This document discusses cerebral aneurysms and subarachnoid hemorrhage. It notes that ruptured cerebral aneurysms account for 75% of subarachnoid hemorrhages, which affect 27,000 Americans per year. The majority of cerebral aneurysms occur at specific locations on major cerebral vessels. Ruptured aneurysms have high rates of morbidity and mortality, while unruptured aneurysms have lower risks if left untreated. The document discusses risks factors, classifications, complications including vasospasm, and approaches to treatment and anesthesia management for patients with cerebral aneurysms and subarachnoid hemorrhage.
Perioperative Management of Hypertensionmagdy elmasry
Hypertension is most common medical reason for postponing surgery.How important is peri-operative hypertension?Hypertensive comorbidities associated with adverse perioperative outcomes .New Guidelines for managing patients with high blood pressure before surgery
Consequences of anesthesia on blood pressure regulation.
Comprehensive presentation on intra arterial blood pressure with a good insight into the the basic physics and brief look into the risks and complications.
Perioperative Management of Hypertensionmagdy elmasry
Hypertension is most common medical reason for postponing surgery.How important is peri-operative hypertension?Hypertensive comorbidities associated with adverse perioperative outcomes .New Guidelines for managing patients with high blood pressure before surgery
Consequences of anesthesia on blood pressure regulation.
Comprehensive presentation on intra arterial blood pressure with a good insight into the the basic physics and brief look into the risks and complications.
Ventricular septal rupture (VSR) is a rare but lethal complication of myocardial infarction (MI).
Bimodal peak
Range: few hours 2 weeks
Average time to rupture
2-8 days
Time course may be accelerated by thrombolysis, possible related to intramyocardial hemorrhage
Renal artery stenosis is the leading cause of secondary hypertension and may lead to :
Resistant (refractory) hypertension,
Progressive decline in renal function, and
Cardiac destabilization syndromes (Flash pulmonary edema, recurrent heart failure, or acute coronary syndromes)
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
6. More than 90% of cerebral aneurysm occur at the
following locations-
1-The origin of the posterior communicating artery
2- The region of the anterior communicating artery
3- Middle cerebral artery bifurcation
4- apex of basilar artery
5- internal carotid artery bifurcation.
7.
8. Acquired vascular lesions secondary to
degenerative changes in the muscular and elastic
components of the vessel wall.
Usually occuring at the branching points of the
major cerebral vessels.
A deficiency of type III collagen in arteries is
assosiated with SAH.
9. Congenital influences may play a role.
Disease processes associated with an increased
risk of IA
Polycystic kidney
Hypertension
Coarctation of the aorta
Ehler- Danlos syndrome
Fibromuscular disease
smoking
10. Small – less than 12 mm 78%
Large – 12-24 mm 20%
Giant - 24mm 2%
Majority of aneurysms that bleed are less than 1
cm of diameter.
Aneurysms that are less than .5 cm diameter
have less risk of bleeding.
12. Causes increase ICP
Increased ICP causes decrease CBF
Bleeding stops with decreased CBF
Decreased consciousness
2 clinical scenarios are seen typically
Return to normal ICP and CBF with return of function
High ICP continues with low CBF
13. Grade 0 - Aneurysm is not ruptured
Grade 1 - Asymptomatic, min. headache and sl. nuchal
rigidity
Grade 2 - Moderate to severe headache, nuchal rigidity, but
no neurologic deficit other than cranial nerve palsy
Grade 3 - Drowsiness, confusion, mild focal deficits
Grade 4 - Stupor, mild or severe hemiparesis, possible early
decerebrate rigidity, vegetative disturbances
Grade 5 - Deep coma, decerebrate rigidity, moribund
appearance
14. WFNS Grade GCS Score Motor Deficit
I 15 Absent
II 13-14 Absent
III 13-14 Present
IV 7-12 P or A
V 3-6 P or A
15. It is very important to assess the degree of SAH.
There are different grading scales for this
purpose.
Modified Hunt and Hess grading scale is most
commonly used because of ease of application.
Extent of vasospasm is related to the amount of
subarachnoid blood present.
CT scan is graded according to the Fisher grade
16. Grade 1 – No blood detected
Grade 2- Diffuse thin layer of subarachnoid
blood ( vertical layers less than 1 mm thick)
Grade 3 – Localised clot or thick layer of
suarachnoid blood( vertical layer = 1 mm thick)
Grade 4 – Intracerebral or intraventricular blood
with diffuse or no subarachnoid blood
17. The clinical management of cerebral aneurysms
centers on the reduction of risk of hemorrhage in
uruptured cases and of repeat hemarrhage in
SAH.
The major complications of SAH are –
1- Aneurysmal rebleeding
2- delayed cerebral ischemia secondary to
vasospasm
18. Incidence of rebleeding is 14-30 % .
Peak incidence at the end of the first week of
SAH.
High risk of rebleed during angiography
Assosiated with high rate of mortality and
morbidity.
19. Blood pressure control is of critical importance
in reduction of risk of rebleeding.
Antifibrinolytic agents have been used
successfully to control rebleeding
20. Vasospasm is the leading cause of morbidity and
mortality in patients who initially survive SAH
Radiological evidence of vasospasm is noted in upto
70% of patients .
Clinical vasospasm occur in almost 30% of patients
Clinical vasospasm occur after 4-9 days of SAH
It typically does not occur after 2 weeks of
aneurysmal rupture.
21. Pathological changes occur are contraction of
vascular smooth muscles and thickening of the
vessel wall
Prostaglandins , biological amines , peptides , cyclic
neucleotides , calcium , lipid peroxidation and free
redicals are implicated .
Conventional cerebral angiography , xenon-
enhanced CT and transcranial doppler is used to
confirm the presence of vasospasm
22. There is a correlation between the amount of
subarachnoid blood after aneurysmal rupture and
the occurrence and severity of vasospasm
Because of this , extensive removal of subarachnoid
blood by early surgery is attempted to decrease the
incidence of vasospasm.
Nimodipine , a calcium channel blocker is
successfully used .
23. Triple H therapy – hypertension , hypervolumia
and hemodilution is used in treatment of
vasospasm.
A new method for symptomatic vasospasm
includes use of cerebral angioplasty to dilate
constricted major cerebral vessels.
26. Assesment of patients neuroloical condition and
clinical grading of SAH
A review of patient,s intracranial pathological
conditions including CT scan and angiograms.
Monitoring of ICP and transcranial doppler
ultrasonography.
27. Evaluation of patients other systemic functions
, premorbid as well as present
Systems known to affected by SAH
Communication with the neurosurgeon regarding
positioning and special monitoring
Optimisation of patient,s condition by correcting
any biochemical and physiological condition
28. To assess the CNS , as we have discussed before
there are grading scales-
1. Modified Hunt and Hess grading
2. WFNS grade scale
3. Fisher grading of CT scan
29. The greater the clinical grade , more likely
vasospasm , elevated ICP , impaired autoregulation
and disordered response to hypocapnia will occur
Worse clinical grade is also assosited with cardiac
arrythmia , myocardial dysfunction , hypovolumia
and hyponatremia.
30. ECG abnormalities
Very common
Many changes seen
cannon t wave, Q-T prolongation, ST changes
Autonomic surge may in fact cause some
subendocardial injury from increase myocardial wall
tension
31. Cardiac dysfunction does not appear to affect
morbidity or mortality (studies from Zaroff and
Browers)
Prolonged Q-T with increased incidence of
ventricular arrhythmias
PVC’s are seen in 80%
ECG changes occur during the first 48 hrs of SAH and
correlate with amount of intracranial bleed.
32. ECG changes reflect the severity of neurogenic
damage and have not shown to contribute
perioperative mortality and morbidity
The decision to operate should not be influenced
by these ECG changes.
33. Hydrocephalous
Seizures
13%
Vasospasm may be cause
Increased risk of rebleed
Treat and prophylaxis
Headache, visual field changes, motor
deficits
34. SIADH
Cerebral salt wasting syndrome
release of naturetic peptide
hypovolemia, increased urine NA and volume
contraction
Distinguish between the two and treat
accordingly
35. Neurogenic pulmonary edema
1-2% with SAH
Hyperactivity of the sympathetic nervous system
Pneumonia in 7-12% of hospitalized patients with
SAH
36. 0-3 days post bleed appears to be optimal
Improved outcome within 6 hours of rupture
despite high H/H grade
If delayed, should be done after 10 days post
bleed after fibrinolytic phase
The results are worst with surgery performed
between 7 to 10 days.
37. Avoid abrupt changes in BP
Maintain CBF with normal to high blood pressure
Avoid increase of ICP
Assess immobility & vital signs control
Achieve brain relaxation
Allow for swift emergence & neurologic assessment
Be prepared for disaster
38. Arterial blood pressure- beat to beat monitoring
of MAP
ECG- myocardial ischemia/ arrhythmia
Pulse oximetry- systemic hypoxia
EtCO2- trend monitor for Paco2/ detection of VAE
Temperature- via oesophageal lead; to allow
modest, passive hypothermia(~35o C)
Urine output- adequacy of renal function &
hydration
39. Blood glucose/ serum electrolytes/ osmolality
-particularly if mannitol is used
Hemoglobin & hematocrit- to estimate extent
of bleeding/ permissible blood loss
Jugular venous bulb monitoring- adequacy of
cerebral perfusion & oxygenation
EEG- CMR/ cerebral ischemia/ depth of
anaesthesia
40. Evoked potentials- intactness of specific CNS
pathways
Transcranial oximetry- noninvasive information
on regional cerebral oxygenation
TCD ultrasonorgaphy
41. TCD is a indirect measure CBF
It is unreliable as a measure of CBF in patients of
SAH because of changes in vessel diameter
But it has become valuable for diagnosing
vasospasm noninvasively before the onset of
clinical symptoms
TCD has been successfully used in the
perioperative management of patients with
cerebral aneurysm.
42. Continuous TCD monitoring may improve the safety
of induced hypotension by correlating the blood
velocity change to the decline in the blood
pressure.
It has been used perioperatively to confirm the
diagnosis of aneurysmal rupture.
43. Patients should receive their regular dose of
nimodipine and dexamethasone
Tab Loarazepam 1-2 mg and tab rantac 150
should be given in night before surgery
To relieve anxiety inj midazolam in incremental
dose of 1 mg is given in the morning of surgery.
44. There is risk of rupture of aneurysm at the time
of induction due to high blood pressure during
tracheal intubation
As a general principle , the patients blood
pressure should be reduced by 20-25% below the
baseline value and hypertensive response to the
tracheal intubation should be alleviated.
45. Another useful approach is to balance the risk of
ischemia from a decrease in CPP against the
benefit of a reduced chance of aneurysmal
rupture from a decrease TMP.
Conceptually induction phase is consisting of 2
parts
Induction to achieve loss of consciousness
Thiopental ( 3- 5 mg/kg ) or propofol (1-2.5
mg/kg ) in combination with fentanyl (3-7 ug/kg)
or sufentanil(.3-.7 ug/kg) is suitable
46. Other alternatives include etomidate (.3-.4 mg/kg)
and midazolam ( .1-.2mg/kg)
Prophylaxis against rise in BP during laryngoscopy
Many agents have been used successfully to
alleviate hypertensive response of intubation.
Fentanyl ( 5-10 ug/kg)
Sufentanil ( .5-1 ug/kg)
Esmolol (.5 mg/kg)
Labetolol (10-20 mg)
Intraveous or topical lidocaine (1.5-2 mg/kg)
Second dose of thiopental ( 1-2 mg/kg)
47. Intravenous adjuncts are preferred in patients
with poor SAH grades whereas deep inhalational
anesthetics are preferred in patients with good
SAH grades.
48. Choice of muscle relaxant
Vecuronium is most hemodyanamically stable
and suitable muscle relaxant.
Succinylcholine causes incease in ICP.
Atracurium may cause hypotension.
Pancuronium causes tachycardia and
hypertension
49. The location and size of aneurysm generally
determine the position of patient.
Anterior circulation aneurysm are usually
approached using fronto-temporal incision with the
patient in supine position
Basilar tip aneurysms are approached using
subtemporal incision with the patient in lareral
position
50. Vertebral and basilar trunk aneurysms approached using
suboccipital incision with the patient in sitting or park
bench position
Avoid extreme positioning (extreme rotation or flexion
of neck to avoid IJV compression)
Padding/ fixing of regions susceptible to injury by
pressure/ abrasion/ movement -groin, breasts, axillary
region
-falling extremities
-knees kept in mild flexion to prevent
backache postoperatively
Mild head-up position (to aid venous cerebral drainage)
51. Elevation of contralateral shoulder by wedge/ roll
(to prevent brachial plexus stretch injury if head is
turned laterally)
Meticulous attention to specific problems in prone/
lateral/ parkbench/ sitting positions
Care of ETT –easy intraoperative accessibility
-fixed & packed securely to
prevent accidental extubation, or abrasions
resulting from movement
52. Care of eyes- taped occlusively to prevent corneal
damage (from exposure/ irrigation with antiseptic
solutions)
APPLICATION OF SKULL PIN HOLDER FRAME
Pain- provides maximal nociceptive stimulus
- must be blocked adequately by
i. deepening of anaesthesia (i.v. bolus of
thiopentone 1mg/kg or propofol 0.5 mg/kg)
ii. analgesia (i.v. bolus of fentanyl 1-3
mcg/kg or alfentanil 10-20 mcg/kg or remifentanil 0.25-1
mcg/kg)
53. iii. local anaesthetic infiltration at pin site
iv. antihypertensive β-blockers e.g.
Esmolol 1 mg/kg or Labetalol 0.5-1 mg/kg
VAE- may occur with pin insertion
54. Positioning of Anaesthetist
-optimal patient monitoring
-access to airway/ intravenous & intraarterial
lines
55. The goals during maintainance of anesthesia are --
To provide a relaxed or ‘slack’ brain that will allow
minimum retraction pressure
To maintain perfusion to the brain
To reduce TMP if necessary during dissection of the
aneurysm and final clipping
Allow prompt awakening and assessment of
patients with good SAH grades
56. Maintenance
CHOICE OF TECHNIQUE
Volatile agents Intravenous agents
Advantages Controlability/ predictability/ early
awakening
Good control of CBF, ICP, & brain
bulk
-cerebrovasoconstriction
↓ in ICP
Disadvantages Poor control of CBF, ICP, & brain
bulk
-cerebrovasodilation
↑ in ICP
Prolonged/ unpredictable
awakening
May interfere with D/D of delayed
awakening
May require emergent CT scan
to rule out surgical complications
Type of
surgery
Simple, low risk of ↑ed ICP Complex, high risk of ↑ed ICP
57. Maintenance
CHOICE OF TECHNIQUE
Volatile agents Intravenous agents
Early institution of
moderate
hyperventilation
Mandatory Optional
Concurrent use with
N2O
Ideal agent
Usually avoided
-synergistic effects in ↑ing CBF &
CMR
-if used, ensure ↓in ICP by
i. hyperventilation
Ii. osmotic diuretics
Iii. BP control
Iv. adequate positioning/ cerebral
venous drainage
v. lumbar drainage
Vi. Use of < 1 MAC (e.g. < 1.15% of
isoflurane)
No
Can be used without
significant problems
Yes
58. Fluid Therapy
Fluid therapy should be guided by intraoperative blood
loss, urine output and CVP/PAWP
The aim is to maintain normovolumia before
aneurysmal clipping and slight hypervolumia and
hypertension after clipping.
Avoidance of hyperglycemia (worsens consequences of
cerebral ischemia)
59. Avoidance of hypoosmolality – can cause brain
oedema
i. Target osmolality: 290-320 mOsm/kg)
ii. Colloid oncotic pressure plays no significant role
in brain oedema
iii. Avoidance of glucose-containing & hypoosmolar
solutions (e.g. Ringer’s lactate, 254 mOsm/kg)
Preferred solutions – crystalloids: 0.9% NaCl
colloids: 6% HES (304 mOsm/kg)
60. Hematocrit- Target for >28%
Warming of I.V. solutions– may be avoided to
permit establishment of mild hypothermia (~350 C)
for neuroprotection
-must be essentially warmed at the end of
procedure to ensure normothermia for emergence
from anaesthesia
61. Hemodynamic control
-Undesirable CNS arousal & hemodynamic activation may
occur despite adequate depth of anaesthesia &
analgesia
-Consider use of i. Esmolol (1mg/kg: initial dose)
ii. Labetalol (0.5-1mg/kg: initial
dose)
iii. Clonidine (0.5-1mcg/kg: initial
dose)
Moderate hypothermia (~350C)
-may confer a degree of brain protection if ischemic
event occurs
62. Prevention
1. No over hydration
2. Sedation/ analgesia/ anxiolysis
3. Avoidance of application of any noxious stimulus with
sedation/ local anaesthesia
4. Head-up position
5. Osmotic agents (mannitol/ hypertonic saline)
6. β-blockers/ clonidine/ lignocaine
63. 7. Adequate hemodynamics: MAP, CVP, PCWP, HR
8. Adequate ventilation: PaO2>100mmHg;
PaCO2~35mmHg
9. Minimal possible intrathoracic pressure
10. Hyperventilation on demand (before induction)
11. Use of total I.V. anaesthestic agents for induction
& maintenance
12. Avoidance of cerebral vasodilators (e.g.
nitroglycerine)
64. Treatment
1.Hyperventilation
2.Osmotic agents
3.CSF drainage (if ventricular/ lumbar catheter in situ)
4.Augmentation of anaesthesia with I.V. anaesthetic
agents (e.g. propofol, thiopentone, etomidate)
5.Adequate muscle relaxation
6. Venous drainage (head-up/ avoidance of PEEP/
reduction of inspiratory time)
7.Mild controlled hypertension (if autoregulation is
present)
65. 5-7 minutes of occlusion with prompt reperfusion
are usually well tolerated but this duration is
insufficient for clipping difficult or giant aneurysms
A number of regimens have been used to extend
the occlusion duration
High dose Mannitol 2g/kg
SENDAI COCKTAIL - mannitol (500 ml of 20%
solution) + vitamin E (500 mg) + dexamethasone
(50 mg)
66. Pharmacological metabolic suppression by
thiopentone ( 5-6 mg/kg) or etomidate (.4-.5
mg/kg)
Etomidate is preferred over thiopental due to
greater hemodyanmic stability
Moderate hypothermia has also been to extend the
duration of tolerable occlusion
67. If the surgical procedure is uneventful , SAH grade I
and II patients should be extubated.
Because hypertensive therapy is useful in reversing
delated cerebral ischemia from vasospasm , modest
level of postoperative hypertension (<180mm hg )
should not be aggressively treated.
Depending on preoperative ventilatory status and
duration and difficulty of surgical procedure
68. SAH grade III patients may or may not be extubated.
Patients with preoperative SAH grade IV and V
usually require postoperative ventilatory support and
neurointensive care.
69. In the postoperative period blood pressure should be
maintained above 140-150 mm hg and less than 180
mm hg.
To distinguish residual anesthesia from surgical
cause following general guidelines are useful
1- Anesthesia causes global depression and any new
focal neurological deficit should alert to a surgical
cause
70. 2-The effect of potent inhaled anesthetics should
have larly dissipated after 30-60 minutes
3- patients whose pupils are midsized and having no
respiratoty depression are unlikly to experience a
narcotic overdose.
4- unequal pupils not present before surgery always
suggest a surgical cause.
Neurological assessment should be done every 15
minutes in the recovery room.