SPINAL ANESTHESIA-Technique And Clinical Pearls..

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LARYNGOSCOPE AND ITS COMPLICATIONS

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MANAGEMENT OF ACCIDENTAL EXTRAVENOUS INJECTION OF I/V INDUCTION AGENT

EXTRA VASCULAR/SUBCUTANEOUS INJECTION:

1. Most I/V induction agents (and especially barbiturates because of their alkalinity) are irritant when injected extravascularly.
2. The extent of pain and damage depends upon the volume and concentration of the injection. These can vary from minor irritation and erythema to sever pain, tissue necrosis to sloughing
3. Pain can be elevated by infiltrating the area with 1% lignocaine (without vasoconstrictor), the penetration of which can be assisted by addition of hyaluronidase.
4. Vasodilation and comfort are aided by warm compressed and simple analgesics.

INTRA-ARTERIAL INJECTION:

1. This can lead to serious damage to the blood supply of the affected limb with permanent ischemic sequelae.
2. The consequences of intra-arterial injection of other drugs such as antibiotics can be just as disastrous as those of barbiturates
3. The classic response is immediate and agonizing pain shooting down the arm into hand and fingers. The severity is such that it is unlikely to be caused by any other event during induction
4. The pain may subsequently last for a short time, be persistent or return later, presumably because of attacks of vascular spasm.
5. After the pain, the limb blanches, the pulse disappears and the limb then becomes mottled and cyanosed.
6. An intense chemical arteritis develops and there may be crystal deposition in small vessel.
   

MANAGEMENT:

1. On suspicion, immediately stop the injection
2. Leave the needle or cannula in vein.
3. Into the artery inject lignocaine 100 mg and papavarine 40 mg in 10-20 ml of saline
4. Give 4000 IU heparin I/V (unless otherwise contraindicated or unless a sympathetic block is to be done immediately
5. Keep the limb warm to encourage vasodilation
   
6. Consider the sympathectomy by local anesthetic e.g. stellate ganglion block.
7. Long term management depends upon the extent of damage and may involve limb salvage surgery or plastic reconstruction
   

I/V INDUCTION OF GENERAL ANESTHESIA - SUMMARY

BASIC PRINCIPLE:-

1. From the patients"s view point,induction of anesthesia is very important time, partly because anxiety is maximal especially in unpremeditated person. So, there should not be any UNDUE DELAYS and that the ENVIRONMENT IS PEACEFUL, gives an impression of confidence and HAS NO DISTRACTING NOISES.
2. The basic principle is to induce anesthesia in a PROPERLY EQUIPPED ENVIRONMENT WITH A PROPERLY TRAINED ASSISTANT. Anesthesia should NEVER be induced WITHOUT SUPPORT.
3. All routine patients should be induced with an ECG, PULSE OXIMETER AND A NIBP cuff in place
4. There should be a RELIABLE I/V ACCESS.
   

ELECTIVE I/V INDUCTION:-

1. A great advantage to the anesthesiologist is the RAPID PASSAGE from consciousness to the plane of surgical anesthesia with few excitation side effects.
2. Doses of I/V induction agents are predictable for population, but not for individuals. TITRATION TO RESPONSE is the key to success for individual patient
3. PRE OXYGENATION is often recommended and is MANDATORY for emergency cases and patients with difficult airway.
4. Pain on injection if experienced, make sure that injection is not going S/C or intra-arterial.
5. The GREATER THE DOSE of drug and the FASTER the injection rate, the quicker the sleep is induced and the MORE ADVERSE the physiological SIDE EFFECTS.Practical experience is the best guide as to how fast to induce anesthesia in particular patient, the less fit responding BEST to SLOW INDUCTION
6. ALWAYS ALLOW SUFFICIENT TIME for the induction agent to act in patient with a SLOW CIRCULATION TIME.
7. Remember that an I/V induction administers a potent drug to a patient and from then onwards, the anesthesiologist has no control over the subsequent actions and pharmacology of the agent. This contrasts with the volatile agents which can be removed by ventilation.
   

ALTHOUGH MINIMAL MONITORING IS REQUIRED, NOTHING REPLACES A VIGILANT ANESTHESIOLOGIST WITH HIS OPEN EYES AND EARS AND THE FINGER ON THE PULSE OF THE PATIENT.

CLINICAL PEARLS:

1. It is a bad practice and produces a risk of AWARENESS for relaxants to be given before consciousness is lost.
2. It is vital, once consciousness is lost, to achieve immediate control of airway and to ensure a continued supply of oxygenated gas to the lungs.
3. The insertion of an oral airway should not be done in an unrelaxed patient in a lighter plane of anesthesia
4. Patient fails to go to sleep when:

• the cannula is not in the vein
• There is venous obstruction (e.g, inflated tourniquet)
• The wrong drug has been given.
• The drug is taking an unusually long time to reach its target receptors because THE CARDIAC OUTPUT is SERIOUSLY LOW.
• It is very easy TO OVERDOSE SICK PATIENTS BY FAILING TO WAIT LONG ENOUGH FOR A RESPONSE.
  

SUXAMETHONIUM---A NECESSARY EVIL

Suxamethonium (sch) still enjoys popularity, despite a long list of side effects, because it is the only ULTRA RAPID onset, ULTRA SHORT duration NMBA (neur0 muscular blocking agent) available.
NEUROMUSCULAR EFFECTS:
1. The drug depolarizes pre-synaptic, post-synaptic and extra junctional. however, when the receptor is in contact with agonist for a long time, it ceases to respond to the agonist. Normally, this DESENSITIZATION process does not take place because of rapid breakdown of Ach (acetylcholine) (< 1 m sec). However, Sch remains at the end plate for much longer time and desensitization develops.
Another possible mechanism is the inactivation of sodium channels in junctional and pre-junctional areas, which occur when the membrane remains depolarized. This inactivation prevents the propagation of action potential
2. Within 1 min after sch injection and before the paralysis manifest, "FASCICULATIONS", as a result of depolarization of nerve terminal produced by activation of pre-synaptic receptors are observed.
3. In masseter muscle, a sustained increase in tension that may last for several minutes can be observed. This increase in masseteric tone, may lead to imperfect intubation conditions. Masseter spasm may be an exaggerated form of this response.
CHARACTERISTICS OF DEPOLARIZING BLOCKADE:
1. Sch blockade is potentiated by inhibitors of acetylcholinesterase, such as neostigmine.
2. After administration of 7-10 mg/kg or 30-60 minutes exposure of sch, train of four and tetanic fade becomes apparent. Neostigmine can antagonize this block which is termed a PHASE-11 BLOCK.
PHARMACOLOGY:
1.Sch is rapidly hydrolyzed by plasma cholinesterase
2.Subparalyzing dose upto 0.3-0.5 mg/kg reach their maximal effect within 1.5-2 minutes at adductor pollicis muscle and within 1 minute at more central muscles, such as masseter and laryngeal muscles. With larger doses (1-2 mg/kg), abolition of twitch response can be reached even more rapidly.
SIDE EFFECTS:
1. CARDIOVASCULAR:

• Bradycardia is more common in children
• Even ASYSTOLE, after a 2nd dose of sch especially in pediatric and elderly patients can occur
  
• The parasympathetic effects can be attenuated with atropine or glycopyrrolate
  
• Sch increases catecholamine release.
  

2.FASCICULATIONS:

• These are more common especially in muscular adults after the rapid injection of sch. These can be prevented by:

1. a small dose of non-depolarizing muscle relaxants (ndmr) given 3-5 minutes before sch is effective. Rocuronium (0.03mg/kg, that is 10%of ED95), atracurium (0.02 mg/kg) are effective in decreasing the incidence of fasciculations. After these ndmr, the dose of sch must be increased from 1 mg/kg to 1.5 or even 2 mg/kg because of the antagonism between depolarizing and non-depolarizing muscle relaxants.
2. Other drugs such as diazepam, lidocaine, fentanyl, magnesium etc.have also been used to prevent fasciculations
3. "SELF- TAMING", that is the administration of small (10 mg) dose of sch one minute before the intubating dose, does not appear to be effective and has largely been abandoned.
   

3. MUSCLE PAINS:

• Generalized aches and pains, similar to the myalgesia that follow violent exercise, are common 24-48 hours after sch administration
• They are more common in young and ambulatory patients.
• Pre-curarization dose of ndmr and lidocaine(1-1.5 mg/kg) are effective in preventing pain.

4. INTRA-GASTRIC AND INTRA CRANIAL PRESSURE are increased by the administration of sch.
5. INTRA-OCULAR PRESSURE:

• IOP increases by 5-15 mm Hg after injection of sch has lead to the widespread recommendation to avoid sch in open eye injuries.
• Inadequate anesthesia, elevated systemic blood pressure and insufficient neuro muscular blockade during laryngoscopy and tracheal intubation might also increase IOP

7. HYPERKALEMIA:

• Serum potassium increases by 0.5 to 1 mEq/L after the injection of sch.
• Severe hyperkalemia, occasionally leading to cardiac arrest has been described in patients after major denervation injuries, spinal cord transactions, peripheral denervation, stroke, trauma extensive burns and prolonged immobilization with disease.
  
• This hyperkalemia may be related to the potassium loss via a proliferation of extra junctional receptors.

ABNORMAL PLASMA CHOLINESTERASE:
1. Plasme cholinesterase activity is reduced in;

• Pregnancy
• Liver disease
• Uremia
• Malnutrition
• Burns
• Oral contrceptives

These conditions usually lead to a slightly clinically unimportant increase in duration of action of sch
2. Plasma cholinesterase activity is reduced by neostigmine so that the duration of sch given after neostigmine, but not after edrophonium is increased.
3. In some patients plama cholinesterase is absent or an abnormal form of enzyme is present. Only patients with HOMOZYGOUS for the condition have prolonged paralysis (3-6 hours) after usual dose of sch(1-1.5mg/kg)
In heterozygous group patients, the duration of action is only slightly prolonged compared with normal individuals
4. Whole blood or fresh frozen plasma can be given to accelerate sch metabolism in patients with low or absent plasma cholinesterase. The best course of action is probably MECHANICAL VENTILATION OF LUNGS until full recovery of neuromuscular function can be demonstrated. Neostigmine is unpredictable in reversal of abnormally prolonged sch blockade and is best avoided.
CLINICAL USES:

• To facilitate tracheal intubation.
• It is especially indicated for the rapid sequence induction when the patient presentw with a full stomach and there is possibility of aspiration of gastric contents