Refractory Hypotension Under Neuraxial Anesthesia for Cesarean Delivery
Neuraxial anesthesia, including spinal and epidural techniques, is widely used for cesarean deliveries due to its efficacy and safety. However, it is not without risks, one of which is hypotension. Aortocaval compression syndrome, also known as supine hypotensive syndrome, is a common cause of hypotension in pregnant women, particularly in the supine position under neuraxial anesthesia. This syndrome occurs when the uterus compresses the inferior vena cava and aorta, leading to reduced venous return and cardiac output. The clinical manifestations include hypotension, tachycardia, nausea, dizziness, and syncope. Moreover, it can compromise uteroplacental perfusion, potentially leading to fetal morbidity or mortality. This case report discusses a 33-year-old pregnant woman with rheumatoid arthritis (RA) who experienced refractory hypotension during cesarean delivery under combined spinal-epidural anesthesia, despite aggressive vasopressor therapy.
The patient, a 33-year-old G4P1 woman weighing 80 kg and 165 cm tall, was at 38+6 weeks of gestation. She had a history of RA for 11 years and had been taking oral prednisone (10 mg) every morning for over 5 years. She had previously undergone an elective cesarean section without complications. During this pregnancy, her RA was stable, and she had no low back pain or spinal deformities. Preoperative evaluations, including echocardiography, electrocardiogram (ECG), liver and kidney function tests, coagulation studies, and blood platelet analysis, were all normal. On the day of surgery, she voluntarily stopped taking prednisone as instructed by her doctor.
In the operating room, the patient’s vital signs were stable: heart rate (HR) 85 beats/min, blood pressure (BP) 120/75 mmHg, and oxygen saturation (SpO2) 98%. Combined spinal-epidural anesthesia was chosen due to the absence of contraindications. The patient was positioned in the left lateral position for the procedure. A smooth puncture at the L3-4 interspace was followed by the administration of 2.2 mL of 0.5% hypobaric bupivacaine into the subarachnoid space. Upon returning to the supine position, the patient suddenly exhibited extreme irritability, sweating, palpitations, and extreme discomfort. She even sat up and shook her limbs. Immediate interventions included repositioning her in a semi-reclining position, manually displacing the uterus to the left, and administering supplemental oxygen. Despite these measures, her HR increased to 134 beats/min, and her BP dropped to 110/94 mmHg. The sensory block level was assessed at T12.
Large doses of phenylephrine and ephedrine were administered intermittently, but the patient’s BP continued to decline, reaching a nadir of 70/26 mmHg. The maximal sensory block level was T6, and bilateral lung sounds were clear and symmetrical. The patient remained awake but irritable. Arterial blood gas analysis revealed the following: pH 7.31, pCO2 31.3 mmHg, base excess (BE) -7 mmol/L, HCO3- 18.5 mmol/L, K+ 3.3 mmol/L, Na+ 138 mmol/L, hematocrit (HCT) 29%, hemoglobin (Hb) 9.9 g/L, oxyhemoglobin saturation (SO2) 100%, and glucose 7.3 mmol/L. Despite rapid rehydration, large doses of phenylephrine (2.1 mg) and ephedrine (48 mg), and the administration of 200 mg hydrocortisone, the patient’s BP only transiently recovered to 130/76 mmHg before dropping again to 55/38 mmHg. Additional doses of phenylephrine (1.1 mg) and ephedrine (36 mg) were administered, after which her BP normalized, and she felt more comfortable. The total treatment included 3.2 mg phenylephrine, 84 mg ephedrine, 200 mg hydrocortisone, 1500 mL crystalloid, and 500 mL colloid. The BP fluctuations lasted over 20 minutes.
Once the patient’s condition stabilized, the cesarean delivery was promptly completed, resulting in the successful delivery of a baby girl with Apgar scores of 10-10-10. The mother recovered well postoperatively.
Aortocaval compression syndrome is typically managed by manual displacement of the uterus, fluid resuscitation, and vasopressors. Most pregnant women have compensatory mechanisms that increase systemic vascular resistance and HR to mitigate the effects of aortocaval compression. However, in rare cases, these measures may be insufficient, leading to severe hypotension or even cardiovascular collapse. A review of the literature revealed four similar cases of severe hemodynamic instability in pregnant patients under neuraxial anesthesia. These cases highlighted that emergent cesarean delivery may be the most effective intervention when refractory hypotension persists despite aggressive vasopressor therapy.
In this case, the patient’s refractory hypotension was initially attributed to excessive block height and supine hypotensive syndrome. However, the sensory block level (T6) and the administration of rapid rehydration and vasopressors ruled out these causes. The patient’s history of RA and long-term prednisone use raised the possibility of adrenal crisis. Although the administration of hydrocortisone led to a transient improvement in BP, the subsequent drop suggested that adrenal crisis was not the primary cause. The patient’s clinical presentation and exclusion of other potential causes led to the diagnosis of severe aortocaval compression.
The management of this case had a notable shortcoming: the delay in performing an emergent cesarean delivery. The prolonged hypotension lasting over 20 minutes posed a significant risk to the fetus. This case underscores the importance of considering emergent cesarean delivery in cases of refractory hypotension resistant to vasopressors, especially when aortocaval compression is suspected.
In conclusion, aortocaval compression syndrome is a critical condition that can lead to severe hypotension in pregnant women under neuraxial anesthesia. While most cases can be managed with standard interventions, refractory hypotension may require emergent cesarean delivery to ensure maternal and fetal safety. Clinicians must be vigilant in recognizing and managing this syndrome to prevent adverse outcomes.
doi.org/10.1097/CM9.0000000000000250
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