Summary

In study session VIII you learnt

• The first 5 to 10 minutes after administration of the spinal anesthetic are the most critical time in adjusting the level of anesthesia when hyperbaric or hypobaric solutions are used. The level of anesthesia should be examined frequently.
• Ways to examine the level of anesthesia include rubbing the skin with cotton soaked with ethyl alcohol, then check whether the patient feels cold sensation or not (for sympathetic blockade). The other way is to prick the skin slightly with a blunt needle, and check whether the patient feels tenderness or not (the pin prick test) sensory level.
• The next 10 to 20 minutes are also the most critical in assessing the cardiovascular responses to spinal anesthesia. Frequent measurements of blood pressure and heart rate will allow early recognition of any degree of hypotension.
• After surgical anesthesia levels and cardiovascular stability have been achieved, the anesthetist may evaluate whether supplemental drugs should be administered to make the patient comfortable.
• It is essential to monitor the respiration, pulse and blood pressure closely. The blood pressure can fall precipitously following induction of spinal anesthesia, particularly in the elderly and those who have not been adequately preloaded with fluid. Bradycardia is quite common during spinal anesthesia particularly if the surgeon is manipulating the bowel or uterus.
• Management of hypotension includes raising the legs, increase the speed of the intravenous infusion, atropine 0.5 to 1 mg intravenously if heart rate is decreased, vasoconstrictors (ephedrine or adrenaline) should be given immediately if the hypotension is severe.
• The most likely cause of transient respiratory arrest during high spinal anesthesia is ischemia of respiratory centre secondary to hypotension.
• High levels of neural blockade can occur readily following spinal anesthesia can be caused by administering an excessive dose, failure to reduce standard doses in selected patients (e.g., the elderly, pregnant, obese, or very short), or unusual sensitivity or spread of local anesthetic. Treatment of high spinal is supportive (oxygenation, ventilation, and maintaining blood pressure and heart rate) until the spinal wears off.
• Nausea and vomiting can be treated by avoiding hypotension, reassurance, deep breathing and antiemetic
• The voiding mechanism is mediated through sacral autonomic fibers, which are the last to regain function after spinal anesthesia which causes post operative urinary retention. A painful distended bladder needs catheterization.
• The most widely accepted explanation for the cause of post spinal head ache is that the leakage of CSF through the hole in the dura mater lowers the pressure in the subarachnoid space. The incidence of spinal headaches is related to the size of the needle.
• A clinically significant spinal hematoma can occur following spinal or epidural anesthesia, particularly in the presence of abnormal coagulation or bleeding disorder.
• Bleeding in the subarachnoid/epidural space will result in the compression of neural tissue. Urgent referral and surgical decompression must occur within 8-12 hours of onset to avoid permanent injury.
• Systemic toxicity is most likely to occur when large amounts of local anesthetics are injected intravascularly and is somewhat likely to occur when injections are made near large blood vessels.
• Clinical features of systemic toxicity include feeling of lightheadedness and dizziness followed frequently by visual and auditory disturbances such as difficulty in focusing and tinnitus, slurring of speech, shivering, coma and convulsion may occur according to severity. Hypotension bradycardia and cardiac arrest may also occur.
• Management of toxicity is directed to maintain clear air way, oxygenation, ventilation and cardiovascular support in the forms of vasopressors and intravenous fluid