From Andreas Vesalius To Endotracheal Anesthesia

The safe anaesthetic management requires diligent efforts in maintaining an intact functional airway. Endotracheal intubation has been one of the best ways of achieving this goal. Intubation of the trachea for the purpose of resuscitation is three centuries older than anaesthesia itself.  Andreas Vesalius in 1543 reported the first tracheal intubation in an animal (1). In his landmark book published in 1543, De humani corporis fabrica, he described an experiment in which he passed a reed into the trachea of a dying animal whose thorax had been opened and maintained ventilation by blowing into the reed intermittently (2,3). Vesalius wrote that the technique could be life saving.

Human endotracheal intubation was first done by Curry in 1792 (4). At that time, no laryngoscope was invented and intubation was done by tactile method. Frederich Trendelenburg in 1868 manufactured the first cuffed tracheostomy tube (“Trendelenburg’s tampon”) and in 1871 performed the first endotracheal anaesthetic in humans via tracheostomy (1). In 1880, William Macewen, Scottish orthopaedic surgeon started placing metal tubes inside the trachea orally in conscious patients by digital palpation and saw the advantage of this “orotracheal intubation” over tracheostomy. In his paper entitled "clinical observations on the introduction of tracheal tubes by the mouth instead of performing tracheotomy or laryngotomy', he describes in addition two cases of endotracheal intubation lasting at least 36 h. He can, therefore, be said also to have performed the first long-time intubation (5). In 1887, an American paediatrician, Joseph O'Dwyer, described a method of oral tracheal intubation and published a detailed account of 50 patients with croup treated by intubation, 12 (24%) of whom survived (6).

Ivan Magill and Stanley Rowbotham together, they laid the foundations of tracheal anaesthesia (7). In 1922 at the Queen Hospital for Facial and Jaw Injuries in the UK, Ivan Magill and Stanley Rowbotham were working on development of techniques to administer anaesthesia to patients with facial injuries. At the time, the best available method for general anaesthesia in facial surgery was by endotracheal insufflation through the mouth or nose. This involved the use of a gum elastic catheter placed into the pharynx, through which air was driven by a motorised pump with the addition of vaporised ether from Shipway Apparatus heated in hot water (8).

During an extensive surgery on a deformed jaw of a soldier, a catheter had been passed through the nose. However, the deformity and contracture of the lower jaw prevented adequate expiration and the patient's breathing became laboured. Magill passed a second tube through the patient's nose which entered the trachea alongside the catheter which was followed by immediate relief in respiration. These findings later contributed to use of endotracheal intubation during anaesthesia (9).

Blind nasal intubation was first developed and described by Magill in 1928, with a demonstration given to the Society of Anaesthetics (Liverpool) in 1932 (9). Great achievement was recorded in the field on endotracheal anaesthesia during the First World War and post war period. The contribution of Ivan Magill and Stanley Rowbotham was the hallmark of endotracheal anaesthesia since 1934.

References:

1. Ezri T, Evron S, Hadad H, Roth Y. Tracheostomy and endotracheal intubation: a short history. Harefuah. 2005 Dec; 144(12): p. 891-3.
2. Baker AB. Artificial respiration, the history of an idea. Med Hist. 1971 Oct; 15(4): p. 336–351.
3. Garrison DH., Hast MH. The Fabric of the Human Body,An Annotated Translation of the 1543 and 1555 Editions of “De Humani Corporis Fabrica”: Northwestern University; 2003.
4. Paul AK. Essentials of Anaesthesiology. 7th ed.: Jaypee Brothers; 2006.
5. Brandt L, Pokar H, Schütte H. 100 years of intubation anesthesia. William Macewen, a pioneer of endotracheal intubation. Anaesthesist. 1983 May; 32(5): p. 200-4.
6. Opinel A, Gachelin G. French 19th century contributions to the development of treatments for diphtheria. J R Soc Med. 2011 Apr; 104(4): p. 173–178.
7. Condon H, Gilchrist E. Stanley Rowbotham. Twentieth century pioneer anaesthetist. Anaesthesia. 1986 Jan; 41(1): p. 46-52.
8. Magill I. Blind nasal intubation. Anaesthesia. 1975 Jul; 30(4): p. 476-9.
9. McLachlan G. Sir Ivan Magill KCVO, DSc, MB, BCh, BAO, FRCS, FFARCS (Hon), FFARCSI (Hon), DA, (1888-1986). Ulster Med J. 2008 Sep; 77(3): p. 146–152.

oxygen delivery

Awake Intubation (procedure in brief) 

Succinylcholine vs Rocuronium

	Succinylcholine	Rocuronium
Chemical structure	Structurally two acetyl choline molecules joined together	Aminosteroid
Classification	Depolarising neuromuscular blocker	Non-depolarising neuromuscular blocker
Fasciculation	Yes ( causes post-op myalgia)	No
Metabolism	·         Rapidly metabolised by pseudocholinesterase ·         Duration of action prolonged in Pseudocholinesterase deficiency	·         Eliminated primarily by liver and slightly by kidney ·         Elimination half life longer as compared to Sch.
Dosage	·         Used for intubation only now-a-days ·         1-1.5 mg/kg iv ·         4-5 mg/kg im (onset delayed)	·         Used for both intubation as well as during maintenance ·         Intubation: 0.6-1.2mg /kg iv ·         Intubation: 1mg/kg im (infants) and 2mg/kg im (children) àonset delayed (3-6min) ·         Maintenance: 0.15 mg/kg every 20 mins ·         Continuous infusion: 5-12µg/kg/min
Onset of action after iv induction dose (onset to maximum twitch depression)	30-60secs	60-90 secs
Duration of action	3-5 mins (phase 1 block)	·         Duration of action (duration to return to ≥ 25% of control twitch height): 20-35 min ·         Clinical duration (duration to return to Train-of-four >0.9): 55-80 min
Reversal with Sugammadex	Not possible	Possible Dose: ·         4 mg/kg iv when recovery has reached 1-2 post-tetanic counts ·         2 mg/kg iv if recovery has occurred upto reappearance of T2 ·         Immediate reversal: 16 mg/kg iv (recovery of T4/T1 ratio to 0.9 by 1.5 min)
Systemic effects	·         Causes bradycardia (especially when a second dose is given after 3-8mins) ·         Hyperkalemia (increases K+ by 0.5 mEq/L) ·         Transient increase in intracranial, intraocular and intragastric pressure	·         Mostly cardiostable ·         Mild vagolytic
Malignant hyperthermia risk	Yes	No
Use in burn patients	Avoid beyond 2 days till 2 yrs after burn (risk of hyperkalemia)	Can be used safely
Apnoea time (time available until critical desaturation occurs in the absence of ventilation after administration of the drug)	Less (because of fasciculation which uses up oxygen)	More
Paediatric usage	Usually avoided especially in case of unknown/undiagnosed myopathy	Can be used safely
Shelf life	Stable at room temperature for upto 14 days	Stable at room temperature for upto 12 weeks

Awake Intubation (procedure in brief)

Halothane vs Sevoflurane

	Halothane	Sevoflurane
Chemical structure	Halogenated alkane	Fluorinated methyl isopropyl ether
Odour	Both drugs have a sweet odour
Preservative for storage	Yes (thymol)	No
Blood: gas partition coefficient	High (2.4) Slower rate of induction and recovery	Lower (0.69) Rapid induction and recovery
MAC	0.75 (more potent)	2 (less potent)
CNS effects	·         Hypoxic ventilator drive is severely depressed by halothane. ·         Blunts autoregulation and increases cerebral blood flow. ·         Maximum increase in CBF among currently used volatile agents	Causes an increase in CBF but to a lesser extent as compared to halothane.
CVS effects	Causes more severe cardiac depression ·         Direct myocardial depression resulting in dose dependent decrease in BP ·         Decreases coronary blood flow due to fall of BP ·         Attenuates Baroreceptor reflex thus blunting the ability to maintain cardiac output by increasing heart rate (like an inhalational β-blocker) ·         Sensitized heart to arrythmogenic effects of catecholamines (epinephrine).	More cardiac stable ·         Comparatively less depression of myocardial contractility ·         Mild decrease in systemic vascular resistance at equipotent dose ·         Does not sensitize the heart to catecholamines.
Hepatic effects	·         Decreases hepatic blood flow ·         Hepatotoxic especially on frequent repeated exposure—halothane hepatitis	·         Decreases portal venous flow but, increases hepatic artery flowà so overall, hepatic blood flow is maintained
Renal effects	·         Decreases renal blood flow, GFR and urinary output ·         Reduction in renal blood flow is more as compared to reduction in GFR resulting in an increase in filtration fraction	·         Slight decrease in renal blood flow, GFR and urine output—comparatively to a lesser degree ·         Reacts with dry barium hydroxide (baralyme) resulting in production of Compound A—found nephrotoxic in animal studies.
On children	·         Less emergence reaction ·         Less nausea/vomiting postoperative	·         More emergence reaction ·         Comparatively more nausea/vomiting postoperative
Upper limit of concomitant epinephrine use	1.5 mcg/kg	4.5mcg/kg
Drug interactions	·         Potentiates non-depolarising neuromuscular blockers ·         Exaggerated myocardial depression when used with beta blockers (eg propranolol) and calcium channel blockers (eg verapamil) ·         Increased lability of BP when used in patients receiving tricyclic antidepressants and monoamine oxidase inhibitors ·         Increased incidence of arrhythmia when combined with aminophylline	·         Potentiates non-depolarising neuromuscular blockers ·         Otherwise, significant drug interaction among other commonly used drugs in clinical practice
Malignant hyperthermia	Both drugs can trigger an attack

Awake Intubation (procedure in brief)

i-gel vs LMA Classic

i-gel	LMA classic
2nd generation Supraglottic device	1st generation Supraglottic device
Cuffless device made of medical grade thermoplastic elastomer	Cuffed device made of made of medical grade silicone
An anatomic seal with pharyngeal, laryngeal and perilaryngeal anatomy is created by conforming with these structures at body temperature	Seal is achieved by inflating the cuff
Single use device. So increases the cost of therapy	Multiple use device. Can be used upto 40 times
It has an added drain tube for passing gastric tube thus reducing risk of aspiration	No gastric drainage facility
Chance of gastric insufflations less	more
Easy insertion technique—steep learning curve	Requires comparatively more training and practice
Absence of cuff—so insertion and removal rapid	Takes comparatively more time
Complete seal may take some time to develop as the device warms up to body temperature	Seal is immediate after inflation of the cuff
Less suitable for head and neck procedures because of bulky rigid stem	Comparatively more suitable for such procedures because of smaller diameter circular stem
Large transverse diameter—prevents rotation in the mouth	Susceptible to rotation

Awake Intubation

First intubation for providing anaesthesia was reported by Dr. William Macewan in 1878.

Preliminaries:

· Airway assessment

During the preoperative visit take a detailed history and physical examination to assess the difficulties that may come during the process and help in planning management.

· Psychological preparation.....

Awake Intubation (procedure in brief)

Hofman degradation

Hofmann degradation is a spontaneous process in plasma at normal pH and temperature and does not depend on any circulating enzyme. In a Hofmann elimination reaction, a quaternary ammonium group is converted to a tertiary amine by cleavage of a carbon-nitrogen bond.

This is a pH- and temperature-dependent reaction in which higher pH and temperature favor elimination. Among drugs used in anesthesia, Atracurium besylate and its 1R‐cis, 1R′‐cis isomer (cisatracurium) undergo Hofmann elimination. This unique pharmacological property provides an organ‐independent degradation pathway.

Atracurium is a bis-benzyltetrahydroisoquinolinium with isoquinolinium nitrogens connected by a diester-containing hydrocarbon chain. The presence (in duplicate) of two-carbon separations between quaternary nitrogen and ester carbonyl provides the basis for a Hofmann elimination reaction.

The marketed form of atracurium has 10 isomers. These isomers have been separated into three geometric isomer groups that are designated cis-cis, cis-trans, and trans-trans according to their configuration about the tetrahydroisoquinoline ring system. The ratio of the cis-cis, cis-trans, and trans-trans isomers is approximately 10 : 6 : 1.

Atracurium is metabolised via Hofmann elimination and nonspecific ester hydrolysis (60%-90%). Laudanosine is the major metabolite of both pathways of metabolism of atracurium, with Hofmann elimination resulting in two molecules of laudanosine and ester hydrolysis resulting in one molecule of laudanosine for every molecule of atracurium that is metabolized.

Cisatracurium is the 1R cis–1′R cis isomer of atracurium and represents about 15% of the marketed atracurium mixture by weight but more than 50% in terms of potency or neuromuscular blocking activity. Cisatracurium is metabolized by Hofmann elimination. It is approximately four times as potent as atracurium, but unlike atracurium, it does not cause release of histamine in the clinical dose range.

In contrast to atracurium, nonspecific plasma esterases do not seem to be involved in the clearance of cisatracurium. Hofmann elimination accounts for 77% of the clearance of cisatracurium, whereas renal clearance is responsible for another 16%. Because of the greater potency of cisatracurium, laudanosine quantities produced by Hofmann elimination are 5 to 10 times lower than in the case of atracurium, thus making this not an issue in practice.