Management of Intraoperative Spinal Anesthetic Complications
Management of Intraoperative Spinal Anesthetic Complications
Spinal anesthetic complication can occur from the local anesthetic, techniques and both. 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. Warning signs of falling blood pressure include pallor, sweating, nausea or feeling generally unwell. Bradycardia is quite common during spinal anesthesia particularly if the surgeon is manipulating the bowel or uterus.
Management of Hypotension
Hypotension is due to vasodilation and a functional decrease in the effective circulating volume. The treatment is, therefore, to reverse the vasodilatation with vasoconstrictor drugs and increase the circulating volume by giving fluids. All hypotensive patients should be given oxygen by mask until the blood pressure is restored.
A simple and effective way of rapidly increasing the patient's circulating volume is by raising their legs thus increasing the return of venous blood to the heart. This can either be done manually by an assistant or by tilting the lower half of the operating table. Tilting the whole operating table head down will also achieve the same effect, but is unwise if a hyperbaric spinal anesthetic has been injected as it will result in the block spreading higher and the hypotension becoming more severe. If an isobaric spinal solution has been used, tilting the table at any time will have very little effect on the height of the block.
Increase the speed of the intravenous infusion to maximum until the blood pressure is restored to acceptable levels and, if the pulse is slow, give atropine o.5 to 1 mg intravenously. Vasoconstrictors should be given immediately if the hypotension is severe, and to patients not responding to fluid therapy. The following vasopressors are recommended during spinal hypotension
Ephedrine is probably the vasopressors of choice. It causes peripheral blood vessels to constrict and raises the cardiac output by increasing the heart rate and the force of myocardial contraction. It is safe for use in pregnancy, as it does not reduce placental blood flow. Ephedrine is generally available in 25 or 30mg ampoules. It is best diluted to 10mls with saline and then given in increments of 1-2ml (2.5-6mg) titrated against the blood pressure. Its effect generally lasts about 10 minutes and it may need repeating. Alternatively, the ampoule may be added to a bag of intravenous fluid and the rate of infusion altered to maintain the desired blood pressure. It can also be given intramuscularly but its onset time is delayed although its duration is prolonged. Larger doses are necessary when it is given intramuscularly.
Epinephrine/Adrenaline: Available as 1mg/ml (1:1,000) and 1mg/10ml (1:10,000) ampoules. Dilute 1ml of 1:1,000 adrenaline to at least 10ml with saline and give increments of 50mcg (0.5ml of 1:100,000) repeating as necessary. Monitor the effect of epinephrine/adrenaline closely - it is a very powerful drug but only lasts a few minutes. It may be used during spinal anesthesia if hypotension does not respond to ephedrine or when it is not available.
The most likely cause of transient respiratory arrest during high spinal anesthesia is ischemia of medullary respiratory neurons secondary to decreases in blood pressure and cardiac output severe enough to impair cerebral blood flow. The character of spontaneous respirations serves as a valuable indication of the adequacy of medullary blood flow during high spinal anesthesia. It is therefore advisable to let patients breathe spontaneously during high spinal anesthesia rather than to control ventilation.
High levels of neural blockade can occur readily following spinal anesthesia 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 Spinal anesthesia ascending into the cervical levels causes severe hypotension, bradycardia, and respiratory insufficiency. Unconsciousness, apnea, and hypotension resulting from high levels of spinal anesthesia are referred to as a "high spinal" or "total spinal." Patients often complain of dyspnea and have numbness or weakness in the upper extremities. Nausea with or without vomiting often precedes hypotension.
Treatment of High Spinal Is Supportive Until the Spinal Wears Off
- Once it is recognized patients should be reassured, oxygen supplementation may need to be increased, and bradycardia and hypotension should be corrected.
- Treatment of an excessively high neuraxial block involves maintaining an adequate airway and ventilation and supporting the circulation. When respiratory insufficiency becomes evident, in addition to supplemental oxygen, assisted ventilation, intubation, and mechanical ventilation may be necessary.
- Hypotension can be treated with rapid administration of intravenous fluids and as described above with positions and vasopressors.
- If respiratory and hemodynamic control can be readily achieved and maintained after high or total spinal anesthesia, surgery may proceed. Apnea is often transient, and unconsciousness may leave the patient amnestic without adverse recall.
Treatment of Nausea & Vomiting
- Treat the cause. The main cause of nausea is hypotension. (See above for treatment.)
- Encourage deep breathing.
- Phenargan: - IV slowly (if the patient's blood pressure is within normal limits) or IM.
- Metoclopramide 10 mg IV or IM.
- Ondansetron 4 mg. IV.
Systemic Toxicity of Local Anesthetics
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. Local anesthetics exert anticonvulsive effects at low concentrations, where as they are potent convulsants at higher concentrations. Local anesthetics have exactly the same membrane stabilizing effect on the cells of the heart and brain as they have on peripheral nerve fibers.
Clinical Features of Systemic Toxicity
- Subjective CNS symptoms include feeling of lightheadedness and dizziness followed frequently by visual and auditory disturbances such as difficulty in focusing and tinnitus. Disorientation numbness of the tongue or circumoral structure and occasional feelings of drowsiness may also occur.
- Objective signs of CNS toxicity are usually excitatory in nature and include slurring of speech, shivering, muscular twitching, and tremors initially involving muscles of the face and distal parts of the extremities. Ultimately, generalized convulsions of a tonic - clonic nature occur. If a sufficiently large dose of a local anesthetic agent is administered systemically, the initial signs of CNS excitation are followed rapidly by a state of generalized CNS depression. Seizure activity ceases and respiratory depression and ultimately respiratory arrest occur. Occasionally in some patients CNS depression may occur without a preceding excitatory phase, particularly if other CNS depressant drugs have been used concomitantly.
- Effects on the CVS: The cardiovascular effects of local anesthetics occur either directly because of inhibition of autonomic pathways during regional anesthesia (high spinal) or because of direct depressant action on cardiac or vascular smooth muscle or on the myocardial conducting system. The primary site of action is the myocardium, where decreases in electrical excitability, conduction rate, and force of contraction occur. As the blood concentration of local anesthetic agents approaches the cardio toxic level, a fall in B/P is usually the first sign of a systemic effect on the CVS. The combined peripheral vasodilation, decreased myocardial contractility, and depressant effect on cardiac rate and conductivity will lead to cardiac arrest and circulatory collapse. In addition, certain agents such as bupivacaine may precipitate potentially fatal ventricular fibrillation. The cardiovascular system is more resistant than central nervous system.
Treatment of Systemic Toxicity (ABCD)
If toxic reactions occur, early detection and prompt support of ventilation and circulation are necessary. When local anesthetic induced seizures occur, hypoxia, hypercarbia, and acidosis develops rapidly. Furthermore, these metabolic changes greatly increase the toxicity of local anesthetics. At the first signs of toxicity, oxygen must be delivered immediately. Administration of oxygen alone, by bag and mask, is often all that is necessary to treat seizures. However, if seizure activity interferes with ventilation or is prolonged, anticonvulsant drug therapy is indicated
- Airway: Establish clear airway; suction, if required
- Oxygen with face mask
- Encourage adequate ventilation (prevent cycle of acidosis, increased uptake of local anesthetic into CNS, and lowered seizure threshold)
- Artificial ventilation, if required
- Elevate legs
- Increase I.V. fluids if blood pressure is decreased.
- CVS support drug if decreased blood pressure persists or decreased heart rate
- Cardio -version if ventricular arrhythmias occur
- CNS depressant
- Diazepam 5-10mg, I.V.
- Thiopental 50 mg I.V., incremental doses until seizures cease
Muscle relaxant: Succinylcholine 1 mg/kg, if inadequate control of ventilation with above measures (requires artificial ventilation and may necessitate intubation)
- Atropine 0.6 mg, I.V., if heart rate is decreased
- Ephedrine, 12.5-25 mg, I.V, to restore adequate blood pressure
- Epinephrine for profound cardiovascular collapse
Prevention of Systemic Toxicity: The best treatment for toxic reactions is prevention.
- Patient evaluation: -Identification of significant systemic disease, age, and other factors, to permit individualization of local anesthetic dose
- Premedication: -Diazepam or other appropriate CNS depressant in moderate dosage
- Resuscitative drugs (diazepam or thiopentone, succinylcholine, atropine, vasopressors)
- Equipment (oxygen administration and suction equipment, airways, laryngoscope, endotracheal tube)
- Ensure adequate I.V. available
- Discard any cloudy solutions or those containing crystals
- Physically separate neural blockade tray from any other drugs
- Personally check dose of local anesthetic and vasoconstrictor
- Use test dose, 5 - 10% of total dose
- Aspirate frequently and discard solution colored by blood
- Monitor cardiovascular signs
- Constant verbal contact with patient past time of peak plasma concentration
Treatment of allergy: If anaphylaxis occurs it is vital to give O2 immediately followed by adrenalin 50 - 100 μg (0.5 - 1 ml. of 1:10000 solution) intravenously. Additional supportive measures include steroids, bronchodilator, infusion of fluids and antihistamine