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2010

Dr Azam's Notes in Anesthesiology


Second Edition

Renal, Urology & History

Dr. Mohammed Azam Danish


Consultant Anesthesiologist & Critical Care Specialist

www.DrAzam.com

Dr Azam's Notes In Anesthesiology


-Second Edition

2010

Dr Azams Notes in Anesthesiology


2nd Edition

Renal, Urology & History


By
Dr. Azam
Consultant Anesthesiologist & Critical Care

www.DrAzam.com

Dr Azam's Notes In Anesthesiology


-Second Edition

2010

PREFACE
This book grew from notes first written in 2003 - 2004 from the students at the J J M
Medical College in Davangere.
There are many textbooks to choose from when preparing for the Anesthesiology
examination. The candidate suffers not from the lack of information but rather from
being inundated with it. The candidate then has the task of information sorting and
data compression to memorize and utilize all this information.
Graphic representation of data is an excellent form of data compression; figures or
drawings are frequently asked about at the viva examination, particularly since the
candidates understanding of a problem comes across most clearly when drawing a
figure or a using a picture. Figures are also a good way of approaching a topic.
I constructed parts of Dr Azams Notes in Anesthesiology for Postgraduate
students when preparing for the Anesthesiology examination and later when
preparing for tutorials.
Dr Azams Notes is aimed primarily at trainees in Anesthesia though more
experienced practitioners may find it useful as a refresher in recent concepts and
advances
Dr Azams Notes is not a substitute for the major anesthesiology text books but
concentrates on principles of management of the most challenging anesthetic cases.
The format is designed to provide easy access to information presented in a concise
manner. I have tried to eliminate all superfluous material. Selected important or
controversial references are presented as well as suggestions for further reading.
Some relate more to basic principles, physiology, pharmacology, etc. bookwork.
Others are more practical in nature, discussing the principles of anesthetic techniques
for certain high-risk situations.
Dr Azams Notes have been created keeping the Postgraduate needs while preparing
for the exams, and also help in his day to day practice. I am sure that Dr Azams Notes
will not only help him to secure highest marks but also help him to gain knowledge to
its full.

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Dr Azam's Notes In Anesthesiology


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2010

NOTICE
Anesthesiology is an ever-changing field. Standard safety precautions must be
followed, but as new research and clinical experience broaden our knowledge, changes
in treatment and drug therapy may become necessary or appropriate. Readers are
advised to check the most current product information provided by the manufacturer
of each drug to be administered to verify the recommended dose, the method and
duration of administration, and contraindications.
However, in view of the possibility of human error or changes in medical sciences,
neither the author nor the publisher nor any other party who has been involved in the
preparation or publication of this work warrants that the information contained
herein is in every respect accurate or complete, and they disclaim all responsibility for
any errors or omissions or for the results obtained from use of the information
contained in this work. Readers are encouraged to confirm the information contained
herein with other sources. It is the responsibility of the licensed prescriber, relying on
experience and knowledge of the patient, to determine dosages and the best treatment
for each individual patient. Neither the publisher nor the editor assumes any liability
for any injury and/or damage to persons or property arising from this publication.

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Dr Azam's Notes In Anesthesiology


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2010

DEDICATION
To Mohammed Shafiulla, my father, my oxygen,
companion, and best friend; for being my major pillar of
support and making this vision a reality. Thank you for your
continual sacrifices with boundless love and limitless
gratitude, for the sake of your children. I owe you a debt I
can never repay.

I also would like to thank my mom (Naaz Shafi), my wife

(Roohi Azam), my two lovely kids (Falaq Zohaa &


Mohammed Izaan), for their support, ideas, patience, and
encouragement during the many hours of writing this book
my Collegues Dr Rajshekar Reddy & Dr Sachin for their
support.
Finally, I would like to thank my teachers. The dream begins
with a teacher who believes in you, who tugs and pushes and
leads you to the next plateau, sometimes poking you with a
sharp stick called "truth."

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Dr Azam's Notes In Anesthesiology


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2010

Contributions
01.
02.
03.
04.
05.
06.
07.
08.
09.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.

Dr. Rajshekar Reddy UAE


Dr. Surendra UAE
Dr. Nagaraj Chandy Hubli
Dr.Kusuma Bangalore
Dr Sachin Doijode London
Dr Chandrashekar Bangalore
Dr Sidhu Bangalore
Dr Ravindra B K Bangalore
Dr Harshavardhan Mangalore
Dr Anil Kumar Tamil Nadu
Dr Mashooda Kerla
Dr Anusuya Bangalore
Dr Sudhir Bangalore
Dr Uma Davangere
Dr Rajeev UAE
Dr Surendra UAE
Dr Shivananda Shimoga
Dr Soujanya Bangalore
Dr Aslam Faris Kerla
Dr Nandakumar Tamil Nadu
Dr Anuradha Bangalore
Dr Arun G Pai Kerla
Dr Geetha Bangalore

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Table of Contents
PREFACE .......................................................................................................................................................... 3
NOTICE ............................................................................................................................................................... 4
DEDICATION .................................................................................................................................................... 5
CHAPTER 1 - MANAGEMENT OF UROENDOSCOPIC ........................................................................................ 11
PROCEDURES IN GERIATRICS ......................................................................................................................... 11
CHRONOLOGICALLY, GERIATRIC PATIENTS CAN BE CLASSIFIED AS FOLLOWS: ....................................................................... 12
PHYSIOLOGY OF AGEING IS DETERMINED BY: .................................................................................................. 12
PHYSIOLOGIC CHANGES ASSOCIATED WITH AGING ......................................................................................... 13
CARDIOVASCULAR SYSTEM ......................................................................................................................... 13
ANATOMICAL AND PHYSIOLOGICAL CHANGES IN RENAL SYSTEM. ..................................................................................... 25
PHARMACOKINETICS AND PHARMACODYNAMICS IN ELDERLY ....................................................................... 30
PREOPERATIVE EVALUATION ........................................................................................................................... 37
CHAPTER 2 - KIDNEY COCKTAIL ...................................................................................................................... 42
CHAPTER 3 - ACUTE RENAL FAILURE .............................................................................................................. 44
DEFINITION OF RENAL DYSFUNCTION AND ITS DIAGNOSIS .............................................................................................. 44
Urinary output ............................................................................................................................................. 44
CAUSES:.............................................................................................................................................................. 46
PRE RENAL........................................................................................................................................................... 46
PERIOPERATIVE CONSIDERATIONS............................................................................................................................. 47
PHYSICAL EXAMINATION AND PREPARATION FOR SURGERY ............................................................................................ 49
TABLE 5: TREATMENT OF HYPERKALEMIA................................................................................................................... 54
CHAPTER 4 - TURP.......................................................................................................................................... 57
DEFINITION ...................................................................................................................................................... 57
ANATOMY AND PATHOPHYSIOLOGY OF HYPERTROPHIC PROSTATE NERVE SUPPLY AND PAIN CONDUCTIVE PATHWAYS: .............. 57
Anesthetic problems:................................................................................................................................... 59
Preoperative evaluation. ............................................................................................................................. 60
Anesthesia ................................................................................................................................................... 62
Table 1: approximate doses of local anesthetic for regional block ............................................................. 63
TRANSURETHRAL RESECTION OF THE PROSTATE (TURP) .............................................................................................. 66
Physiological changes during the lithotomy position. ................................................................................. 66
Non electrolyte solution: .......................................................................................................................... 67
COMPLICATIONS OF TURP: .................................................................................................................................... 68
POSTOPERATIVE COMPLICATIONS: ............................................................................................................................ 69
TURP SYNDROME: ................................................................................................................................................ 69
PATHOPHYSIOLOGY AND CLINICAL FEATURES OF TURP SYNDROME: ................................................................................ 71
SIGNS AND SYMPTOMS OF HYPONATREMIA ................................................................................................................ 73
TREATMENT OF TURP SYNDROME: .......................................................................................................................... 74
CHAPTER 5 - GUIDELINES FOR PREOPERATIVE INVESTIGATIONS AND LABORATORY TEST ABNORMALITIES. . 86
COMPLETE BLOOD COUNT....................................................................................................................................... 86

Dr Azam's Notes In Anesthesiology


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2010

COAGULATION PROFILE. (INR AND APTT) ................................................................................................................. 86


BLOOD GLUCOSE LEVEL .......................................................................................................................................... 87
LIVER FUNCTION TESTS ........................................................................................................................................... 87
ECG. .................................................................................................................................................................. 88
ECG CRITERIA FOR MYOCARDIAI ISCHAEMIA: .............................................................................................................. 88
PULMONARY FUNCTION TESTS: ................................................................................................................................ 90
BEDSIDE TESTS OF FUNCTIONS; ................................................................................................................................ 90
ARTERIAL BLOOD GAS. ........................................................................................................................................... 92
Recommended test guidelines for asymptomatic patients: ........................................................................ 93
IMPLEMENTING ACCURACY AND EFFECIENCY IN PREOPERATIVE EVALUATION ........................................ 94
CHAPTER 6 - HISTORY OF ANESTHESIA ......................................................................................................... 107
CHAPTER 7 - SOME OUTSTANDING CONTRIBUTORS TO THE SCIENCE AND ART OF ANESTHESIA ................. 110
SIR-IVAN-MAGILL (1888-1986) ....................................................................................................................... 110
JOHN SILAS-LUNDY (1894-1973) .................................................................................................................... 111
Contributions: ............................................................................................................................................ 111
HENRY EDMUND GASKIN BOYLE (1875-1941) .......................................................................................... 112
CONTRIBUTIONS: ................................................................................................................................................ 112
HAROLD RANDALL GRIFFITH (1896-1985) ................................................................................................ 113
CARL-KOLLER (1857-1944) ............................................................................................................................. 113
JOSEPH T. CLOVER (1825-1882) ..................................................................................................................... 115
SIR FREDERICK-HEWITT (1857-1916) ............................................................................................................. 116
HELMUT-WEESE (1897-1954) ........................................................................................................................ 116
WILLIAM-STEWART HALSTED......................................................................................................................... 117
CONTRIBUTIONS: ................................................................................................................................................ 117
WILLIAM-THOMAS, GREEN-MORTAN (1819-1868) ....................................................................................... 118
JOHN-SNOW (1813-1858) .............................................................................................................................. 119
CONTRIBUTIONS TO ANESTHESIA: ........................................................................................................................... 120
JAMES-YOUNG SIMPSON (1811-1870) ........................................................................................................... 120
AUGUST KARL-GUSTAV BIER (1861-1949) ...................................................................................................... 121
ARTHUR E. GUDEL .......................................................................................................................................... 122
CONTRIBUTION:.................................................................................................................................................. 122
STAGES OF ANESTHESIA: ....................................................................................................................................... 122
JOSEPH PRIESTLEY (1733-1804) ..................................................................................................................... 123
HUMPHRY DAVY (1778-I829) ......................................................................................................................... 124
HENRY HILL HICKMAN (1800-1830)................................................................................................................ 124
HORACE WELLS (1815-1848) .......................................................................................................................... 125
SIR WILLIAM MACEWEN (1847-1924) ............................................................................................................ 126
HEINRICH FRIEDRICH WILHELM BRAUN (1862-1934) .................................................................................... 127
ARTHUR LAWEN (1876-1958) ........................................................................................................................ 127
GASTON LABAT (1877-1934) .......................................................................................................................... 128
RALPH MILTON WATERS (1883-1979) ............................................................................................................ 128
HELMUT WEESE ............................................................................................................................................. 129
SIR ROBERT REYNOLDS MACINTOSH (1897-1989) ......................................................................................... 129

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Dr Azam's Notes In Anesthesiology


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2010

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Chapter 1 - MANAGEMENT OF UROENDOSCOPIC


PROCEDURES IN GERIATRICS
Geriatrics is a medial sub-specialty that focuses on the care of elderly patient i.e.
more than 65 years of age.
Survival past the years of full somatic maturity and young adulthood is
associated with progressively increasing inter individual variability. Precise assessment
and appropriate management of elderly surgical patients represent a great challenge to
all medical healthcare providers. Physiological changes that accompany the process of
ageing contribute to an increased perioperative risk for older persons who have to
undergo anesthesia and surgery. To minimize these risks, through knowledge about
physiological changes is necessary. It should also be remembered that chronological age
is not the same as biological age because of difference in the ageing process.
Elderly patients who maintain greater than average functional capacities are said
to be PHYSIOLOGICALLY YOUNG. When function declines at an earlier age and at a
more rapid rate, then those elderly patients can be considered to be
PHYSIOLOGICALLY OLD.

Variability in the rate at which organ system function changes with increasing age
explains the presentation of patients as physiologically Young or old.

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Chronologically, geriatric patients can be classified as


follows:
ELDERLY people in the age group of 65 to 74 years.
AGED are the people in the age group of 75 to 84 years.
VERY OLD these are the people more than 85 years of age
Ageing arises from damage to DNA and sub cellular components resulting in
changes in anatomical structure and physiological functioning of the body.

PHYSIOLOGY OF AGEING IS DETERMINED BY:


Genetic factors
Environmental factors Ex: smoking, alcoholism, dietary habits, stress, diseases, physical
injury etc.
Ageing leads to a progressive decline in the resulting organ function, impaired
functional reserve, quick occurrence of functional disability which takes longer time to
get cured. Functional reserve represents the interference between resting basal and
maximal organ function, Organ system functional reserve declines markedly with
increasing age. Ageing is associated with loss of physiologic reserve in all organ systems,
increasing the vulnerability to disease and decreases the ability to compensate for
stress.
Chronic diseases associated with ageing further limit baseline function Eg: COPD,
IHD, HTN, DM, etc. Atypical presentation of a disease is common in elderly and it
diagnosis and worsens the outcome. Elderly are at increased risk of untoward reactions
to medications, anesthetic agents, medical and surgical interventions.

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Various pathophysiological changes of ageing affecting major organ system are as


follows:

PHYSIOLOGIC CHANGES ASSOCIATED WITH AGING


Pulmonary
Lung volumes increase FRC increase VC RV
PaO2
Ventilatory drive with hypercapnea
Ventilator drive with hypoxemia
Lung compliance
Cardiovascular
Basal heart rate
Maximal heart rate
Circulating norepinephrine levels
Circulating epinephrine levels
Response to adrenergic stimulation
Receptor density to
Incidence of valvular disease
= Increased

Renal
Renal blood flow
Glomerular filtration rate
Gastrointestinal
Hepatic blood flow
Hepatic mass
Musculoskeletal
Muscle mass
Total body water
Bone density
Body fat
Incidence of osteoarthritis
Neurologic
Cortical neurons
Cerebral blood flow except
with disease then

= decreased = no change

CARDIOVASCULAR SYSTEM
Cardiovascular changes that occur with ageing are more important to the
anesthesiologist than any of the age related physiological changes, as most of the
intravenous and inhalational anesthetic agents to some extent are CVS depressants.
Various changes seem are:
1. Decreased Beta receptor responsiveness.
2. Stiffening of connective tissue in the arteries, veins and heart.
3. Increase in the activity tissue in the arteries, veins and heart.
4. Gradual myocyte death without replacement.
5. Decreased responsiveness to atropine.

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1. Decreased Beta receptor responsiveness:


This is due to decrease in the affinity of Beta agonists to the receptors and efficacy of the
post receptor coupling responsible for muscle contraction. The density of Beta
receptors however remains constant. Effects of decreased Beta receptor sensitivity
include:
Reduced responsiveness of the heart to exercise i.e. inability to raise heart rate
(decreased maximal H.R.). Gradual increase in ejection fraction even with heavy
exercise (in contrast to rapid increase seen in young adults) Decreased maximal
oxygen consumption (10% per decade)
Decreased cardiac responsiveness to baroreflex, but the vasoactive component is
as effective as in young adults.
Decreased contractility of the ventricles.
Due to these reasons, the elderly heart becomes more dependent on ventricular
filling to increase its output and thus it is less tolerant to hypovolemia.

2. Connective tissue stiffening.


Proteins in the connective tissue are altered because of free radical attack and
glycosylation. Damaged proteins are replaced mostly by collagen because, elastin
production decreases with age. Even though it is produced, it is of poor quality. Hence
the connective tissue becomes stiff.
High blood sugar levels in diabetic patients also produce glycosylation induced damage
to the connective tissues and hence they are more prone for this stiffening and its
consequences.
a. Effects of stiffening of arterial connective tissue.
b. Systemic hypertension, increased after load and increase in the workload of left
ventricle causes left ventricular hypertrophy and decrease in maximal coronary
blood flow.
c. Effects of stiffening of venous connective tissue.
d. Buffering action of veins to maintain a constant central blood volume due to their
flexible nature will be lost. This will reduce the venous return and atrial
pressure. As elderly heart is more dependent on cardiac filling to maintain
cardiac output, they are at risk for changes in blood volume and posture.
e. Effects of stiffening of myocardial connective tissue.
f. Increase in End Diastolic Volume (EDV) due to decreased contractility.
g. Heart remains relatively full because of increased EDV
h. Increase in atrial pressure leading to pulmonary congestion
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Ventricular filling becomes more dependent on atrial pressure. This is because,


prolonged contraction and slowed relaxation of ventricles diminishes early
ventricular filling, and loss of atrial kick further contributes to this.
Quality of ventricular contraction is not impaired, thus despite an increase in
systolic blood pressure, the resting ejection fraction remains unaltered.

3. Increase in the activity of sympathetic nervous system this is due to:


- Increase in the amount of norepinephrine release.
- Increase in systemic vascular resistance (0.5% increase/yr)
- Slightly increased Alpha receptor response.
- But sympathetic mediated vasoconstrictor response is as effective as in young
adults.
Gradual myocyte death
Myocyte cannot regenerate and get replaced by hypertrophy of remaining cells
contributing to the ventricular hypertrophy seen in elderly. Fibrosis and attrition of
myocytes will limit electrical conductivity in the elderly heart both in the myocardium
and in the specialized components of conduction system.
This is evidenced as conduction abnormalities like ---- Prolonged PR interval and to some extent increased QRS and QT intervals.
- Decrease in QRS and T wave amplitude.
- T wave inversion especially in leads, I, a VL, V5 and 6
- Progressive LAD and appearance of benign RBBB.
- First degree heart block.
- Left anterior hemi block
- Attrition of pacemaker cells in SA node leads to decrease in heart rate.
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5. Decreased response to atropine


There will be decrease in vagal tone as the age advances; hence there is less vagal
stimulation to be removed by the atropine.
Summary of major age-related changes in the structure and function of the
cardiovascular system
Myocardium
Decreased inotropic response to beta adrenoceptor stimulation
Decreased chronotrophic response to beta-adrenoceptor stimulation
Minimal concentric ventricular hypertrophy
Decreased in intrinsic heart rate, increased atrial ectopic
Hemodynamics
Resting cardiac output reduced in proportion to metabolic needs
Widening of arterial pulse pressure
Elevated SVR and impedance to ejection of stroke volume
Lower maximal heart rate with compensatory increase in EDV during
exercise
No change in ejection fraction
Integrated cardiovascular functions
Tissue perfusion to all vascular beds well maintained
Reduced autonomic homeostasis
Greater dependence on preload
Decreased beta-adrenoceptor responsiveness
EDV, end-diastolic ventricular volume, SVR, systemic vascular resistance.

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Physiological and Anatomical Changes in Respiratory System


Morphological or Structural changes
Functional correlation
Loss of muscular support to the pharynx
Upper airway obstruction
Peripheral differentiation and decreased
CNS reflex activity.
Loss of protective airway reflexes i.e.
Decreased alveolar surface area
coughing/swallowing makes patient
( Breakdown of alveolar septe)
more prone for aspiration.
Increase in interstitial connective tissue
Decreased diffusing capacity for O2 and
and duct ectasia
CO2. Increase in physiological dead space
Decreased volume of pulmonary capillary Increase in anatomical dead space
bed and loss of elastic recoil of lung
Decrease in diffusing capacity for O2 and
parenchyma and small airways.
CO2.
Increased proteolysis of elastin and
Increase mean pulmonary artery pressure
decreased elastin/collagen ratio
and PVR
Changes in composition of surfactant
Tracheobronchial instability leading to
impaired FEV1 and maximum, breathing
capacity.
Decreased intrinsic recoil, early closure of
smaller airways.
Barrel shaped rigid chest wall
Reduced elastic recoil
Decreased strength of respiratory muscles

Changes in lung volumes

V/Q mismatch P(A-a) O2 increased


Vd/Vt increased
Closing capacity = FRC
(In supine posture by 44 yrs in erect
posture by 60 yrs)

Decrease in metabolic and immune functions


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MAJOR AGE-RELATED CHANGES


IN RESPIRATORY STRUCTURE AND FUNCTION
Lung parenchyma
Reduced total alveolar surface area
Reduced elastic recoil
Loss of tracheobronchial structural integrity
Decreased metabolic and immune functions
Lung volumes
Minimal changes in FRC (increased FRC)
Some reduction of TLC (stature dependent)
Increased RV
Decreased VC
Increased small airway closure
Pulmonary mechanics.
Increased lung compliance
Minimal change in total pulmonary compliance
Decreased FEV1
Increased work of maximal breathing
Decreased MBC
Gas exchange
Impaired V/Q matching
Increased P(A-a)O2
Increased VD/VT
Control of ventilation,
Normal resting PaCO2
Deceased ventilator response to hypoxia
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Decreased ventilatory response to hypercapnea


Increased sleep-related disruption of ventilation, apnoea, periodic ventilation
Increased sensitivity to narcotic-induced ventilatory depression.
FEV1, forced expiratory volume; FRC, functional residual capacity, MBC, maximal breathing
capacity; (P(A-a)O2, alveolar-arterial oxygen gradient; PaCO2, arterial carbon dioxide partial
pressure; V, residual volume; TLC, total lung capacity; VC, vital capacity; VD/VP dead
space fraction; V/Q, ventilation/perfusion.
STRUCTURAL CHANGES AND THEIR FUNCTIONAL CORRELATES IN THE AGED LUNGS
AND THORAX
System Morphology / structure
Function
Lung
Alveolar surface (intraalveolar Diffusing capacity physiologic dead
fenestration = pores of Kohn )
space
Interstitial connective tissue
Anatomic dead space
duct ectasia (enlarged
respiratory bronchioles and
alveolar ducts)
Tracheo-bronchial instability with early
Proteolysis of elastin (crossclosure of small airways, increased
linking ), altered location and
compliance (barrel-shaped chest wall,
orientation of elastic fibers
flat diaphragm), changes in lung
elastin / collagen ratio ,
volumes, ventilation/ perfusion
surfactant (+ altered
mismatch with progressive impairment
composition)
of arterial oxygenation
Thorax Stiffness (calcification of ribs
Tidal volume , respiratory frequency
and vertebral joints)
Loss of respiratory muscle mass
Maximum voluntary respiratory
pressure
Morphological or Structural changes
Thorax
Calcification of ribs and vertebral joints
Loss of respiratory muscle mass mainly
fast twitch muscle fibres (type II)
Decreased diaphragmatic efficiency
Scanty cilia

Functional correction
Stiffening of chest wall (decreased TV)
Decreased electromygraphic (EMG)
activity by 50% in skeletal muscles.
Decreased MBC.
Poor cough.
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Various changes seen in lung volumes are as shown in the diagram below

Control of ventilation and Gas exchange:


Ventilator response to decreased PaO2 and PaCO2 is decreased by 50% by 70
years of age. Decreased CNS activity. Decreased neuronal output to respiratory muscles.
There is increase in sleep related disruption in ventilation. Hence more prone for sleep
apnoea. Elimination of CO2 is unaffected, hence resting PaCO2 is normal.
Arterial oxygenation is impeded because of V/Q mismatch which occurs due to
- Increase in physiological and anatomical dead space.
- Early airway closure in small bronchioles leading to uneven distribution of
inspired gas.
- Decrease in diffusing capacity of O2 because of increased interstitial connective
tissue and loss of alveolar surface.
- Attenuation of hypoxia induced pulmonary vasoconstriction and hypocapnic
bronchoconstriction because of stiffening of connective tissue in the vasculature
and airways.
Therefore PaO2 decreases by 5 mmHg per decade from the age of 20 years. Significant
reduction occurs at 40-75 years when it remains stable at 83 mmHg.

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PHYSIOLOGICAL AND ANATOMICAL CHANGES IN NERVOUS SYSTEM.


MAJOR AGE RELATED CHANGES IN CENTRAL NERVOUS SYSTEM STRUCTURE
AND FUNCTION
Brain anatomy
Progressive loss of neurons in gray matter and within neurotransmitter
synthesizing areas
Modest atrophy of white matter (late in geriatric era)
Increased intracranial cerebrospinal fluid volume
Substantial (but variable) progressive reductions in hemispheric metabolic
activity
Cerebral circulation
Auto regulation and local metabolic coupling maintained in healthy subjects
Modest decline in mass-specific (ml/100g/min)global and regional blood flow
Substantial (but variable) progressive reductions in total (ml/min)hemispheric
blood flow
Neurophysiology
Reduced neuronal density
Reduced brain and spinal cord neurotransmitter activity
Simplification of synaptic interconnections.
Decreased plasticity and impaired recovery from neuronal injury
Neurological characteristics
Crystallized intelligence and implicit memory well maintained
Deafferentiation and impaired speed of processing of sensory input
Progressive decline in fluid intelligence
Decreased anesthetic requirement.
Anesthesia is a transient state of deliberate drug induced coma. Any plan for
anesthetic management, therefore, produces extensive and profound disruption of CNS.
The effect of ageing on the nervous system, determine what adjustments of the
anesthetic plan will be most appropriate for an elderly patient.

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1) Changes in brain.
Neurons are postmitotis cell therefore they are not replaced when they get injured or
die. Total brain weight declines by 10-30% by the age of 80 years mainly there is
decline in grey matter. Cerebral metabolism and O2 demand is reduced mainly because
of decreased neuronal tissues mass.
Cerebral blood flow is reduced by modest degree but its auto regulation is well
maintained. Regional cerebral blood flow mainly depends on local metabolic and
neuronal activity and it remains unchanged. But diseases that alter cortical function
may uncouple local brain blood flow form metabolic requirement of the tissues they
perfuse. Cerebral glucose utilization is also decreased.
Reductions in neuronal density and declining neuro transmitter synthesis reduce
requirements for specific hemispheric global (CBF) and regional grey matter (CBF)
brain blood flow. Hemispheric cerebral metabolic requirements for oxygen (CMRo2
ml/100gm/min) will decline nonlinearly.

2) Changes in spinal cord and peripheral nerves


Neuronal loss is similar to that seen in the brain.
There is a universal and progressive loss of sensitivity and vigour in both mono and
polysynaptic spinal cord motor reflexes. These changes combined with reduced muscle
mass and decreased strength, reduced sensitivity and precision of joint proprioception
exert adverse consequences on gait and balance and limit normal daily physical activity.
Attrition of neurons in cerebellum, decreased visual and auditory activity will also
contribute to this and makes elderly more prone for disequilibrium falls. Velocity of
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peripheral nerve conduction decreases by 0.15 m/sec/yr. impairment of corticospinal


transmission increases the time needed between intention and onset of voluntary
motor activity.
a. Affernetation: There is progressive global differentiation and generalized reduction
of intellectual functions.
b. Visual function: Degenerative changes in the optic nerve and progressive
hardening and yellowing of the lens will decrease the visual acuity, producing
presbyopia. Visual field gets compromised both in size and sensitivity. Colour
discrimination gets diminished.
c. Auditory function: There are progressive impairments of hearing and speech
discrimination.
Taste and olfactory sensations are also diminished
d. Touch and pain: There is an increase in threshold for pain and touch perception.
Ageing increases perception thresholds for all forms of sensory input.
3) Changes seen at neuromuscular junction.
There is a decline in the number and density of motor neuron/endplate units and also
thickening of muscle motor endplate and loss neurotropic support. Increase in the
number and variety of cholinergic receptors at the endplate and surrounding areas
offsets the age relate decline in the number of motor endplates and therefore despite
loss of skeletal muscle mass, dose requirements of NM blocking drugs are not reduced.
Motor neuron degeneration leads to: Skeletal muscle atrophy reducing its dynamic
strength. (isometric strength is well maintained). Disseminated neurogenic atrophy
responsible for age related changes in the NMJ. Thickening of post junctional membrane
and its spread beyond the usual endplate areas because of age related deficiency of
Cyclic GMP, generate a typical extrajunctional cholinergic receptors. There is also
impairment of acetyl choline synthesis and release. Thus it is difficult to predict the
release of acetyl choline following electrical stimulation of motor neuron. Hence, there
is less pharmacodynamic change even though there is proliferation of motor end plate /
increased receptors.
4) Intelligence and memory
Recall of needed facts is slower and less precise. The ability to sustain attention span is
reduced. Memory retrieval is reduced because of decreased neurotransmitter activity.
Implicit memory remains intact (short term memory). Sementic/explicit long term
memory is increased. Episodic memory (experiences) reduced. Pseudodementia: due to
stress and destruction imposed memory dysfunctions in elderly. Crystallized
intelligence is not affected. Eg: Language skills and personality. Fluid intelligence is
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diminished Eg: Short term memory, Visual and auditory reaction time, immediate
processing of information.
5) Sleep and plasticity.
Total average time in bed increases but there are arousal periods during the sleep. Early
awakening in the morning is seen. Rapid eye movement (REM) sleep is well maintained
but deeper stage III and slow wave sleep pattern are compromised.
Upper airway obstruction, apnoea and hypoventilation are common during sleep
leading to hypoxia induced disturbances in CVS and CNS metabolism. Nocturnal
ventilator response to CO2 remains unchanged. Circadian rhythm of adrenocortical
steroid release related sleep pattern does not change much.
6) Autonomic nervous system
The autonomic reflex responses are gradually impaired in the elderly. The speed
and magnitude of the response are low and they find it difficult to maintain homeostasis
under stress. They respond poorly to sudden changes in posture, hypovolemia and do
not increase their heart rate in response to stress as readily as a young adult. The
mechanism for this is a decrease in the number of receptors as well affinity of receptors
to the agonists.
7) Thermoregulation
Elderly are more prone for perioperative hypothermia because of:
- Frail constitution
- Reduced metabolic rate
- Reduced subcutaneous fat layer
- Major and long operations.
- Impaired thermoregulation i.e.
- Delayed and less vigorous compensatory mechanisms:
Eg: cutaneous vasoconstriction, shivering etc
Adverse effects of hypothermia:
- CNS depression
- Depression of ventilator drive which may extend postoperatively to produce
postoperative somnolence and hypoxia
- Prolonged drug action.
- Precipitates negative post operative nitrogen balance and accelerates protein
catabolism.
- This compromises wound healing and surgical recovery.
- Impairment in coagulation.
- Immune dysfunction.
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Leftward shift of ODC


Vigorous compensatory mechanisms for hypothermia can precipitate myocardial
ischemia by increasing O2 demand.

Prevention by using:
Warm IV Fluids, heating blankets, warmed water mattresses and forced air warming.

Anatomical and physiological changes in renal system.


Renal tissue mass reduces because of atrophy of renal tissue and reduction in the
number of nephrons. Renal tubules appear to be obliterated. Proximal convuluted
tubule (PCT) becomes shorter. This and associated loss of glomerular surface, is the
reason for well preserved functional capacity for glomerular filtration relative to
tubular absorption. GFR is decreased by 6-8% per decade up to 8th decade and then
more rapidly thereafter.
Renal cortical blood flow decreases because of overall reduction in renal tissue
vascularity and increase in renal vascular resistance (only functional). Blood flow to the
renal medulla is well preserved. Effect on auto regulation of RBF is unknown.
Production of creatinine is itself reduced because skeletal muscle mass. Hence
serum creatinine concentration represent the point of equilibrium between the rate at
which creatinine is generated and the rate at which it is both filtered and excreted into
the urine and may not accurately reflect renal functions/functional reserve. Therefore
normal serum creatinine concentration in the aged patient does not imply that renal
functional reserve will be adequate to maintain homeostasis of circulating blood volume
and electrolyte stores perioperatively.
Ability to respond appropriately and completely to the metabolic acidosis is decreased
because of:
- Decreased ability to acidify the urine.
- Delayed excretion of acid load
- Reduced rate of synthesis of bicarbonate.
Sodium homeostasis is well maintained. But they cant reduce the urinary
sodium loss at faster rate response to ADH is lowered. Raised Se. K and blood
urea levels are seen.
Functional hypoaldosteronism, reduced thirst sensation increased levels of atrial
natriuretic peptide, (ANP) depressed response of juxtra glomerular apparatus
(JGA) to Beta receptor stimulation leading to reduced renin angiotensin response
(by 50%) and decreased arginine vasopressin (AVP) are some other functional
impairments seen in elderly population. Decreased AVP and increased ANP lead
to depressed thirst mechanism.
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Both volume of urine produced and the fraction of total daily creatinine excreted
during sleep is increased. This effect combined with age related reduction in
urinary bladder capacity predisposes to nocturia.
In conclusion, loss of renal tissues mass and reduced GFR due to the decline of
nephron functional reserve, unaltered osmorecetpor/ACP responsiveness, are
probably responsible for the age related impairment of water homeostasis.
Hence, fluid restricted elderly surgical patients are at increased risk of
dehydration and hypernatremia.
SUMMARY OF MAJOR AGE-RELATED CHANGES IN RENAL AND HEMATOLOGICAL
STRUCTURE AND FUNCTION
Kidney
Modest by variable loss of renal tissue mass, especially in cortices
Marked decline in renal blood flow and glomerular filtration rate
Slight increase in filtration fraction
Glomerulotubular balance well maintained
Reduced tubular responsiveness to hormones that conserve salt and water
Decreased acid excretion
Blood
Normal erythrocyte, platelet, and leukocyte indices
Reduced erythropoietic functional reserve
Normal coagulation and haemostasis
Decreased fibroinolytic reserve, predisposition to infection and autoimmune
phenomena
Pharmacokinetics
Decreased renal clearance of hydrophilic drugs and metabolites
Slightly reduced plasma protein binding of xenobiotics
Increased apparent drug potency and high plasma drug concentrations due to
delayed redistribution of parenteral drugs from plasma

Haematological changes:
Volume of bone marrow is reduced, but the functional remains normal when there is
adequate supply of iron, folic acid and Vit. B12. Flexibility of RBC is decreased,
compromising small vessel perfusion especially in patients in shock or with
polycythemia and with conditions of acute hemoconcentration. RBC fragility is
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increased. Degenerative changes in RBC morphology associated with age related


changes in its activity will lead to increase in ESR. 2-3 DPG is decreased leading to left
shift of Oxygen Dissociation Curve. Chronic nutritional anaemia may also present which
decreases tissue O2 delivery. Enhanced platelet mediated homeostasis. Small increase in
intrinsic clotting factors. Slight decrease in antithrombin III. All these changes make
elderly prone for pulmonary thromboembolism i.e. prothrombotic.
Immune function:
There is thymic involution and diminished function of T lymphocytes. Little effect is
seen no macrophages and nonself immune discrimination increasing the incidence of
autoimmune disorders. All these changes predispose elderly to perioperative infections.
Changes in endocrine system:
There is little change in the plasma levels of most of the hormones. But the rate of
turnover is decreased. There will be progressive impairment in the capacity to
metabolise a glucose load. Declined pancreatic function increases the incidence of
glucose intolerance and diabetes mellitus in elderly. Hence intraoperative glucose
administration should be limited in elderly surgical patients. Intraoperatively blood
glucose levels should be measured frequently.
Diminished plasma renin concentration by 30-50% leading to reduction in
plasma aldosterone levels. Altered renin-aldosterone system increases the risk of
development of hyperkalemia.
Impaired release of stimulating hormones Eg. ACTH, TSH by the releasing factors i.e.
TRF, somatotropin and adrenocortical hormones. Subclinical hypothyroidism is seen in
13.2% of elderly females which manifests as increase in TSH. Slower synthesis and
degradation of hormones Eg. T3 and TSH.
Changes in GIT
Decreased lower oesophageal sphincter tone, along with delayed gastric emptying time
and decreased absorption of nutrients produces anaemia and chronic nutritional
deficiency in the elderly. They may present as full stomach patients, increasing the
chances of aspiration.
Changes in hepatobiliary system
Liver size reduces by 40% by the age of 80 years. Hepatic blood flow and splanchnic
blood flow also decline proportionately. Decline in hepatic function is characterized by:
reduced activity of many microsomal enzymes as well as pseudocholinesterase and
reduced levels of plasma proteins.

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Changes in body composition and metabolism.


Women tend to gain body fat throughout adulthood and hence maintain their total body
weight. Even as lean tissue mass and skeletal elements are lost, whereas most men loose
body both weight and stature by 8th decade.
a) Stature and body habitus:
There is a progressive reduction of height. Accumulation of adipose tissue seen in the
middle years is followed by accelerated loss of subcutaneous and intramuscular fat in
geriatric population, osteoporosis and demineralization leads to biphasic changes in
total body weight.
b) Body composition:
There is a decrease in lean tissue mass, skeletal muscle mass and loss of metabolically
active organ tissues, blood flow and decreased intracellular water content. However
circulating blood volume is maintained.
c) Tissue functions:
Little qualitative changes in metabolic activity (BMR is 40% of that in 20 yrs by 70 yrs)
Atrophy and fibro calcification of elastic and mechanically specialized tissues Eg. Skin,
Eye, large arteries etc. altered tissue receptor agonist interactions for neurotransmitters
and trophic hormones. Decrease in immune response.
K. Musculoskeletal changes:
Skin atrophies with age and is prone to trauma from adhesive tape. Electrocautery pads
and ECG electrodes. Veins are often frail and easily ruptured by intravenous infusions.
Decreased mass and strength of bones with or without osteomalacia or osteoporosis
makes elderly more prone for fractures and hence careful positioning is required during
anesthesia. Arthritic joints may interfere with positioning or regional anesthesia
techniques. Poor dentition may affect mask ventilation. Loose tooth may pose problem
during intubation.

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SUMMARY OF MAJOR AGE-RELATED CHANGES IN BODY COMPOSITION AND


METABOLISM
Stature and body habitus
Progressive reduction of height
Osteoporosis and demineralization (especially in women)
Accumulation of adipose through middle adult years but accelerated loss of
subcutaneous and intramuscular fat during geriatric era
Biphasic changes in total body weight

Body composition
Decreasing skeletal muscle mass throughout adulthood (especially in sedentary
men)
Loss of metabolically active organ (e.g., liver, kidney) lean tissue mass and blood
flow.
Decreased intracellular water
Maintained circulating blood volume (aerobically active, normotensive older
adults)
Tissue functions
Little qualitative changes in metabolic activity
Atrophy and fibrocalcification of elastic and mechanically specialized tissues (skin,
eye, large arteries)
Altered tissue receptor/agonist interactions for neurotransmitters and trophic
hormones
Pharmacokinetics
Increased alpha-phase drug concentrations
Delayed redistribution of drugs from plasma to affect compartments in the
biophase
Reduced elimination clearance for drugs undergoing hepatic or renal biotransformation
Increased steady-state distribution volumes for lipophilic drugs
Prolonged elimination half-times

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PHARMACOKINETICS
ELDERLY

AND

2010

PHARMACODYNAMICS

IN

Ageing produces both pharmacokinetic and pharmacodynamic changes


Pharmacokinetics:
The relationship between drug dose and plasma concentration. It deals with
what body does to the drug and it includes drug absorption, tissue distribution,
metabolism and elimination.
Pharmacodynamics:
The relationship between concentration and clinical effect. It explains what a
drug does to the body.
T 1/2 of any drug depends on two factors.
VD
=
volume of distribution
Cl
=
clearance
T =
0.693 x VD
Cl

Drug dose

Absorption
Distribution
Binding
Metabolism
Excretion

Plasma
Concentratio
n

Distribution
Diffusion
Binding

Physiological state
Pathological changes
Other drugs

Tissue
concentratio
n

Drug
response

Pharmac
o
Kinetic
factors

Pharmac
o
Dynamic
factors

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Volume of distribution affected by total body water, protein content and body fat
content.
Elderly people have increased body fat decreased serum protein levels and total
body water. This will increase the volume of distribution for lipid soluble drugs,
decreasing their plasma concentration. Conversely, water soluble agents have less
volume of distribution, hence higher plasma concentration. Because of increased
volume of distribution of lipid soluble agents, they have longer duration of action, hence
delayed recovery and also they have to be used in smaller doses. Clearance for
intravenous agents depends on the efficiency of hepatic metabolism and renal
elimination and for inhalational agents it depends on the efficiency of cardiopulmonary
system function.
Renal and hepatic function decline with age, so the drugs which depend upon
their clearance on the function of these two organs may show prolonged duration of
action. Increased elimination half life make them susceptible for cumulative drug
effects, Age related decline in CNS function make elderly more sensitive to drugs is also
reduce. Altered plasma protein binding also effects distribution and elimination of a
drug. Ageing causes decrease in serum albumin level and increase in acid glycoprotein
(which binds to basic drugs). Protein bound drugs cannot interact with end organ
receptors and are unavailable for metabolism or excretion.
Anesthetic implications of various physiological changes:
It is difficult to elicit proper history because of decreased visual auditory acuity
as well as impaired memory. These changes can also contribute for post operative
confusion. Elderly may present with nutritional anaemia (which increase perioperative
CNS mortality and morbidity by increasing demand for increased cardiac output).
Anaemia will be less responsive to iron therapy. Decreased lean tissue mass and fat
reduces their body weight. They are shorter and may be kyphotic because of reduced
intervertebral spaces. Poor dentition poses problems during airway management.
Delayed gastric emptying and associated decreased airway reflexes make them prone
for aspiration. They arrive to the operating room with increased sympathetic activity
because of anxiety and pain. There may be difficulty in canulation and homeostasis
because of fragile veins. Careful handling during positioning is necessary. Elderly are
more dependent on increased sympathoadrenal activity for maintenance of their basal
activity than young adults. Hence GA/SA induced disintegration of Sympatho adrenal
activity may be dangerous in them especially if autonomic response is already
compromised by HTN/other CVS pathology.

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They are volume dependent yet volume intolerant hence:


Small changes in blood volume can result in considerable changes in blood
pressure (BP) Normal physiological stresses like postural shift may cause sudden
hypotension. Enhanced pressure changes are seen with excessive sodium
intake/restriction or diuretic therapy. Because of reduced autonomical homeostasis
there may be rapid changes in hemodynamics which may affect tissue perfusion.
Therefore, continuous and accurate monitoring of cardiopulmonary function and
oxygenation is must. They may not respond to hypotension by sudden increase in
HR/SVR. Hypotension is less responsive to inotropes. If sustained hypotension and the
use of peripheral vasoconstrictor drugs can be avoided, graded pharmacological
sympathectomy produced by neuraxial local anesthetics largely prevent renal
vasoconstriction and may minimize reduction of renal blood flow during recovery from
surgery. Both general anesthesia (GA) and regional anesthesia (RA) cause oliguria.
Perioperative blood/blood component transfusion is indicated for:
Maintenance of adequate O2 carrying capacity. Restoration of coagulation,
preservation of blood viscosity is required for long term hemodynamic stability.
Aggressive blood replacement with homologus blood depresses the immune system.
They are less suitable for autologus blood donation (decreased RBC reserve).
No specific anesthetic technique appears to be specifically indicated for elderly
patients, nor should age itself be considered a major risk factor that predisposes to
permanent post operative neurological dysfunction. Elderly show increased sensitivity
to anesthetic agents, sedatives and narcotics. Hence they should be used in
lesser/titrated doses. Duration of action of most of the drugs is prolonged because of
decreased rate of metabolism and prolonged elimination. Decreased albumin level
causes increased levels of free fraction of the drugs which bind to it Eg.
Thiopentone/Diazepam/Midazolam etc. delayed recovery after GA is mainly because of
increased sensitivity of CNS to the depressant effect of anesthetic agents. Use drugs
whose pharmacokinetic characteristics are less influenced by the process of ageing Eg:
propofol/desflurane During intubation/extubation sympathetic response should be
blocked to prevent CVS and CNS mortality.
No change or slight increase in the dose requirement of neuromuscular blockers.
Duration of block is prolonged. Return of effective neuromuscular transmission
following reversal is indistinguishable from young adults. Prolonged
Acetylcholinesterase
activity,
because
of
delayed
clearance
of
neostigmine/physostigmine may predispose to late post operative bradyarrhythmias.
Little effect on plasma cholinesterase is seen. Hence action of scholine is not affected.
Anesthesia causes reduction in FRC thus decreasing pulmonary compliance.
There will be increase in Vd/Vt because of alterations in regional lung mechanics and
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anesthesia induced modification of the lung, thorax and abdominal unit, but not by
increase in true shunt. Hence this hypoxia wont respond to increase in PEEP or
hyperventilation/use of large tidal volume/intermittent sigh/by increasing
concentration of delivered O2. N2O can disrupt neurological function within the cerebral
cortex causing cognitive disorder.
With regional epidural anesthesia, lesser dose of local anesthetic is required.
Greater cephalad spread is seen, maximum plasma concentration is attained sooner and
recession of block is more rapid. This is because of: Increase in rigidity of the space
(decreased spread through the intervertebral space) decreased local resistance to L.A
and more rapid vascular absorption. Duration of spinal anesthesia is slightly increased,
but spread of anesthesia is indistinguishable from that seen in young adults. Incidence
of cauda equine syndrome is high, PDPH incidence is decreased. More prone to
neurotoxic injury by lidocaine because of decreased CSF volume or spinal canal stenosis.
Bradycardia produced intraoperatively is less responsive to atropine.
Post operatively:
They are more prone for pulmonary atelectasis, sleep apnoea, obstruction of
airway and aspiration pneumonia because of diminished airway reflexes and increased
periodic breathing during sleep. They maintain O2 delivery by increasing O2 extraction
not by increasing cardiac output. Hypoxia can precipitate myocardial ischemia. Hence,
post operative O2 supplementation is must. They are more susceptible to acute
respiratory failure and their MBC is less. Hence, it will be difficult to wean them from
the ventilator. Good post operative analgesia should be provided to avoid pain and
anxiety induced precipitation of MI, stroke etc. High antibiotic coverage is must.
Adequate nutrition, fluid and electrolyte balance should be maintained.
Maximum residential depression of nervous system occurs during the second
day of GA in both young and elderly. Transient confusion and disorientation may persist
for a longer duration. Ultimate recovery of intact neurological function is more difficult
to re-establish promptly in the elderly surgical patient than in the young. Pre-existing
CVS and cerebrovascular diseases are also contributory factors for the post operative
neurological dysfunction along with anesthetic agents and techniques.
It should be remembered that:
There are no specific principles/guidelines to the perioperative management of the
geriatric patient that will guarantee rapid emergence or uncomplicated neurological
outcome

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ANESTHESIA FOR ENDOUROLOGICAL PROCEDURES


Endoscopic surgeries largely replacing incisional surgeries in urology. Economic
considerations, patient convenience and advances in instrumentation have all
supported the trend towards endoscopy in urologic surgery.
COMMON ENDO UROLOGIC PROCEDURES DONE ARE:
Cystourethroscopy.
Internal optical urethrotomy.
Ureteroscopy
Placement of ureteral stent.
Distal stone manipulation/laser lithotripsy.
Transurethral resection of prostate.
Balloon dilatation of the prostate.
Transurethral resection of bladder tumours.
Extracorporeal shock wave lithotripsy.
Percutaneous nephrostomy, nephroscopy and urethroscopic nephrolithotomy.
Advantages of endoscopic procedures:
Elderly patients in the high risk group requiring urologic procedures can be
managed with local anesthetic techniques. Minimal tissue trauma. Need for GA is greatly
reduced and hence it is associated complications too. Duration of hospital stay has
reduced from 1-2 weeks after open surgical procedures to only 24 hours in endoscopic
procedures. Post operative morbidity and mortality is less.
Different Anesthetic Options Available:
I. Local Anesthesia.
Local anesthetic 2% lidocaine jelly infiltrated into the lower urinary tract under direct
vision. While doing urological procedures, bladder should be maintained in undistended
form. To achieve this, resectoscope with the ability for continuous irrigation is used or a
suprapubic catheter is placed for aspiration.
II. Sedoanalgesia:
This type of analgesia gives emphasis on sedation and analgesia. Various combinations
of drugs are used. Sedatives: Benzodiazepines Eg. Midazolam they give hypnosedation
and amnesia.
Analgesics: pethidine or Topical 2% lidocanine jelly.
Method: Give Inj. Midazolam 0.1-0.12 mg/kg 20-30 min. before surgery. Wait for 10-15
min. and then give Inj. Pethidine 1-1.5mg/kg or apply lidocaine jelly locally. In elderly,
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the dosage of Midazolam is reduced to 30-60% if the patient is still anxious; Inj.
Midazolam is given in 1 mg IV increments.
For Biopsy/Diathermy/Incision:
1% lidocaine with adrenaline (1:200.000) is infiltrated into the area.
The advantage of this technique is that is more safe and has got high acceptancy.
Patient can be discharge within 1 hour after the procedure.
Spinal/Epidural anesthesia:
Bupivacaine, with or without narcotics are used in various concentrations. 0.25% is
found to be least toxic.
Advantages:
Minimal physiological disturbances. Provides adequate muscle relaxation of
pelvic floor, perineal and thigh muscles. Can diagnose over hydration, bladder
perforation, visual disturbances and change in consciousness early. More useful if Xrays are to be taken during cystoscopic examination. Since patients can be asked to
cooperate by holding their breath at the proper time.
Complications:
Hypotension, high or total spinal, headache, backache, meningitis etc are seen
with regional block PDPH is rare in elderly. Transient hearing loss not seen with
epidural anesthesia, because of transmission of decreased CSF pressure to the inner ear
through the cochlear duct
General Anesthesia:
Is indicated when:
Regional anesthesia fails.
Regional anesthesia is contraindicated.
Patient is unco-operative/anxious.

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CONTROVERSY BETWEEN GENERAL/REGIONAL ANESTHESIA


There is lots of controversy that, which anesthesia is suitable for elderly patients.
Researchers have recently studied different aspects of the controversy as follows:
General
Regional
anesthesia
anesthesia
Mortality and Morbidity.
Intra operative hypotension
Greater
Post operative hypertension
Other complications
Like Myocardial ischemia
Pulmonary embolism
Cerebrovascular accidents
Not much
TIA
Difference
Biliary/Renal dysfunction
Not
much
Need for post op ventilation
difference
Cognitive function
Blood Loss
Heat loss

Surgical stress
Immunological changes

Post operative pain relief

No
significant No significant
difference
Difference
More
Decreased heat
Production.
Therefore
if
unwarmed
irrigating fluid is
used, heat loss
will be more.
No change in Cortisol levels seen in
both groups
Decreased
Smaller
lymphocyte and elevation
in
lymphocyte
glucose
responsiveness
Need
post Can give post
operative
pain operative
medication early analgesia with
and
very epidural
frequently
catheter insitu
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PREOPERATIVE EVALUATION
History:
In the workup of any patient, the history is of paramount importance. This is
particularly true in urology. History helps us to know whether the disease is acute or
chronic and directs towards that specific investigations to be done.
HISTORY OF PRESENTING ILLNESS
Various enquiries in particular to the patient with urological problems are:
History of:
Coexisting diseases Eg: IHD, HTN, Asthma, TB etc.
Previous hospitalization.
Other surgical procedures
Blood transfusions.
Cognitive dysfunction/malignancy/gait disturbances
Alcohol/smoking habits.
Bladder habits.
Family history of DM/HTN/IHD/TB etc.
Present/past medications with regard to indication, dosage, frequency duration
and any allergic drug reactions.
Drugs commonly prescribed for the elderly patients:
Drug
Adverse effect or drug interaction
Diuretics
Hypokalemia
Hypovolemia
Digitalis
Cardiac dysrhythmias
Cardiac conduction disturbances
Beta antagonists
Bradycardia
Congestive heart failure
Bronchospasm
Attenuation of autonomic nervous system activity
Centrally
acting Attenuation of autonomic nervous system activity
antihypertensive
Decreased MAC
Tricyclic antidepressants
Anticholinergic effects
Cardiac dysrrhythmias
Cardiac conduction disturbances
Increased MAC
Lithium
Cardiac dysrrhythmias
Prolongation of muscle relaxants
Antidysrrhythmic
Prolongation of muscle relaxants agents
Antibiotics
Prolongation of muscle relaxants

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PHYSICAL EXAMINATION
I. General physical examination.
Look
for
appearance,
behaviour,
gait,
speech,
presence
of
anxiety/depression/confusion. Presence/absence of pallor, cyanosis, clubbing,
lymphadenopathy, periorbital and pedal oedema, dehydration etc. Examine the spine
for any deformity. Check tone of anal sphincter. Elicit achillis tendon and
bulbocavernous reflexes. Assess-nutritional status, body mass index, skin fold thickness.
Assess Airway:
Check mouth opening, neck movements, buccal pad of fat
Look for dentition loose teeth,
Look if there is any vertebrobasilar insufficiency,
Grade airway by mallampatti scoring system.
II. SYSTEMIC EXAMINATION
Respiratory system
Cardiovascular system
C.N.S. with regard to intelligence and memory as well.
Detailed neurological survey has to be done to uncover sensory or motor
impairment that will account for residual urine or incontinence.
Per-abdomen:
Look for any organomegaly, free fluid, lymphnode enlargement especially,
hypogastric, external iliac, preaortic etc. Which can present as abdominal mass? Also
palpate left supraclavicular LN as testicular and prostatic malignancies metastasise
here.
INVESTIGATIONS:
History and physical examination directed testing, markedly improves the
effectiveness of preoperative preparation and assists in the formation of appropriate
anesthetic plan.
Various tests to be done on an elderly surgical patient should be primarily
determined by the surgical procedure and by the type and severity of pre-existing
disease and the extent of functional compromise.
Hb% TC, DC, ESR.
Complete haemogram, BT. CT
Peripheral blood smear: May show hypochromic anaemia in case of chronic
pyelonephritis, uremia and carcinoma.
Urine: Albumin, Sugar,Micriscopy, Culture, pH, specific gravity
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ECG
RBS
Renal function tests:
Blood urea, serum creatinine,
Creatinine clearance
Serum electrolytes.
Roentogenography examinations of urinary tract
USG, CT Scan, Radioisotopic studies and endoscopic examination depending on
the need.
RISK ASSESSMENT.
Risk factors for postoperative mortality in elderly surgical patients:
ASA Physical status
III & IV

Surgical procedures

Major &/or emergency procedures

Co-existing diseases

Cardiac. Pulmonary diseases Diabetes mellitus,


Liver and Renal impairment

Functional status

<1-4 metabolic equivalent

Nutritional status

Poor, Albumin <35%, Anaemia

Place of residence

Not living with family

Ambulatory status

Bedridden.

PREOPERATIVE PREPARATION:
Elderly are associated with certain psychological stresses which make them
anxious or depressed and increases the risk of post operative delirium, confusion,
cognitive dysfunctions and dysfunctions and depression, thus delying the recovery.
These stresses include
Fear of loss of normal functioning.
Fear of long term hospitalization/death.
Fear of operative and anesthetic procedures.
Awareness of financial burden.

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These can be minimized by preoperative counselling during the pre-operative visit.


Correct anaemia/malnutrition if any.
Control co-existing diseases.
Ask to stop smoking at least for 8 weeks prior to Surgery
Train them in cough and lung expansion techniques.
Premedication:
Normal adult premedication doses may produce exaggerated effect in elderly
patients as they are more sensitive to drug effects. This may create unwanted confusion
and agitation in them. Hence premedication should be light.
ANXIOLYTICS:
Benzodiazepines with lesser sedative effect and shorter duration of action are
preferred and prescribed one day before surgery. they include: Tenazepam and
Triazolam
Anticholinergics: If at all needed, glycopyrolate is the drug of choice.
Antihypertensive/cardiac drugs/anticonvulsant drugs/antiasthmatic
drugs/various hormonal preparations which the patient is on are to be continued till
the morning of surgery.
In diabetic patients morning dose of insulin OHGA to be skipped.
Prophylaxis to prevent aspiration: Inj.metaclopramide 10 mg and Inj. Ranitidine
50mg IV half an hour before surgery.
MONITORING DURING ANESTHESIA:
Because of limited physiological reserves and a reduced margin of error in
elderly patients, monitoring generally should be more intense than for younger patients.
But every monitoring technique has a cost benefit relationship that must be assessed
individually in view of the patients age. Physical status and proposed surgical
procedure.
Various monitors used are:
Pulse oximeter-pulse rate SPO2, pulse volume, rhythm.
NIBP
ECG
UOP
ETCO2
Temperature.

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Chapter 2 - KIDNEY COCKTAIL


During renal transplant operation once the transplant anatomies are completed,
the early onset of urine output i.e. renal function is paramount.
Several measures can be used to stimulate urine production and improve
transplant kidney viability.
Some centers infuse a kidney viability when suturing of the vascular
anastamosis begins. It is infused at a rate to be completed just before anastamosis is
completed.
The constituents of the kidney cocktail are
600 ml of 0.45 of Dextrose 0.45 of Normal saline
37.5 g of Albumin
37.5 g of Mannitol
80mg of Frusemide (for cadaveric kidneys).
Albumin:
Has been found to improve the graft function it acts by improving the oncotic pressure
and thus expanding the intravascular volume.
Mannitol:
Acts by expanding the intravascular volume reducing cellular swelling, increasing
tubular urine flow, and reducing the potential for tubular obstruction.
Scavenges free radicals and increases release of intra renal prostaglandins.
Diuretics:
Frusemide Loop diuretics block the chloride pump in the thick ascending Loop of
Henley and increase resistance against ischemic injury.

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Chapter 3 - ACUTE RENAL FAILURE


Introduction
Acute renal failure (ARF) is seen commonly in the perioperative period and in the ICU. It
is associated with a high morbidity and mortality (oliguric 50-80% and non oliguric 1040%). It is therefore imperative to either prevent its occurrence or recognize its
presence and treat it as soon and as efficiently as possible.

Definition of renal dysfunction and its diagnosis


Urinary output
Traditionally oliguria is defined as a urine output of less than 0.5 mlkg-1hr-1 or 400
mlday-1. Anuria is defined as less than 50 ml per day. However, a reduction in the urine
output need not necessarily mean renal failure. It may just be an external sign of an
underlying process such as hypotension and hypovolemia which needs correction.
Restoration of blood pressure and blood volume may increase the urine output showing
that the kidney is in perfect condition.
Urine-analysis. The presence of blood may suggest the presence of an embolic
phenomenon and a large number of casts in acute tubular necrosis. Also look for protein
and myoglobin. However, 'dirty' results on urinalysis are common in critically ill
patients.
Blood Urea Nitrogen (BUN) is the breakdown product of protein and in the presence
of acute renal failure it typically rises by about 10 -15 mg/dl/day. However it must be
remembered that the BUN level varies directly with protein intake and increases in the
presence of gastrointestinal bleeding, sepsis and corticosteroid administration (and falls
in starvation, malnutrition, and muscle wasting and liver disease). Thus interpretation
of BUN values must rely more on the change over time rather than on absolute values
taking into account concomitant conditions such as those mentioned above as well as
other measures of renal failure.
Creatinine is the breakdown product of muscle and its level rises by 1 to 2 mgdl-1day-1
in acute renal failure. Its absolute value and change over time is a much more reliable
indicator of underlying renal function than the BUN levels. (Values higher than 2 mgdl 1day-1 may be seen in rhabdomyolysis)
Creatinine Clearance. Normal creatinine clearance is 120 mlmin1. A crude estimation
of the creatinine clearance may be obtained by the following formula.

CrCl (ml/min) =

(140-age) x weight
(kg)
72 x serum Cr (mg/dl)

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This equation is simply the ratio of the expected amount of muscle breakdown (taking
age and weight into account) to the breakdown product present in the serum multiplied
by a 'fudge factor' of 72. Women being smaller the resulting value is multiplied by 0.85
for females. However in acute renal failure with rapidly failing kidneys this formula may
overestimate creatinine clearance and a more accurate estimation is required. This may
be done by collecting urine over a period of time, usually 24 hours but in the ICU
situation even 2 hours has been shown to yield accurate results and may be more
practical ads well. The following equation is then used
Urine sodium and osmolality. When perfusion of the kidneys is reduced, sodium
reabsorption increases and excretion decreases and a urine sodium of less than 20
meqL-1 results (urine osmolality >400 mosmolkg-1). This may occur in hypovolemia due
to dehydration or haemorrhage, or from decreased forward flow as is seen in patients
with cardiac failure. Urinary sodium concentrations of less than 10 meqL -1 may be seen
in patients with hepatorenal syndrome or very severe hypo perfusion.

Urine [Cr] (mg/dl) x volume


(ml/min
Plasma [Cr] (mg/dl)
When there is an acute injury to the kidney, as in acute tubular necrosis, sodium
CrCl (ml/min) =

reabsorption is impaired and there is an increase in sodium excretion resulting in


urinary sodium levels of greater than 20 meqL-1 or even greater than 40 meqL-1 (urine
osmolality <400 mosmolkg-1).
Note that the above numbers are meaningless if diuretics have been given, Occasionally
a combination of factors like hypovolemia in addition to chronic renal failure may make
the interpretation of urinary sodium levels difficult. In these cases fractional excretion
of sodium may help determine whether the cause is renal or prerenal.
Fractional Excretion of Sodium

Fe Na = Urine [Na] / plasma [Na]


Urine [Cr] / plasma [Cr]

X 100

A fractional excretion of sodium of less than 1 % occurs in prerenal failure


(hypovolemia and cardiac failure) and that of more than 2% in renal failure (e.g. acute
tubular necrosis)
Abdominal ultrasound can help differentiate chronic causes (small kidneys
hypertension and chronic renal failure, normal or large kidneys diabetes and
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amyloidosis) and obstructive causes (large dilated pelvis and ureters). It can also
estimate renal perfusion using Doppler ultrasound.
Nuclear scans are useful in case of suspected embolus or vascular compromise.

Causes:
Investigations to help differentiate pre renal and renal causes of renal failure
Investigation
Urinary sodium (meqL-1)
Fractional excretion of sodium (%)
Urine osmolality (mosmL-1)
Urine creatinine / plasma creatinine
Urine/plasma osmolality

Pre renal
<20
<1
>400
>40
>1.5

Renal
>40
>2
250 - 300
<20
<1.1

Pre renal
Hypoperfusion due to any cause makes the kidney concentrate urine, decreases the
urine output and causes the BUN and creatinine to rise. The BUN level usually, but not
always, rises out of proportion to the creatinine level and a ratio of 20:1 is achieved.
Therefore prerenal failure is most often not a failure at all but a normal response on the
part of the kidney to an inadequate perfusion. Common causes include hypovolemia,
congestive cardiac failure and extreme vasodilation. Treating the precipitating cause
may rapidly and completely reverse the rise in BUN and creatinine levels. Genuine renal
injury may only occur if there is a superimposed insult like exposure to a nephrotoxic
agent. Serum Potassium may be elevated
Renal or intra-renal failure classically falls into 3 categories: Tubular failure
(including acute tubular necrosis), interstitial nephritis and glomerulonephritis and
vasculitis. However, it is probably more helpful to classify intrarenal failure according to
the causes of renal damage as enumerated in Table.

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causes of oliguria
Pre renal
Hypovolemia
Hypotension
Poor cardiac output
Pre existing renal damage
Renal vascular disease
Renal vasoconstriction
Sepsis

Renal
Hypoxia
From pre renal causes
Renal vein thrombosis
Nephrotoxins
Aminoglycosides
Amphotericin
Chemotherapeutic agents
NSAIDS
Contrast media (beware
in diabetes and multiple
myeloma)
Tissue injury
Haemoglobinuria
Myoglobinuria
Uric Acid (tumour lysis)
Inflammatory nephritides
Glomerulonephritis
Interstitial nephritis
Polyarteritis
Myeloma

2010

Post Renal
Bladder neck
obstruction
Blocked drainage
system
Pelvis surgery
Prostatic enlargement
Raised intra-abdominal
pressure
Renal or uretric
Calculi
Clots
Necrotic papillae

Post renal: This occurs when there is an obstruction to renal flow anywhere distal to
the pelvis. Obstruction is always the most likely diagnosis when there is anuria.
For this is to occur either ureters, or the urethra should be obstructed. It is commonly
seen in patients with retroperitoneal or pelvic pathology and abdominal ultrasound is a
good diagnostic tool. Do remember to check the patency of the Foleys catheter.

Perioperative considerations
It is important to understand the pathogenesis of renal failure. Though the kidneys
receive 25% of the cardiac output, they only get 10% of the total body oxygen uptake.
Renal auto regulation does take care of the GFR over a wide range of blood pressures
and glomerular ultra filtration is a balance between vasodilators and vasoconstrictors.
However, of the blood that the kidneys receive the glomeruli receive 90-95% while the
medulla only receives 5-10%. Oxygen extraction on the other hand is much greater in
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the medulla due to active water and salt reabsorption. Thus the medulla is more prone
to hypoxic damage.
The occurrence of perioperative renal failure depends upon the surgery, preoperative
and intraoperative haemodynamics and renal conditions (diabetic patients have a 10
fold greater risk of renal deterioration in the presence of hypovolemia). All intravenous
and volatile induction agents affect renal function by decreasing cardiac output and
blood pressure. Extradural block (or high spinal) up to the level of T4 reduces
sympathetic tone to the kidneys, resulting in a decrease in RBF and GFR. Mechanical
ventilation with positive pressure also decreases renal blood flow. Major surgery with
extensive third space losses can lead to hypovolemia and renal hypoperfusion.
Thus the progression of renal failure may take one of three paths as seen in Fig. 1,
Exclusion of pre renal and post renal causes make intrinsic renal failure the most likely
cause. This is often associated with an increased morbidity and mortality.

Fig. 1: Pathogenesis of acute renal failure

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Risk factors for developing renal failure. The successful prevention of perioperative ARF
depends on the identification of patients who are at risk for developing ARF as seen in
Table 3.
Table 3: Risk factors
Patient factors
Perioperative factors
Advanced age
Hemodynamic instability- hypotension
Major vascular surgery (AAA)
Hypovolemia(oliguria)
Atherosclerosis
Diuretic therapy
Coronary artery bypass and other
Surgical oedema
cardiac surgery
Preoperative starvation
Hypertension
Gastric aspiration/vomiting
Congestive cardiac failure
Peritonitis/ ileus/obstruction
Biliary surgery / jaundice
Diarrhoea/bowel preparation
Chronic renal disease
Prolonged tissue exposure
Cirrhosis liver
Blood loss
Diabetes mellitus
Hypoxia
Myeloma
Tissue damage and inflammation
Nephrotoxic drugs
Ischaemia and reperfusion
Pre-eclampsia /eclampsia Sepsis
Major burns
Polytrauma
Muscle breakdown
Pancreatitis
Massive blood transfusions and
Transfusion reactions

Physical examination and preparation for surgery


Check the adequacy of hydration, cardiac output and blood pressure. Also look at the
daily intake and output charts.
Use a large bore cannula for intravenous fluid resuscitation and administer oxygen.
Essential preliminary monitoring includes an electrocardiogram, noninvasive blood
pressure monitoring and pulse oximetry. Invasive arterial monitoring and central
venous pressure monitoring should be then considered. Echocardiography and
pulmonary artery wedge pressure monitoring are helpful, if available.
Shift to the ICU for monitoring and preoperative stabilization if required.
Prevention of further deterioration of renal function and maintenance of adequate renal
output (1-2 ml per kg - non oliguric renal failure).
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Preoperative rehydration is essential especially in those patients who are


significantly dehydrated e.g. those with large bowel obstruction or sepsis. Aim to
measure and maintain the CVP at 10-15 cm H2O. The response to a fluid bolus (250-500
ml of normal saline) over 10-15 minutes may help to differentiate between hypovolemia
per se and acute tubular necrosis, while more invasive monitoring is got ready (CVP,
Pulmonary artery catheterization and echocardiography may be required.) Some
authors suggest that we aim to maintain a mean arterial blood pressure of at least 50
mmHg, which is the lower limit for renal auto regulation. But most authors suggest
maintaining a higher blood pressure - a mean of >70 mmHg in normal patients and >85
mmHg in hypertensive patients using inotropes if necessary.
If intra abdominal pressure is raised more than 20 mmHg (normal 0-17 mmHg)
anuria can result from direct compression on the renal pelvis. This is seen in 30% of
emergency laparotomies and is very common after massive intra abdominal bleeding
such as leaking abdominal aortic aneurysms, intestinal distension, paralytic ileus and
ascitis. Improvement in renal function only occurs after decompression. The probable
mechanisms for a decrease in cardiac output and thus the GFR in these cases are as
follows: reduced venous return, compression of the renal vein with reflex renal artery
vasoconstriction, elevation of renal tubular pressure with a decrease in the filtration
gradient and an increase in rennin, aldosterone and ADH production.
Intra abdominal pressure may be measured via the bladder. Instil 50 ml saline into the
bladder via a Foley's catheter, clamp it off and measure the manometric pressure of the
fluid within the bladder via a needle inserted into the catheter lumen
Raised intra abdominal pressure may also give rise to a false high CVP leading to under
filling of the patient.
On first recognition of deteriorating renal function immediately eliminate or
appropriately reduce the dose of nephrotoxic drugs like gentamicin and vancomycin
(measure levels where possible) and change amphotericin to fluconazole if possible.
Nephrotoxins and nephrotoxic drugs, which could precipitate renal failure
Nephrotoxic drugs
Nephrotoxins
ACE inhibitors
Haemoglobin
Aminoglycosides
Myoglobin
Amphotericin-B
Bilirubin
Aspirin
Uric acid
Cisplatin
Cyclosporine
Assoc. with crystal production
Low molecular weight Dextrans
Acyclovir
Non steroidal antiinflammatory drugs
Methotrexate
Indinivir
Triamterene
If the blood pressure is normal and hypovolemia is not an issue drastically cut
down on the IV fluid therapy, thereby preventing a fluid overload.
The use of dopamine and diuretics remains controversial.
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Reduce the administration of acid (commonly administered in the form of 0.9%


sodium chloride solution which has a pH of 5), potassium, magnesium and
phosphates in maintenance IV and enteral feeds.

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Avoid NSAIDs in the post op period


Start enteral feeds as early as possible and maximize enteral nutrition, as there is now
evidence that outcomes are better in patients on enteral rather than parenteral
nutrition.
Other management issues Use of diuretics
The rationale for their use rests on the assumption that they decrease oxygen
consumption in the tubular cells by inhibiting trans cellular sodium transport and thus
prevents ischemic cell injury. In addition, loop diuretics may vasodilate cortical vessels
and improve oxygenation. Finally augmentation of tubular blood flow may reduce
intratubular obstruction and back leak of filtrate thus rapidly accelerating resolution of
ARF. However, in patients with established ARF several studies have shown no benefit
of loop diuretics.
It is believed that the outcome of non-oliguric renal failure is better than oliguric renal
failure. However, in a recent retrospective survey of critically ill patients with ARF
diuretic use was associated with an increased risk of death and non recovery of renal
function. The author suggested that the adverse outcome was due to either direct
deleterious effects of diuretics or indirect effects owing to a delay in the recognition of
the severity of ARF and institution of dialysis support. Other authors believe that
diuretics may also prove harmful as frusemide can cause interstitial nephritis and
hearing loss.
Therefore, diuretics should be used cautiously in critically ill patients and no patient
should be given frusemide unless they are adequately filled and the systemic arterial
pressure is adequate as an already damaged kidney may be profoundly injured by a
relatively mild decrease in perfusion pressure. Frusemide has been given in a bolus of
20 - 40mg. In patients with established renal insufficiency (raised serum creatinine) and
sustained oliguria this treatment should be withdrawn. However, in responders 250 mg
may be given as an infusion over an hour as infusions are more effective and less toxic
than bolus doses. Mannitol 0.5 to 1gkg-1 may also be given
Use or Dopamine
Low dose dopamine (1 to 3 gkg-1 per min) increases diuresis and natriuresis in
healthy experimental animals and humans. These effects are not seen uniformly in the
critically ill. However after extensively reviewing the data available the same authors
came to the conclusion that the use of dopamine in renoprotective doses should be
abandoned as there was no evidence supporting its effectiveness in preventing ARF and
it should not be used as a panacea for oliguria. In addition, dopamine can precipitate
serious cardiovascular and metabolic complications such as depression of the
respiratory drive, triggering of tachyarrhythmias, causing myocardial ischemia,
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accelerating intestinal ischemia, depression of anterior pituitary hormones and


decreased T-cell function.
Noradrenaline:
It improves mean arterial pressure and glomerular filtration. This is especially seen in
high output-low resistance septic shock. Urine flow reappears with restoration of
systemic haemodynamics and renal function improves without the use of low dose
dopamine or frusemide. This fact supports the hypothesis that renal ischaemia
observed during hyperdynamic septic shock is not worsened by nor adrenaline infusion
and even suggests that this drug may effectively optimize renal blood flow and renal
vascular resistance.
Adrenaline
In patients who fail to respond to fluid administration and other vasopressor adrenaline
can increase arterial pressure primarily by increasing cardiac index and stroke volume.
However, adrenaline has detrimental effects on splanchnic blood flow and causes
transient decreases in pHi and increases the PCO2.
Dobutamine may be used to improve cardiac output. However, it causes peripheral
vasodilatation and is usually used along with noradrenaline.
The use of Fenoldopam is also controversial
Calcium channel blockers.
During ischaemia, calcium channels open resulting in vasospasm. It is believed that
calcium channel blockers exert direct vascular effect with preservation of renal auto
regulation and enhanced recovery of RBF, GFR and natriuresis among other effects.
However it must be remembered that calcium channel blockers in high doses may
compromise the haemodynamic status in critically ill patients.
Specific pharmacological treatments6 have been used in cases of acute renal failure
associated with sepsis. Examples of these include Anti-TNF- therapy, inhibition of
platelet-activating factor, inhibition of nitric oxide synthase, endothelin antagonism,
inhibition of arachidonic acid metabolism, natriuretic peptides, inhibition of leukocyte
adhesion, inhibition of coagulation and growth factors -the details of whose use is
beyond the scope of this article
Emergency management of raised serum potassium
Treatment should be initiated if the serum potassium is > 6.5 mmol. L or ECG changes
are present. Intervention is important as cardiac compromise may occur.

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Table 5: Treatment of hyperkalemia


Onset of Duration
Side effects
effect
or action
Calcium IV Directly antagonizes Immediate Brief
Avoid if being
Gluconate
5- effects of potassium on
treated
with
10ml of 10% the heart
digitalis
solutionChloride 3-5 ml
of 10% solution
Insulin 15 U Shifts potassium into Prompt
4-6 hours Hyperglycaemia,
actrapid
in cells
hypoglycaemia
100ml
20%
dextrose over
30-60 mins
Beta
agonist Shifts
potassium Prompt
Short
Requires
salbutamol
5 Intracellularly
nebulizer
mg nebulized
Sodium
Shifts potassium into Prompt
Short
Possible serum
bicarbonate 50- cells
overload
100 mEq IV esp.
if acidotic
Ion
exchange Removes
potassium l-2hours
Sodium
resin Calcium from the body
overload
resonium 15G
PO/30G
PR
8hrly
Dialysis
or Removes
potassium Prompt
Requires
haemofiltration from the body
vascular access
Treatment

Mechanism of action

Other complications of renal failure include severe metabolic acidosis which is dealt
with by dialysis
Dialysis
Dialysis may be emergent or elective. The indications for dialysis are volume overload,
hyperkalemia, severe acidosis, and uremia (with a change in mentation, pericarditis,
pleuritis or bleeding). Emergency dialysis is rarely required in hospitalized patients. In
the ICU set up BUN and creatinine clearance is assessed daily and dialysis is usually
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started when the BUN level exceeds 100 mgdl-1 or the creatinine clearance is less thanl5
mlmin-1. (these figures are arbitrary and vary from centre to centre).
There are four contemporary modes of dialysis:
Peritoneal Dialysis (PD, not usually considered in the post operative general surgical
patient with abdominal pathology or respiratory compromise).
Haemodialysis (HD, difficult to do especially in the hypotensive post operative or septic
patient, requiring vasopressor support).
Continuous Arterio Venous Haemofiltration (CAVH, relies on an adequate pressure
head, has no external apparatus to control flow or provide warning and requires the
insertion of a wide bore catheter into an artery which may result in bleeding, an
aneurysm, thrombosis and clot formation).
It has been largely replaced by Continuous Veno Venous Haemofiltration CVVH, is a
slow method of solute and fluid removal, results in a largely haemodynamically stable
milieu and can remove a large quantity of cytokines which may reduce the incidence or
progression of multi-organ failure. The newer machines have improved safety features
such as an air detector and a pressure monitor. They do however require one on one
nursing and frequent, 4-6 hourly, and potassium assessment. They are capable of
removing up to 10 litres of fluid at one sitting and are often helpful in weaning from
mechanical ventilation and shortening ICU stay.

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Chapter 4 - TURP
INTRODUCTION
The prostate is a secretary organ wrapped around the urethra between the urinary
bladder and pelvic floor. The common conditions affecting the prostate are benign
prostatic hypertrophy (BPH) and cancer. BPH is an aging process, due to excessive
cellular growth of both glandular and stromal elements of gland, which leads to bladder
out flow obstruction and complications include recurrent infections, stone formation,
Haematuria and impairment of renal function. BPH in patients with prostate gland
(size) weighing less than 40 50 gm.

DEFINITION
TURP, it is the modified cystoscopic technique in which hypertrophied lateral and
median lobe of the prostate gland is excised with an electrical cautery. Bleeding being
controlled with coagulation current, Continuous irrigation is needed for distending the
bladder and to wash away blood and dissected prostatic tissue.

Anatomy and Pathophysiology of hypertrophic prostate


Nerve supply and pain conductive pathways:
Organ

Sympathetic Parasympathetic

Spinal levels of pain


conduction

Bladder

T11 L2

S2 - 4

T11 L2 (Dome)
S2 4 (neck)

Prostate

T11 L2

S2 - 4

T11 L2, S2 4

L1 - 2

S2 - 4

S2 4

Penis
Urethra

and

Parasympathetic fibers are the main motor supply to the bladder except trigone of
bladder. The afferents carrying, sensation of stretch and fullness of bladder are
parasympathetic, where as pain, touch and temperature sensations are carried by the
sympathetic nerves. Sympathetic fibers are predominantly alpha adrenergic in the
bladder base and the urethra, and beta adrenergic in the bladder dome and lateral wall.

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The prostate is a pear shaped gland consists of four closely integrated zones- the
anterior, peripheral, central and preprostatic zones. Each zone is made up of secretary,
smooth muscle, and fibrotic tissue. All zones are enclosed in one capsule. The gland is
rich in blood supply. Arteries and veins penetrate the prostatic capsule and branch
inside the gland. The venous sinuses adjacent to, the capsule are particularly large.
As early as the fourth decade of life, nodules begin to develop in the preprostatic zones,
forming one middle, two laterals, and one anterior and posterior lobe. The middle and
posterior lobes are most commonly associated with BPH and lateral lobe associated
with malignancy causing urinary tract obstruction.

Anesthetic problems:
Patients presenting for prostate surgery are elderly and have co-existing morbidities.
Cardiovascular and respiratory problems are common, and they are often on various
medications. Prostatic surgery carries a high risk of intraoperative bleeding, and so
ideally, all patients should have blood taken for cross matching. Anticoagulant drugs
such as aspirin and non-steroidal antiinflammatory drugs should be stopped 10 days
prior to surgery. Patients on warfarin must be considered on an individual basis in
conjunction with their physician. Those requiring continuous anticoagulation may need
to change to intravenous heparin, which can then be stopped for the duration of
surgery.
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Preoperative evaluation.
Preoperative evaluation is to know their general -condition, functional capabilities of
specific disease and drug intake, which enable to make judgment for the acceptance of
surgery, permits treatment of pre-existing disease, allow appropriate lab testing
to
be performed to access the expected perioperative and intraoperative problem and
their management.
Incidence of systemic medical disorders in TURP patients.
Disorder
Incidence %
Cardiac disease
67
Cardiovascular
50
Abnormal ECG
77
COPD
29
Diabetes mellitus
8
Routine history, including alcohol intake, smoking and drug history.
Physical examination: Pallor, cyanosis, clubbing, icterus, lymphadenopathy,
oedema, pulse rate respiratory rate and blood pressure.
Examination of all organ systems (cardiovascular system, Respiratory system
and CNS).
Airway assessment: Mallampatti grading, Dentition- loose tooth, denture. Loss of
buccal pad of fat- difficult in approach to induction or maintenance by mask.
Risk factors:
Obesity, Smoking, Malnutrition, Recent/Chronic infections, Alcoholism, DM, Malignancy
and Drugs
Investigations:
i. Urine for albumin, sugar and microscopy including culture and sensitivity.
ii. Haemogram, blood sugar.
iii. Renal function tests: blood urea and serum Creatinine
iv. ECG.
v. X-ray of Chest and kindneys.
vi. Serum electrolytes.
vii. USG of kidney, bladder and prostate.
viii.
Prostatic specific antigen (PSA).
ix. 2D Echo-abnormal ECG with relevant history of angina and IHD.
x. Pulmonary function tests.
xi. Liver function tests. In selected cases.
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Premedication: To alleviate Preoperative anxiety. If the patient is on antihypertensive


and anti anginal drugs, continue until the time of surgery to prevent rebound
hypertension and tachycardia
Sedative like benzodiazepines in reduced dose. Tab Diazepam 5 mg at HS.
H2 receptor antagonist like Ranitidine 150mg at HS on day before surgery and 3
hours before surgery to increase gastric pH and to reduce gastric volume.
Analgesics like opiates. Eg. Fentanyl 1to 2g/kg IV
Anticholinergics like Atropine 0.02 mg/kg iv, or Glycopyrrolate (0.01mg/kg/IV)
Intra-operative monitoring:
1.

Pulse oximetry

2.

ECG

3.

Noninvasive blood pressure monitoring

4.

Temperature.

5.

End tidal CO2+ analyzer if general anesthesia is administered.

6.

Central venous pressure line. (in case of RVF)

7.

Swan - ganz catheter: for pulmonary capillary wedge pressure, pulmonary


artery pressure.(in case of LVF)

Intravenous fluids: Normal saline is the appropriate choice for TURP, to decrease any
effects of dilutional hyponatremia. Fluids should be given cautiously, because these
patients are at risk of fluid overload. Remember impaired renal function and during
surgery, the irrigating fluid will be absorbed.
Blood loss is a complication of radical prostatectomy or for very large prostates.
Isovolemic haemodilution may be used to reduce the use of allogenic blood. Prostatic
tissue contains many,a receptors, and so a-adrenergic agonists (e.g. methoxamine) may
be used to decrease blood loss.

Thromboprophylaxis should be considered for those undergoing radical


prostatectomy and for any patients who may have difficulty in mobilizing
postoperatively with small doses of heparin 5000 units subcutaneously two or
three times daily in patients with moderate risk. (Advanced age, malignancy,
cardiac disease, varicose vein and obesity patients are more prone for DVT)

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Anesthesia
Regional anesthesia is used for prostatic surgery. A surgical block to the level of T10 is
required, and the caudal, subarachnoid (spinal) or epidural routes may be used. The
addition of short-acting opiates (e.g. Fentanyl) will reduce the dose of local anesthetic
needed to provide an adequate block. Epidural or combined spinal and epidural
anesthesia with an epidural catheter is the preferred regional method and can be used
postoperatively for pain relief.
Spinal anesthesia: Block should be up to Tl0

Provides adequate anesthesia for the patient and good relaxation of the pelvis
floor and the perineum.

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Caudal and sacral blockade:


Used effectively for prostate surgery.
Haemodynamic stability is main advantage.
Used effectively in high risk patients undergoing laser prostatectomy.
In laser prostatectomy bleeding is minimal (50 to 70ml), hence copious amount
of irrigation fluid is not needed, thereby bladder distension is avoided.

Table 1: approximate doses of local anesthetic for regional block


Anesthetic
Spinal
anesthesia

Epidural
anesthesia
Caudal
anesthesia

Dose without Dose with Dose


of
Fentanyl
Fentanyl
Fentanyl
0.5% hyperbaric (heavy) 2.5 ml
2.0 ml
20cg
bupivacaine
0.5% isobaric bupivacaine 3 ml
2.5 ml
20 cg
2% lidocaine
2 ml
1.5 ml
20 cg
5% hyperbaric (heavy) 1.5 ml
1 ml
20 cg
lidocaine
0.5% bupivacaine
20 ml
15 ml
100 cg
Local anesthetic

2% lidocaine (can add 20 ml


1:200 000 adrenaline)
0.5% bupivacaine
25 ml

15 ml

100 cg

20 ml

100 cg

2% lidocaine (can add 25 ml


1:200 000 adrenaline

20 ml

100 cg

General anesthesia:
Necessary in patients who require ventilatory or Haemodynamic support.
In patients with uncontrolled Hypertension and IHD
When there is contraindication to regional anesthesia.
Patient's refusal for regional anesthesia.
- Pre oxygenation with 100% of oxygen for at least 5 min.
- Injected slowly to avoid circulatory depression.
- Slow onset of anesthesia due to sluggish circulation.
- Delayed elimination due to retarded metabolism.
- Titrate, the dose required.
- Signs of effect should be observed rather than giving preselected standard dose.
Inducing agents: Common inducing agents are, Thiopentone, Midazolam, Propofol, and
Etomidate. Propofol may be close to an ideal induction agent because of its rapid
elimination.
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Relaxation: Relaxed with inj. Scoline 1.5 - 2mg/kg


Laryngoscopy and Endo tracheal intubation: Patients usually edentulous, it makes
easy Laryngoscopy, but rigidity of cervical spine and atrophy of mandible may cause
difficulty in intubation.
Maintenance: After induction, controlled ventilation with muscle relaxants. Adequate
anesthesia with N2O, O2 and analgesia without the risk of hypoxia. Protect lungs from
aspiration by cuffed ETT. Because, progressive decrease in reactivity of protective
airway reflexes in elderly.
Inhalation agents: Decrease in MAC value by 4% for each decade of age above 40
years. Eg. MAC of Halothane at 80 years is 0.64%.
Onset of action will be more rapid if cardiac output is depressed. Whereas it will be
delayed if there is significant ventilation - perfusion miss match abnormality.
Recovery from anesthesia with a volatile anesthesia may be prolonged, because of an
increased volume of distribution (increased body fat), decreased metabolism of
halothane by decreased hepatic function and decreased pulmonary gas exchange.
Myocardial depressant effects of volatile anesthesia are exaggerated in elderly patients.
The rapid elimination of Desflurane may, make it the inhalation anesthesia of choice for
elderly patients.
Muscle relaxants: Commonly used are,
Rocuronium (0.4- 0.9mg/kg iv for induction, 0.15mg/kg iv for maintenance),
Vecuronium (loading dose. 0.08 - 0.l mg/kg iv for induction, initially 0.04 0.06mg/kg for maintenance, later 0.01- 0.015mg/kg ),
Atracuronium (induction dose 0.4-0.5 mg/kg, maintenance dose 0.08-0.1mg/kg,)
Two fold prolongation in onset of NM block in elderly patients due to decrease cardiac
output and slow muscle blood flow.
Reversal: Neostigmine 0.5 mg/kg and Glycopyrrolate 0.01mg/kg.
Perioperative problems:

1.

Difficult in maintaining airway, due to


o Loss of buccal pad of fat
o Edentulous patients or loose tooth with poor supportive tissue
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Difficult intubation.
Cervical arthritis/ rheumatoid arthritis.
Difficult in visualization of glottic opening during direct Laryngoscopy.

3.

Deficiency in circulating blood volume, electrolyte imbalance and impaired


oxygen transport (hemorrhage, dehydration, ischemia, and acidosis) may impair
the patient reversibility.

4.

Care should be taken during Laryngoscopic examination to avoid over extension


of neck, because of increase chances of vertebro - basilar arterial insufficiency.

Advantages of Spinal anesthesia over General anesthesia


A change in mental status in a conscious patient provides early indication of fluid
over load and electrolyte disturbances.
Sympathetic blockade - increases venous capacitance and peripheral pooling of
blood thereby decreasing the excessive fluid absorption and circulatory
overload.
It reduces blood loss by reducing blood pressure during surgery.
Incidence of deep vein thrombosis is decreased.
Increased blood flow resulting from the sympathetic blockade may play a role in
reducing DVT formation.
Regional anesthesia decreases the hyper coagulable tendency in the
postoperative period and helps to maintain normal coagulation and platelet
function. It is believed to be due to modulation of the neuro -endocrine response
to tissue injury. There is evidence that hemostasis of the neuroendocrine system,
as well as the immune response Js better preserved after regional anesthesia, as
compared to general anesthesia.
It provides postoperative analgesia and thus reduces the incidence of
postoperative hypertension and tachycardia.
Postoperative lung infection is less with regional anesthesia.

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Transurethral Resection of the Prostate (TURP)


TURP is the primary treatment for symptomatic BPH. The resectoscope is introduced
through a modified cystoscope into the bladder and the tissue protruding into the
prostatic urethra is resected.
Prostatic capsule is suaully preserved. If the capsule is violated large, amounts of
irrigation solution are absorbed into circulation and the periprostatic and
retroperitioneal spaces.
Position:
Lithotomy position is commonly used for urological procedure. TURP is
usually performed in the lithotomy position with slight trendelenburg tilt.
When putting a patient in the lithotomy position, both legs should be moved together
gently due to delicate bone and degenerative joints to prevent fractures and strain on
the pelvic ligaments. The anterior superior iliac spins are on a level with the break in the
table. The patient will be in good lithotomy position when the both legs are supported
on the stirrups. Adequate padding of parts required to prevent peripheral nerve
injuries.

Physiological changes during the lithotomy position.


Decreased pulmonary compliances.
Cephaled shift of the diaphragm.
Decreased lung volume- RV, FRC, TV, VC.
Cardiac preload increases- Exacerbate congestive cardiac failure.
Irrigating fluid: Ideally an irrigation solution for TURP should be, Isotonic,
Nonconductive, nonhemolytic (hemolysis does not occur, if enter into circulation),
Neutral visual Density (Surgeons view not distorted), Non-toxic, Easy to sterilize, and
Inexpensive. Unfortunately, such a solution does not exist.
Distilled water: Is electrically inert and inexpensive and has excellent optical
properties, solution is extremely hypotonic.
Absorption of large amount of water leads to dilutional hyponatremia.
Haemolysis of Red Blood Cells, shock and renal failure.
CNS symptoms ranging from confusion to convulsion and coma.
The clinical signs of acute hemolysis are sudden prostration, chills, clammy skin, tight
chest, and bronchospasm. Massive hemolysis reduces the oxygen carrying capacity and
raises the potassium and free haemoglobin blood levels. Cause of death in these patients
is ventricular fibrillation caused by the hyperkalemia. The free Hemoglobin in the blood
tends to precipitate in renal tubuli and cause renal failure.
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Normal saline and ringer lactate:


It is well tolerated when absorbed intravascularly.
Electrolyte solutions highly ionized and facilitate the dispersion of high
frequency current from resectoscopy.

Non electrolyte solution:


Solution
Glycine 1.2%
Glycine 1.5%
Sorbitol 3.5%
Mannitol 5%
Glucose 2.5% (4%)
Urea 1%
Cytal (Sorbitol 2.7% + Mannitol 0.54%

Osmolality (mosm/g)
175
220
165
275
139
167
178

Of these, Cytal and Glycine are the two most commonly used solutions. To maintain the
transparency, these solutions are purposely prepared moderately hypotonic. (Normal
serum Osmolality is 280 to 300 mosm/Lit)
Non-electrolyte solution prevents dissipation of diathermy current during resection.
Complications are very much reduced but CNS symptoms, over hydration caused by
circulatory overload and decreased plasma osmolality remain as complication.
Properties of commonly used irrigating solutions for transurethral resection
procedures:
Osmolality
Solution
Advantages
Disadvantages
(MOSM/L)
Distilled water
0.0
Improved visibility
Hemolysis,
Hemoglobinemia,
Hemoglobinuria
Hyponatremia
Glycine (1.5%)
220
Less
likelihood
of Transient postoperative
Transurethral Resection visual
syndrome,
syndrome
Hyperammonemia
Hyperoxaluria
Sorbitol (3.3%)
165
Same as Glycine
Hyperglycemia, possible
Lactic acidosis Osmotic
diuresis
Mannitol (5%)
275
Isosmolar solution Not Osmotic
diuresis
metabolized
possibility of actute
intravascular
volume
expansion.

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During TURP, both intravascular and extra vascular absorption occurs.


Amount of fluid absorption depends upon the following factors:
The height of the container of irrigating solution above the surgical table
(prostate) determines the hydrostatic pressure, driving fluid into prostatic veins
and sinuses, usually 40 cm. When the height exceeds 60 cm, significant volume
absorption can occur. (<60cm)
Longer duration of surgery.(<60min)
Venous pressure in the prostate.
Number of venous sinuses opened during resection.
Large prostatic glands have rich venous networks that promote entry of
irrigation solution into peri -prostatic and retro-peritoneal space.(<60gm)
Excessively distended bladder during surgery facilitates absorption.
The hydrostatic pressure of the irrigating fluid should limit to 60 cm H2O
(<60cmH2O)
Intravascular absorption occurs when the pressure of the irrigating fluid exceeds
the open venous sinusoid pressure. Extra vascular absorption occurs when
perforation of the prostatic capsule occurs.
Normally absorbed at about 20 ml/min, average of 1-1.5 liters, but absorption of
upto 4-5 liters has been recorded. The average weight gain by the end of surgery
is 2 kg. in clinical practice, it is almost impossible to assess the volume of
absorption.
The volume of irrigating solution absorbed can be estimated by the following
equation.

Complications of TURP:
Anesthetic complications:
Hypotension
Bradycardia. And Cardiac dysrhythmias
Hypoxia
Impeded respiratory muscle excursion
Reflex of stomach contents
Lower compartment syndrome in prolonged
surgery
Deep vein thrombosis

Surgery related complications:


Circulatory overload
TURP Syndrome
Hypo Osmolality
Glycine and Ammonia toxicity
Hypothermia
Bladder perforation
Bleeding and coagulopathy
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Backache
Transient bacteremia and septicemia.
Peripheral nerve injury common personeal nerve, sciatic and femoral nerves.
Sciatic nerve by, exaggerated knee extension, thigh flexion and external hip
rotation.
Femoral nerve by, adduction and rotation of the thigh.
Common peroneal nerve by compression between fibula and stirrups.
Posterior tibial nerve by stirrups compression.
Saphenous nerve by compression between stirrups and medical malleolus.

Postoperative complications:
Bleeding and clots in catheter- urinary retention.
UTI - septicemia.
Thrombophlebitis.
Pain and neurapraxia in lower limb nerves.
Incontinence.
Retrograde ejaculation.
Erectile dysfunction.
Hypothermia.

TURP syndrome:
TURP syndrome is a general term used to describe a wide range of neurologic and
cardiopulmonary symptoms and signs caused by intravascular absorption of hypotonic,
bladder irrigating fluids during the procedure. In conscious or sedated patients, the
sudden onset of restlessness should raise the suspicion of TURP syndrome. TURP
syndrome may occur as quickly as 15 min after resection begins or upto 24 hours postoperatively. Incidence is 2%.
Etiology is metabolic encephalopathy due to intravascular absorption of irrigating
fluids.The signs and symptoms of the TURP syndrome are:
Cardiopulmonary
Hematologic and Renal
Central nerves system
Hypertension,
Hyperglycemia,
Nausea / Vomiting,
Reflex Bradycardia,
Hyperglycinemia,
Confusion,
Dysarrhythmias, CCF,
Hyperammonemia,
Restlessness,
Respiratory distress,
hyponatremia,
Blindness,
Pulmonary oedema,
Hypoosmolality,
Lethargy/Paralysis,
Hypoxemia, cyasnosis,
metabolic acidosis,
dilated/Non reactive Pupils,
Hypotension,
hemolysis/anemia,
Seizures
shock,
acute renal failure,
coma and Death.
death
Death
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Pathophysiology and clinical features of TURP syndrome:


Pathophysiology
Fluid over load

Clinical features
Hypertension, Bradycardia, arrhythmias, angina, pulmonary
oedema and hypoxemia, ventricular failure and hypotension.
Water intoxication or Confusion and restlessness, twitching or seizures, lethargy or
Hypoosmolality
coma; dilated or sluggish pupils, papilloedema, low voltage
ECG, hemolysis.
Hyponatremia
CNS changes as above reduced inotropy, widened QRS
complex, low voltage ECG, T wave inversion in ECG.
Glycine toxicity
Nausea and vomiting, headache, transient blindness, loss of
light and accommodation reflexes (blink reflex preserved),
myocardial depression, ECG changes.
Hemolysis
Anemia, acute renal failure, chills, clammy skin, chest
tightness and bronchospasm, hyperkalemia resulting in
malignant arrhythmias or bradyasystole
Coagulopathy
Severe bleeding, primary fibrinolysis, disseminated
intravascular coagulation.
Glycine 1.5%:
(HO2-CCH2-NH2). A non-essential amino acid, which functions as
inhibitory Neurotransmitter. Glycine has a distribution similar to that of gamma amino
butyric acid (GABA); the latter is an inhibitory neurotransmitter in the brain. It has been
suggested that Glycine is also major inhibitory transmitter acting in the spinal cord and
brain system.
Normal plasma Glycine is 13 -17 mg/L. Glycine half-life is 85 min.
Glycine absorption has been shown to cause an average of 17.5% decrease in cardiac
output. The administration of the amino acid arginine reverses the myocardial
depressing effect of Glycine.
Glycine toxicity in patients undergoing TURP is uncommon, probably because most of
the absorbed Glycine is retained in the periprostatic and retroperitoneal spaces. Where
access to circulation is limited.

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Glycine may cause encephalopathy and seizures via its ability to potentiate the effect of
N methyl D aspartate (NMDA), an excitatory neurotransmitter. Magnesium exerts a
negative control on the NMDA receptor and hypomagnesemia caused by dilution may
increase the susceptibility to seizures.
For this reason, a trial of magnesium therapy may be indicated in patients who develop
seizures during TURP.
The most common metabolites of Glycine are Ammonia, Glyoxylic acid and Oxylic acids.
In some patients, excessive absorption of Glycine during TURP leads to
Hyperammonemia and hyperoxalurea. Hyperoxalurea could compromise renal function
in patients with co-existing renal disease, as it is often present in elderly patients
undergoing TURP.
Hyperammonemia: The signs and symptoms usually appear within one hour after
surgery. Typically, the patient becomes nauseated, vomits and then become comatose.
Deterioration in cerebral function has been documented at ammonia concentration
exceeding150 mol/L. The Hyperammonemia tends to occur postoperatively, probably
because Glycine absorption from the periprostatic space continues after surgery.
Ammonia is metabolized primarily in the liver. Ammonia increased in liver dysfunction
and in Arginine deficiency.
Prophylactic administration of Arginine or Ornithine prevents hyper ammonia.
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Transient blindness: is one of the more alarming complications of TURP. It is seen


with absorption of Glycine during TURP. It is probably secondary to its inhibitory action
in retina and cerebral oedema. Loss of vision may occur any time from 30 min after the
start of surgery upto 6 hours after surgery completed. The patient complaints of blurred
vision and of seeing halos around objects. Examination of eyes reveals dilated and
unresponsive pupils, perception of light and blink reflex are preserved. Intraocular
pressure and optic discs remain normal. Postoperatively TURP related blindness
gradually resolves and the eyesight returns to normal within 8 to 48 hours after
surgery, when the blood Glycine returns below 50mg/L.
Hyponatremia: Sodium is a ubiquitous electrolyte that is essential for proper function
of excitatory cells, those of the heart and brain. Extreme reduction in, serum sodium
level alters brain, cardiac and renal function.
Hyponatremia results from intravascular absorption of large amount of electrolyte free
solutions. Symptoms are related to the degree of hyponatremia and the speed with
which this develops.

Signs and symptoms of Hyponatremia


Serum Sodium ECG Changes
CNS
(mEq/L)
120
Widened QRS
Restlessness and confusion
115
Widened QRs/elevated St segment
Nausea and / or semi coma
110
Ventricular tachycardia/fibrillation
Seizure and coma
During TURP, serum sodium level typically falls, 3 to 10 mEq/L. However, the
correlation between the severity of the hyponatremia and the amount of irrigation
solution absorbed during surgery is in-consistent. The fall in serum sodium level is
directly proportional to the rate at which the irrigation solution is absorbed, rather than
total amount absorbed.
Acute symptomatic hyponatremia requires prompt treatment. In such instances,
correction of plasma Na+to more than125mEq/L is usually sufficient to alleviate
symptoms.
Very rapid correction of hyponatremia has been associated with demyelinating lesion in
the Pons (central pontine rnyelinolysis), resulting in serious permanent neurological
sequelae.
Hypo Osmolality: Crucial physiological derangement leading to CNS dysfunction. Blood
brain barrier is impermeable to sodium, but permeable to water. Cerebral oedema
caused by acute Hypoosmolality can increase intracranial pressure, which results in
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Bradycardia and hypertension by the Cushing reflex. Apparently, the hypervolemia and
hyponatremia that often accompany TURP promote cerebral oedema and this in turn
raises intracranial pressure and provokes neurological symptoms.

Treatment of TURP syndrome:


Ensure oxygenation and circulatory support.
Terminate the surgery as soon as possible.
Restrict fluid and Administer loop diuretic eg. Furosemide.
Immediately obtain the fallowing laboratory tests: Hematocrit, serum electrolyte,
Creatinine and glucose concentration, serum Osmolality, arterial blood gas and
12 lead ECG.
Institute the invasive monitoring and provides supportive therapy to maintain
circulation, pulmonary function and to prevent renal failure.
Treat severe symptoms of hyponatremia (if serum Na+ < 120mEq/Lit) with
hypertonic saline (3% or 5% at the rate less than 100ml/hour (1-2 ml/kg/hr).
And discontinue when serum Na' >120mEq/Lit. If the serum sodium
concentration is less than 100mEq/L, severe CNS side effects of hyponatremia
and hypo-Osmolality are evident, or reduced inotropy results in cardiovascular
collapse.
Administer iv Midazolam in 1-3 mg or Diazepam 3-5mg, incremental doses to
treat twitching or seizures; a barbiturate 50 - 100 mg, may be added if seizure
persist, if still seizure persist phenytoin 10-20 mg/kg iv. (Not faster than
50mg/min).
A trial magnesium therapy may be indicated in patients who develop seizure.
And in whom Glycine containing irrigating solution was used.
Auscultate chest and obtain chest radiograph to detect pulmonary oedema.
Intubate and mechanically ventilate the patient at the earliest evidence of
pulmonary oedema.
Transfuse packed red blood cells as necessary.
If bleeding continues, investigate for DIC or primary fibrinolysis. DIC is treated
with crystalloids and blood products to achieve hemodynamic stability and
normal coagulation. Primary fibrinolysis responds well to E - Amino Caproic
Acid administered as an IV infusion of 3 - 5 gm in the first hour, followed by
continuous IV infusion at 1 gm /hour until the bleeding is controlled.

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Prevention of TURP syndrome:


Limit resection time to less than one hour.
Keep the prostatic capsule intact until the end of resection.
Maintain irrigation fluid height less than 60 cm above the prostate gland (30 cm
at the beginning of resection and 15 cm in the final stages of resection).
If intravesical pressure are maintained below 15 cm H2O absorption of fluid is
minimal.
When venous sinuses are opened during the procedure the level of irrigating
fluid should be lowered and Inj. Furosemide administered
Measure serum electrolyte levels during and after the resection.
Use regional anesthesia and very light or no sedation to allow early detection of
changes in the patients mental status.
Blood loss: Hypertrophied prostate is highly vascular and operative bleeding usually is
significant. The blood is washed in to the draining bucket and mixed with ample
quantities of irrigating fluid. Hence, estimation of blood loss is quite inaccurate and
extremely difficult.
5 to 20 ml/gm of prostate, resected. Or 2 to 4 ml/min of resection is an average blood
loss.
Blood loss increased in:
Prolonged operation time.
Number of sinuses opened during resection.
The size of the gland.
Prostatic inflammation from repeated or recent catheterization.
Increased vascularity.
Presence of infection.
Dilutional thrombocytopenia resulting from excessive absorption of irrigation
solution.
Increased systemic fibrinolysis caused by plasmin and urokinase during prostate
resection from prostatic tissue (release of plasminogen activators from the
prostate, which converts plasminogen into plasmin). During and immediately
after TURP, these agent cause local fibrinolysis and promote bleeding from the
raw surface of the prostate gland. The existence of a local Fibrinolytic
mechanism is supported by the observation that prophylactic administration of
anti Fibrinolytic agent reduces bleeding from prostatic bed.
Others believe that the fibrinolysis secondary to Disseminated Intravascular
Coagulation triggered by the systemic absorption of resected prostatic tissue.
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Which is rich in thromboplastin, characteristically, the platelet count and


fibrinogen blood level are abnormally low. At autopsy, multiple micro thrombi
are observed in various parts of the body. The high level of fibrin degradation
products found in the blood of these patients is caused by secondary fibrinolysis,
which commonly accompanies DIC.
BLADDER PERFORATION:
Perforation usually occurs during difficult resection and most often made by the cutting
loop or knife electrode, sometimes by the tip of the resectoscope, over distention of
bladder, unexpected movement by the patient or cough or difficult or traumatic
instrumentation. (Bleeding which obscures the surgeon's vision .
If bladder wall is chronically inflamed, previously irradiated or thin and stretched, is
more prone to perforation.
Signs and symptoms:
Bradycardia.
Hypotension.
Restlessness.
Diaphoresis, nausea, abdominal pain and hiccups.
Dyspnoea.
Shoulder pain.
Extra peritoneal perforation: - Pain in the, per-umbilical, inguinal and suprapubic
region. Additionally the urologist may notice the irregular return of irrigating fluid.
Intra peritoneal perforation:- Perforation through the wall of bladder.
- Large extra peritoneal perforation, extend into the peritoneum. Symptoms, related to
the diaphragmatic irritation. Pain referred to upper part of the abdomen, precordial
area, shoulder region or neck.
- Other signs and symptoms are pallor, sweating, nausea, vomiting, abdominal rigidity,
hypotension etc.
Management:
Stop surgery and achieve hemostasis.
Treat hypotension with IV crystalloids, vasopressors and ionotropes.
Obtain a Hematocrit. Start blood transfusion if brisk bleeding continues. Occult
blood loss into the intraperitoneal or retroperitoneal space may occur.
Perform a Cystourethrogram to locate the perforation.
For most perforations suprapubic cystotomy, an indwelling Foley's catheter and
occasionally ureteral stents are sufficient. In some instances, immediate
explorative laparotomy may be necessary to control bleeding and repair the
perforation.
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Prevention:
Avoid over distention.
Avoid rough instrumentation.
Avoid patient movement and
Avoid extensive prostate or bladder tumour resection at one sitting.
Transient bacteremia and septicemia:
The prostate harbors many bacteria, which can be a source of introperative and
post-operative bacteremia via prostatic venous sinuses.
This risk is further increased by the presence of an indwelling catheter.
About 30% of patients undergoing TURP have infected urine preoperatively, and
half of them sustain bacteremia post-operatively.
Hypothermia:
Irrigating fluids stored at room temperature are frequently used during TURP.
Heat loss due to irrigation and significant absorption of this fluid may result in a
decrease in patient's body temperature and cause shivering.
Several liters of irrigation solution pass through the bladder during TURP, which
can reduce body temperature at the rate of 1 degree per hour. About half of all
patients undergoing TURP become hypothermic shivering at the conclusion of
surgery.
Use of warmed irrigating solutions has been shown to be efficacious in reducing
this heat loss and resultant shivering. But warming of fluids might cause
increased bleeding due to vasodilatation. And operating whenever possible in a
warm environment.
Use of systemic and intrathecal opioids decreases post-operative shivering from
cold.
Conclusion:
TURP remains the gold standard for the treatment of men with BPH. Improvement in
surgical technique, perioperative monitoring of fluids and electrolytes, anesthetic care
and the availability of video endoscopy have diminished intra operative and post
operative morbidity and mortality. The incidence of complication of transurethral
surgery is inversely proportional to the experience of surgeon.
PREOPERATIVE EVALUATION FOR ELECTIVE SURGERIES
Introduction: The anesthetic
preoperative evaluation includes the acquisition of
medical information and assessment of the patient's physiologic status but also offers
brief opportunity to help to alleviate the patient and family's anxiety or fear about
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impending anesthesia and surgery. The anesthetic preoperative evaluation should be


done by anesthesiologist earlier in days, not on the day of surgery or not before surgery.
Objectives: The ultimate goals of preoperative and preprocedure medical assessment
of patients who are to undergo anesthesia care are to reduce the morbidity of surgery,
to increase the quality but decrease the cost of perioperative care and to return the
patient to desirable functioning as quickly as possible.
Traditionally these goals have been facilitated by a preoperative meeting between the
patient and the anesthesiologist. This meeting has six specific purposes.
1. To obtain appropriate information about the patient's medical history and
physical and mental conditions in order to determine which tests and
consultations are needed.
2. Guided by patient choices and the risk factors uncoverccl by the medical history
to choose the care plans to be Followed.
3. To obtain informed consent
4. To educate the patient about anesthesia, perioperative care, and pain treatments
in the hope of reducing fear or anxiety and facilitating recovery. Because fear
can influence like this.
Stage of fear
Increased by
Decreased by
Apprehension
Nontherapuetic approach
Therapeutic approach

Irritability of nervous
Excitement stimulants
Rest and adequate sleep in
system
hospital sedatives

Resistance to anesthesia
Chronic alcoholism smoking Premedication
1. To make perioperative care more efficient and less expensive.
2. To utilize the operative experience to motivate the patient to more optimal
health and thereby improve perioperative and / or long term out come.
Risk assessment: The overall risk for surgical complications depends on individual
factors and the type of surgical procedure. Eg: Advanced age, co-existing diseases like
respiratory, cardiac, malnutrition and diabetes mellitus. With respect to type of surgery,
urgent and emergency procedures constitute higher risk situations than elective
procedure.
High risk referred to here is primarily surgical procedure derived risk of
cardiac/pulmonary complications. Cardiovascular complications are more common in
adults, and pulmonary complications are more common in children.
American society of anesthesiologists physical status classification:
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Status
ASA class 1. Normal healthy patient

Disease level
No organic, physiological, biochemical or
psychiatric disturbance. Or, Normal.
ASA class 2. No. functional limitation
Mild to moderate systemic disturbance
that may be related to the reason for
surgery, Eg. Mild heart disease, DM, mild
HTN< anesmia, old age, obesity and mild
chronic bronchitis.
ASA Class 3. Some functional limitation
Severe systemic disturbances that may or
may not be related to the reason for
surgery. Eg. Angina, severe DM, Cardiac
failure.
ASA Class 4. Functionally incapacitated
Severe systemic disturbance that is life
threatening with or without surgery. Eg.
Marked cardiac insufficiency, persistent
angina, and severe respiratory, renal or
hepatic insufficiency.
ASA class 5. Patient who is not expected to Moribund patient who has little chance of
survive with or without surgery in 24 hrs
survival but is submitted to surgery as a
last resort (resuscitative effort)
ASA class 6. Brain dead patient
Dead patient brought for organ removal
for transplant purpose.
Emergency operation (E)
Any patient in whom an emergency
operation required.
Medical problems discovered on preanesthetic evaluation that could prompt a change in
patient management.
History:
1. History of present illness and its treatments. Including indications for surgery.
And history of recent infections like URTI or Pneumonia.
2. When the patient last visited with her/his primary care physician.
3. Exercise tolerance, including activity level. Most important is to determine the
patients cardiovascular reserve. To know this, ask about maximum amount, the
patient can walk or the greatest number of floors patient can climb without the
need to stop ability to do 4 metabolic equivalents (MET) of exercise.

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Estimated energy requirements for various activities/ To assess LV Function


Clinically
Metabolic equivalents
Activity
(METs)
1. 1 MET
Can take care of himself, can eat, dress. and use the toilet, can
walk indoors around the house, can walk a block or two on
level ground at 2 to 3 mph (3.2 to 4.8 km/h)
2 4 MET
- Can climb a flight of stairs or walk up a hill.
- can walk on level ground at 4 mph (6.4 km/h)
- Can run a short distance.
- Can do heavy work around the house such as scrubbing floor
or moving heavy furniture.
- Can participate in moderate recreational activities such as
golfing, bowling, dancing, double tennis, or throwing a baseball
or foot ball.
III. 10 MET
Can participate in strenuous sports such as swimming, single
tennis, foot ball, basketball or skiing.
The equivalent of walking 5 city block or climbing two flights of stairs at a reasonable
rate without having) to stop correlates in multiple studies with better preioperative
outcome.
History of prior illness like, chest pain, palpitation, cough with expectoration,
breathlessness, PND, orthopnea, asthma or COPD
Also history should he asked to the patient to identify any diseases of Hepatic
and gastrointestinal disease. Bleeding problems, renal disease, endocrine
disturbances, neurological disease (CNS + PNS), and musculoskeletal disease,
psychiatric and dermatologic disease. And history of surgery.
Family history and Social history including alcohol and tobacco use and
cessation.
Medications and causes for their use and allergies. Medications including over
the counter and herbal products to define a preoperative medication regimen,
anticipate potential drug interactions, and provide clues to underlying disease.
The ability to review previous anesthetic records is helpful in detecting the
presence of a difficult airway or to confirm previous uneventful intubations, a
history of malignant hyperthermia and the individual's response to surgical
stress and specific anesthetics.
The anesthesiologist should determine when the patient last taken food as well
as note the sites of preexisting intravenous cannulae, and invasive monitors.

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Physical examination:
GPE: Examination of eyes for abnormal movement and skin for signs of jaundice,
cyanosis, nutritional abnormalities like anaemia (pallor) and dehydration. Fingers are
checked for clubbing. Look for the built of patient, weight and height.

Figure 5-22. A: Mallampati classification of oral opening. B. Grading of the laryngeal


view. A difficult orotracheal intubation (Grade III or IV) may be predicted by the
inability to visualize certain pharyngeal structures (Class III or IV) during the
preoperative examination of a seated patient (Reproduced, with permission, from
Mallampati SR: clinical signs to predict difficult tracheal intubation (hypothesis) can
anaesth Soc J 1983; 30:316)
Examination of leas for bruising, edema, mobility, sensation and adequacy of hair
growth (or skin texture) as signs of circulatory competence.
Vitals:

Pulse including Carotid and jugular pulses. R.R. and Temp.


Arterial - BP in both arms.

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Airway : A Basic concern of the anesthesiologist is always the patients airway.


The ability to flex the base of the neck and extend the head.
Assessment of ability to open mouth.
Examination of oral cavity including dentition, and for presence of high arched
and narrow palate.
The Mallampatti classification has become the standard for assessing the
relationship of the tongue size relative to the oral cavity.
Airway Classification system:
Class
Direct visualization patient seated
Laryngoscopic view
0
Tip of epiglottis is seen
I
Soft palate, fauces, uvula, pillars seen plus Entire glottic seen
posterior Pharyngeal wall
II
Soft palate, fauces, uvula seen,
Posterior commissure seen
III
Soft palate, base of uvula seen
Tip of epiglottis
IV
Only hard palate seen
No glottal structure seen
Other indicators of difficult intubation include a thyromental distance less than
6.5 cm and a sternomental distance < 12.5 cm.
Mentohyoid distance :
Grade 1:6 cm or more
Grade 2: 2-4 cm. Laryngoscopy is difficult.
Grade 3: < 4 cm
None of the published clinical tests provide either 1009' sensitivity or 100% specificity.
The combination of Nlallampatti score with either the thyromental or the sternomentai
distance provides positive predictive value upto 100%.
Cardiovascular (CVS). Chest for heart sounds, heaves, thrusts, pulsations, murr1nu-s,
gallops, (3rd and 4th heart sounds suggestive of congestive heart failure).
Lung (R S). Chest auscultation of' the bases of' the lung for subtle rales, for ronchi,
wheezes sounds and other sounds indicative of lung disease.
Plus those aspects specific to the patient's condition or planned procedure, such as a
sensory nerve examination if a regional block is planned.
In traumatized patients, rheumatoid arthritis, or Down syndrome patients,
assessment of cervical spine is critical.
A functional assessment of cardiopulmonary system may reveal key features that
warrant preoperative intervention or further evaluation.

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The 2002 ASA preoperative testing advisory:


No test, but rather a physician review, stating that "this patient is in optimal shape for
daily living" is usual for patients undergoing minimally invasive surgery.
Types of surgical procedures for which anesthesia may be administered
Type
General definition
Specific Examples
I or Low risk
Minimally invasive procedures that
Cataract extraction, diagnostic
have little potential to disrupt
arthroscopy, postpartum
normal physiology and are
interval tubal ligation, breast
associated with only rare
surgery, superficial surgery,
periprocedure morbidity, related to endscopy.
the anesthetic. These procedures
rarely require blood administration,
invasive monitoring and / or
postoperative management in a
critical care setting.
II or Intermediate
Moderately invasive procedure that Carotid endarterectomy, head
risk
have modest or intermediate
and neck surgery, transurethral
potential to disrupt normal
resection of the prostate and
physiology. These may require
abdominal and thoracic
blood administration, invasive
surgery, laparoscopic
monitoring, or postoperative
cholecystectomy, orthopaedic
management in a critical care
surgery.
setting.
III or High risk
Highly invasive procedure that
Emergency surgery, anticipated
typically produce significant
increased blood loss, total hip
disruption of normal physiology.
replacement, open aortic valve
These procedures commonly require replacement and posterior
blood administration, invasive
fossa craniotomy for aneurysm.
monitoring, or postoperative
Peripheral vascular surgery.
management in a critical care
setting.

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History

Concern / area to evaluate

Airway perceived, as
difficult to intubate
Asthma

Head, eyes, ears, nose, throat,


airway: Prior anesthesia outcomes
Pulmonary disease

DM, insulin
dependent

Endocrine, metabolic, diabetes

Drug abuse

Social history

Gastro esophageal
reflex or hiatus
hernia

Gastrointestinal disease hiatus


hernia

Heart disease: valve


disease, risk of sub
actute bacterial
endocarditis
Malignant
hyperthermia
history, family
history, or suspected
potential history
Monoaminooxidase
inhibitors

Antibiotic prophylaxis

Pacemaker or

Cardiovascular disease

Prior anesthetic or surgery history

CNS / Physchiatric / medication

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Anesthesia plans that may


require extra time
Obtain fibreoptic equipment,
obtain skilled help
Optimize therapy, use
bronchodilators: Possibly
extubate during deep
anesthesia
Discuss insulin management
with patient and primary care
doctor, monitor blood glucose
intra-operatively, and
determine presence of
autonomic neuropathy and
plan management
appropriately, such as
administration of
metaclopamides and PACU or
ICU stay.
Consider HIV testing: Prescribe
medications to avoid
withdrawal symptoms in
preoperative period
Administer H2 antagonists or
oral antacids and use rapid
sequence induction of
anesthesia or use awake
intubation techniques and
obtain appropriate equipment.
Arrange for antibiotic
administration 1 hour prior to
surgery.
Obtain clean anesthesia
machine, use appropriate
technique and precaution.
Have agents to treat malignant
hyperthermia available.
Discontinue therapy
preoperatively if patient is not
suicidal, plan for pain therapy
perioperatively
Evaluate cause for pace maker
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automatic
implantable cardiac
defibrillator

electrocardiogram

Peripheral motor
neuropathy
Pregnancy or
uncertain pregnancy
status

Cns disease ; Neurological deficit

Pulmonary
tuberculosis

Pulmonary disease, tuberculosis

Renal insufficiency

Genitourinary disease

Genitourinary / pregnancy

2010

implantation obtain
repolarizing equipment or
magnet. Use lectrocautery with
altered position. Use bipolar
electrocautery
Avoid depolarizing muscle
relaxants.
Monitor foetal heart rate, use
roal antacids, adjust induction
of anesthesia, determine status
of pregnancy.
Use disposable breathing circuit
or clean equipment. Ensure
adequate treatment of patient
prior to surgery.
Monitor fluid status
intraoperatively

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Chapter 5 - GUIDELINES FOR PREOPERATIVE


INVESTIGATIONS AND LABORATORY TEST ABNORMALITIES.
Complete blood count
a)

Age less than 6 months and more than 60 yrs.

b)

History or physical exam suggesting anaemia or bleeding tendency.

c)

Known cardiac, pulmonary or renal disease. malignancy.

d)

As a base line when massive blood loss is anticipated

e)

Suspicion of infection.
Hemoglobin of 9g/dl is adequate for patients over 3 months of age but should
exceed 10g/dl for younger patients.
Asymptomatic anaemia prior to non-blood loss surgery should not be treated
preoperatively. Because patients survive anesthesia and type-A surgery when
hemoglobin levels are about 8g/dl.
Surgically acceptable values: Hematocrit 29% to 57% for men,
27% to 54% for women
White blood cell count - 2400 to 16000/mm3 for both men and women.
Blood grouping and cross matching would be warranted for all patients
undergoing procedure involving possible blood loss of more than 2units/70 kg
body weight.(type B or / and type C surgical procedures).

Coagulation profile. (INR and APTT)


a) Patient on warfarin / heparin'
b) Hepatic disease.
c) Bleeding tendency.
Partial thromboplastin time (P.T.T) and prothrombin time (P.T) are useful tests
for screening patients, who have a history of bleeding. But insignificant for
asymptomatic patients. i.e., pre operative clotting function testing for
asymptomatic patients who have no risk factors for coagulopathy is incapable of
predicting perioperative bleeding.
Patients taking aspirin at a dose of 3 to 10 mg/kg of body weight daily does not
seem to pose a risk of bleeding.
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A patient taking aspirin 2g/70kg of body weight daily, or large closes of aspirin
i.e., more than six 325mg tablets a day should be evaluated. and also those
patients who is consuming aspirin continuously, sufficiently early to ensure that
there is no appreciable level of acetylsalicylic acid in the blood for 24 hours
before surgery. Because this is the period in which acetyl salicylic acid would
have to be absent for the generation of the approximately 50,000 new platelets
/mm3 needed for normal platelet aggregation. Chart 1

Blood glucose level


a) Diabetes patient
b) Patient on corticosteroids or TPN.
c) Positive urine sugar.
d) Age > 40 years

Screening for diabetes may soon shift from random blood glucose levels to
determinations of the concentration of glycosylated hemoglobin (HbA 1c).

e. Renal function tests


a)
b)
c)
d)
e)
f)
g)
h)
i)
j)

Hypertension
Cardiac disease
Diabetes mellitus
Patient on drugs that can affect electrolyte balance eg: diuretics, ACE inhibitors
or drugs whose level may be affected by renal functioneg. Digoxin.
As a baseline for major surgery eg. Aortic aneurysm, Oesophagectomy,
hepatectomy.
Age >60 yrs.
Positive urine albumin
Patient on TPN
Patient having bowel preparation for surgery.
Recent vomiting and diarrhoea.

Liver function tests


a)
b)
c)
d)

Known hepatic disease.


Chronic alcoholic
Hepatitis carrier
Malnourished patient and paticrnt on TPN
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Abnormal hepatic or renal function might change the choice and does of
anesthetic or adjunct drugs.
Albumin level was an important predictor of perioperative morbidity and
mortality in every surgical speciality. Changes in this level after enteral nutrition
have been important predictors of perioperative outcome in malnourished or
otherwise very sick patients. It may therefore time to add this laboratory test for
patients undergoing surgical class C procedure and for patients who have
physiologic age of over 85 are undergoing surgical class B procedure.
Antibody test for hepatitis A and C are useful after infection has occurred, which
reduces the medico legal risks posed by post anesthetic jaundice.

ECG.
a)
b)
c)
d)

Age > 50 yrs (male). > 60 yrs (female)


Cardiac disease eg. Rheumatic carditis
Patients with cardiac risk factors eg: hypertension, vascular disease, diabetes.
Not required if ECG has done in past 3 months. And conditions stable. The
abnormalities on the ECG that have the potential to alter management of
anesthesia are as follows:
Atrial flutter; or fibrillation, first. second and third degree atrioventricular block,
changes in ST segment suggesting myocardial ischaemia or recent pulmonary
einholism, premature ventricular and atrial contractions (greater than 3 per
minute) left or right ventricular hypertrophy. Short P.IZ interval. wolff-park]
nson-white syndrome, myocardial infarction, prolonged QT segment and tall
peaked T waves.
ECG's are indicated for asymptorrmatic patients of average risk, underaoir10
type B or C procedures who are over 40 (men) or 50 (women) years of age.
We know that conditions such as normal blood pressure, regular vigorous
exercise, the absence of exposure to cigarette smoke and control of stress can all
decrease physiologic age by more than 20 years. Therefore we would delay
routine ordering of ECG's for 10 calendar years for any male or female patient for
whom these advantageous conditions apply.

ECG criteria for myocardiai ischaemia:


At least 1 min of J point depression with down sloping or horizontal ST segment,
slowly up sloping STsegment depression. defined as 2mm of ST depression
measured 80 milliseconds from the J point and ST segment elevation. ECG flow
chart3
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ECG patterns indicative of myocardial ischaemia

Figure 27-11 Electrocardiographic (ECG) Criteria for myocardial ischemia consist of 1


mm or more of J-point depression with downsloping or horizontal ST segments; slowly
upsloping St-segment depression, defined as 2 mm of St depression measured 80
milliseconds from the J point; and St-segment elevation. Whereas ST-segment
depression indicates nontransmural ischemia, ST-segment elevation often connotes
more severe degrees of ischemia reflecting transmural injury. The structure of the STsegment slope is predictive of the severity of coronary disease shown angiographically,
with downsloping St depression indicating severe two-and three-vessel coronary artery
disease more often than either horizontal or slowly upsloping St depression does and
ST-segment elevation indicating high-grade, usually aroximal arterial obstruction in
patients without previous myocardial infarction. (Reproduced with permission from
Goldschlager N: Use of the treadmill test in the diagnosis of coronary artery disease in
patients with chest pain. Ann intern Med 97:383, 1982).

Chest X-Ray:
a)

Those with cardiac or irreversible ln11monary disease (not Asthmatics and who
have, not had a chest X-ray in the past 6 months.
b)
Close exposure to TB (family members) in the past year.
Certainly it may be important to know about the existence of the following conditions
before proceeding to anesthesia and surgery. Tracheal deviation or compression,
mediastinal masses. Pulmonary nodules, a solitary lung mass, aortic aneurysm.
Pulmonary oedema, pneumonia, atelectasis, new fractures of the vertebrae, ribs, and
clavicles, dextrocardia, and cardiomegaly. However, the chest radiograph would not
detect the degree of chronic lung disease requiring a change in anesthetic technique any
better than would the history or physical examination.

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Chest radiographs are not warranted for any asymptomtic patients who are less than
75 years of age and free of risk factors. In fact this conclusion may apply to those older
than 75 yrs of age as well.

Pulmonary function tests:


Indications for pre-operative pulmonary evaluation:
History
Physical examination
Smoking history
Cyanosis
Age > 60 yrs
Tachypnea
pulmonary symptoms like persistent cough, Upper airway anomaly
wheezing
Chest wall and spinal deformities
Known lung disease like COPD
Passive expiratory wheezing
Morbid obesity with body Wt. > 20%
Forced expiration time > 3 sec
Thoracic operation scheduled
Generalized weakness
Requirement for single lung anesthesia or
Severe neuromuscular disease
lung resection
Decreased mental status
Upper abdominal operation
Pulmonary function testing continues to play a role in traditional preoperative
evaluation of patients undergoing major surgery. It is simple and risk free

Bedside tests of functions;


1)

Breath holding test

2)

Valsalva test

3)

Respiratory force test or match blowing test

4)

Cough test

5)

Expiratory time heard over trachea

6)

Pulse oximetry

The cornerstone of all pulmonary function testing is clinical spirometry.

1)

Vital capacity

2)

Time expired spirogram


Forced vital capacity (FVC)
Forced Expiratory Volume in 1 second (FEV1)

3)

Maximum breathing capacity or Maximum voluntary ventilation. (MVV)

or
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sniders test
4)

Forced Expiratory flow (FEF):

5)

Flow volume Loops

6)

Carbon monoxide diffusing capacity

Other diagnostic pulmonary function tests:


a.
Measurement of pulmonary arterial and wedge pressure at rest and during
exercise.
b.
Detection of regional disease including presence, location, and extent can be
accomplished by presently available tests. These can show the distribution of
blood to pulmonary capillaries and the matching of gas and blood to an alveolus.
These are
a)

Single breath oxygen test

b)

Single breath xenon test

c)

Screening bronchograph tests

d)

Intravenous tagged albumin / technetium perfusion test.

Pulmonary function tests in restrictive and obstructive lung disease:


Value
Restrictive Disease
Obstructive disease
Definition
Proportional decreases in all Small airway obstruction
lung volumes
expiratory flow

Normal or slightly
FVC

Normal or slightly
FEV1

FEV1/ FVC
Normal

FEF25-75%
Normal

Normal or if gas trapping


FRC

Normal or if gas trapping


TLC

to

Preoperative measures to improve lung function:


Ideally a comprehensive rehabilitation regimen of exercise, nutrition, education, and
most importantly physiotherapy can improve the functional capacity of patients with
significant lung disease.
The treatment regimen is aimed largely at four modalities 1) smoking cessation, 2)
mobilization of secretions 3) therapy for bronchospasm and 4) improved motivation
and stamina.

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The removal of secretion is an important component of preoperative preparation.


Antibiotic therapy, adequate hydration systematically, heating of aerosol therapy
agents. The use of mucolytic agents and expectorants are beneficial.

Arterial blood gas.


a)

Metabolic decompensation eg. DKA

b)

Morbid obesity

c)

Cyanotic congenital heart disease

Cervical spine
a)

Downs syndrome

b)

Rheumatoid arthritis flexion and extension views

c)

Trauma patient

Tests for HIV, pregnancy, Malignant hyperthermia, magnesium deficiency:


The history is still the best tool for limit, testinL7 to only at-risk population e.g., for
pregnancy testing only female patients who believe they may be pregnant.
For malignant hyperthermia syndrome, polymerase chain amplification might be
used in future to screen, in high risk patients
At risk individuals are - Children with a history of myopathies who are
undergoing surgery for strabismus, patients having a family history of problems
with anesthesia, and patients with a history of abnormal (red) appearance,
thermoregulatien and reactions to minor stresses..
Magnesium (Mg) deficiency represents another special situations. Putatively it is
much more common than other iron deficiencies, and Mg treatment has been
advocated as extremely beneficial.
The total serum Mg constitutes less than 1% of total body Mg]
Hypomagnesaemia < 1.2 mEq / lit or < 0.72 mmol / lit.
Some investigators believed that serum magnesium should be measured
routinely in hospitalized patients because of the high prevalence of
hypomagnesaemia. Coupled with difficulty of diagnosing hypomagnesaernia on
clinical grounds alone. If one is going to use Mg empirically, one probably should
have a measure of renal function and should monitor serum Mg levels (or
reflexes in the awake patients).

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Recommended test guidelines for asymptomatic patients:


Age
< 6 Months

Minor surgery
Hb or HCT
(hematocrit)
HB or HCT
(hematocrit)
Hb or HCT

Major surgery
CBC

Hb, or HCt ECG,


Glucose

CBC, Bun Glucose, ECG

65 to 75

HCT, ECG, BUN,


Glucose

CBC, BUN, Chest X-ray


ECG, electrolytes,
Glucose

75 yrs and above

HCT, BUN, glucose,


ECG, chest X-ray

CBC, BUN, Glucose,


ECG, Chest X-ray
Electrolytes.

6 Months 6 yrs
6 yrs to 40 yrs
40 to 65 yrs

Adult female of
childbearing age
group pregnancy
test

CBC
CBC

Medico legal liability:


Extra-testing- not warranted by findings on a medical history does not provide medico
legal protection against liability. Moreover the failure to pursue an abnormality
appropriately, poses a greater risk of medico legal liability than does failure to detect
that abnormality. In this way extra testing increases the medico legal risks to physicians.

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Consequences of using nonselective batteries of perioperative tests:


Consequences
1)
Direct risks to patient
False-positive results (i.e., an erroneous Abnormality
on a radiograph or ECG) may initiate follow up
activities that are harmful to the patient. False negative
results encourage the overlooking of true problems
or instruct a false sense of security.
2)
Indirect risks to patient Diverts physicians attention to nonvital issues
3)
Cost of society
Reduces resources available to care for others.
4)
Cost of physicians
Failure to pursue abnormalities increases, medico legal
risks.

IMPLEMENTING ACCURACY AND EFFECIENCY IN PREOPERATIVE


EVALUATION
The ability of preoperative evaluation of even healthy patients (ASA, Physical status I
and 11) to detect important symptoms and medical history makes its benefit greater
than its risk, Furthermore preoperative evaluation done in advance is ultimately cost
efficient as it minimized expensive delays on the clay of surgery. There are at least three
methods for organizing preoperative evaluation efficiently.
1)
The surgeon, internist, family practioner / physician or / and anesthesiologist,
who seen the patient before a scheduled procedure can obtain the history and
perform the physical examination.
2)
A clinic can be set up in an out patient facility so that these two tasks are
performed early enough to ensure that laboratory tests or consultations can be
obtained without delaying schedules.
Anesthesia preoperative evaluation clinic (APEC) or preoperative and preprocedure
assessment clinic (PPAC)
The preoperative evaluation is often the first encounter a patient has with anesthesia
and health system or hospital based services. Examination facilities, personalized
services and organizational efficiency during the evaluation often influence a patient
perception of the quality of health care at an institution.
The establishment of a centralized anesthesia pre operative evaluation clinic or PPAC,
can be a positive investment for the anesthesia group and the hospital as it becomes a
recognized centre for decreasing perioperative costs, improving the efficiency of clinical
services, implementing clinical pathways that educate and increase market share and
increasing patient and surgeon satisfaction with preoperative and periprocedure
services.

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The PPAC is an integrated partnership having visible alliances with the departments of
anesthesia, nursing, surgery, (OBG) obsterics and gynaecology and always with the
hospital or health system administration.
The anesthesia preoperative evaluation clinic is a constructive partnership working
towards the achievement of common goals. The sharing of resources and budgetary
costs is apportioned.
Goals of the anesthesia preoperative evaluation
clinic:
Decreased cost
Efficient quality service
Enhanced clinical productivity
Timely access to clinic
Enhanced patient education
Patient and surgeon satisfaction
Reduced length of stay in the hospital
Operational goals for a preoperative and
preprocedure assessment clinic (PPAC)
1. To improve patients (clients) perception
of the preoperative evaluation experience by
increasing personalized patient care , comfort and convenience.
2. To provide centralized site for preoperative evaluation.
3. To institute an anesthesia scheduling system for timely patient access and flow.
4. To ensure the presence of an anesthesiologist on site when patients are present.
5. To appoint medical director of the PPAC coordinate all activities.
6. To ensure the availability of medical records and surgical notes at the time of
preoperative evaluation.
7. To decrease logistical shuffling of patients to multiple hospital service areas.
8. To integrate and co-ordinate services through on-site facilities for admitting /
registration, insurance authorization. laboratory test and electrocardiographic
studies.
9. To improve the education of patients and families about the elements of their
surgical procedure and the proposed anesthesia care. Including postoperative
pain control options.
10. To educate patients about what to expect regarding post operative feeding and
discharge needs.
11. To ensure and co-ordinate cost effective ordering of preoperative laboratory and
diagnostic studies.
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12. To provide an anesthesia medical consultation service for evaluation of


medically complex inpatients and out patients.
13. To decrease the number of cancellations and delays in the operative procedures
on the day of surgery.
14. To enlist the skills of a nurse practitioner to assist in pre-operative evaluations
and patient / family education.
15. To develop protocols, policies and clinical pathways
16. To perform quality assurance reviews.
17. To maximize efficiency in operating room function and turnover time by
coordinating all preoperative information at one location.
18. To enhance patient and surgeon satisfaction.
A questionnaire answered by the patient can be used to indicate likely disease process
and appropriate laboratory tests
Sample patient questionnaire for determining which preoperative laboratory tests
should be obtained:
Patient Name: _____________
Age __________
Sl.
Questions
Yes
No
No.
1.
Do you currently take any of the following
medications ?
Aspirin
Anticoagulants
Quinidine, diltiazem, Verapamil nifedepine or
propranolol
Diuretics
Digitalis
Antihypertensive drugs
Immunosuppressive drugs
Steroids
2.
3.

4.

Dont Know

Have you ever been treated for cancer with


chemotherapy or radiation therapy ?
Do you currently have any problems with
youre a) liver, e.g. cirrhosis, hepatitis,
jaundice or malaria ?
b) Kidneys eg. Stone, infection, failure, dialysis
c) Spleen,
d) Blood eg: anemia, leukemia sickle cell
disease
Have you or anyone in your family ever had a
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5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.

2010

serious bleeding problem


Have you received a blood transfusion within
the last 6 months
Have you recently had fever, chills, cold or flue
Have you ever been told, you have sugar or
diabetes ?
Do you wakeup to urinate more than once a
night
Do you have muscle cramps or spasms
Do you have problems with your lungs and
chest
Are you pregnant
Do you have cough or cough with sputum
Do you have epilepsy or fits
Do you have neck or back problems
Have you or any blood relative had problems
related to an operation.
Have you lost weight recently
Are you scheduled to have an operation ? If so
which one ?
What medicine do you take ?
a)
b)
c)
d)
e)
f)
others ________________

Informed consent:
The preoperative assessment culminates in giving the patient a reasonable explanation
of the options available for anesthetic management; general, regional, local or topical
anesthesia, intravenous sedation, or a combination thereof. Monitored anesthesia care,
refers to monitoring the patient during a procedure performed with intravenous
sedation or local anesthesia administered by the surgeon. Regardless of the technique
chosen, consent must always be obtained for general anesthesia in case other
techniques prove inadequate.
Consent must be informed to ensure that the. patient has sufficient information about
the procedure and their risks to make a reasonable and prudent decision whether to
consent. It is generally accepted that not all risks need to be detailed. Only risks that are
realistic and have resulted in complications in similar patients with similar problems. It
is generally advisable to inform the patient that some complication may be life
threatening.

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Anaesthersiology preoperative note:
Date:
Time:
Name:
Age:
Sex M/F
Medical History
Allergies
Intolerance
Drugs use

Preop diagnosis:
Proposed Operation:
Medications
Alcohol

Tabacco

Present problems:
CVS
RS
Diabetes
Neurological

Arthritis/Musculo-skeletal
Renal
Hepatic
Other

Previous anesthetics:
Family hisotyr
Last oral intake
Physical Examination
Temp:
Heart / CVS
Lungs / RS
Airway
Teeth

BP:

PR:

RR:

Extremities
Neurological
Other

Laboratory investigations
HCT / Hb
ECG
Urine
Blood glucose
BUN
Sr. Creatinine HBS Ag
Electrolytes

Ht:
Wt:

2010

NA
Ca

Cl
Mg

Plan : General
Regional
Monitored anesthesia care
ASA class
Signature:

Chest X-ray
Albumin
HIV
K
HCO3
CO2
Invasive monitors
Special techniques.
M.D
(Resident)

(Staff)

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Patient consent
Anesthetic alternatives and risks ranging from tooth damage to life threatening events
have been explained and accepted.
Patients signature

Patient name and address

Anesthetic implications of concurrent disease:


Failure to consult with primary Care physician preoperatively or, before a
complex procedure, is, as risky as not checking the oxygen in the spare cylinder.
Diabetes mellitus: It is important to know the end-organ dysfunction that exists and the
degree of glucose control, (cardiovascular dysfunction, renal insufficiency, joint
collagen tissue abnormalities, limitation in neck neck extension, (difficult intubations
secondary to fixation of the attanto-occipital joint) and poor wound healing).
Inadequate granulocyte production and neuropathies.
During recyional anesthesia, local anesthetic requirements are lower and the risk
of nerve injury is higher. In addition combining local anesthetic with epinephrine
may pose an even greater risk of ischaemic or edematous nerve injury or both.
The most important electrolyte disturbance in diabetic ketoacidosis is depletion
of total body potassium. Phosphorous deficiency in ketoacidosis may give rise to
significant muscular weakness and organ dysfunction.
Obesity:
In obese patients gas exchange may be impaired not only by altered
cardiopulmonary mechanism but also by management of a difficult airway, loss
of functional residual capacity (FRC) and ensuing rapid desaturation when
anesthesia is induced, also by the presence of sleep apnea, chronic respiratory
insufficiency and pulmonary hypertension.CIn obese patients FRC is less than
closing volume and decreased time of safe apnea, before hypoxia occurs.
Obstruction of the airway by the abundant soft tissue in the upper airway
frequently produces hypoxemia and hypercapnia. Obesity significantly increases
the risk of difficult tracheal intubations.
Obese patients have increased volume and acidity of gastric juices
preoperatively. Awake intubation is preferred in obese patients, but one should
be, aware and take precaution of gastro esophageal reflux and the greatest
potential for pulmonary aspiration occur during bucking on an endo tracheal
tube.
Obesity is also a significant risk factor for postoperative hypoxemia.
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Morbid obesity (BMI > 30 kg/m2) is the most common and a major risk factor for
ohstructive sleep apnea (OSA)
Prevalent ECG findings in obese patients are low QRS voltage, left ventricular
hypertrophy or strain, left atrial abnormality and T-wave flattening in the
inferior and lateral leads. In right ventricular hypertrophy or strain - right axis
deviation, right bundle branch block.
The obese may have limited cardiac reserve and poor tolerance for stress
induced by hypotension.
The proper positioning of the patient, placement of monitoring devices and
establishment of intravenous sites are more difficult to accomplish.
Thyroid dysfunction:
We should aim to avoid imposing surgery on any patient whose thyroid function is
clinically abnormal.
In hyperthyroidism anti cholinergic drugs (especially atropine) are avoided as
they interfere with the sweating mechanism and cause
A patient with a large goiter and an obstructed airway can be handled in the
same way as any other patient with problematic airway management.
Preoperative medication should avoid excessive sedation and an airway should
be established often with the patient awake. A firm armored endotracheal tube is
preferable and should be passed beyond the point of extrinsic compression.
In hypothyroidism patients, anesthetic requirement will be decreased and
enlarged tongue may hamper the endotracheal intubation. There is increased
incidence of myasthenia gravis in hypothyroidism patients, and it is advisable to
use a peripheral nerve stimulator to guide administration of muscle relaxants.
Serum calcium level should be monitored because changes in the calcium level
may alter the duration of muscle relaxation. The three substances that regulate
serum concentrations of calcium, phosphorous and magnesium are parathyroid
hormone, calcitonin and vit. D which act on kidney, bone and gut, severe
hypercalcemia can occur in hypolemia. ECG shows shortened PR or QT intervals.
Normal intravascular volume and electrolyte status should be restored before
commencement of anesthesia and surgery.
Hypercalcemia can be corrected by hydration and diuresis. Complications of this
intervention include hypomagnesaemia and hypokalemia.
Hypocalcaemia: Most common cause is hypoalbuminemia. In hypocalcaemia cardiac
contractility is affected. ECG reveals prolongation of QTc interval.

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Hypertension:
Blood pressure mm of Hg:
Category
Systolic
Diastolic
Optimal
< 120
< 80
Normal adult
< 130
< 85
Normal Adolescence
100
75
Normal early children
85
55
Normal infants
70
45
High normal
130-139
85-89
Hypertension
Stage 1
140-159
90-99
Stage 2
160-179
100-109
Stage 3
180
110
Control hypertension to prevent complications. Search for end organ damage
CNS, coronary arteries, myocardium, aorta, carotid arteries, and kidneys and
peripheral blood vessels.
We use such preoperative data to determine the individualized range of values
that we consider tolerable by a particular patient during and after surgery. That
is if BP is 180/100 mm of Hg and heart rate is 96/min on admission without
sighs and symptoms of myocardial ischaemia, we feel confident that the patient
can tolerate these levels during surgery. If during the night. BP decreases to
80/50 mm of Hg and heart rate to -l8/inin and the patient does not awake with
signs of a new cerebral deficit, we believe that the patient can safely tolerate such
levels during anesthesia.
Routinely administer all anti-hypertensive drugs preoperatively, except ACE
inhibitors or angiotensin-11 antagonists. Because ACE inhibitors are associated
with hypotension during induction.
In patients on ACE inhibitor during general anesthesia if refractory hypotension
occurs vasopressin is the drug of choice.
Ischemic heart disease
The presence of coronary artery disease, its severity, and the time of the most
recent myocardial tissue death, the arteries affected, ventricular function and
reserve and the complications and treatment of the disease are important
informations to the anesthesiologist.
Preoperative testing:
Elevated levels of cardiac enzymes
Treadmill exercise testing, bicycle ergometry, dipyridamole thallium imaging,
dobutamine stress test, echocardiography, preoperative Holter monitoring, non
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invasive imaging, the ankle-brachial pressure index cardiac catheterization, also


add information to the history.
Vavular heart disease: Now common are congenital bicuspid aortic stenosis, mitral
valve prolapse, hypertrophic cardiomyopathy and mitral valve insufficiency as a result
of calcification and drug therapy.
NYHA functional classification of heart disease:
Class
Criteria
I No limitation
Ordinary physical activity does not cause undue fatigue,
dyspnea or palpitation
II slight limitation of
Such patients are comfortable at rest. Ordinary activity
physical activity
results in fatigue, palpitation, dyspnea, or angina.
III marked limitation of
Although patients are comfortable at rest, less than
physical activity
ordinary activity will lead to symptoms
IV Inability to carry on any
Symptoms of congestive failure are present even at rest;
physical activity without
with any physical activity increased discomfort is
discomfort
experienced.
Disorders of the Respiratory and Immune system:
Eradicate acute infections and suppress chronic infections by using appropriate
diagnostic measures and antibiotic treatment.
Relieve bronchospasm by using inhaled corticosteroid and bronchodilating
drugs.
In patients with bronchial asthma consider the administration of corticosteroids
beginning at least 48 hours before surgery.
Institute measures to improve sputum clearance and familiarize the patient with
respiratory therapy equipment and postural drainage maneuvers.
Treat uncompensated right ventricular heart failure with digoxin, diuretics,
oxygen and drugs that decrease pulmonary vascular resistance.
The use of low-dose heparin prophylactically to decrease the incidence of venous
thrombosis and pulmonary emboli.
Identify and treat suspected or diagnosed sleep apnea with CPAP or BIPAP.
Encourage reduction or cessation of smoking at least 4 weeks and preferably 8
weeks or more before surgery.
Disease of CNS, Neuromuscular disease and psychiatric disorders:
The patient's ability to answer health history questions practically ensures a
normal mental status. Questions can be directed to exclude the presence of
increased intracranial pressure, cerebrovascular disease, seizure history pre
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existing neuromuscular disease or nerve injuries. Neurological exam may be


cursory in healthy patients or extensive in patients with coexisting disease.
Testing of strength reflexes and sensation may be important in patients if the
anesthetic plan or surgical procedure may result in a change in the condition.
Coma: It is imperative to know the cause of the coma, so that drugs can be avoided that
might worsen the condition or that might not be metabolized because of organ
dysfunction.
Abnormal pupillary response may indicate hypoxia, hypothermia, and local eye
disease or drug intoxication with belladonna alkaloids, narcotics
benzodiazepines or glutethimide.
In neuromuscular disorders anesthetic management consists of minimizing
stress and maintaining normal fluid and electrolyte status and body
temperature.
Liver: A history of jaundice should be noted. If jaundice has occurred after anesthesia it
may be related to volatile agent particularly halothane.
Risk assessment of a patient with hepatic disease can be undertaken using the child
pugh risk index.
Child grade
A

Bilirubin mg/dl
< 2.5
2.5-4
>4
Albumin gm/dl
> 3.5
3-3.5
<3
Prothrombin time (seconds prolonged)
1-4
4-6
>6
Encephalopathy
0
1-2
3-4
Ascites
None
Easy
Difficult
Nutritional status
Excellent
Good
Poor
Operative mortality (Approximate %)
0-10
4-31
19-76
The assessment is based on the sum of a number of key clinical features. Grade A
corresponds to low risk (0-10%) grade B patients should be optimized preoperatively.
Grade C patients should not undergo elective surgery if possible.
Gastro esophageal reflux disorder (GERD):
Consider antacid prophylaxis
Rapid sequence intubation
Antiemetics to control postoperative nausea and vomiting.

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Kidneys:
Renal failure is normally treated with dialysis and renal transplantation. Patients
presenting for elective surgery should be well controlled.
Electrolytes, acid base balance, fluid status must be carefully checked.
A patient with established renal failure should be assessed for anaemia.
It is important to note the fistula (AV) which must be carefully protected during
surgery. Renal excretion of drugs and the metabolites of other will be impaired.
So drugs dosage should be attached.
Musculoskeletal system:
For osteoporosis and painful joints.
Poor mouth opening, an immobile neck, atlanto-occipital instability.
Rheumatoid arthritis:
The skin which is delicate and easily traumatized.
Anaemia which does not always respond to iron.
The lungs for nodules and fibrosis.
Patients are usually on a number of drugs these often have associated side effects
such as DM, HTN, electrolyte imbalance (Corticosteroids) folate deficiency, liver
and pulmonary dysfunction (methotrexate) renal failure and HTN
(cyclosporine). GERD (NSAIDS).
PREOPERATIVE MEDICATION
various goals for preoperative medicine
1. Relief of anxiety
2. Sedation
3. Amnesia
4. Analgesia
5. Drying of airway secretions
6. Prevention of autonomic reflex responses
7. Reduction of gastric fluid volume and increased pH.
8. Antiemetic effects
9. Reduction of anesthetic requirements
10. Facilitation of smooth induction of anesthesia
11. Prophylaxis against allergic reactions.

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Common preoperative medications doses and administration routes


Administration
Medication
Dose (mg)
route
1. Diazepam
Oral
5-20
2. Lorazepam
Oral / im
1-4
3. Midazolam
Im
3-7 (0.05 to 0.2 mg/kg)
iv
Titration of 1.0-2.5 mg doses
4. Morphine
Im
5-15
5. Ranitidine
Oral
50-200
6. Metaclopramide
Oral, im, iv
5-20
7. Atropine
Im, iv
0.3-0.6
8. Glycopyrrolate
Im, iv
0.1-0.3
9. Promethazine (phenergan)
Oral / im / iv
12.5 -20
Conclusion: Our primary goal has to be, efficient delivery of quality care. The
responsibility of anesthesiologist starts from preoperative and pre procedure
assessment. The proposed PPAC facilitates those most sought after-goals, improved
quality of care and reduced costs and increased efficiency. At the same time the
anesthesiologists can lessen their own anxiety about performing the very best
evaluation possible.

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Chapter 6 - HISTORY OF ANESTHESIA


The development of anesthesia since its introduction in 1846 has been erratic, long
periods of stagnation being occasionally broken by improvements and advances. For the
history of pain relief in surgery before 1846 see A History of Anesthesia (Atkinson R. S.
and Boulton T. B.) London: Royal Society of Medicine, 1989.
Anesthesia as we know it today was first used by W.T.G. Morton of Boston in the
US who gave ether at the Massachusetts General Hospital on 16 October 1846 to Gilbert
Abbott. C. W. Long of Georgia had given the same agent several times 4 years previously
but failed to report his work at the time so that this was unknown to Morton. Thus was
Henry Hill Hickman's idea that anesthesia could be produced by the inhalation of gases
and vapours, finally vindicated. Horace Wells, a colleague of Morton, had used nitrous
oxide for the painless extraction of teeth quite successfully in 1844, but his public
demonstration of this practice was a disastrous failure and the gas was temporarily
forgotten. The news of Morton's discovery soon spread throughout the civilized world,
and on 19 December 1846 Francis Boott, a physician, born and trained in the US but
working in London, received news of Morton's discovery and encouraged Mr James
Robinson, a dentist to give ether to a Miss Lonsdale for a dental extraction, Mr Robinson
acting as dentist and anesthetist. A commemorative plaque has now been placed on his
residence at No. 14, Gower Street, London. (On the same day, Dr Scott operated under
ether at the Dumfries and Galloway Infirmary in Scotland.) So successful was this that
Boott persuaded Robert Liston, the University of London's professor of surgery, to
experiment with the new drug. It was tried out with considerable publicity and brilliant
success for the amputation through the thigh of Frederick Churchill's leg at University
College Hospital on 21 December 1846.
The technical difficulties associated with the administration of ether were partly
overcome by the substitution with chloroform by James Young Simpson, professor of
midwifery at Edinburgh University, in the following year. He poured drops of this newer
agent on to gauze held near the face of the patient, so avoiding the inhalers that were
used for ether.
John Snow, a London physician, was the first to attempt some sort of scientific
investigation into the new anesthetic agents and the methods of their administration,
and he devised several pieces of apparatus for delivering to the patient known
percentage concentrations of anesthetic vapour in an attempt to increase their safety.
This work was undertaken because of the reports of deaths associated with anesthesia.
Different uses of the drugs and different methods of administration were adopted in
different countries. Thus chloroform was used more frequently in Scotland, the greater
part of Europe and in the southern states of America, while ether remained the favorite
in England and in the northern states of America. There was much controversy as to
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which was the safer of the two drugs but eventually ether won the day. When in 1858
John Snow, who was England's leading physician anesthetist, died, his place was taken
by J. T. Clover, and partly due to the influence of these two pioneers, the administration
of anesthetics in the UK has always been in the hands of medical men and, as time has
passed, in the hands of specialists in the subject.
Meanwhile, nitrous oxide still had its friends in the US, and in 1863 G. Q. Colton,
who introduced it to Wells, embarked on a campaign of popularization of the gas. Its
disadvantages were difficulty in administration and the asphyxia inseparable from its
use. The latter was partly overcome by Edmund Andrews of Chicago who in 1868 gave
it with 20% oxygen, and by Paul Bert of Paris who gave it under pressure 10 years later.
The first major war in which anesthetics were used was the Crimean War (1854-1855).
It is an interesting fact, however, that even 25 years after Morton introduced the use of
ether in surgery, operations were still being performed in the complete absence of any
form of anesthesia, even in European teaching-Hospitals.
During the next 40-50 years there were few significant changes in anesthesia, but in the
1920s the pace of progress quickened. In the 1920s, ether and chloroform were the
main agents used but ethyl chloride and nitrous oxide were often employed for
induction. Simpsons open drop method was the most popular, while the first Boyle
machine appeared in 1917. One of the early pioneers was Sir Geoffrey Marshall, who
gained experience of anesthesia while serving in the R.A.M.C. in. the First World War.
Before the 1930s the anesthetist administered one or two volatile agents to produce
unconsciousness, muscle relaxation and deafferentation. This gave place to various
techniques of so-called balanced anesthesia and so the amount of toxic drugs to which
the patient was exposed was reduced and the hazard of general anesthesia made less.
Among other innovations were the popularization of endotracheal techniques by Ivan
W. Magill and E. Stanley Rowbotham, the appearance of bromethol (Avertin), divinyl
ether, cyclopropane and trichloroethylene, and the induction of anesthesia by
intravenous barbiturates in the early 1930s. Because of the difficulty of obtaining
relaxation of the jaw and larynx with ether, blind nasotracheal intubation became
increasingly used. Controlled respiration was used with cyclopropane so that when
curare was first tried out by Harold Griffith in Montreal in 1942, the way to deal with
hypoventilation and apnoea was well established, and soon intermittent positivepressure ventilation became routine practice.
Local analgesia made its appearance in 1884 when Carl Koller of Vienna
demonstrated the use of cocaine for topical analgesia in the eye. Infiltration and regional
block followed from this. Spinal analgesia was first described by August Bier in Kiel in
1898 and extradural block by Fernand Cathelin and Jean Athanese Sicard in Paris in
1901 and by Fidel Pages of Madrid in 1921 and Achille Mario Dogliotti of Turin in 1931.
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The two world wars stimulated both surgery and anesthesia, and following each, the
number of doctors who continued their anesthetic work, learnt under service
conditions, into civilian life had a considerable influence on the development of the
specialty.
Technical improvements were slowly accompanied by academic recognition, but
not always by adequate financial rewards. The first examination for the Diploma in
Anesthetics was held in London in 1935 and the first chair in anesthetics was created in
Oxford, with R. R. Macintosh as professor, 2 years later. Ralph Waters was appointed as
the first professor of anesthesia in a university in the US in 1933. In the UK the
recognition of anesthesia as a specialty with full equality with other medical and
surgical specialties was secured in 1948 with the introduction of the National Health
Service, and since then anesthesia has not only kept pace with the rapid advances made
in surgery, but has in many instances enabled these advances to be made. In recent
decades the scope of the anesthetist's work has widened and now takes in not only preoperative assessment and postoperative care, but supervision of intensive therapy
units, pain services, and in many cases research and postgraduate education. An
enormous development in the use of monitoring equipment, some of it highly
sophisticated, has taken place in the last 20 years. Among those workers who remember
clinical anesthesia in the 1930s and early 1940s, few would disagree with the statement
that what is known as 'modern anesthesia' commenced with the introduction of the
muscle relaxants.
Following a joint congress of anesthetists in London in 1951 of which Sir Ivan
Magill was President, and a similar meeting in Paris the same year, it was decided to
form a Federation of Societies of Anesthesiologists and the first Congress of the new
body was held in Scheveningen in Holland in 1955. Other similar congresses have been
held in Toronto (1960), Sao Paulo (1964), London (1968), Kyoto (1972), Mexico City
(1976). Hamburg (1980), Manila (1984), Washington (1988) and The Hague (1992).
Among training courses arranged by the World Health Organization were those of the
Anesthesiology Centre in Copenhagen (1950-1973) and in Manila (under the guidance
of Professor Quintin Gomez).

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Chapter 7 - SOME OUTSTANDING CONTRIBUTORS TO THE SCIENCE


AND ART OF ANESTHESIA

SIR-IVAN-MAGILL (1888-1986)
Ivan-Whiteside Magill was born in Larne, Northern Ireland in an integral part
of UK.
His birth in 1888 took place 42 yrs after Mortons first use of ether and just two
years after the discovery of local analgesia using cocaine.
He attended the grammer school and then became a medical student at Queens
university qualifying in 1913.
He became a house surgeon at the Stanley hospital in Liverpool and with the
outbreak of 1914-1918 war, joined the RAM and served with the Irish-Guards at
the battle of Loos. When peace cane again, Magill posted to the Queens hospital
in Kent.
With a young colleague, Stanley Rowbotham, they started giving anesthesia for
reconstructive operations on the face and jaws in wounded soldiers. Under the
care of Harold-Gilles who later became a world famous pioneer of plasticsurgery.
Here after trial and groon, they first did tracheal intubation first using twonarrow gum elastic tubes. One afferent and the other efferent, for the insufflation
of ether vapour under slight positive pressure, and then employing a single widebore rubber tube for spontaneous breathing.
They are also among the first to develop the technique of nasotracheal intubation
by the so called blind-method.
Those anesthetists, who learnt how to perform blind nasal intubation, soon
realized its great advantages.
In addition intubation provided a clear airway, prevented laryngeal spasm and
enabled the lungs to be protected against foreign material.
Magill devoted big professional life to the administration of anesthetics and was
selected to the staffs of various hospitals in London.
Magill was a man of practical ingenuity and over the years originated developed
many new pieces of equipment and development of technique for the safely of
his patients and the convenience of his surgeons.
He introduced
Magills laryngoscope
Laryngeal forceps

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Magill attachment a simple combination of a breathing tube reservoir bag, and


expiratory valve used for spontaneous respiration.
Magill developed methods of administering anesthetics in thoracic surgery. Employing
endobronchial tube and bronchus blocker for the control of pulmonary secretions and
these techniques for the production of one lung anesthesia greatly contributed to the
development of thoracic surgery in 1920s and 1930s.
He received a very large number of honours and medals including a knighthood
awarded personally by the Queen in 1960, the FRCS (Eng) the honorary, FFARCS, the
DSC of his old university, Henry-Hickman medal from the Royal society of medicine.
In 1920s when Ivan-Magills career began, anesthesia was a little regarded, especially
and those who practiced it. Exclusively attracted little esteem from their colleagues.
He was a leading anesthetist because of his firm character and common sense, his preeminence in clinical anesthesia and his international reputation.

JOHN SILAS-LUNDY (1894-1973)


Birth: He was born in Seattle, Washington
Son of a Doctor.
He took an arts degree in 1917 and qualified in Medicine from the Rush medical
college in Chicago two years later (1919).
After serving as a resident in Chicago hospitals be returned to his birth place and
entered general practice.
In April 1924 he was invited to become head of the department (HOD) of
Anesthesiology at the Mayo-clinic and this be directed for the next-28 yrs
although his connecting with the clinic did not end until 1959.
He became professor in Mayo-Graduate school of medicine in 1934 and was one
of the founders of the American board of Anesthesiology.
He was a prolific writer, and this together with the worldwide reputation of the
mayo-clinic where he worked, soon carried his nine throughout the US and
Europe.

Contributions:
He established the first laboratory of gross-anatomy to be used at the clinic and
this was important for his teaching of the techniques of regional analgesia which
had been stimulated there by Gaston-Lobat.
In 1925 Lundy developed the theory and practice of balanced anesthesia.
Lundy used thiopentone on 18th June 1934 and continued throughout his
professional life to advocate its use. Though, it was used by waters of Madison
first.
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On 1942 be opened the first post anesthesia observation room in the world at St.
Marys hospital Rochester.
Dr. Lundy was the author of the textbook Clinical anesthesia published in 1942,
which deals with the Modern-anesthesia.
Lundy received many medals awards and honours from academic bodies
throughout the world.
He reward from Chicago and continued to practice anesthesia at Seattle.

HENRY EDMUND GASKIN BOYLE (1875-1941)


Birth: born in Barbados
And qualified at Bartholomews hospital, London in 1901 where as a student he
was president of the abemethian society.
Boyle became casualty officer in Bristol and then a returned to St. Bartholomews
as junior resident anesthetist.

Contributions:
In 1912 be became interested in N2O and O2 anesthesia and in 1917 got coxeter,
the instrument maker to copy James-Taylor Gwathmeys gas oxygen machine
which became the first Boyle-apparatus.
He introduced gas oxygen into France for use in anaesthetizing wounded soldiers
in the First World War and for this received the decordation of OBE.
After the First World War, he visited US and brought bailer introduced DAVISSGAG to British throat surgeons.
He was an early user of Magills endotracheal-techniques.
He was elected FRCS and DA in 1935.
A founder member of the association of anesthetists of great Britain and Ireland
in 1932.
In 1907 wrote the first edition of his textbook practical anesthetics the third
edition of which was prepared by his junior colleagues C.Langton Hewer.
Boyle was a character and was universally known as Cockie.
His anesthetic machine, modified in every particular is used in most Britishhospitals today.
Krapp and Taub synthesized a new barbiturate, hexabarbitons later to become
known as Evipan.
Helnut - Weese saw that this might be the long awaited short-acting and safe
agent for induction of anesthesia.
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He was soon able to show that it fulfilled his expectations and in 1932 he
published his results, thus becoming undisputed creator of practical clinical
modern intravenous anesthesia.
He won recognition at the international conference of anesthesia at New-York
in 1938 during which he was elected as an honorary member.
During the II-world war, Weese investigated the possibility of producing a
synthetic plasma volume expander, and as a result, polyvinyl-pyrrolidone
became
available
and
saved
many lives. He died following a fall from a chair
in his
laboratory, an unusual event in a man well used to climbing in the high Alps.

HAROLD RANDALL GRIFFITH (1896-1985)


Harold-Griffith on 23rd January 1942, injected intocostrin intravenously a
preparation containing curorae, to aid muscle relaxation in a patient undergoing
appendicectomy cyclopropane anesthesia at the Homeopathic hospital.
Birth: born near Montreal on 25th July 1896.
Obtained the BA in 1914 and MD CM in 1922.
In this year he also married.
The following year he obtained the MD in homeopathic medicine from the
medical college of Philadelphia.
An interest in anesthesia developed early in his career and after a time be
became chief anesthetist at the Montreal homeopathic hospital where he spent
his active professional life until his retirement in 1966. His father was a medical
director there and his brother surgeon-in-chief.
He developed an expertise in tracheal intubations and along with Ralph-waters
of Madison became a world expert on the use of the new-agent cyclopropane.
Dr. Griffith was a much loved man of modest disposition who was known to his
younger colleagues as Uncle-Hanold.
In later life he received many honours and distinctions including Hickman-medal
from the Royal-society of medicine in London in 1956.
He died of Parkinsons because aged 90 yrs on 7th May 1985.

CARL-KOLLER (1857-1944)
o Carl-Koller was the first medical man to make use and to publicize the
analgesic properties of cocaine to prevent the pain of a surgical-operation.
Birth: He was born in 1857 in Schuttenhofer.
The son of a Jewish businessman.
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Education: He was educated in Vienna, thought of studying law. Served for two
years as a conscript in the imperial army and finally enrolled as a medicalstudent in the University of Vienna.
While still an undergraduate Koller published the results of some highly
regarded experimental pathological investigations into the embryology of the
mesoderm of the chick.
He qualified as a doctor in 1882 at the age of 25 and became a member of the
dept of ophthalmology. In 1884, at the age of 27 be published the analgesic
properties of cocaine.
Koller was dissatisfied with the standards of anesthetists and restlessness cough
and vomiting during surgery. He began to realize that this problem would only
be solved if he could find some drug which, when instilled in to the conjunctival
sac would abolish pain, with this, view, he tried morphine and other sedative
drugs, but of course without success.
Sigmund-Freud who was working in the department neurology investigated a
new drug cocaine: he knew that it deadened mucous membranes but was not
clear to its effects on muscular contraction and asked Koller to do some
experiments to elucidate this problem.
Freud then went on holiday while Koller set to work with cocaine. He started by
applying some to his own tongue and was immediately stuck as others had been
before him, by its strange power to deaden all sensation. He immediately
realized that, this might be the agent be had been looking for to act as a local
analgesic in his eye operations. He quickly get about investigating its analgesic
effects in the experimental pathology laboratory on animals, than on himself on
his friends and lastly on his patients.
He satisfied himself that not only did it works but that it worked extremely well
and lost no time in making his discovery public. He wrote a short a preliminary
report and asked his friend, to read it for him at forthcoming meeting of the
German Ophthalmological Society to be held in Heidelberg, which Koller
himself was not able to attend. His demonstrated with 2% cocaine solution in the
OPD caused a sensation in the meeting. The date was 15th September 1884. The
following month Keller read two full papers became the imperial medical society.
This cocaine news (event) spread throughout Europe and the US and Koller
became a notable figure. But Koller did not get senior post in the academic dept
of eye-surgery.
Koller was, however a restless and somewhat awkward man and decided to try
his luck once more in Vienna but he found it hard.
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Koller fought with sobers and he decided to leave Vienna. He arrived to NewYork in 1888 and where he spent the remainder of his active life. He soon built
up a thriving hospital and private practice and established a solid reputation as
first class ophthalmologist. Koller received many medals, scrolls and
commendations from various academic bodies. Koller was its true begetter. He
died, in 1944 at the age of 86.

JOSEPH T. CLOVER (1825-1882)


After the death of John-Snow, Clover became the leading scientific anesthetic
investigator and practical anesthetist in Britain.
Birth: born in Ayleshan Norfolk and was educated at the Gray-Friars priority
school in Norwich and university college hospital in London.
Clover was present in the operating-theatre at university college hospital on 21
December 1946 when Robert Liston amputated the leg of Frederick-Churchill
when ether was given William Squire, a medical student.
Joseph-Clover was interested in anesthesia from its commencement.
Joseph-Lister was a fellow student.
Became House-surgeon to James-Syme and later RMO at university collegehospital and took FRCS in 1850.
He was the pioneer of the art of completely and immediately removing from the
urinary bladder, the calculus fragments produced by lithotripsy.
He also devised Clovers crutch a simple but effective piece of apparatus for
maintaining a patient in the lithotomy position.
Worked as general practitioner in London (because of poor health) later
specializing in anesthetics, there by helping to fill the vacancy created by the
early death of John-Snow in 1878.
In 1862 be invented a chloroform inhaler which enabled percentage mixtures of
chloroform and air to be accurately measured and administered.
Realizing the dangers of chloroform, clover set to work to make the
administration of ether more simple and easy. This he did by inducing
anesthesia with N2O, later adding ether to the gas.
In 1868 published a paper on the administration of nitrous oxide.
In 1877 he described his portable regulating ether inhaler.
Another of Clovers achievements was his teaching that ether could be safely
given over long periods with anesthesia carried to adequate depth.
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Clover died at the age of 57. He is buried in Brampton cemetery, London, his
grave-being 200 yards from that of John-Snow.

SIR FREDERICK-HEWITT (1857-1916)


Educated at Merchant-Taylors school Christs college, Cambridge he was a
distinguished student there.
Became an anesthetist as defective eyesight prevented him becoming a
consulting physician.
He emphasized that N2O anesthesia is possible without asphyxia and that
chloroform is especially dangerous during induction.
Hewitt modified Junkies chloroform bottle and redesigned Clovers inhaler.
Hewitt invested the first practical machine for giving N2O + O2 in fixed
proportions in 1887.
Hewitt died of gastric neoplasm at Brighton.
His grave lies in Brighton and Preston cemetery.

HELMUT-WEESE (1897-1954)
o Helmut-Weese deserves an honoured place in the history of anesthesia as
the first man to make intravenous induction a safe and practical
procedure.
Birth: he was born in Munich in to a family originating from the German part of
Poland, son of a lecturer in the history of art.
When Helmut-Weese was nine, the family moved to Berne. Where his father
became a private dozent at the university.
He decided to study medicine and attended the universities of Berne, Munich and
Zurich where he qualified.
His first post was internal medicine and then he changed to pharmacology.
He paid particular attention to the study of digitalis wrote a book on it and as a
result, he became well known both inside and outside Germany to physicians as
well as to pharmacologists.

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WILLIAM-STEWART HALSTED
Halsted is famous for his early experiments with new local-analgesic solutions of
cocaine.
Birth: he was born in to a substantial family in the New-York city.
He was educated at Yale-college where his athletic prowess surpassed his
academic abilities.
Decided to study medicine, he entered the college of physicians and surgeons in
New-York in 1874, and graduated 3yrs later.
While a resident at Roosevelt hospital, new-York, in 1878, he became friendly
with William H. Welch.
Next 2yrs be spent in post-graduate studies in Austria and in Germany.
When he returned home, he entered surgical-practice in New-York city.
Halstead was one of the first to recognize the importance of the discovery of
cocaine, and with some of his colleagues commenced to experiment with the new
drug on them.

Contributions:
He originated nerve-block or regional analgesia.
He showed that a reduction in the circulation of a part of the body, by using
Esmarch bandage would prolong the effects of local analgesia.
He demonstrated that, for skin analgesia, Intradermal injection distensionmethod was superior to subcutaneous injection.
He was the first surgeon to block the nerves of the face the brachial plexus, the
internal pudendal and posterior tibial nerves.
In 1886, his-uncontrolled addiction to cocaine led to his admission to a
psychiatric hospital. He seems to have exchanged the craving for cocaine for the
craving for morphine possibly as a result of therapy, and remained off and on, a
morphine addict in the rest of his life.
On discharge from hospital his personality was seen to have changed, and he
now appeared as a slow, meticulous rather morose may who gave great attention
to the smallest detail of what occupied him.
In 1889, Halsted was appointed, the first professor of surgery in Johns-Hopkins
University and chief surgeon to the hospital.
During the next 30 yrs of his life he made his clinic world-famous and became
one of the founding fathers of 20th century surgery becoming mentor, guide,
philosopher and friend to countless young colleagues.

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His enthusiasm for regional analgesia warned and in later life he always
preferred to operate on unconscious patients. He died following a second
operation for gallstones and obstructive jaundice.
e) Among his contributions to surgery were, his radical operation, for the
removal of the whole breast with its lymphatic drainage for the relief of breast
cancer.
f) In 1890, he introduced the use of rubber-gloves in to surgery.

WILLIAM-THOMAS, GREEN-MORTAN (1819-1868)


(W.T.G. MORTON)
Introduction: Morton deserves the chief credit for the introduction of ether as an
anesthetic agent.
Although W.E. Clarke gave ether for a dental extraction in 1842 and Crawford
Williamson-long removed a tumour from the neck of James M. Venable quite
painlessly few months after Clarkes experiment.
By this time Morton was famous and well established.
In science, the credit for a new discovery belongs to the man, who convinces the world,
not to the man to whom the idea first occurs. Morton convinced the world of the
advantages of ether anesthesia and credit for this discovery is his.
Birth: Morton was born at Charlton.
Started working at the age of 16yrs in a printing house; later went into business
but was a failure. As a young man, he suffered the pain of a surgical operation in
Cincinnati.
He studied at the Baltimore-college of dental surgery.
He set up his practice at Farmington, Connecticut and later became a pupil and later a
partner of wells at Hartford.
Morton-separated from Horace Wells, and becoming a medical student in Boston at the
Harvard medical school, was present when wells failed to satisfy the audience as to the
efficiency of nitrous oxide.
Morton never qualified in medicine, but received honorary MD in 1852, Charles T.
Jackson one of Mortons lecturers at Harvard suggested, that ether could be used as
surface analgesic in dentistry.
Morton experimented in dogs to find out the effect of giving ether vapour by inhalation.
Impressed with the ether results, he gave the vapour to Ebon frost for the removal of a
tooth on 30th September 1846. The operation was painless.
After trying on 37 patients. Morton while still a medical student gave demonstration at
the Massachusetts general hospital on 16th October 1846. In what is now the ether
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dome and day is celebrated as ether day. Ether was given to Gilbert Abbott who was
a printer and journalist by Dr. John Collins warren who removed a tumour from the
jaw of his patient Gilbert-Abbott without producing pain.
Oliver Wendell-Holmes professor of anatomy and physiology at Harvard medical
school, said this priceless gift to humanity went forth from the operating theatre of the
Massachusetts-general hospital, and the man to whom the world owes it is; Dr. T.W.G.
Morton.
Much wrangling occurred between Morton and Jackson as who should be given credit
for the discovery.
Fate: Morton was sever in his lifetime officially recognized as the pioneer of ether,
anesthesia. Morton spent his later years forming at Needham, Massachusetts. Morton
died of cerebral-hemorrhage quite suddenly in central part, New-York city on 15 July
1868.
The inscription on his tombstone in mount Auburn cemetery, Boston, composed
by Henry J. Bigelow reads.
Inventor whom, in all time, surgery was agony, by whom pain in surgery was
averted and annulled; since whom, science has control of pain.
History of ether:
It was given in London and Paris in 1846, Robert Liston was the first surgeon to
operate under ether in England.

JOHN-SNOW (1813-1858)
Birth: Born in New York on 15th March 1823.
John-Snow was the eldest of 9 children of a farmer. After Morton, John snow was
the first-whole time anesthetist.
Education: John-Snow started his medical studies at the age of 14 yrs in New-Castle. He
was one of the eight medical students who entered the Newcastle-on-Tyne medical
School at its inception in 1832.
He was a student of Mr. William Hard-Castle.
John-Snow worked at the New castle infirmary and became interested in the
first-cholera epidemic in 1831-1832. In 1836 he migrated to London, traveling on foot
and attended lectures at the Hunterian school of Anatomy in great windmill street and
also at west minister hospital. He passed the M.D. exam in London, and appointed as a
lecturer in forensic medicine at Alder gate school of medicine. He spent rest of his life in
London as a general practitioner.

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Contributions to anesthesia:
1. John-Snow invented an ether inhaler in 1847 and adapted face-piece of Dr.
Francis-Sibson, later he invented his own.
2. Snow became the leading anesthetist in London and wrote a book in On
inhalation of ether in surgical operations. He described five stages or degrees of
anesthesia.
3. He emphasized the importance of knowing depth of anesthesia.
4. John-Snow used chloroform instead of ether, and after knowing that it causes
cardiac failure he invented percentage chloroform inhaler.
5. In 1853 Snow originated the method of chloroform in labor analgesia (pain)
when he acted as an anesthetist at the birth of Queen Victorias 8th child prince
Leopold. He gave his royal-patient 15 minimal doses intermittently on a
handkerchief. The administration lasting 53 mins.
6. John-Snow introduced amylene as an inhalational anesthetic in 1856.
7. In his later years, Snow proved that cholera is a water born disease; he ordered
for the removal of broad-street pump handle in 1854 in London and so
terminated the third cholera-epidemic.
Fate: John Snows health was poor and suffered from phthisis and from nephritis being
treated for the kidney disease by Richard Bright. He experimented with many
substances to see if they pressed anesthetic properties trying many of them on him.
John suffered from paralysis and died on 11th June 1858.
Near the site of pump, in broad wick street, a public house has been named the
John snow. Snows graveyard in Brompton cemetery was restored in 1938 by
anesthetist from Britain and U.S states.

JAMES-YOUNG SIMPSON (1811-1870)


Birth: Born at Bathgate, near Edinburgh.
Education: qualified in 1830, finished his M.D. in 1832. Ejected to chain of midwifery at
Edinburgh, in 1840. Simpson started university career in atmosphere of hostility but his
ability as a lecturer soon attracted large classes of students.
1. Simpson took an interest in a wide range of subjects, including leprosy,
puerperal sepsis and hospital design.
2. He put forward the method of haemostasis by acupressure to promote better
wound healing.
3. James Simpson made many contributions to the literature of archaeology,
becoming the president of the society of antiquaries of Scotland in 1861.
4. Young Simpson is most famous for the introducing of chloroform in 1847.
5. He was the first to use ether in obstetric practice on 19 January 1847.
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6. Liverpool chemist suggested that Simpson should try chloroform as an


anesthetic vapour. Simpson experiment on himself and his assistants, Mathews
Duncan and George Keith, on 4th November 1847 at Simpsons house. Four days
later, chloroform was used clinically and reported to Edinburgh-medical
society.
Thus Simpson introduced a new anesthetic agent as substitute for ether in relief
of pain.
He held that, chloroform has the following advantages over ether; 1) action more
rapid, complete and persistent 2) smaller quantity is required for pain relief 3)
pleasanter 4) cheaper.
Simpson-remained an enthusiastic salesman for chloroform anesthesia.
From 1845 to his death in 1870, Simpson lived at Edinburgh. The dining room
has been preserved as The discovery room and contains some of Simpsons
furniture and possessions. He was buried in the family plot in Warriston
cemetery, Edinburgh.
In its day chloroform was a superb anesthetic, easy to administer, portable,
capable of producing good relaxation and reasonably safe.

AUGUST KARL-GUSTAV BIER (1861-1949)


Birth: Bier was born in Helsen in Waldeck in Germany in 1861.
Education: Graduated in 1889 at Kiel, when he became assistant to the professor of
surgery, Von-Esmarch.
While there he supervised the transition from antiseptic to aseptic techniques in
the operating theatres, he became familiar with the work of a medical colleague at Kiel,
Heinrich Irenaeiu Quincke, who established lumbar puncture as a safe investigation in
routine neurological examination.
In 1898, Bier gave the first deliberate spinal anesthetic and to prove his faith in
the method, Bier allowed his assistant, Dr. Hildebrandt, to inject in to his own theca 2ml
of 1% cocaine solution. Leaving Kiel, Bier became professor of surgery successively at
Greifswald.
I.
In addition to his discovery of spinal-analgesia Bier invented
II.
The method of treating chronic inflammation by the method of passive
hyperemia with Esmarchs bandage.
III.
He was the pioneer of intravenous procaine analgesia
IV.
IVRA for upper and lower limb surgeries with Esmarch bandage.
V.
Bier was one of the great figures of German-surgery as teacher, lecturer and
operator.
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Bier introduced the tin-helmet into the German army in the First World War.
In later life he came to hold unorthodox ideas advocated physical education calisthenics
etc. He died in 1949 at Sauer in the German at the age of 88.

ARTHUR E. GUDEL
Birth: Born in Cambridge city, Indiana
Education: Received his medical education at the Indiana school of medicine.
Qualifying in 1908. Gudel lost three fingers of his right hand at the age of 13 but
nevertheless, be become skilled pianist.
Started as a general practitioner / anesthetist
He became a lecturer in the university of Indiana polis, during which time he was
practicing anesthetist in that city. Gave anesthetics in France during First World
War. Later he went to Los Angles where he became associate clinical professor
of Anesthesiology, at the University of Southern-California School of medicine. A
leading pioneer of American anesthesia.

Contribution:
Administration of nitrous oxide and air for obstetrics and minor surgery.
Description of the anesthetic properties of divinyl-ether
Reintroduction with R.M. waters of a cuffed tracheal tube
Systemization of the signs of inhalational anesthesia (Guedels stages)
Pharyngeal airway
Introduction of controlled respiration using ether
Classic description of the clinical use of cyclopropane.
Bier received the Hickman medal from the Royal society of medicine in 1991.
Distinguished service award of the American society of anesthesiologists in 1951.
There is a Gudel-memorial anesthesia centre in San Francisco, together with an
eponymous lecture established in his honor by the university of California medical
centre in Los-Angeles.
Died in California in 1956

Stages of anesthesia:
1. Stage of analgesia
2. Stage of excitement
3. Stage of surgical anesthesia
a. Regular breathing to cessation of eye movement
b. Commencement of intercostals paralysis
c. Complete (total) paralysis of intercostal paralysis
d. Complete diaphragmatic paralysis
4. Apnoea cardiopulmonary arrest

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JOSEPH PRIESTLEY (1733-1804)


Born in Fieldhead near Leeds, the son of a handloom worker, and brought up in a strict
Nonconformist Calvinistic atmosphere by an aunt. Educated at Batley Grammar School.
Trained as a dissenting minister and took charge of Mill Hill Chapel in Leeds in 1773. He
then became a schoolmaster and experimenter in chemistry, physics and electricity. He
never gave up the phlogiston theory, unlike Lavoisier who discredited it and who was
guillotined during the French Revolution. Next, Priestley spent seven years as librarian
and companion to the second Earl of Shelbourne (1737-1805) at Bowood, and isolated
or identified 'alkaline air' (NH3), 'vitriolic acid air' (SO2), 'dephlogisticated air' (O2) in
1774, a gas given the name of oxygen by Lavoisier (1743-1797) and produced by
heating mercuric oxide with a burning glass; 'dephlogisticated nitrous air' (N2O) in 1773
and 'Nitrous acid air' (NOZ). (One of his teachers, Mathew Turner of Manchester,
described the anesthetic effects of ether in 1744.) He also discovered methane and the
absorption of carbon dioxide (fixed air) by green plants in the presence of sunshine with
the formation of oxygen. By subjecting carbon dioxide to pressure in water he
discovered 'soda water'. He was elected a Fellow of the Royal Society and became a
Doctor of Laws of the University of Edinburgh. From the former institution he received a
Copley Medal for a paper on 'The Different Kinds of Air'. His discoveries led Thomas
Beddoes (1760-1808) of Bristol to experiment with the therapeutic effects of these
'airs'. In 1780 he went to Birmingham to take charge of a Unitarian congregation, The
New Meeting House, and in this city he became a member of the famous Lunar Society,
which brought him into contact with Erasmus Darwin (1731-1802), physician and
grandfather of Charles (1809-1882), James Watt (1736-1818), scientist and inventor
and William Murdoch (1757-1839), engineer and the inventor of gas lighting. He
became a close friend of, and correspondent with Benjamin Franklin (1706-1790),
American printer, inventor and diplomat. He was an opponent of political
discrimination against Dissenters, and on the second anniversary of the fall of the
Bastille (14 July 1789) his chapel, home, scientific apparatus, books and manuscripts
were looted by a High Tory Royalist mob, forcing him to seek refuge in Hackney, near
London. His left-wing political opinions still separated him from his scientific colleagues
so that in 1794 he joined his sons in Northumberland, Pennsylvania. Here, he added
farming to his other activities and soon became a leader of his new community. He died
of oesophageal obstruction in 1804 at the age of 70. A statue to Priestley was unveiled
in Birmingham by Thomas Henry Huxley in 1874 to mark the centenary of the discovery
of oxygen. Hilaire Belloc (1870-1953), the poet, journalist and historian, was a greatgrandson.

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HUMPHRY DAVY (1778-I829)


Born in Cornwall, the son of a wood carver. Became apprenticed to J. B. Borlase,
surgeon, of Penzance, in 1795. At the age of 17 he experimented with nitrous oxide and
the effects of its inhalation. In 1798 Davy became superintendent of Thomas Beddoes's
(1760-1808) Pneumatic Institute in Clifton, Bristol, for the treatment of pulmonary
tuberculosis by inhalation of gases; other gases used were hydrogen, oxygen, 'water gas'
and carbon dioxide. Humphry Davy published his book Researches, Chemical and
Philosophical: Chiefly Concerning Nitrous Oxide (London: J. Johnson, 1800). "On the day
when the inflammation was most troublesome, I breathed three large doses of nitrous
oxide. The pain always diminished after the first four or five respiration. In this, Davy
suggested that nitrous oxide inhalations might be used to relieve the pain of surgical
operations and named it laughing gas. A nitrous oxide container was made by James
Watt (1736-1819) in 1799 to assist this research. The idea was not pursued by
Humphry Davy or anyone else, except for its entertainment value, but his work was
known to, and may have influenced, Gardner Quincy Colton (1814-1898) 44 years later.
In later life, Davy became famous. He invented the miner's safety lamp, was created a
baronet in 1818, and was elected President of the Royal Society in 1820. Among Davy's
colleagues at Bristol was Dr Peter Mark Roget, FRS, famed for his Thesaurus of English
Words and Phrases (1852). Davy prepared nitrous oxide by the method of Berthollet
(1785) by heating ammonium nitrate. He was Faraday's teacher and was the first to
describe sodium and potassium.

HENRY HILL HICKMAN (1800-1830)


Born 27 January 1800 at Lady Halton, Bromfield, in Shropshire. Medical education
received in Edinburgh, but did not graduate there (MRCS, England, 1821). He settled in
practice in Ludlow and later in Tenbury Wells in Worcestershire. He married in 1821.
While at Shifnal, in Shropshire, his interest in gas therapy was aroused, as the village
was the birthplace of Thomas Beddoes. Familiarizing himself with the pioneer work of
Davy, Priestley and Michael Faraday (1791-1867), Hickman returned to Ludlow and
commenced experiments on animals (controlled asphyxiation) in 1825. He was able to
perform surgical operations painlessly on them, by causing them to inhale carbon
dioxide. This was the first work on surgical anesthesia induced by inhaling a gas. His
results where published in a paper, 'A Letter on Suspended Animation' (Ironbridge,
1824), when W. T. G. Morton was a child of 5, but attracted no attention from scientific
men in England. Even Sir Humphry Davy, who was approached by Hickman's friend, T.
A. Knight, FRS, showed no interest. Charles X of France (1752-1827) was appealed to in
1828, and the French Academy of Medicine agreed to investigate Hickman's results, but
nothing came of the matter. Baron Dominique Jean Larrey (1766-1842), one of
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Napoleon's surgeons, however, gave Hickman some encouragement. Hickman died


prematurely, aged 29, at Tenbury Wells, and was buried in Bromfield churchyard,
Shropshire, where, in 1930, a memorial was erected in the porch by the Anesthetic
Section of the Royal Society of Medicine, unveiled by Sir St Clair Thompson and
dedicated by the Bishop of Hereford (Br. Med. J. 1930, 12 April). The first allusion to
Hickman in recent times was in an article by C. J. S. Thompson in the Br. Med. J. 1912, 1,
843.

HORACE WELLS (1815-1848)


Born in Hartford, Connecticut. In 1844, on 10 December. Gardner Q. Colton (18141898), a travelling lecturer in chemistry, gave a demonstration of the effects of inhaling
nitrous oxide at Hartford. Connecticut. Horace Wells, a local dentist was present and
noticed that a young shop assistant, Samuel Cooley, while under the influence of the gas,
banged his shin and made it bleed, but stated afterwards that he experienced no pain.
Wells persuaded Colton to try the gas during a dental extraction, and on the following
day; 11-December 1844, the experiment was carried out "with Colton as anesthetist,
John M. Riggs (1810-1885) as dentist and Wells as patient. It was a big success "A new
era in tooth pulling", according to Wells. Wells learnt from Colton the method of
manufacture of nitrous oxide and used, it in his denial practice on 15 patients. It was
administered from an animal bladder through a wooden tube into the mouth, while the
nostrils were compressed. Later he went to Boston to interest a larger audience in his
discovery. He demonstrated the method to the students of Harvard Medical School, in
the class of Dr John Collins Warren (1778-1856), but the patient complained of pain; the
affair was a fiasco and Wells was hissed out of the room as a fraud. Morton and Charles
I. Jackson (l805-1880) were present at this operation in January 1845. Wells returned to
Hartford and continued to use the gas, but the introduction of ether gradually ousted
nitrous oxide. In 1847 Wells published his letter 'A History of the Discovery of the
Application of Nitrous Oxide Gas, Ether, and Other Vapours to Surgical operations. In
1847 he opened a dental office in New York City but soon afterwards Wells gave up
dentistry, became a chloroform addict, travelled around the country with a troop of
performing canaries, and was Incarcerated in jail after be spattering a New York
prostitute, with sulphuric acid, while recovering from self-administered chloroform. He
committed suicide by cutting his femoral artery, aged 33.
Colton reintroduced the use of nitrous oxide in dentistry in 1863, at New Haven.

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SIR WILLIAM MACEWEN (1847-1924)


Born in Rothesay in the Isle of Bute, Scotland, on 22 June 1847 youngest of 12
children and son of a sea captain, just 7 months after Simpson's introduction of
chloroform. A medical student in the University of Glasgow, he qualified in 1869
and proceeded to the MD degree 3 years later. While the Regius Professor of
surgery, Joseph Lister, was developing his system of antiseptic surgery, Macewen
became his dresser and this association with the great man had a profound effect
on Macewen's subsequent professional development. Following resident
appointments in the Royal Infirmary, he was appointed medical superintendent
of the Belvedere Fever Hospital, where he had the harrowing experience of
treating patients suffering from respiratory obstruction due to laryngeal
diphtheria, an experience which led him to his great discovery of oral laryngeal
intubation. Leaving the Fever Hospital he went into general practice and became
a parochial medical officer but gradually his interests centred on surgery and he
obtained appointments at both the Glasgow Royal Infirmary and Western
Infirmary, culminating in his nomination to the chair as Regius Professor of
surgery in the University of Glasgow in 1877. a post he was to fill with great
distinction for the next 15 years. He was invited to become the first professor of
surgery at the new Johns Hopkins Hospital in Baltimore, but refused it, the post
going to William Stewart Halsted. On the accession of King Edward VII in 1902,
he was knighted. Macewen became president of the British Medical Association
in 1922 and of the International College of Surgeons when it met in London the
following year. A tall, handsome, impressive personality who tolerated fools
badly, and went his own way.
His numerous surgical contributions included the diagnosis and treatment of
cerebral abscess, surgery of the brain, the spine, chest and bones. He was an
early exponent of aseptic surgery in which sterilization of instruments and
dressings was carried out by heat.
He was the pioneer of oral and nasal tracheal intubation as an alternative to
tracheotomy, performing the manoeuvre by touch in the conscious patient. He
first used rubber and gum elastic catheters in the treatment of laryngeal
diphtheria, later metal and 'flexometallic tubes' during operations on the base of
the tongue and pharynx in I878. A sponge was packed round the superior
laryngeal aperture and chloroform and air administered through the tube, thus
protecting the lungs from contamination.
In addition to his great technical advances. Macewen paid constant attention to
teaching his students the rudiments of safe anesthesia, a form of tuition
uncommon at that time. He remained a great believer in chloroform anesthesia.
He became a Surgeon Rear-Admiral and Consultant to the Royal Navy in Scotland
in 1914.

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HEINRICH FRIEDRICH WILHELM BRAUN (1862-1934)


Braun has been called 'the father of local analgesia' and he coined the term 'conduction
anesthesia'. He was born in Rawitch in Poland in 1862. and although intending to
become a musician, he graduated in medicine in 1887 in Dresden, and after a period as
assistant to Karl Thiersch (1822-1895) in Leipzig and Richard von Volkmann (18301889) in Halle, whose niece he married in 1888, became director of the Deaconess
Hospital in Leipzig where his interest in local analgesia was developed, having been
stimulated by Max Oberst (1849-1925) of Halle. In 1902 he introduced the use of
adrenaline in local analgesic solutions of cocaine, and in 1905 became the pioneer of the
new drug procaine. In this year also appeared the first edition of his classic textbook,
Local Anesthesia; the eighth edition was published in 1933. He preferred conduction
(nerve) block to Schleich's infiltration. Braun was appointed to direct the new hospital
at Zwickau in 1906, and here he passed the remainder of his professional life. He
introduced dental local analgesia into Germany. He described the anterior approach to
the coeliac plexus (anterior splanchnic block) and was the inventor of the Braun splint.
He was also interested in general anesthetics but realized their danger and devised an
apparatus for the safe administration of chloroform and ether vapour was president of
the German Surgical Society in 1924 and retired in 1928.

ARTHUR LAWEN (1876-1958)


Lawen was born in 1876 in Waldheim in Saxony, and qualified at Leipzig in 1900. He
became in Leipzig a pupil of Heinrich Braun and later of Friedrich Trendelenburg
(1844-1924) and Erwin Payr (1871-1976) of Griefswald. He held senior posts at Leipzig
and Marburg and was appointed professor of surgery at Konigsberg in East Prussia
where his chief work was done. In 1912 he employed curare to reduce the amount of
ether needed for relaxation, in an attempt to reduce the incidence of postoperative
pulmonary complications, which were then thought to be due to ether vapour. This
work was interrupted by the First World War. Lawen was the first to describe
paravertebral conduction anesthesia, and in 1910 he was the first to show that
extradural analgesia was a safe and practical form of pain relief in pelvic and abdominal
surgery. For this he used large volumes of 1.5 or 2% procaine solution with sodium
bicarbonate, injected through the sacral hiatus. He did a great deal to popularize local
analgesia, tracheal intubation and artificial respiration. After 1945 he became a refugee
from East Germany, having lost his sons, his possessions and his university chair during
the war. He died in 1958, aged 82.

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GASTON LABAT (1877-1934)


Born in the Seychelles and graduated at Montpellier, Took up the study of medicine at
the age of 37 in 1914 after running a successful pharmacy in Mauritius. Became
anesthetist to Victor Pauchet (1869-1936), surgeon to the St Michael Hospital in Paris,
and was co-author with Pauchet of the later editions of the latter's book. Was invited to
the Mayo Clinic in 1920 and-became special lecturer on regional anesthesia there.
Wrote his classic book Regional Anesthesia: Its Technique and Clinical Application in
1922. Subsequently became clinical professor of surgery (anesthesia) at New York
University and worked at the Bellevue Hospital. Founded American Society of Regional
Anesthesia in 1923. Died in October 1934 in New York, A third (posthumous) edition of
his book was published in 1967, edited by J. Adriani, and a fourth in 1985.
His book, outstanding in its time, had a great influence on the development and
acceptance of regional analgesia. In 1922 its main readers were surgeons. Only in later
years was regional analgesia practised by anesthetists.

RALPH MILTON WATERS (1883-1979)


Born in North Bloomfield, Ohio, of Anglo-Scottish descent. Became a student at Western
Reserve University in Cleveland in 1903 and after taking an arts degree became MD in
1912. Settled in general practice in Sioux City in Iowa, married and remained there for 5
years. Gradually became interested in anesthesia and the basic sciences so that by 1916
anesthesia came to occupy much of his time and he decided to specialize; an unusual
step to take at the time. He opened a private clinic as a commercial venture with an
operating room and facilities for minor surgery, where he gave the anesthetics; one of
the first 'day-stay' clinics in the US. In 1923, he acquired an anesthetic practice in
Kansas City where he remained for 3 years. He hurt his back, lifting an overweight
patient, and as a result had to spend 6 months in a brace. On recovery he visited John S.
Lundy (1884-1973), chief anesthetist at the Mayo Clinic, and on his way home stopped
off with friends at Madison. Here he met Chauncey Leake (1896-1978) the
pharmacologist, and Erwin Schmidt, professor of surgery, and as a result he was invited
in 1927 to take charge of anesthesia at the new Hospital of the State of Wisconsin at
Madison, which opened in 1924. He became in turn assistant professor, associate
professor and in 1933 full professor of anesthesia with clinical charge of anesthesia in
the university hospitals. This was the first such post in the US. He had a long and
distinguished career and his clinic became one of the leading centres of anesthesia in
the world. He visited Europe and the UK in 1936 and was awarded the Hickman Medal
by the Royal Society of Medicine in London in 1938. He retired in 1949 and was
succeeded by Alexander MacKay and then by Sidney Orth in 1952. His pupils included
Drs Rovenstine, Gillespie, Hingson, Lucien Morris, Gordh, Apgar, Neff and many others.
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His contributions to the growing specialty were numerous and important and he wrote
more than a hundred papers. Among the more noteworthy arc the following: insistence
on proper training programmes for young anesthetists; encouragement on careful note
keeping during anesthesia by means of punch-cards; the introduction of cyclopropane
into anesthetic practice; the development of the to-and-fro carbon dioxide absorption
system; a re-evaluation of chloroform; pioneering use of thiopentone in 1934;
endobronchial intubation.
He exercised a great influence on anesthesia in the US and in the UK during 1930-1950
and trained many anesthetists who later occupied important posts in universities in the
US and in Europe. He was one of the most important founding fathers of anesthesia as
we know it today. He received numerous medals, citations and honours from academic
bodies throughout the world and lived to enjoy 30 years of retirement, latterly growing
citrus fruit in Florida, where he died in Orlando on 19 December 1979.

HELMUT WEESE
Deserves an honoured place in the history of anesthesia as the first man to make
intravenous induction a safe and practical procedure. He was born in Munich into a
family originating from the German part of Poland, and the son of a lecturer in the
history of art. When he was nine, the family moved to Berne where his father became a
privatdozent at the University. Switzerland had a great influence on his development.
He decided to study medicine and attended the Universities of Berne. Zurich and
Munich where he qualified. His first post was in internal medicine under von Romberg,
and then he changed to pharmacology in 1925 and worked with W. Straub. He did well
in the new discipline and in his own turn became privatdozent. He paid particular
attention to the study of digitalis, wrote a book on it and as a result, became well known
both inside and outside Germany to physicians as well as to pharmacologists. When in
1928, F. Eicholtz who had previously described the effects of bromethol (Avertin)
moved to Konigsberg and then to

SIR ROBERT REYNOLDS MACINTOSH (1897-1989)


Born at Timaru, New Zealand Robert Macintosh travelled to Britain when the First
World War broke out and joined the Royal Fying Corps only to become a prisoner of
war. He-Qualified in medicine from Guy's Hospital in 1924 and after abandoning a
career in surgery became a successful dental anesthetist In London. In 1937 he moved
to Oxford to become the first Nuffield Professor of Anesthetics in the University, the first
such chair in Europe. He built up a renowned department in Oxford, undertaking clinical
work, teaching and the development of anesthetic apparatus. He secured the
appointment anesthetic sisters and nurses, wrote text books noted for their clarity and
encouraged the practice of regional analgesia. Essential of general anesthesia which he
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wrote with Dr Freda Bannister, was the first anesthetic book to be published by
Blackwell Scientific Publications Ltd, in 1941. Robert Macintosh was first and foremost
a clinical anesthetist and his name became "associated with many practical pieces of
equipment, the most famous being the Macintosh laryngoscope. He had an enormous
and worldwide influence on the evolution of anesthesia. He travelled to many countries,
including the underdeveloped ones, and his work was recognised by bestowal of
honorary degrees from Universities in Argentina, France and Poland. He was made an
Honorary Fellow' of the Faculties of Anesthetists in England, Ireland and Australia and
an Honorary Doctor of Science in the University of Wales. He was knighted in 1955.
The Corporate Organization of Anesthesia in Britain.
The Society of Anesthetists was founded in 1893 by J. F. W. M. Silk (1878-1943) of
King's College Hospital, and forty anesthetists joined it. First president, Woodhouse
Braine (1837-1907) of Charing Cross Hospital, with Silk as Honorary Secretary and
Dudley W. Buxton (1855-1931) of University College Hospital, as Treasurer. Published
first volume of Transactions in 1898. In 1908 was incorporated into the Anesthetic
Section of the new Royal Society of Medicine. The first society of anesthetists in the
world which had as its object the discussion of problems of anesthesia and the
advancement of the science and art of the subject. The Scottish Society of Anesthetists
dates from 1914.
The Association of Anesthetists of Great Britain and Ireland was founded in 1932 to
perform functions that could not be performed by the Anesthetic Section of the Royal
Society of Medicine. These were (and are): to promote the development and study of
anesthetics and their administration and the recognition of the administration of
anesthetics as a specialized branch of medicine; to co-ordinate the efforts and activities
of anesthetists; to represent anesthetists and to promote their interests; to promote
the establishment of diplomas and degrees in anesthesia; to encourage and promote cooperation and friendship between anesthetists; and to do all such lawful things as may
be incidental or conducive to the attainment of such objects. The first president was
Henry Featherstone (1894-1967) of Birmingham with W. Howard Jones of Charing
Cross Hospital as Secretary and Z. Mennell (1876-1959) of St Thomas Hospital, London
as Treasurer. At this time there were only fifty specialist anesthetists in the whole of the
UK.84 (For a description of the 'Arms' of the Association, see Boulton T. B. Anesthesia,
1974, 29, 627.)
The Faculty of Anesthetists of the Royal College of Surgeons of England was created in
1948 at the request of the Association of Anesthetists. The Fellowship (FFARCS) was
proposed in 1946 and the first examinations Qheld in 1953. A. D. Marston (1891-1962)
of Guy's Hospital was the first dean.

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The College of Anesthetists was created in 1989 when a new charter allowed the Faculty
of Anesthetists to evolve to collegiate status. It became The Royal College of Anesthetists
in 1992.
The Faculty of Anesthetists of the Royal College of Surgeons in Ireland was founded in
1959. The first examination for its fellowship taking place in 1961.

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