during late pregnancy because they can cause premature closure of the ductus arteriosus and oligohydramnios.
●Sedation – Sedation is often required to tolerate mechanical ventilation. There are few reports comparing benzodiazepines with other anxiolytic agents during pregnancy. Midazolam is theoretically superior to lorazepam based upon the observation of teratogenic effects in animal studies of lorazepam; however, the clinical importance of these findings is unclear. Propofol crosses the placenta and may be associated with neonatal respiratory depression. Data on the clinical use of propofol for pregnant critically ill patients is limited to case reports, so its use should be limited until more prospective data is available [78,79]. There are no studies evaluating the safety and effectiveness of dexmedetomidine in the critically ill obstetric patient.
●Neuromuscular blockade – Use of neuromuscular blocking agents should be avoided unless the patient has refractory respiratory failure despite aggressive sedation. Minimal data are available regarding which neuromuscular blocking agent to use for pregnant patients who require it to facilitate mechanical ventilation. Cisatracurium may be preferable as a first-line agent, based upon the observation that it is not affected by renal or hepatic dysfunction [80,81]. By contrast, pancuronium can accumulate in the setting of hepatic dysfunction . (See "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults".)
Consultation with an obstetrician and a pharmacist who specializes in the care of pregnant patients may be helpful to facilitate the use of these agents in the intensive care unit (ICU) [74,75,83-86]. A neonatologist should also be present at delivery because analgesics, sedatives, and neuromuscular blocking agents can cause respiratory depression in the newborn. Ventilatory support may be needed for the newborn until the effects of the drugs wear off .
The use of analgesics, sedatives, and neuromuscular blocking agents in critically ill adults is reviewed separately. (See "Sedative-analgesic medications in critically ill adults: Selection, initiation, maintenance, and withdrawal" and "Neuromuscular blocking agents in critically ill patients: Use, agent selection, administration, and adverse effects" and "Pain control in the critically ill adult patient".)
Vasopressors — Vasopressors and inotropes can vasoconstrict uterine blood vessels, reducing fetal blood flow. Thus, other interventions should be used initially to manage hypotension, such as administration of intravenous fluids and placing the patient in the left lateral decubitus position to prevent compression of the inferior vena cava by the gravid uterus. Hypotension that persists despite these initial interventions requires vasopressor therapy, since sustained maternal hypotension decreases uterine blood flow. (See "Use of vasopressors and inotropes".)
There is a paucity of clinical studies with no consensus about which is the best vasopressor for maternal hypotension or shock due to critical illness. In addition, the 2021 sepsis treatment guidelines published by the Society of Critical Care Medicine do not specifically address the care of pregnant patients. However, we agree with others that following these guidelines is reasonable for the management of maternal hypotension from septic shock [42,43,88,89]. Thus, we consider norepinephrine as the first-line vasoactive agent in pregnant patients who fail to respond to early aggressive volume resuscitation. Although norepinephrine can reduce uterine blood flow, there are no data to suggest that norepinephrine has an adverse effect on the well-being of the fetus [42,90]. Thus, we consider this risk to be outweighed by the benefit of maternal resuscitation [43,88].
For pregnant patients with refractory shock, the best second-line agent is unknown. However, indirect evidence from randomized trials of vasopressors for hypotension caused by spinal anesthesia suggest that phenylephrine may a reasonable second-line agent . Animal models have shown that ephedrine, phenylephrine, norepinephrine, and epinephrine all increase maternal blood flow. In contrast, ephedrine is the only agent to increase uterine blood flow in animals; all other agents induce vasoconstriction of uterine blood vessels [90-96]. Despite this finding in animals, in human studies ephedrine has been associated with fetal acidosis and phenylephrine is associated with maternal bradycardia [91,96]. Since phenylephrine is not associated with fetal acidosis and maternal bradycardia is easily monitored, we prefer phenylephrine as a second-line agent for septic shock in pregnancy.
The benefits of hydrocortisone in pregnant patients with septic shock are also unstudied. Nonetheless, hydrocortisone can be considered in patients with refractory septic shock who are poorly responsive to both aggressive fluid resuscitation and vasopressor therapy . Unless these conditions are met, we advise against the routine use of corticosteroids in the management of pregnant patients with sepsis or septic shock.
Monitoring — All pregnant patients should undergo conventional ICU monitoring. This usually includes continuous assessment of the heart rate, cardiac rhythm, oxyhemoglobin saturation, and respiratory rate, as well as frequent evaluation of the blood pressure and temperature.
Invasive hemodynamic monitoring is occasionally helpful, especially when hypoxemic respiratory failure (eg, pulmonary edema) is accompanied by hypotension and/or renal failure. In these situations, hemodynamic measures can help determine the volume status, which is essential for administration of the optimal balance of intravenous fluids, diuretics, and vasoactive medications [89,97]. (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults".)
Invasive hemodynamic monitoring is generally accomplished using a central venous catheter to measure the central venous pressure. Pulmonary artery catheters are rarely needed. Interpretation of hemodynamic measures must consider the expected physiologic changes of pregnancy. (See "Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes" and "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults".)
Arterial catheterization may be helpful if the blood pressure is labile or frequent arterial blood gases are needed. (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation" and "Arterial blood gases".)
Pregnant individuals should have fetal heart rate and uterine monitoring, the frequency of which depends upon the gestational age of the fetus and the clinical scenario.
Bedside critical care ultrasound is emerging as a useful tool in the assessment of the hypotensive critically ill patient . Transthoracic echocardiography (TTE) may assist in the differentiation of life-threatening hypotension in the critically ill obstetric patient . For example, bedside TTE allows the rapid identification of right ventricular versus left ventricular heart failure thereby allowing the timely administration of appropriate therapy or pursuit of additional testing.
SUMMARY AND RECOMMENDATIONS
●Epidemiology – Fewer than 2 percent of individuals require admission to an intensive care unit (ICU) during pregnancy or the peripartum period (the last month of gestation and the first few weeks after delivery). Both maternal and fetal mortality are high when critical care is required. (See 'Incidence and mortality' above.)
●Etiologies – The most common indications for ICU admission during pregnancy or the peripartum period are postpartum hemorrhage and the hypertensive disorders (severe preeclampsia or eclampsia). Other indications include cardiovascular disease, venous thromboembolism, acute respiratory failure, infection, hepatic disease (eg, acute fatty liver, the HELLP syndrome [hemolysis, elevated liver enzymes, and low platelets], viral hepatitis), thrombotic microangiopathy (TMA), posterior reversible encephalopathy syndrome, and diabetic ketoacidosis. (See 'Cardiovascular disease' above and 'Venous thromboembolism' above and 'Hemorrhage' above and 'Preeclampsia or eclampsia' above and 'Acute respiratory failure' above and 'Infection/sepsis' above and 'Liver disease' above and 'Thrombotic microangiopathy' above and 'Posterior reversible encephalopathy syndrome' above and 'Diabetic ketoacidosis' above.)
●Hypertension – For pregnant patients who require acute blood pressure control for hypertension (eg, severe preeclampsia or eclampsia), we suggest labetalol, hydralazine, or nicardipine rather than other agents (Grade 2B). Due to potential harm to the fetus, angiotensin-converting enzyme inhibitors and nitroprusside should be avoided during pregnancy. (See 'Preeclampsia or eclampsia' above.)
●Supportive care – Supportive care refers to interventions that sustain life and prevent complications but do not treat the cause of the critical illness. Many of these interventions are not different from those of nonpregnant patients and are discussed separately. (See "Nutrition support in critically ill patients: An overview" and "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention" and "Deep vein thrombosis and pulmonary embolism in pregnancy: Prevention".)
•Mechanical ventilation – Mechanical ventilation is similar for pregnant and nonpregnant females. The major pregnancy-specific considerations are related to the arterial carbon dioxide tension (PaCO2). The target PaCO2 should be between 30 to 32 mmHg, PaCO2 values <30 mmHg or >40 mmHg should be avoided. A reasonable arterial oxygen tension target goal is 70 mmHg or above. (See 'Mechanical ventilation' above.)
•Sedation – Most drugs used for analgesia, sedation, and paralysis cross the placenta. Thus, the possible adverse effects of the various agents on the fetus (including teratogenic potential) must be considered when selecting an agent. Consultation with an obstetrician and a pharmacist who specializes in the care of pregnant patients may be helpful. A neonatologist should be present at delivery because analgesics, sedatives, and neuromuscular blocking agents can cause respiratory depression in the newborn. (See 'Sedation' above.)
•Vasopressors – Interventions other than vasopressors should be used initially to manage hypotension, including the administration of intravenous fluids and placing the patient in the left lateral decubitus position. Hypotension that persists despite these initial interventions warrants the initiation of a vasopressor, since sustained maternal hypotension decreases uterine blood flow. (See 'Vasopressors' above.)
For pregnant patients who require vasopressor therapy, we suggest norepinephrine as the initial agent, rather than ephedrine, epinephrine, or dopamine (Grade 2C). For patients with refractory shock despite norepinephrine, we suggest the use of phenylephrine rather than ephedrine (Grade 2C). (See 'Vasopressors' above.)
•Monitoring – All patients should undergo conventional ICU monitoring. Invasive hemodynamic monitoring is occasionally helpful, especially when there is hypoxemic respiratory failure (eg, pulmonary edema) accompanied by hypotension and/or renal failure. This is generally accomplished using a central venous catheter to measure the central venous pressure, rather than a pulmonary artery catheter. (See 'Monitoring' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Peter F Clardy, MD, who contributed to earlier versions of this topic review.
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟