10 General and Specific Complications and Treatment Measures
10.1 Vasovagal Syncope
Vasovagal syncope and orthostatic collapse are associated mainly with a drop in blood pressure, tinnitus, pallor, nausea, and, in some cases, short-term clouding of consciousness or loss of consciousness. The symptoms are mostly harmless and quickly reversible. Anxiety and sometimes state of sobriety also often play a role.
10.1.1 Treatment
Placing the patient in a horizontal position and general measures, such as calming the patient, generally improve symptoms. Vasovagal reactions often occur during the first session in a series of local anesthetic treatments (Hanefeld et al 2005). It is nevertheless necessary to consider more serious causes (see below) as a differential diagnosis.
10.2 Intravascular Administration of Local Anesthetics and Glucocorticoids
Generally speaking, free local anesthetic that is not bound to proteins interacts with all electrically excitable membranes following its spread into the plasma, blocking the highly specific sodium channels of the membrane. Depending on the concentration of the local anesthetic, all excitable cell systems may be affected.
Other than the local tissue toxicity (nerves, muscle) of some agents, or methemoglobinemia following prilocaine administration, the main side effects of local anesthetics affect the central venous and cardiovascular systems (Table 10‑1). When the substance-specific limit value of the local anesthetic is exceeded following accidental intravenous injection and overdose, or unexpectedly rapid resorption, symptoms arise that are associated with an increase in plasma concentration of the free substance.
Type of toxicity | Effects |
Systemic toxicity | Effects on CNS Cardiovascular |
Local tissue toxicity | Neurotoxicity Myotoxicity |
Hematological toxicity | Methemoglobin production (prilocaine) |
Anaphylactoid reaction | Monoester type LA >>> amino amide type |
Abbreviations: CNS, central nervous system; LA, local anesthetics. | |
The development of clinical symptoms is highly dependent on the following factors:
Speed of uptake.
Plasma concentration.
Type of local anesthetic chosen.
Injections administered into the arteries leading to the brain (vertebral artery, carotid artery) result in sudden and sometimes extremely high concentrations in the central nervous system (CNS), with immediate symptoms. The injection of local anesthetics into peripheral arteries or veins results in a comparatively slower uptake.
10.2.1 Central Nervous System
The initial symptoms are those of CNS hyperexcitability; the symptoms of CNS depression develop later (Table 10‑2). The symptoms may increase gradually, or may attain a high level immediately.
Hypoventilation results in a decrease in pH owing to increased respiratory acidosis (CO2 retention) and sometimes hypoxia-related metabolic acidosis. In this case, the local anesthetic is released from the plasma protein and the amount of free, active local anesthetic in the plasma increases. More anesthetic can be found in the CNS as a result of the increased hypercapnic brain circulation, and it accumulates in the brain because ions are trapped in their active form in acidotic cells. This in turn accelerates the vicious cycle of symptoms. The risk is generally greatest with highly potent (receptor avidity!) and very long-acting local anesthetics such as bupivacaine and ropivacaine.
Treatment
Treatment should follow the guidelines for effective cardiovascular resuscitation, and the necessary expertise and equipment for this must therefore always be readily available. The prognosis is generally good if CNS symptoms are treated rapidly and appropriately.
10.2.2 Cardiac Circulatory System
The cardiac circulatory system generally seems more resistant to the systemic action of local anesthetics. CNS symptoms typically arise at lower plasma levels than cardiac circulatory symptoms. However, this does not apply equally to all local anesthetics. There is significantly less difference when using long-acting agents, such as bupivacaine, in particular, compared with the mid-acting local anesthetics (lidocaine, mepivacaine, prilocaine). Indirect cardiac circulatory effects via the CNS (bradycardia, arrhythmia, and sympathicolysis) must be differentiated from the direct effects (negatively dromotropic, inotropic, and suppression of the pacemaker function in the sinoatrial nodes). Modern local anesthetics, such as ropivacaine or S-bupivacaine, have proven to be better in this respect. Cases of noncardiopulmonary resuscitation have been reported only for bupivacaine. Fig. 10‑1shows the symptoms depending on the time and dosage.
Treatment
Treatment is limited to symptomatic measures such as the administration of oxygen and, if necessary, artificial respiration, the administration of fluids, and vasopressors if required. If necessary, resuscitation is carried out according to the standards of the European Resuscitation Council (ERC).
10.3 Intrathecal Administration of Local Anesthetics and Glucocorticoids
When local anesthetics are accidentally injected into the subdural or subarachnoid space, the local anesthetic can reach the intracranial region and bind to the central neuronal structures, to an extent depending on the volume and dose. The typical symptoms arising from this are also known as “total spinal anesthesia” (classically arising from an overdose of intrathecal local anesthetic during spinal anesthesia or from unnoticed intrathecal injection of local anesthetic during peridural anesthesia).
Symptoms of “total spinal anesthesia”:
Coma.
Dilated, unreactive pupils.
Central apnea.
Arterial hypotension (vasomotor failure) up to cardiovascular arrest.
The risk is higher during anesthetic interventions near the spinal cord, and typically during paravertebral, intercostal, stellate, celiac, and thoracic and abdominal sympathetic ganglia blocks. Total spinal anesthesia has even been described following ophthalmological and ENT blocks.
10.3.1 Treatment
Treatment is symptom-related. Emergency equipment must be kept available throughout the procedure.
Treatment for intrathecal local anesthetic:
Stop further addition of local anesthetic.
Free airways, administer oxygen, artificial respiration, intubate.
Support cardiovascular system.
Obtain intravenous access.
Rapid, bold administration of fluids (e.g., balanced electrolyte solution) + hydroxyethyl starch (e.g., 6% hydroxyethyl starch [HES] 130/0.4).
Catecholamine administration (e.g., norepinephrine or epinephrine 0.5–1 mg IV).
When resuscitation according to the guidelines of the ERC is carried out immediately, and when complications such as aspiration, hypoventilation, and/or hypoxia are prevented, the prognosis that the central block will recede is good (depending on the dose and type of local anesthetic administered).
Note
The intrathecal application of glucocorticoids is not known to have any acute life-threatening side effects.
10.4 Anaphylactoid Reaction—Anaphylactic Shock
Anaphylactoid reactions are immunological or paraimmunological reactions associated with the release of typical mediators—serotonin, slow-reacting substance of anaphylaxis (SRS-A), bradykinin, arachidonic acid metabolites, platelet-activating factor, and histamine. These reactions should be considered as potentially life-threatening, and require rapid and adequate treatment.
The clinical reaction is to be expected especially within 30 minutes of exposure to allergens; sometimes it may occur immediately. The severity of the reaction is often inversely proportional to the latency time. Severe reactions can lead to cardiovascular arrest without any prior warning.
Anaphylactoid reactions are clinically divided into five levels of severity (Table 10‑3). These levels are not based on the pathological mechanism of the original reaction. The symptoms range from trivial skin efflorescence, mild to severe respiratory and cardiovascular symptoms, or smooth muscle spasms (in the hollow viscera), to immediate and sudden respiratory and cardiac arrest. Symptoms can potentially begin at any level of severity and then subside, persist, or increase.
10.4.1 Treatment
The initial treatment (see Table 10‑3) consists of stopping the influx of allergens immediately. Obviously, this is not possible after the injection of a local anesthetic.
Even when symptoms are mild, IV access should be obtained right away and kept open by using a large-bore needle for the infusion of a balanced electrolyte solution. Oxygen should be administered prophylactically (this is obligatory for more severe reactions). It is advisable to administer histamine-receptor blocking agents (e.g., dimethpyrindene 4 mg and cimetidine 200 mg) via the IV line. However, their action is not likely to be visible within the first 30 minutes. The same applies to glucocorticoids (e.g., prednisolone 250 mg).
If there is a significant drop in blood pressure, the energetic administration of fluids is indicated, e.g., a pressure infusion of HES 130/0.4, 6%, 500 to 2,000 mL.
The IV administration of epinephrine (0.05–0.2 mg; ampules up to 1 mg, diluted 1:10) is indicated in all reactions from level 2 upwards. This has an immediate vasopressor (α-effect), broncholytic (β-effect), and specific antiallergic effect. The patient must be immediately intubated and, if necessary, resuscitated according to the standards of the ERC when respiratory failure (level 3) or respiratory and cardiac arrest occur.
In some cases, swelling of the pharyngeal–laryngeal mucosa may be so great that a cricothyrotomy is required to obtain an artificial airway. Laryngeal obstruction is the most common cause of death in cases of anaphylaxis. It is therefore important to pay attention right away to the symptom of “lump in the throat” (Tryba et al 1994; Madler et al 1998; Hoffmann et al 2001).
As far as emergency tactics go, if a resuscitation team is available, it is preferable to alarm them at an early stage. From level 1 reactions onward, the patient should be referred to a hospital emergency department. A high degree of caution is recommended, because of the unpredictability and possibly rapid development of presenting symptoms. Regrettably, there is no consensus between specialties with regard to the prophylactic provisions of expert personnel, equipment, and safety levels.
Note
Anaphylactoid reactions may in principle always arise following the administration of local anesthetics.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
