Complications Associated with Excessive Responses to Appropriately Placed Drug
Exaggerated dermatomal spread of neural block-ade can occur readily with either spinal or epidural anesthesia. Administration of an excessive dose, failure to reduce standard doses in selected patients (eg, the elderly, pregnant, obese, or very short), or unusual sensitivity or spread of local anesthetic may be responsible. Patients may complain of dys-pnea and have numbness or weakness in the upper extremities. Nausea often precedes hypotension. Once exaggerated spread of anesthesia is recog-nized, patients should be reassured, oxygen supple-mentation may be required, and bradycardia and hypotension should be treated.
Spinal anesthesia ascending into the cervical levels causes severe hypotension, bradycardia, and respiratory insufficiency. Unconsciousness, apnea, and hypotension resulting from high levels of spi-nal anesthesia are referred to as a “high spinal,” or when the block extends to cranial nerves, as a “total spinal.” These conditions can also occur follow-ing attempted epidural/caudal anesthesia if there is accidental intrathecal injection . Apnea is more often the result of severe sustained hypoten-sion and medullary hypoperfusion than a response to phrenic nerve paralysis from anesthesia of C3–C5 roots. Anterior spinal artery syndrome has been reported following neuraxial anesthesia, presumably due to prolonged severe hypotension together with an increase in intraspinal pressure.
Treatment of an excessively high neuraxial block involves maintaining an adequate airway and ventilation and supporting the circulation. When respiratory insufficiency becomes evident, in addi-tion to supplemental oxygen, assisted ventilation, intubation, and mechanical ventilation may be necessary. Hypotension can be treated with rapid administration of intravenous fluids, a head-down position, and intravenous vasopressors. Bradycar-dia can be treated early with atropine. Ephedrine or epinephrine can also increase heart rate and arterial blood pressure. If respiratory and hemodynamic control can be readily achieved and maintained after high or total spinal anesthesia, surgery may proceed.
Examination of data from the ASA Closed Claim Project identified several cases of cardiac arrest dur-ing spinal anesthesia. Because many of the reported cases predated the routine use of pulse oximetry, many physicians believed oversedation and unrecog-nized hypoventilation and hypoxia were the causes. However, large prospective studies continue to report a relatively high incidence (perhaps as high as 1:1500) of cardiac arrest in patients having received a spinal anesthetic, Many of the cardiac arrests were preceded by bradycardia, and many occurred in young healthy patients. Examination of this problem identified vagal responses and decreased preload as key factors and suggests that patients with high baseline vagal tone are at risk. To prevent this from occurring, hypovolemia should be corrected. Prompt drug treatment of hypo-tension and bradycardia are recommended. Many clinicians will not allow the heart rate to fall below 50 beats per minute during spinal anesthetic blockade.
Local anesthetic block of S2–S4 root fibers decreases urinary bladder tone and inhibits the voiding reflex. Epidural opioids can also interfere with normal voiding. These effects are most pronounced in male patients. Urinary bladder catheterization should be used for all but the shortest acting blocks. If a cath-eter is not present postoperatively, close observation for voiding is necessary. Persistent bladder dysfunc-tion can also be a manifestation of serious neural injury, as discussed below.
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