Spinal Anesthesia

A. Anatomy

Spinal anesthesia targets the spinal cord, which arises from the foramen magnum and extends to the conus medullaris, typically ending around the third lumbar vertebrae (L3) in adults. The spinal column is protected by three layers: the dura mater, arachnoid mater, and pia mater. The subarachnoid space, where the spinal anesthetic is administered, contains cerebrospinal fluid (CSF), spinal nerves, and the arachnoid and pial vessels. The arachnoid membrane provides significant resistance to drug diffusion, accounting for approximately 90% of the barrier.

The epidural space lies outside the dura mater and is bounded by the ligamentum flavum, lamina, and spinous processes. It is important to distinguish between the epidural and subarachnoid spaces, as the needle placement determines the type of anesthesia administered.

Key anatomic landmarks for spinal anesthesia include the iliac crests, which can be used to approximate the L4-L5 interspace. The spinal needle is commonly inserted at the L3 or L4 level in adults to avoid the termination of the spinal cord.

B. Indications

1. Lower abdominal and pelvic surgeries: Spinal anesthesia is suitable for surgeries below the umbilicus, such as hernia repairs, gynecological and urological procedures.
2. Lower extremity surgeries: This includes orthopedic procedures and lower limb surgeries.
3. Cesarean sections: It provides adequate analgesia and muscle relaxation while allowing the mother to remain awake and participate in the birth.

C. Contraindications

Absolute contraindications:
1. Patient refusal or inability to cooperate and maintain a still position.
2. Coagulation disorders or use of anticoagulants, which increase the risk of spinal hematoma.
3. Local infection at the injection site.

Relative contraindications:
1. Sepsis: Due to the risk of spreading infection to the central nervous system.
2. Neurological conditions: Such as myelitis, which can be exacerbated by invasive procedures.
3. Intracranial hypertension: As spinal anesthesia can cause a sudden drop in systemic vascular resistance and increase intracranial pressure.
4. Severe spinal or spinal cord deformities: These may lead to complications in needle placement and drug distribution.
5. Cardiovascular conditions: Stenotic heart valve lesions and severe hypertrophic cardiomyopathy can be poorly tolerated due to the hemodynamic changes associated with spinal anesthesia.
6. Lack of anesthesiologist experience: This may increase the risk of complications.

D. Equipment

1. Patient monitors: ECG for heart rhythm monitoring, pulse oximeter for oxygen saturation, and a blood pressure cuff to assess circulation.
2. Resuscitation equipment: Oxygen supply, bag and mask for ventilation, and suction to clear the airway if needed.
3. Sterile environment: Sterile gloves, mask, gown (if required), and a clean field are essential to prevent infection.
4. Intravenous access: To administer fluids and medications during the procedure.
5. Sterile prep solution: Typically Betadine or a non-iodine alternative for skin preparation.
6. Spinal needle: Small gauge (24-26 gauge) for minimizing trauma.
7. Sterile drapes: To maintain the sterility of the area.
8. Local anesthetic: For skin infiltration to reduce pain during the spinal block.
9. Syringes: A small syringe for local anesthetic and a 3-5 mL syringe for the spinal anesthetic agent.
10. Anesthetic agent: Typically a local anesthetic with or without additives like epinephrine or opioids to prolong the block and enhance analgesia.
11. Bandage: For securing the needle site post-procedure

Emergency Drugs for Sedated Patients (AAPD Guidelines)

In the context of pediatric dentistry and sedation, it is crucial to be prepared for potential emergencies that may arise during or after sedation. The following is a list of emergency drugs that may be needed to rescue a sedated patient, along with their indications and uses.

Emergency Drugs

1. Albuterol for Inhalation

   • Indication: Bronchospasm or asthma exacerbation.
   • Use: Administered via nebulizer or metered-dose inhaler to relieve bronchospasm.

2. Ammonia Spirits

   • Indication: Syncope or fainting.
   • Use: Inhaled to stimulate respiration and increase alertness.

3. Atropine

   • Indication: Bradycardia or asystole.
   • Use: Increases heart rate by blocking vagal effects on the heart.

4. Diazepam

   • Indication: Seizures or severe anxiety.
   • Use: Administered intravenously or intramuscularly for rapid sedation or seizure control.

5. Diphenhydramine

   • Indication: Allergic reactions or anaphylaxis.
   • Use: Antihistamine for allergic symptoms; may also be used for sedation.

6. Epinephrine (1:1,000 and 1:10,000)

   • Indication: Anaphylaxis or severe asthma attack.
   • Use: 1:1,000 for intramuscular injection; 1:10,000 for intravenous administration in cardiac arrest.

7. Flumazenil

   • Indication: Benzodiazepine overdose.
   • Use: Reversal agent for sedation caused by benzodiazepines.

8. Fosphenytoin

   • Indication: Status epilepticus.
   • Use: Anticonvulsant for seizure control, administered intravenously.

9. Glucose (25% or 50%)

   • Indication: Hypoglycemia.
   • Use: Administered intravenously to rapidly increase blood glucose levels.

10. Lidocaine

    • Indication: Cardiac arrhythmias or local anesthesia.
    • Use: Antiarrhythmic agent for ventricular arrhythmias; also used for local anesthesia.

11. Lorazepam

    • Indication: Anxiety or seizures.
    • Use: Sedative and anticonvulsant, administered intravenously or intramuscularly.

12. Methylprednisolone

    • Indication: Severe allergic reactions or inflammation.
    • Use: Corticosteroid for reducing inflammation and managing allergic reactions.

13. Naloxone

    • Indication: Opioid overdose.
    • Use: Opioid antagonist to reverse respiratory depression and sedation caused by opioids.

14. Oxygen

    • Indication: Hypoxia or respiratory distress.
    • Use: Administered to improve oxygen saturation and support respiratory function.

15. Racemic Epinephrine

    • Indication: Croup or severe bronchospasm.
    • Use: Administered via nebulization to reduce airway swelling and improve breathing.

16. Rocuronium

    • Indication: Neuromuscular blockade for intubation.
    • Use: Non-depolarizing neuromuscular blocker for facilitating intubation.

17. Sodium Bicarbonate

    • Indication: Metabolic acidosis or hyperkalemia.
    • Use: Administered intravenously to correct acidosis and manage elevated potassium levels.

18. Succinylcholine

    • Indication: Rapid sequence intubation.
    • Use: Depolarizing neuromuscular blocker for quick intubation.

Pharmacodynamics of Nitrous Oxide

Overview

Nitrous oxide (N2O), commonly known as "laughing gas," is an inhalational anesthetic used primarily for its analgesic and anxiolytic properties. Understanding its pharmacodynamics is crucial for safe and effective use in clinical settings.

Pharmacodynamics

1. CNS Depression:

   • Nitrous oxide produces nonspecific central nervous system (CNS) depression.
   • While it is classified as an inhalational general anesthetic, it provides limited analgesia, making surgical anesthesia unlikely unless concentrations that produce anoxia are reached.

2. Potency:

   • Nitrous oxide is the weakest of all inhalation agents, with a minimum alveolar concentration (MAC) of approximately 105%.
   • The MAC is a measure of the potency of an inhalation agent, defined as the concentration required to produce immobility in 50% of patients in response to a surgical stimulus.

3. Effects at Various Concentrations:

   • 30% to 50% Concentration:
     • Produces a relaxed, somnolent patient who may appear dissociated and is easily susceptible to suggestion.
     • Some patients may experience amnesia, but there is typically little alteration in learning or memory.
   • Greater than 60% Concentration:
     • Patients may experience discoordination, ataxia, giddiness, and increased sleepiness.
     • It is recommended that the concentration of nitrous oxide should not routinely exceed 50% to avoid adverse effects.

4. Titration:

   • One of the advantages of nitrous oxide is its ability to be easily titrated.
   • It can be increased for stimulating procedures (e.g., injections) and decreased during less stimulating periods (e.g., restorations).

Physiological Considerations

1. Entrapment in Gas-Filled Spaces:

   • Nitrous oxide can become entrapped in gas-filled spaces such as the middle ear, sinuses, and gastrointestinal tract.
   • This can lead to increased middle ear pressure, which is generally insignificant in patients with normal Eustachian tube function but can induce pain in patients with acute otitis media.

2. Contraindications:

   • Acute Otitis Media: Use should be avoided in patients with this condition due to the risk of increased middle ear pressure and pain.
   • Severe Behavioral Problems and Emotional Illness: Patients who are uncooperative or have a fear of "gas" may not tolerate nitrous oxide well.
   • Claustrophobia: Patients with this condition may feel uncomfortable with the nasal hood placement.
   • Maxillofacial Deformities: Conditions that prevent proper placement of the nasal hood can contraindicate its use.
   • Nasal Obstruction: Conditions such as upper respiratory infections, nasal polyps, or a deviated septum can hinder effective administration.
   • Chronic Obstructive Pulmonary Disease (COPD): Patients with COPD may have difficulty with nitrous oxide due to respiratory issues.
   • Pregnancy: Caution is advised when using nitrous oxide in pregnant patients.
   • High Oxygenation Situations: Situations where high oxygenation is inadvisable, such as during Bleomycin therapy, contraindicate the use of nitrous oxide.

Pain: sensory and emotional experience associated with actual or potential tissue damage

1. Components: sensory (objective characteristics of pain e.g., location, duration, intensity; thermal, mechanical, or chemical) and motivational/affective (associated with past experience, fear, suffering, anxiety, culture)

2. Anatomy and physiology: nociceptors specialized to convey noxious stimuli (mechanical, chemical, thermal) 

a. Hyperalgesia: exaggerated pain response to stimulus that was previously painful. 

i.  Primary: nociceptors in area of tissue damage fire or due to algesic chemicals (bradykinin, SP, etc.)

ii.  Secondary: absence of local causes so due to changes in CNS that result in nociceptor firing (e.g., referred pain due to convergence)

b. Allodynia: pain caused by stimulus that is normally innocuous (non-painful); e.g., abcess- just touch, hurts

c. Fiber types: local anesthetics target Ad and C fibers

i.  A-b: myelinated cutaneous mechanoreceptor (25-50 m/s); innervates Ruffini endings

ii.  A-d: myelinated nociceptor that mediates sharp, well-localized pain (10-30 m/s)

iii. C: have Schwan cells but no myelin; nociceptor that mediates dull, poorly-localized pain (<2.5 m/s)

d. Neurotransmitters:

i.  Excitatory: glutamate (most common, works on NMDA receptors), substance P (SP, p for pain; act at neurokinin, NK, receptors), calcitonin G-receptor peptide (CGRP; co-released with SP), prostaglandins (products of cyclooxygenase), and kinins

ii.  Inhibitory: GABA (amino acid; hyperpolarizes neurons so ¯ pain sensation), monoamines (e.g., seratonin, NE), and opioids (e.g., endorphins- give runner’s high; 3 made by body: 1) b-endorphin, 2) dynorphin, 3) enkephalins; 3 receptors: 1) mu- most important for pain, 2) delta, and 3) kappa)

Treatment:

a. Opioids: indicated for moderate to severe acute (post-op) pain, chronic cancer pain, or as sedative/pain reliever during general anesthesia.  A narcotic = sleep-inducing.

i.  Mechanism of action: bind opioid receptor in spinal cord and brainstem (mu, d, and kappa; found in periaqueductal grey- area in brain with tons of opioid receptors, when activated ® ¯ pain), inhibit peripheral nociceptors, activate descending pain control system, improve affective components of pain

ii.  Side-effects: euphoria, sedation, respiratory depression, nausea/vomiting, constipation (especially with elderly), addiction, tolerance (does not remain once drug removed)

b. NSAIDS (non-steroidal anti-inflammatory drugs): indicated for mild to moderate pain that has inflammatory component, fever.  Aspirin first made in 1853 from parts of willow bark.

i. Mechanism of action: inhibits cyclooxygenase (COX) which makes prostaglandins and other inflammatory agents.  Anti-pyretic (fever-reducing) actions mediated by effects on hypothalamus- center of brain that regulates body T.

ii. Side effects: since acidic- nausea, vomiting (rare), GI bleeding, prolonged bleeding time since inhibit platelets.  Warnings if ulcer history, combining NSAIDS (® ringing in ears), and flu/chicken pox in children ® risk of Rie syndrome (fatal brain inflammation)

c. Tylenol (acetaminophen): analgesic and anti-pyretic but no significant effect on inflammation.   OD kills liver.

d. Muscle relaxants: don’t act directly on muscles; indicated for myofascial pain (muscle/CT pain) but not analgesic (not good for pain control)

i. Mechanism of action: depends on drug but most ­ GABA-mediated signals in spinal cord

ii. Side-effects: sedation, weakness

e. Anti-depressants: low-doses indicated for chronic pain that is unresponsive to conventional analgesics, 1st choice for some types of neuropathic pain.  Side effects: sedation, xerostomia, CV effects.

i.  Mechanism of action: activate descending pain control systems ® pre-synaptic a-2 receptor to ­ monoamine (NE, seratonin) in brain ® inhibit SP, glutamate, etc. release from peripheral nociceptors.

4. Descending pain modulatory pathways: neuronal cell bodies in brainstem send projections to dorsal horn where release NT that inhibit incoming pain info or decrease sensitivity of neurons in dorsal horn to that info.  Opioids and antidepressants act in part by these pathways.