Final FRCA, 28/06/05
Final FRCA Exam Questions:
(my friend had these questions for his exam).
Long case
36y male with neurofibromatosis presents with convulsions he also hadright sided homonymous hemianopia for last few weeks.
He is a smoker andalcoholic.
O/E consious, appropriate, no focal neurology other than the eye sight.PR 56/min BP 140/90mmHg.
ECG- Right axis deviation, Up slurring of ST in V4&V5.
CXR-RUL collapse consolidation and a well circumscribed mass in the midzone.
FBC Unremarkable except MCV89
BioChem Unremarkable except high
ALPCT posterior cranial fossa tumour looks malignant.
Nerosurgens want todo a craniotomy
Questions
1.Summarise
2. Planned/ Emergency
3.Differential diagnosis Lung mets/ Nerofibromatosis
4.what is the % of Nerofibromatosis becoming malignant
5.What is R/homonymous hemianopia6.Alcohol intake what is the recommendation
How much is a unit of alcohol
7.ECG description
8.CXR description
9.Why MCV high/ Causes of high MCV
10.Why ALP high in this Pt normal billirubin
11.What other investigation you need
12. Will you proceed with the case
13. Principal of neurosurgery
14.What is the position for this surgery
Short Cases
74yRuptured aortic aneurysm while in the ward
What will you do now?How do you resuscitate circulation?
What will you do?
How much blood will you requestHow much will you resuscitate?How do you proceed?
Where will you anaesthetise?Take me through the process?
What induction agent will you use?Difference between Ketamine and Etomidate?What monitoring will you use
Do you need arterial line to start the caseHow do you monitor clotting
What is the principal of thrombo elastogram
When do you expect problems
How do you treat intra operative hypertension
26y Thoraxoscopic
Sympathectomy for hyperhydrosis
What do you see in the CXR- Pneumothorax
What else do you see- Subcutaneous emphysema
How to detect pneumothorax on the tableWhat do you do immediatelyHow do you insert chest drainWhere do you insert
Do you apply suction
25yMytonica Dystrophica
What are featuresMode of inheritanceOnsetWhat are the problems for anaesthetists
What is the principal of anaesthetic managementWhat is pathology associated
Basic science viva
Physics
Define Laminar flow/ Turbulant flow
Hagen Poiseulle’s formulae
Factors affecting turbulent flow & howWhat is the relevance to anaesthetistReynaulds number
Variable orifice flow meterPrinciple and relevance
Anatomy
Nerve supply of the foot Femoral nerve root valueRelation ship of those nerve to the ankle Ankle block performanceMaximum dose CalculationComplication
Pharmacology
Benzodiazepine action how do they actGABA recetor MidazolamEffects/ Side effects Uses
Continuos infusion
Context sensitive half life define
Normal half life of midazolam
Physiology
Draw clotting cascadeWhat is the role of the plateletsWhat is the importance of tissue factor
Fibrinolytic system
My viva questions, Dec 06
long case
middle aged Downs man for cataract, very anxious, has ASD, loud P2, XRC with prominent pulmonary veins, ECG with RAd and Rt sided strain, patient SOB.
questions
1. summary
2.how would you proceed
3.how would cardiologist treat (diuretics)
4. how would you manage GA?
Short clinical scenarios
1. Failed needle toracocentesis for tention pneumothorax XRC
diagnosis, reasons for failure, what would you do next?
2. IVDU for operation- all routine questions from exam books
3. Prone position- all routine questions
Clinical science viva
1. Physiscs- everything about cautery
2. physiology/pharmac- ICT/ how different anaesthetic agents affect ICT?
3. Organ donation issues, neonates?
Saturday, March 17, 2007
Cardiff SpR interviews
SpR Interview questions 1.
1. Presentation on any non-medical topic for 5 minutes.
2. What was the most useful course you attended?
3. Tell about the latest situation you called consultant for. Why was it necessary to call consultant?
4. Do you think we really need RCTs?
5. Tell about one audit which changed your practice.
6. What are your weaknesses?
7. Tell about cleanyourhands campaign.
8. Tell when you decided to do Anaesthetics?
9. Roll of internet in I & T.
10. when would you be available for job if offered?
Cardiff Interview for SpR 2Anaesthetics, Dec 05.
Panel 1
Presentation For 5 minutes.
15 minutes for preparation
Is it appropriate to deny the elective treatment for patients with self-inflicted co-morbidity?Related questions on presentation- Insurance, privatisation, finances ect.
CVTell your greatest achievement.
Tell why people would remember you in your last job.
Where would you prefer to work as a consultant?(A small DGH/ big teaching hospital)
What are you going to do during your SpR training?(Anything specific?)
Looking back at your career, what would you do differently than this CV?Little bit about sub-speciality interests.
Panel 2
Actor scenario-Explain the mum of a child who needs to go to ITU for suxamethonium apnoea after appendicectomy.Related theoretical questions on suxamethonium apnoea.
Clinical management question-
Paediatric transfer-Will you do it?What should be the competencies?What preparation would you make?
NHS and management question-What do you think of the idea of resident on-call consultant?
Panel 3
Research paper critical appraisal-What is the gold standard method?
Why a particular method has been used as a gold standard in this study?
What is Alfa, Beta error?What is study power?
What is Null hypothesis?Why Bland-Altman analysis is used in this study?Tell about this research study?What would you do this if you were the journal editor?
Audit, teaching, training-What is audit?Which national audit has made difference to quality of care?Which local audit in your hospital has made difference to quality of care?What do you need to get results from audit project?Why audits fail?
Panel 4
Dummy scenario-VentilationIntubationClinical judgementClinical decision making-
Adult for TKR on elective basis, what preparation, what anaesthetic options, details of regional and GA with emphasis on decision making.
SpR interview questions 3
SpR Anaesthetics Interview questions- Cardiff Rotation, September interviews.
1. Tell me something for which you are/will be remembered (school days activities, college etc..).
2. Should the health services be target oriented?
3. Who should monitor the training?
4. Obstetrics failed intubation protocol?
5. Caeserian section classification- grades?
6. Obstetric epidural procedure?
7. Pre-assessment clinic details.
8. Actor who was worried about cancellation of his hernia operation due to LRTI.
9. Research paper critical appraisal- in details.
10. How would you access journals?
11. Statistical techniques for comparison of & gt;2 study groups.
12. Do audits really help? Give example from your work place.
13. Severe COAD with INR 1.5- case management for hernia operation.
14. What if INR of 2 (on warfarin for artificial valve) and cardiologist advises stable haemodynamics throughout operation?
15. Dummy skills.
SpR Interview questions 4
My Interview for SpR
interview panels-
Panel 1- (20 minutes)
I was given a topic for presentation (15 min for preparation)-
How would you prevent cross infections in hospital?
(5 minute presentation).Related questions-Role of media in spread of health awareness. Will it be effective way to spread the message? How?
CV- important aspects of my CV?How are you planning to complete your ITU training?
Panel 2- (20 minutes)
Research paper discussion (They sent me a paper published recently in Anaesthesia journal- Critical appraisal of the paper).Related questions-Research, study, trials, prospective/ randomisation/ Double blind?Teaching & training-What are ideal teacher qualities?What are different teaching methods?What are different learning methods?Who do you learn?What is audit cycle?My audit?Do you know any recent audit which has made significant impact at national level/
Panel 3- (20 minutes)
Actor station-Actor (patient) was worried about the awareness under anaesthesia. I had to talk and explain him.Patient asked me the incidence of awareness (I didn’t know)(He kept asking- would you guarantee that I won’t be aware under anaesthesia?
Related questions- what would you do to prevent awareness? What is MAC? Monitoring to prevent awareness.Does it work?
NHS administration-Nurse anaesthetist- what do you think?Would they dilute our junior doctor’s training?Would it have a problem of profession demarcation between nurse anaesthetist and us.There is already scarcity of nurses, if you use up nurses for your fields then what would be the result?
EWTD-How would it affect you as a trainee? What are your solutions for that?How the consultants should improve their knowledge and skills apart from day to day working?
Panel 4- (12 minutes)
Clinical scenarios-
1.Sim man (computerised dummy with airway connected to monitoring system, which could adjust the sats according to your ventilation efficiency. Mask ventilation and dummy intubation .
Scenarios.2.Post operative hypotension, details of assessment, differentials, treatment.
1. Presentation on any non-medical topic for 5 minutes.
2. What was the most useful course you attended?
3. Tell about the latest situation you called consultant for. Why was it necessary to call consultant?
4. Do you think we really need RCTs?
5. Tell about one audit which changed your practice.
6. What are your weaknesses?
7. Tell about cleanyourhands campaign.
8. Tell when you decided to do Anaesthetics?
9. Roll of internet in I & T.
10. when would you be available for job if offered?
Cardiff Interview for SpR 2Anaesthetics, Dec 05.
Panel 1
Presentation For 5 minutes.
15 minutes for preparation
Is it appropriate to deny the elective treatment for patients with self-inflicted co-morbidity?Related questions on presentation- Insurance, privatisation, finances ect.
CVTell your greatest achievement.
Tell why people would remember you in your last job.
Where would you prefer to work as a consultant?(A small DGH/ big teaching hospital)
What are you going to do during your SpR training?(Anything specific?)
Looking back at your career, what would you do differently than this CV?Little bit about sub-speciality interests.
Panel 2
Actor scenario-Explain the mum of a child who needs to go to ITU for suxamethonium apnoea after appendicectomy.Related theoretical questions on suxamethonium apnoea.
Clinical management question-
Paediatric transfer-Will you do it?What should be the competencies?What preparation would you make?
NHS and management question-What do you think of the idea of resident on-call consultant?
Panel 3
Research paper critical appraisal-What is the gold standard method?
Why a particular method has been used as a gold standard in this study?
What is Alfa, Beta error?What is study power?
What is Null hypothesis?Why Bland-Altman analysis is used in this study?Tell about this research study?What would you do this if you were the journal editor?
Audit, teaching, training-What is audit?Which national audit has made difference to quality of care?Which local audit in your hospital has made difference to quality of care?What do you need to get results from audit project?Why audits fail?
Panel 4
Dummy scenario-VentilationIntubationClinical judgementClinical decision making-
Adult for TKR on elective basis, what preparation, what anaesthetic options, details of regional and GA with emphasis on decision making.
SpR interview questions 3
SpR Anaesthetics Interview questions- Cardiff Rotation, September interviews.
1. Tell me something for which you are/will be remembered (school days activities, college etc..).
2. Should the health services be target oriented?
3. Who should monitor the training?
4. Obstetrics failed intubation protocol?
5. Caeserian section classification- grades?
6. Obstetric epidural procedure?
7. Pre-assessment clinic details.
8. Actor who was worried about cancellation of his hernia operation due to LRTI.
9. Research paper critical appraisal- in details.
10. How would you access journals?
11. Statistical techniques for comparison of & gt;2 study groups.
12. Do audits really help? Give example from your work place.
13. Severe COAD with INR 1.5- case management for hernia operation.
14. What if INR of 2 (on warfarin for artificial valve) and cardiologist advises stable haemodynamics throughout operation?
15. Dummy skills.
SpR Interview questions 4
My Interview for SpR
interview panels-
Panel 1- (20 minutes)
I was given a topic for presentation (15 min for preparation)-
How would you prevent cross infections in hospital?
(5 minute presentation).Related questions-Role of media in spread of health awareness. Will it be effective way to spread the message? How?
CV- important aspects of my CV?How are you planning to complete your ITU training?
Panel 2- (20 minutes)
Research paper discussion (They sent me a paper published recently in Anaesthesia journal- Critical appraisal of the paper).Related questions-Research, study, trials, prospective/ randomisation/ Double blind?Teaching & training-What are ideal teacher qualities?What are different teaching methods?What are different learning methods?Who do you learn?What is audit cycle?My audit?Do you know any recent audit which has made significant impact at national level/
Panel 3- (20 minutes)
Actor station-Actor (patient) was worried about the awareness under anaesthesia. I had to talk and explain him.Patient asked me the incidence of awareness (I didn’t know)(He kept asking- would you guarantee that I won’t be aware under anaesthesia?
Related questions- what would you do to prevent awareness? What is MAC? Monitoring to prevent awareness.Does it work?
NHS administration-Nurse anaesthetist- what do you think?Would they dilute our junior doctor’s training?Would it have a problem of profession demarcation between nurse anaesthetist and us.There is already scarcity of nurses, if you use up nurses for your fields then what would be the result?
EWTD-How would it affect you as a trainee? What are your solutions for that?How the consultants should improve their knowledge and skills apart from day to day working?
Panel 4- (12 minutes)
Clinical scenarios-
1.Sim man (computerised dummy with airway connected to monitoring system, which could adjust the sats according to your ventilation efficiency. Mask ventilation and dummy intubation .
Scenarios.2.Post operative hypotension, details of assessment, differentials, treatment.
Saturday, October 28, 2006
Arterial blood pressure
www.medicineteacher.blogspot.com
Measurement
History
Hales 1733
Riva-Rocci 1896
Cushing 1901
Direct method
Sites
Procedure
Components
Frequency response <40Hz/<20Hz required
Resonance, damping
Other uses- waveform, temperature, dye, blood sampling
Indirect methods
Mercury/aneroid manometer- palpation, oscillation, auscultation (Korotkoff sounds), Pulse detector, Doppler probe.
Oscillotonometer- two cuffs: inflation, pulse detection
Automatic measuring devices- single cuff for inflation & pulse detection
Indirect methods
Finapress device- cuff around finger, continuous measurement
Continuous arterial tonometry- continuous, pressure transducer over radial artery, its output is proportional to BP, periodic calibration needed.
Details
Direct method
Manometer with cuff
Oscillometry- Most common clinical method
Finapress method
Doppler probe/arterial tonometry
Errors NIBP
Detection of Korotkoff sounds
Cuff size
Zero/calibration errors
Errors IABP
Damping- high resonance and critical damping ideal; bubbles, canula, tap, tubing reduce the natural frequency of the system
Complaint catheter wall- damping
Clots- reduce resonant frequency- damping
Zeroing errors
www.medicineteacher.blogspot.com
www.medicineteacher.blogspot.com
Measurement
History
Hales 1733
Riva-Rocci 1896
Cushing 1901
Direct method
Sites
Procedure
Components
Frequency response <40Hz/<20Hz required
Resonance, damping
Other uses- waveform, temperature, dye, blood sampling
Indirect methods
Mercury/aneroid manometer- palpation, oscillation, auscultation (Korotkoff sounds), Pulse detector, Doppler probe.
Oscillotonometer- two cuffs: inflation, pulse detection
Automatic measuring devices- single cuff for inflation & pulse detection
Indirect methods
Finapress device- cuff around finger, continuous measurement
Continuous arterial tonometry- continuous, pressure transducer over radial artery, its output is proportional to BP, periodic calibration needed.
Details
Direct method
Manometer with cuff
Oscillometry- Most common clinical method
Finapress method
Doppler probe/arterial tonometry
Errors NIBP
Detection of Korotkoff sounds
Cuff size
Zero/calibration errors
Errors IABP
Damping- high resonance and critical damping ideal; bubbles, canula, tap, tubing reduce the natural frequency of the system
Complaint catheter wall- damping
Clots- reduce resonant frequency- damping
Zeroing errors
www.medicineteacher.blogspot.com
Addison's
Addison’s disease
www.medicineteacher.blogspot.com
Addison’s
Glucocorticoid deficiency
Mineralocoeticoid deficiency usually
Primary, secondary
Acute, chronic, acute on chronic
Autoimmune mostly
clinically
Low BM
Postural hypotension
N V D weight loss
Pigmentation
Reduced hair
May not be obvious until stressed
Reduced calcium very rare
lab
Low Na, high K & urea
Low BM
Elevated ACTH
SST- 250 microgram, 0, 30, 60 min cortisol level, >580 ug excludes diagnosis
Reduced renin activity
Reduced aldosterone
adrenal crisis
Precipitated by stress
Hypotension, low Na, High K, low BM
Can present similar to septic shock
Hypovolaemic picture
treatment
ITU
Hydrocortisone 200 mg stat, 100 mg qds
Fluid resuscitation
Glucose resuscitation
Inotropes
Dexamethasone if diagnosis not clear, as doesn’t interfere with cortisol level.
hypercalcaemia
Increased bone resorption
Hyperparathyroidism
Malignancy- metastasis, PTH like peptides, lymphoma, mm
Paget’s disease
Immobilisation
Increased GIT abs-
Intake- milk alkalli, antacids, Ca
Excess Vit D- vit D, TB, sarcoidosis, lymphoma
Decreased Output-
Renal failure
Thiazides
FHH
www.medicineteacher.blogspot.com
www.medicineteacher.blogspot.com
Addison’s
Glucocorticoid deficiency
Mineralocoeticoid deficiency usually
Primary, secondary
Acute, chronic, acute on chronic
Autoimmune mostly
clinically
Low BM
Postural hypotension
N V D weight loss
Pigmentation
Reduced hair
May not be obvious until stressed
Reduced calcium very rare
lab
Low Na, high K & urea
Low BM
Elevated ACTH
SST- 250 microgram, 0, 30, 60 min cortisol level, >580 ug excludes diagnosis
Reduced renin activity
Reduced aldosterone
adrenal crisis
Precipitated by stress
Hypotension, low Na, High K, low BM
Can present similar to septic shock
Hypovolaemic picture
treatment
ITU
Hydrocortisone 200 mg stat, 100 mg qds
Fluid resuscitation
Glucose resuscitation
Inotropes
Dexamethasone if diagnosis not clear, as doesn’t interfere with cortisol level.
hypercalcaemia
Increased bone resorption
Hyperparathyroidism
Malignancy- metastasis, PTH like peptides, lymphoma, mm
Paget’s disease
Immobilisation
Increased GIT abs-
Intake- milk alkalli, antacids, Ca
Excess Vit D- vit D, TB, sarcoidosis, lymphoma
Decreased Output-
Renal failure
Thiazides
FHH
www.medicineteacher.blogspot.com
Monday, August 14, 2006
Final FRCA part 1
Acute Pain management:
Acute pain---spectrum---Chronic pain
May not fit exactly in one group
Scope of acute pain services increasing
Neuropathic pain can present within hours- as acute pain
Certain surgeries more prone to develop chronic pain- link between acute post-op pain and chronic pain. Potentiation of dorsal horn neurones in acute situation if persists longer- chronic pain.
Study of 5000 chronic pain patients- 22.5% were due to surgery, 17.5% were trauma related.
Complications of severe post op acute pain-
Epidural- reduces all these risks
Pain medicine is gaining special interest
Dead Space measurement:
A Invasive
B Non-invasive
a. SBT-CO2 (Fowler’s)
b. Bohr’s
c. Bohr-Enghoff
d. Kouloris/Romero method
a. Fowler’s - Single breath technique using CO2 measurement- FCO2 plotted against expired volume. Three phases of graph obtained. Phase 1- airway deadspace, 2- interface between airway/alveolar space mixing, 3-alveolar gas expired.
Midpoint of phase 2 by Fowler’s method will give anatomical Vd. 85ml in intubated pt, it is diffusive boundry, so varies with breath holding, end-inspiratory pause.
Phase 3 slope- upward (causes- i. well ventilated units empty first (mixed with N), ill ventilated ones empty later- pure CO2; ii. More CO2 keeps coming into lung from circulation as expiration continues)
PE- normal slope, but large VD
R-L shunt-- normal slope, but large VD
Intrapulmonary shunting- steep phase 3, large Vd.
b. Bohr’s - Assuming that last part of expirate represents alveolar air- Bohr’s deadspace can be calculated.
c. PaCO2 in ABG can be used to calculate the FCO2 of alveolar gas in equilibrium with arterial blood. This FCO2 value can be used in dead space equation- Bohr-Enghoff equation.
d. Kouloris/Romero method- non-invasive, combines impairment of CO2 elimination by airway and alveolar deadspaces.
Bohr-Enghoff method- Only simple clinical method where Vd increases with increasing severity of V/Q mismatch.
Diagrams- SBT_CO2, Kouloris/Romero Vd
Fluid absorption in endoscopic surgery-
Fluids used-
Glycine 1.5%
Mannitol
Sorbitol
NS
Sterile water
Surgeries performed-
TURP
TURBT
TCRE
Cystoscopy
Arthroscopy
Renal stone surgery
Rectal tumour
Vesical ultrasonic lithotripsy
Mechanism of fluid absorption-
Absorption- if irrigation fluid pressure more than 1.5 Kpa- TURP, TCRE
Extravagation- intra/extra peritoneal- renal stone surgery
Risk factors-
Smoking
Prostate cancer= benign disease
Extent of resection
Duration
Capsular perforation
Damage to venous sinuses
Fibroid resection in TCRE
Incidence-
1-8% mild to moderate TURS
Identification method (definition of TURS) affects incidence-
i. severity score- 1, 2, 3, CVS/CNS symptoms
ii. intra-op/post-op symptoms Vs amount of fluid absorbed
Symptoms-
Prickling sensation
Restless
Headache
Bradycardia
Hypotension
Feeling bad
Chest pain
Nausea
Vomiting
Poor UOP
Vision disturbed
HT
Reduced LOC
Diarrhoea
Abd pain
Confusion
Coma
Death
Severe TURS
CNS-92%
CVS-54%
Eye-42%
GIT- 25%
ARF- 21%
Death-25%
PK & PD-
Glycine-
Non-essential aa
0.3 mmol/l
Cheap, non allergic
T1/2 distri- 6 min
T1/2 elim 40 min-hours- dose dependent
BBB restricted
Liver metabolism- ammonia, 5-10% unchanged in urine
Osmotic diuresis
5-8 mmol/l visual disturbance
>10 N V
20-80 fatal
Mannitol
Glucose isomer
3 & 5%
Short distri T1/2
T ½ el 100 min
100 unchanged in urine
Osmotic diuresis
0.5-1% solution not diuretic
Few or no symptoms on absorption into circulation
Sorbitol
T1/2 dist 6 min
T1/2 el 33 min
Glucose+ fructose
Sorbitol- no reports of TURS
Sorbitol+mannitol- five case reports
Plasma dilution mannitol>mannitol+sorbitol> glycine 1.5%
Sorbitol & glycine enter cells and absorb water by osmosis- IV dehydration, cell swelling.
Pathophysiology
Haemodynamics- transient raised CVP, SOB, pulmonary edema, then hpokinetic haemodynamics phase- brady, hypovol, hypotension, reduced CO.
Heart- brady, ST-T depression, reduced conductivity, collapse
Blood- Reduced proteins, Na, osmolality, PaO2; increased K, urosepsis.
Brain- depression due to edema, Ammonia (>100micromol/l) glycolic acid, glyoxilic acid, glutamate, hyperglycinaemia; cerebral herniation
NS- >50 ml/kg absorption- few CNS symptoms.
Mannitol- ok
Sorbitol- fructose intolerance, lactic acidosis, enceph in presence of liver failure.
Kidney- diuresis, natriuresis, hpotension, urosepsis- renal infaction due to hypoperfusion, Increased ADH
Extravagation
ECF dissolves in this fluid, hyponatraemia, brady, hypovol, hypotension, reduced CO
Comparisons
Animal studies- glycine worst outcome
Volunteers-More CVS/CNS symptoms with glycine than other 2
Clinical- Glycine 1% = 1.5% more symptoms like nausea than mannitol; for CVS all = but > than mannitol+sorbitol
Measurement of fluid absorption-
Serum Na- repeated measurements, practical difficulty
Volumetric fluid balance- input+ output; practically difficult- but good to detect extravagation
Gravimetry- theatre table with facility to weigh patient
CVP- transient rise, so not useful; >500ml absorption in <10 min for change.
Isotope measurement- safety issue
Ethanol- similar to Isotope measurement, 1% ethanol
Sensitivity 75ml/10 min of surgery.
If > 75ml/10 min of surgery- increased absorption
Extravagation- Gravimetry, Volumetric fluid balance; other methods late detection- 15-20 min
Prevention-
Surgeon education
Duration
Lower fluid bag-60 cm
Low pressure irrigation- bladder canula suprapubically or special port in resectoscope to keep fluid draining
Alternate techniques- bipolar resectoscope, vaporisation
Drugs- vasoconstrictors, harmoes for rndometrial size reduction
Treatment-
Vision- spontaneous resolution
N, V- antiemetics
CVS support- atropine, Ca, fluid replacement if hypovolaemia, hypotension
Hypertonic saline if Na < 120 mmol/l, evidence based.
Raise Na by 1mmol/l/hr
Frusemide- only if pulmonary edema and spont diuresis doesn’t occur, not routinely.
Extravagation-
Same as above + may need surgery- will remove electrolyte- Hypertonic saline required.
Acute pain---spectrum---Chronic pain
May not fit exactly in one group
Scope of acute pain services increasing
Neuropathic pain can present within hours- as acute pain
Certain surgeries more prone to develop chronic pain- link between acute post-op pain and chronic pain. Potentiation of dorsal horn neurones in acute situation if persists longer- chronic pain.
Study of 5000 chronic pain patients- 22.5% were due to surgery, 17.5% were trauma related.
Complications of severe post op acute pain-
Epidural- reduces all these risks
Pain medicine is gaining special interest
Dead Space measurement:
A Invasive
B Non-invasive
a. SBT-CO2 (Fowler’s)
b. Bohr’s
c. Bohr-Enghoff
d. Kouloris/Romero method
a. Fowler’s - Single breath technique using CO2 measurement- FCO2 plotted against expired volume. Three phases of graph obtained. Phase 1- airway deadspace, 2- interface between airway/alveolar space mixing, 3-alveolar gas expired.
Midpoint of phase 2 by Fowler’s method will give anatomical Vd. 85ml in intubated pt, it is diffusive boundry, so varies with breath holding, end-inspiratory pause.
Phase 3 slope- upward (causes- i. well ventilated units empty first (mixed with N), ill ventilated ones empty later- pure CO2; ii. More CO2 keeps coming into lung from circulation as expiration continues)
PE- normal slope, but large VD
R-L shunt-- normal slope, but large VD
Intrapulmonary shunting- steep phase 3, large Vd.
b. Bohr’s - Assuming that last part of expirate represents alveolar air- Bohr’s deadspace can be calculated.
c. PaCO2 in ABG can be used to calculate the FCO2 of alveolar gas in equilibrium with arterial blood. This FCO2 value can be used in dead space equation- Bohr-Enghoff equation.
d. Kouloris/Romero method- non-invasive, combines impairment of CO2 elimination by airway and alveolar deadspaces.
Bohr-Enghoff method- Only simple clinical method where Vd increases with increasing severity of V/Q mismatch.
Diagrams- SBT_CO2, Kouloris/Romero Vd
Fluid absorption in endoscopic surgery-
Fluids used-
Glycine 1.5%
Mannitol
Sorbitol
NS
Sterile water
Surgeries performed-
TURP
TURBT
TCRE
Cystoscopy
Arthroscopy
Renal stone surgery
Rectal tumour
Vesical ultrasonic lithotripsy
Mechanism of fluid absorption-
Absorption- if irrigation fluid pressure more than 1.5 Kpa- TURP, TCRE
Extravagation- intra/extra peritoneal- renal stone surgery
Risk factors-
Smoking
Prostate cancer= benign disease
Extent of resection
Duration
Capsular perforation
Damage to venous sinuses
Fibroid resection in TCRE
Incidence-
1-8% mild to moderate TURS
Identification method (definition of TURS) affects incidence-
i. severity score- 1, 2, 3, CVS/CNS symptoms
ii. intra-op/post-op symptoms Vs amount of fluid absorbed
Symptoms-
Prickling sensation
Restless
Headache
Bradycardia
Hypotension
Feeling bad
Chest pain
Nausea
Vomiting
Poor UOP
Vision disturbed
HT
Reduced LOC
Diarrhoea
Abd pain
Confusion
Coma
Death
Severe TURS
CNS-92%
CVS-54%
Eye-42%
GIT- 25%
ARF- 21%
Death-25%
PK & PD-
Glycine-
Non-essential aa
0.3 mmol/l
Cheap, non allergic
T1/2 distri- 6 min
T1/2 elim 40 min-hours- dose dependent
BBB restricted
Liver metabolism- ammonia, 5-10% unchanged in urine
Osmotic diuresis
5-8 mmol/l visual disturbance
>10 N V
20-80 fatal
Mannitol
Glucose isomer
3 & 5%
Short distri T1/2
T ½ el 100 min
100 unchanged in urine
Osmotic diuresis
0.5-1% solution not diuretic
Few or no symptoms on absorption into circulation
Sorbitol
T1/2 dist 6 min
T1/2 el 33 min
Glucose+ fructose
Sorbitol- no reports of TURS
Sorbitol+mannitol- five case reports
Plasma dilution mannitol>mannitol+sorbitol> glycine 1.5%
Sorbitol & glycine enter cells and absorb water by osmosis- IV dehydration, cell swelling.
Pathophysiology
Haemodynamics- transient raised CVP, SOB, pulmonary edema, then hpokinetic haemodynamics phase- brady, hypovol, hypotension, reduced CO.
Heart- brady, ST-T depression, reduced conductivity, collapse
Blood- Reduced proteins, Na, osmolality, PaO2; increased K, urosepsis.
Brain- depression due to edema, Ammonia (>100micromol/l) glycolic acid, glyoxilic acid, glutamate, hyperglycinaemia; cerebral herniation
NS- >50 ml/kg absorption- few CNS symptoms.
Mannitol- ok
Sorbitol- fructose intolerance, lactic acidosis, enceph in presence of liver failure.
Kidney- diuresis, natriuresis, hpotension, urosepsis- renal infaction due to hypoperfusion, Increased ADH
Extravagation
ECF dissolves in this fluid, hyponatraemia, brady, hypovol, hypotension, reduced CO
Comparisons
Animal studies- glycine worst outcome
Volunteers-More CVS/CNS symptoms with glycine than other 2
Clinical- Glycine 1% = 1.5% more symptoms like nausea than mannitol; for CVS all = but > than mannitol+sorbitol
Measurement of fluid absorption-
Serum Na- repeated measurements, practical difficulty
Volumetric fluid balance- input+ output; practically difficult- but good to detect extravagation
Gravimetry- theatre table with facility to weigh patient
CVP- transient rise, so not useful; >500ml absorption in <10 min for change.
Isotope measurement- safety issue
Ethanol- similar to Isotope measurement, 1% ethanol
Sensitivity 75ml/10 min of surgery.
If > 75ml/10 min of surgery- increased absorption
Extravagation- Gravimetry, Volumetric fluid balance; other methods late detection- 15-20 min
Prevention-
Surgeon education
Duration
Lower fluid bag-60 cm
Low pressure irrigation- bladder canula suprapubically or special port in resectoscope to keep fluid draining
Alternate techniques- bipolar resectoscope, vaporisation
Drugs- vasoconstrictors, harmoes for rndometrial size reduction
Treatment-
Vision- spontaneous resolution
N, V- antiemetics
CVS support- atropine, Ca, fluid replacement if hypovolaemia, hypotension
Hypertonic saline if Na < 120 mmol/l, evidence based.
Raise Na by 1mmol/l/hr
Frusemide- only if pulmonary edema and spont diuresis doesn’t occur, not routinely.
Extravagation-
Same as above + may need surgery- will remove electrolyte- Hypertonic saline required.
Monday, August 07, 2006
Glutamine for ITU nutrition
www.medicineteacher.blogspot.com
Functions glutamineGlutamine becomes an essential amino acid in the human body during times of stress including critical illness and after major trauma or surgery.
Glutamine is the most abundant free amino acid in the extracellular and intracellular compartments, contributing to more than 50% of the body
’s free amino acid pool (Young 2001).
Supports rapidly proliferating cells, such as lymphocytes and enterocytes
à important to immune and intestinal integrity.
Acid-base homeostasis.
Nitrogen and ammonium carrier.
Glutamine levels during illness
ICU patient mortality has been shown to be significantly higher for patients with low plasma glutamine levels
(Oudemans-van Staaten, et al. 2001).
Animal studies
Predominantly rat studies have showed that glutamine:
Limits intestinal permeability
Reduces gut atrophy
Preserves intestinal and extraintestinal IgA levels
Decreases intestinal proinflammatory cytokine production
Early human research on glutamine
Many researchers have studied replacement of glutamine, either parenterally or enterally, assuming this could lead to improved patient outcomes.
Until 2003, published trials were small: each enrolled between 35 to 84 patients.
Some studies suggested lower infection rates and perhaps improved mortality.
A meta-analysis by Novak et al. (2002) showed inconclusive results. Parenteral glutamine showed a trend towards reduced mortality as well as fewer infectious complications but no reduction in length of stay.
Enteral Glutamine
Hall et al. (2003): prospective, triple blinded study in a 10 bed ICU in Perth, Australia.
363 patients; 20g/day enteral glutamine.
No difference in: mortality at 6 months
severe sepsis
infections
consumption of inotropes.
Enteral Glutamine Cont.
Schulman et al. (2005): prospective, unblinded study involving 185 patients admitted to a surgical and trauma ICU in Charlottesville, Virginia, USA.
Patients were sequentially assigned to either standard enteral feeds or 20-40g/day glutamine supplemented feeds.
No significant difference in in-hospital mortality or secondary end points (there was a trend towards higher mortality in the glutamine group).
Why no benefit with enteral glutamine?
The proposed benefit of glutamine for human cells may also extend to bacteria.
Animal studies have demonstrated an increased growth rate of bacteria when incubated in the presence of glutamine.
(Kajikawa 2002).
Parenteral Glutamine
Dechelotte P: French study involving 114 patients in 16 ICUs.
Prospective, double-blind, controlled, randomized trial.
Received 0.5g/kg/day glutamine parenterally.
↓
infection rate: 0.45 vs 0.71 infections per patient (p <>
↓
pneumonia: 10 vs 19 patients (p <>
↓
hyperglycaemia: 20 vs 30 patients (p <>
Early death rate and 6-month survival were not different.
Survivors at 6 months: glutamine group 72%, control 83%.
Have the studies been
giving enough glutamine?
Most naturally occurring food proteins contain 4-8% of their amino acid residues as glutamine; hence, the daily consumption of glutamine is usually less than 10g. The optimal dose of glutamine is unknown
(Hall et al. 2003).
What about glutamine use
in other areas of medicine
?
Studies in:
Premature infants
Bone marrow transplants
Inflammatory bowel disease
Show similar lack of benefit.
Costs
Glutamine 10g 50ml bag
£15.96Glutamine 20g 100ml bag £
29.60
Kabiven 9 bag
£31.75
Last year, Ysbyty Gwynedd spent
£12 000 on Kabiven 9.
Therefore adding 20g of glutamine would almost double the cost of enteral feeding.
Conclusions
There is insufficient evidence to conclusively determine whether glutamine supplementation for ICU patients is beneficial.
The best evidence so far indicates that there is likely to be no benefit.
The additional cost can not be justified.
References
Dechelotte P, Hasselmann M, Cynober L, et al. L-alanyl-L-glutamine dipeptide
– supplemented total parenteral nutrition reduces infectious complications and glucose intolerance in critically ill patients: The French controlled, randomized, double-blind, multicenter study. Crit Care Med 2006;34:598-604.Hall JC, Dobb G, Hall J, de Sousa R, Brennan L, McCauley R: A prospective randomized trail of enteral glutamine in critical illness 2003;29:1710-1716.
Kajikawa H, Mitsumori M, Ohmomo S: Stimulatory and inhibitory effects of protein amino acids on growth rate and efficiency of mixed ruminal bacteria. J Diary Sci 2002;85:2015-2022.
Oudemans-van Staaten HM, Bosman RJ, Treskes M, et al: Plasma glutamine depletion and patient outcome in acute ICU admissions. Intensive Care Med 2001; 27:84-90.
Novak F, Heyland DK, Avenell A, et al: Glutamine supplementation in serious illness: A systematic review of the evidence. Crit Care Med 2002; 30:2022-2029.
Schulman AS, Willcutts KF, Claridge JA, et al. Does the addition of glutamine to enteral feeds affect patient mortality?. Crit Care Med 2005 Vol. 33, No. 11.
Young VR, Ajami AM. Glutamine: The emperor or his clothes? J Nutr 2001; 131(9 Suppl):2449S-2459S.
The End. Thank you.
Thursday, August 03, 2006
Addison's disease
Addison’s disease
Addison’s
Glucocorticoid deficiency
Mineralocoeticoid deficiency usually
Primary, secondary
Acute, chronic, acute on chronic
Autoimmune mostly
clinically
Low BM
Postural hypotension
N V D weight loss
Pigmentation
Reduced hair
May not be obvious until stressed
Reduced calcium very rare
lab
Low Na, high K & urea
Low BM
Elevated ACTH
SST- 250 microgram, 0, 30, 60 min cortisol level, >580 ug excludes diagnosis
Reduced renin activity
Reduced aldosterone
adrenal crisis
Precipitated by stress
Hypotension, low Na, High K, low BM
Can present similar to septic shock
Hypovolaemic picture
treatment
ITU
Hydrocortisone 200 mg stat, 100 mg qds
Fluid resuscitation
Glucose resuscitation
Inotropes
Dexamethasone if diagnosis not clear, as doesn’t interfere with cortisol level.
hypercalcaemia
Increased bone resorption
Hyperparathyroidism
Malignancy- metastasis, PTH like peptides, lymphoma, mm
Paget’s disease
Immobilisation
Increased GIT abs-
Intake- milk alkalli, antacids, Ca
Excess Vit D- vit D, TB, sarcoidosis, lymphoma
Decreased Output-
Renal failure
Thiazides
FHH
Addison’s
Glucocorticoid deficiency
Mineralocoeticoid deficiency usually
Primary, secondary
Acute, chronic, acute on chronic
Autoimmune mostly
clinically
Low BM
Postural hypotension
N V D weight loss
Pigmentation
Reduced hair
May not be obvious until stressed
Reduced calcium very rare
lab
Low Na, high K & urea
Low BM
Elevated ACTH
SST- 250 microgram, 0, 30, 60 min cortisol level, >580 ug excludes diagnosis
Reduced renin activity
Reduced aldosterone
adrenal crisis
Precipitated by stress
Hypotension, low Na, High K, low BM
Can present similar to septic shock
Hypovolaemic picture
treatment
ITU
Hydrocortisone 200 mg stat, 100 mg qds
Fluid resuscitation
Glucose resuscitation
Inotropes
Dexamethasone if diagnosis not clear, as doesn’t interfere with cortisol level.
hypercalcaemia
Increased bone resorption
Hyperparathyroidism
Malignancy- metastasis, PTH like peptides, lymphoma, mm
Paget’s disease
Immobilisation
Increased GIT abs-
Intake- milk alkalli, antacids, Ca
Excess Vit D- vit D, TB, sarcoidosis, lymphoma
Decreased Output-
Renal failure
Thiazides
FHH
Wednesday, May 31, 2006
Measurement of cardiac output
Sangram Patil
Cardiac output
§ Definition
§ Determinants
§ Ideal device
§ Gold standard- thermo dilution technique of PAC.
Clinical assessment
§ Low organ perfusion
§ CNS
§ Metabolic acidosis
§ R/S
§ GUT
§ CVS
§ CRT
Techniques
§ Fick partial rebreathing method
§ Dye dilution
§ Thermo dilution
§ Arterial pulse contour analysis
§ Combined Li dilution APCA
§ Thoracic impedance
§ Doppler ultrasound technique
Dye dilution
§ Diagram
§ Graph
§ CO= Computer analysis of AUC for concentration-time curve.
§ Indocyanine green
§ Lithium dilution technique.
Thermo dilution
§ Most widely used.
§ Technique
§ Recent advance- Continuous CO measurement.
§ Status
Arterial waveform analysis
§ Pulse contour analysis- PiCCO (aortic).
§ Arterial cannulation- pulse contour analysis.
§ CVP line- transcardiopulmonary thermo dilution CO measurement for calibration.
§ Beat to beat calculation of CO from AUC.
§ Problems-abnormal waveforms, arrhythmias.
Combined Li dilution-APCA
§ Li dilution-calibration.
§ APCA-Beat to beat CO calculation.
§ LiDCO
§ PulseCO
§ SVR, SV, CO.
Fick Partial rebreathing method
§ Fick principle + CO2 elimination--NICO
§ CO2 elimination = V CO2/ CaCO2 - CvCO2
§ V CO2, CaCO2, CvCO2
§ Technique
§ ETT+IPPV, Rebreathing valve cycles through 2 phases- baseline (non RB), second phase (rebreathing), CO2 / flow sensor, ratio of change in CO2 elimination- calculated as CO.
Thoracic electrical bio-impedance
§ Flow from ventricle to aorta changes the electrical impedance.
§ Xiphoid electrode, neck electrode.
§ Not good correlation with thermo dilution.
§ Problems- age, fluid shifts, pulmonary oedema, myocardial ischemia, electrical interference.
Doppler ultrasound
§ Velocity of BF in descending aorta
§ Frequency of reflected US is changed depending on flow velocity in aorta.
§ V= 2.F0 / (C). (Fd). (Cosine incident angle).
§ > 20 degree angle- underestimates V.
§ Sites- suprasternal, trachea, Oesophagus
§ Oesophageal- Doppler transducer, M mode transducer, SV, 70% CO, ETT.
TOE
§ Sophisticated endoscopic probe.
§ Doppler ultrasound technique.
§ CO, V function, Wall motion abnormality, anatomy, valve function.
§ Doppler- velocity across valve. AUC for flow- velocity curve gives VIT ( velocity time integral)
§ 2DECHO- valve cross sectional area, CSA.
§ SV =VTI . CSA
§ CO= SV. HR
Advantages
Cardiac output
§ Definition
§ Determinants
§ Ideal device
§ Gold standard- thermo dilution technique of PAC.
Clinical assessment
§ Low organ perfusion
§ CNS
§ Metabolic acidosis
§ R/S
§ GUT
§ CVS
§ CRT
Techniques
§ Fick partial rebreathing method
§ Dye dilution
§ Thermo dilution
§ Arterial pulse contour analysis
§ Combined Li dilution APCA
§ Thoracic impedance
§ Doppler ultrasound technique
Dye dilution
§ Diagram
§ Graph
§ CO= Computer analysis of AUC for concentration-time curve.
§ Indocyanine green
§ Lithium dilution technique.
Thermo dilution
§ Most widely used.
§ Technique
§ Recent advance- Continuous CO measurement.
§ Status
Arterial waveform analysis
§ Pulse contour analysis- PiCCO (aortic).
§ Arterial cannulation- pulse contour analysis.
§ CVP line- transcardiopulmonary thermo dilution CO measurement for calibration.
§ Beat to beat calculation of CO from AUC.
§ Problems-abnormal waveforms, arrhythmias.
Combined Li dilution-APCA
§ Li dilution-calibration.
§ APCA-Beat to beat CO calculation.
§ LiDCO
§ PulseCO
§ SVR, SV, CO.
Fick Partial rebreathing method
§ Fick principle + CO2 elimination--NICO
§ CO2 elimination = V CO2/ CaCO2 - CvCO2
§ V CO2, CaCO2, CvCO2
§ Technique
§ ETT+IPPV, Rebreathing valve cycles through 2 phases- baseline (non RB), second phase (rebreathing), CO2 / flow sensor, ratio of change in CO2 elimination- calculated as CO.
Thoracic electrical bio-impedance
§ Flow from ventricle to aorta changes the electrical impedance.
§ Xiphoid electrode, neck electrode.
§ Not good correlation with thermo dilution.
§ Problems- age, fluid shifts, pulmonary oedema, myocardial ischemia, electrical interference.
Doppler ultrasound
§ Velocity of BF in descending aorta
§ Frequency of reflected US is changed depending on flow velocity in aorta.
§ V= 2.F0 / (C). (Fd). (Cosine incident angle).
§ > 20 degree angle- underestimates V.
§ Sites- suprasternal, trachea, Oesophagus
§ Oesophageal- Doppler transducer, M mode transducer, SV, 70% CO, ETT.
TOE
§ Sophisticated endoscopic probe.
§ Doppler ultrasound technique.
§ CO, V function, Wall motion abnormality, anatomy, valve function.
§ Doppler- velocity across valve. AUC for flow- velocity curve gives VIT ( velocity time integral)
§ 2DECHO- valve cross sectional area, CSA.
§ SV =VTI . CSA
§ CO= SV. HR
Advantages
Wednesday, May 24, 2006
Non-obstetric surgery during pregnancy
Anaesthesia for non-obstetric surgery during pregnancy
Dr.Sathish Krishnan
YG
Introduction
1-2% of pregnant women undergo anaesthesia during their pregnancy for surgery unrelated to delivery
M.C – Appendicitis,ovarian cyst,trauma.
Physiological and pharmacological changes important.
Goals
Maintain normal maternal physiological function
Maintain uteroplacental flow and O2 delivery.
Avoid unwanted drug effects on the fetus
Avoid oxytocic effects
Avoid awareness during G.A
Use regional when possible
Preanaesthetic assessment
Liase with obst & neonatalogist
U.S –if delivery is imminent
Symptoms of cardiac disease & ECG changes are common in pregnancy.
Radiology- minimise fetal exposure.
Relevant blood tests
Premeds-always include aspiration prophylaxis
Avoid NSAIDS.
Drugs
Teratogenic effects- 15th -56 days of gestation
Studies- no increase in teratogenecity but increase in abortion, growth restriction and LBW
Problems were due to primary disease and surgery and not due to anaesthesia
Benzodiazepines not teratogenic & single dose is safe.
GESTATION
No elective surgery during pregnancy
Only tubal ligation in first 6 weeks after delivery
Emergency surgery-regardless of gestational age
Preserve the life of mother
If possible-surgery delayed until 2nd trimester- reduced abortion & teratogenecity - but no firm evidence.
Nonviable fetus
Same principles as for pregnant patient
Coagulopathy risk- should be corrected
Anaesthesia for conception & 1st trimester
IV sedation for invitro fertilisation, should not interfere with fertilisation & embryo development
Propofol – sedation, regional or G.A.N20 avoided
6-8 weeks-physiological changes occur , supplementary O2, hyperventilation.
Airway management- may be difficult. Nasal airways avoided
Reduced pseudocholinesterase (30%), balanced by increase in Vd.
Aspiration prophylaxis from beginning of 2nd trimester
Lower anaes.requirements.reduced MAC (30%) ,IV drugs in lower doses
Fetus assessed by U.S before & after surgery
Regional whenever possible
2nd Trimester
Aortocaval compression from 20 weeks (may be before)
Lateral displacement of uterus
Risk of intravascular injection
Reduce dose of LA
Hypercoagulable state-prophylaxis
3rd Trimester
C.section before major surgery
Surgery delayed for 48 hrs to allow steroid therapy for fetal lung maturation
Regional for section and then converted to GA if needed
Volatile agents in small doses- to prevent uterine atony
Lactation may be supressed, contraindications for breast feeding are patients on ergot, lithium etc
Fetal monitoring
After 24-26 weeks, FH should be monitored
Difficult in obese or abdominal surgery
Inhalation agents cause decrease in FHR variability
Plan of action if fetal distress diagnosed
Minimal uterine manipulation
No evidence to use prophylactic tocolytics
Anaesthetic technique
No evidence to show that regional is better than GA in terms of outcome
Regional minimises fetal drug exposure, airway management is simpler, blood loss reduced & overall risk is less to both mother & fetus
Risk of regional is hypotension- reduce uterine blood flow
Recent studies show that it is more important to treat the blood pressure than to worry about agent
GA only by well trained anaesthetist
Laparoscopic surgeries
Pregnancy is no longer a contraindication for LAP surgeries
Study in Sweden- 2 million deliveries- favoured lap surgeries than open surgeries
Why? Less exposure of fetus to toxic agents, small incisions, less pain, less analgesic needed, rapid recovery & mobilisation.
C02 pneumoperitoneum - risk of hypoxemia, hypercarbia & hypotension.
THANK YOU
Dr.Sathish Krishnan
YG
Introduction
1-2% of pregnant women undergo anaesthesia during their pregnancy for surgery unrelated to delivery
M.C – Appendicitis,ovarian cyst,trauma.
Physiological and pharmacological changes important.
Goals
Maintain normal maternal physiological function
Maintain uteroplacental flow and O2 delivery.
Avoid unwanted drug effects on the fetus
Avoid oxytocic effects
Avoid awareness during G.A
Use regional when possible
Preanaesthetic assessment
Liase with obst & neonatalogist
U.S –if delivery is imminent
Symptoms of cardiac disease & ECG changes are common in pregnancy.
Radiology- minimise fetal exposure.
Relevant blood tests
Premeds-always include aspiration prophylaxis
Avoid NSAIDS.
Drugs
Teratogenic effects- 15th -56 days of gestation
Studies- no increase in teratogenecity but increase in abortion, growth restriction and LBW
Problems were due to primary disease and surgery and not due to anaesthesia
Benzodiazepines not teratogenic & single dose is safe.
GESTATION
No elective surgery during pregnancy
Only tubal ligation in first 6 weeks after delivery
Emergency surgery-regardless of gestational age
Preserve the life of mother
If possible-surgery delayed until 2nd trimester- reduced abortion & teratogenecity - but no firm evidence.
Nonviable fetus
Same principles as for pregnant patient
Coagulopathy risk- should be corrected
Anaesthesia for conception & 1st trimester
IV sedation for invitro fertilisation, should not interfere with fertilisation & embryo development
Propofol – sedation, regional or G.A.N20 avoided
6-8 weeks-physiological changes occur , supplementary O2, hyperventilation.
Airway management- may be difficult. Nasal airways avoided
Reduced pseudocholinesterase (30%), balanced by increase in Vd.
Aspiration prophylaxis from beginning of 2nd trimester
Lower anaes.requirements.reduced MAC (30%) ,IV drugs in lower doses
Fetus assessed by U.S before & after surgery
Regional whenever possible
2nd Trimester
Aortocaval compression from 20 weeks (may be before)
Lateral displacement of uterus
Risk of intravascular injection
Reduce dose of LA
Hypercoagulable state-prophylaxis
3rd Trimester
C.section before major surgery
Surgery delayed for 48 hrs to allow steroid therapy for fetal lung maturation
Regional for section and then converted to GA if needed
Volatile agents in small doses- to prevent uterine atony
Lactation may be supressed, contraindications for breast feeding are patients on ergot, lithium etc
Fetal monitoring
After 24-26 weeks, FH should be monitored
Difficult in obese or abdominal surgery
Inhalation agents cause decrease in FHR variability
Plan of action if fetal distress diagnosed
Minimal uterine manipulation
No evidence to use prophylactic tocolytics
Anaesthetic technique
No evidence to show that regional is better than GA in terms of outcome
Regional minimises fetal drug exposure, airway management is simpler, blood loss reduced & overall risk is less to both mother & fetus
Risk of regional is hypotension- reduce uterine blood flow
Recent studies show that it is more important to treat the blood pressure than to worry about agent
GA only by well trained anaesthetist
Laparoscopic surgeries
Pregnancy is no longer a contraindication for LAP surgeries
Study in Sweden- 2 million deliveries- favoured lap surgeries than open surgeries
Why? Less exposure of fetus to toxic agents, small incisions, less pain, less analgesic needed, rapid recovery & mobilisation.
C02 pneumoperitoneum - risk of hypoxemia, hypercarbia & hypotension.
THANK YOU
medicine teacher
Hi friends,
Thank you for your interest in this website.
Most of the time our academic work goes unnoticed. Even we tend to forget about it after some time, though it is there with us in floppy or flash disc. Most of our academic material is for presentation or teaching a small or large group of audience.
Once the presentation is done nothing usually happens to the prepared material unless we are very enthusiastic to submit the same for publication in journals or books.How about publishing these presentations in the form of website? This will keep our hard work alive for ever.
Another aspect is we can have access to this material anywhere and anytime.On website, this material is open to the whole world. Sharing our knowledge and hard work with others on such a broad scale is excellent idea, isn’t it?
I would encourage you to contribute to this website by sending me your presentations or any other academic material. It might be your lecture, personal notes or audit work, or case presentation. You can send me without disclosing patient identity or department identification.
I wont be publishing any diagrams or photographs on this website, so no problem with copy rights.
Do let me know your suggestions and forward me as much material as you can.
Thank you again.
Dr S Patil
SpR Anaesthetics
All Wales rotation
UK
sangram@doctors.org.uk
Thank you for your interest in this website.
Most of the time our academic work goes unnoticed. Even we tend to forget about it after some time, though it is there with us in floppy or flash disc. Most of our academic material is for presentation or teaching a small or large group of audience.
Once the presentation is done nothing usually happens to the prepared material unless we are very enthusiastic to submit the same for publication in journals or books.How about publishing these presentations in the form of website? This will keep our hard work alive for ever.
Another aspect is we can have access to this material anywhere and anytime.On website, this material is open to the whole world. Sharing our knowledge and hard work with others on such a broad scale is excellent idea, isn’t it?
I would encourage you to contribute to this website by sending me your presentations or any other academic material. It might be your lecture, personal notes or audit work, or case presentation. You can send me without disclosing patient identity or department identification.
I wont be publishing any diagrams or photographs on this website, so no problem with copy rights.
Do let me know your suggestions and forward me as much material as you can.
Thank you again.
Dr S Patil
SpR Anaesthetics
All Wales rotation
UK
sangram@doctors.org.uk
Thursday, May 18, 2006
Neurocritical Care
Neurosurgery & neurocitical care
www.medicineteacher.blogspot.com
Unresolved issues
•IV versus inhalational
•Nitrous oxide
•Opioids
•Sitting Position
•Hypothermia
•Hyperventilation
•Hypotension
•Triple H therapy
•Colloid versus crystalloid
•HS, mannitol, steroids
•Non-anaesthetic drugs
IV versus inhalational
•Sevoflurane
•Propofol
•Etomidate
•Thiopental
•Research studies- failed to show any difference
Nitrous oxide
•Opponents
•Proponents
•Research studies- no specific study.
•Avoid in- air in ventricles, risk of embolism, pneumocephalus, reduced IC compliance & need of high FiO2
Opioids
•Morphine
•Fentanyl
•Sufentanyl
•Remifentanyl
Sitting position
•Risk of VAE
•Benefits
•Studies- relatively low incidence of complications reported
•Careful patient selection, expert anaesthetic team, intra-operative monitoring
Mild hypothermia
•Mild hypothermia, 2-3 degree Celsius
•Moderate to severe hypothermia
•Research studies- conflicting results
•NABIS- no benefits
•IHAST- no benefits
•Head injury with raised ICT- clear benefit
•Immediate management of cardiac arrest- helpful
Hyperventilation
•Logic behind this
•Studies- Cochrane library report
•PaCO2 >4.0 kPa
•Routine hyperventilation avoided except as a rescue measure for herniation of brain
Induced hypotension
•Induced hypotension for global cerebral effect- not used now
•In past brief periods of controlled hypotension for surgical dissections and aneurysm clippings
•Temporary clipping of major feeding vessel
•Research- Controversy over which is better
•Clip might cause ischaemia as well plus interference with surgical field.
Triple H therapy
•Hypervolaemia
•Hypertension
•Haemodilution
•Controversies- when, what fluids, how much BP, for how long
•Oxygen carrying capacity
Crystalloid versus colloid
•Volume required
•Response time
•Duration of effect
•Interference with clotting, allergy
•CPP
•ICT
HS Mannitol Steroids
•HS
•Mannitol
•Steroids
•Research evidence
Non-anaesthetic drugs
•Nimodipine
•Mg
•Remacemide
Summary
•Nitrous oxide use is controversial
•Limited indications for hypothermia
•No routine hyperventilation
•Strict BM control
•Nimodipine, remacemide might be helpful
•Modern trend is minimally invasive surgery, awake procedures (functional neurosurgery)
•Modern technology like TCD ultrasound, JB oximetry, NIRS, laser Doppler flowmeter
www.medicalaudits.blogspot.com
www.medicineteacher.blogspot.com
Unresolved issues
•IV versus inhalational
•Nitrous oxide
•Opioids
•Sitting Position
•Hypothermia
•Hyperventilation
•Hypotension
•Triple H therapy
•Colloid versus crystalloid
•HS, mannitol, steroids
•Non-anaesthetic drugs
IV versus inhalational
•Sevoflurane
•Propofol
•Etomidate
•Thiopental
•Research studies- failed to show any difference
Nitrous oxide
•Opponents
•Proponents
•Research studies- no specific study.
•Avoid in- air in ventricles, risk of embolism, pneumocephalus, reduced IC compliance & need of high FiO2
Opioids
•Morphine
•Fentanyl
•Sufentanyl
•Remifentanyl
Sitting position
•Risk of VAE
•Benefits
•Studies- relatively low incidence of complications reported
•Careful patient selection, expert anaesthetic team, intra-operative monitoring
Mild hypothermia
•Mild hypothermia, 2-3 degree Celsius
•Moderate to severe hypothermia
•Research studies- conflicting results
•NABIS- no benefits
•IHAST- no benefits
•Head injury with raised ICT- clear benefit
•Immediate management of cardiac arrest- helpful
Hyperventilation
•Logic behind this
•Studies- Cochrane library report
•PaCO2 >4.0 kPa
•Routine hyperventilation avoided except as a rescue measure for herniation of brain
Induced hypotension
•Induced hypotension for global cerebral effect- not used now
•In past brief periods of controlled hypotension for surgical dissections and aneurysm clippings
•Temporary clipping of major feeding vessel
•Research- Controversy over which is better
•Clip might cause ischaemia as well plus interference with surgical field.
Triple H therapy
•Hypervolaemia
•Hypertension
•Haemodilution
•Controversies- when, what fluids, how much BP, for how long
•Oxygen carrying capacity
Crystalloid versus colloid
•Volume required
•Response time
•Duration of effect
•Interference with clotting, allergy
•CPP
•ICT
HS Mannitol Steroids
•HS
•Mannitol
•Steroids
•Research evidence
Non-anaesthetic drugs
•Nimodipine
•Mg
•Remacemide
Summary
•Nitrous oxide use is controversial
•Limited indications for hypothermia
•No routine hyperventilation
•Strict BM control
•Nimodipine, remacemide might be helpful
•Modern trend is minimally invasive surgery, awake procedures (functional neurosurgery)
•Modern technology like TCD ultrasound, JB oximetry, NIRS, laser Doppler flowmeter
www.medicalaudits.blogspot.com
Friday, May 12, 2006
Post cord transection
Sangram Patil
Spinal cord anatomy
Physiology
Blood supply-
Single ASA, 2 small PSAs
Essentially no collateral supply between the two
Segmental vessels, large distance between them- watershed area between upper thoracic and lumbar region. Artery of Adamkiewicz (T8-L3).
Regulation of SC blood flow
SC perfusion pressure
Auto regulation- abolished by trauma
Pathophysiology of acute cord injury (ASCI)
Primary injury
Original impact and compression of SC.
No treatment
Secondary injury
Ischemia triggered by primary injury, and other mechanisms.
Systemic effects of ASCI
CVS, R/S, GIT, GUT, Temperature, CNS, Skin.
CNS- Central/ Anterior/Posterior/ Hemi section/ complete transection
Chronic cord injury/ transection
Spinal Shock
Autonomic dysreflexia
Other CVS changes
Blood Volume
Abnormal Valsalva response- no plateau, no overshoot.
Orthostatic hypotension- gradual adaptation d/t autoreg.
Increased renin-angiotensin response- salt-water retention.
Continued..
Respiratory system
C1/2, C3/4, lower cervical- intercostal.
Reduced VC- might recover to some extent;
Increased WOB, reduced ERV/FVC (better in head up position).
Abdominal muscle paralysis- cough, atelectasis, V/Q mismatch.
Muscles
Increased Ach receptors, K changes with suxamethonium.
Spasticity- due to intact spinal reflex arc below the level of lesion.
Bones
Reduced density below the level.
Temperature- perception, regulation.
Continued..
Skin-
decubitus ulcers, common reason for operations in them.
Blood-
Anaemia, DVT.
GUT-
emptying, shock-reflex phase (detrusor-sphinctor dyssynergia), predisposed to Renal Failure.
GIT- emptying delayed
Chronic Pain- 60% of them.
Anaesthetic implications:
Pre-anaesthetic checklist
Anaesthesia
Standby anaesthesia
Risk of AD- cervical injury, history of AD, urological procedures.
Spasm- proprioceptive/ cutaneous stimuli cause spasm of muscles.
Patient wish- IV sedation is a choice.
Previous procedures done as standby anaesthesia.
General anaesthesia
Premedication
Sedatives, nifedipine 10 mg S/L.
Monitoring- routine, CVP/PAC.
Drugs-reduced circulating BV, small VOD for anaesthetics, more sensitive to IV agents, reduced ability to tolerate CVS effects, reduced renal clearance.
Propofol is well established now, ketamine- spasm, NDMR single dose usually sufficient.
Sux- avoid 3days to 9months.
Induction- large vein, preload, RSI not routine.
Maintenance- IPPV, risk of more drop in CO with IPPV.
Positioning- pressure points
Fluids- preload, meticulous attention to balance.
Anticholinergics at induction for low HR.
Temperature
Autonomic dysreflexia- Halothane, enflurane/ isoflurane equally well. Increase the depth under GA.
Spasm- increase depth, relaxants rarely.
Penile erections- metaraminaol, increase depth.
Recovery- temperature, respiration. AD may occur in recovery.
Pregnancy- Increased changes of SCI, reduced CVS/RS reserve when there is increased demand
Regional anaesthesia..
Reliable prevention of AD with spinal.
Difficult to decide level of block
Dose-response relationship is not well established.
Epidural not very satisfactory blockade.
Procedures usually needing anaesthesia
Spine fixation
Intrathecal baclofen infusion apparatus
Ant sacral root stimulators, phrenic nerve pacing.
Urological procedures
Limbs, ulcers.
Other procedures.
Spinal cord anatomy
Physiology
Blood supply-
Single ASA, 2 small PSAs
Essentially no collateral supply between the two
Segmental vessels, large distance between them- watershed area between upper thoracic and lumbar region. Artery of Adamkiewicz (T8-L3).
Regulation of SC blood flow
SC perfusion pressure
Auto regulation- abolished by trauma
Pathophysiology of acute cord injury (ASCI)
Primary injury
Original impact and compression of SC.
No treatment
Secondary injury
Ischemia triggered by primary injury, and other mechanisms.
Systemic effects of ASCI
CVS, R/S, GIT, GUT, Temperature, CNS, Skin.
CNS- Central/ Anterior/Posterior/ Hemi section/ complete transection
Chronic cord injury/ transection
Spinal Shock
Autonomic dysreflexia
Other CVS changes
Blood Volume
Abnormal Valsalva response- no plateau, no overshoot.
Orthostatic hypotension- gradual adaptation d/t autoreg.
Increased renin-angiotensin response- salt-water retention.
Continued..
Respiratory system
C1/2, C3/4, lower cervical- intercostal.
Reduced VC- might recover to some extent;
Increased WOB, reduced ERV/FVC (better in head up position).
Abdominal muscle paralysis- cough, atelectasis, V/Q mismatch.
Muscles
Increased Ach receptors, K changes with suxamethonium.
Spasticity- due to intact spinal reflex arc below the level of lesion.
Bones
Reduced density below the level.
Temperature- perception, regulation.
Continued..
Skin-
decubitus ulcers, common reason for operations in them.
Blood-
Anaemia, DVT.
GUT-
emptying, shock-reflex phase (detrusor-sphinctor dyssynergia), predisposed to Renal Failure.
GIT- emptying delayed
Chronic Pain- 60% of them.
Anaesthetic implications:
Pre-anaesthetic checklist
Anaesthesia
Standby anaesthesia
Risk of AD- cervical injury, history of AD, urological procedures.
Spasm- proprioceptive/ cutaneous stimuli cause spasm of muscles.
Patient wish- IV sedation is a choice.
Previous procedures done as standby anaesthesia.
General anaesthesia
Premedication
Sedatives, nifedipine 10 mg S/L.
Monitoring- routine, CVP/PAC.
Drugs-reduced circulating BV, small VOD for anaesthetics, more sensitive to IV agents, reduced ability to tolerate CVS effects, reduced renal clearance.
Propofol is well established now, ketamine- spasm, NDMR single dose usually sufficient.
Sux- avoid 3days to 9months.
Induction- large vein, preload, RSI not routine.
Maintenance- IPPV, risk of more drop in CO with IPPV.
Positioning- pressure points
Fluids- preload, meticulous attention to balance.
Anticholinergics at induction for low HR.
Temperature
Autonomic dysreflexia- Halothane, enflurane/ isoflurane equally well. Increase the depth under GA.
Spasm- increase depth, relaxants rarely.
Penile erections- metaraminaol, increase depth.
Recovery- temperature, respiration. AD may occur in recovery.
Pregnancy- Increased changes of SCI, reduced CVS/RS reserve when there is increased demand
Regional anaesthesia..
Reliable prevention of AD with spinal.
Difficult to decide level of block
Dose-response relationship is not well established.
Epidural not very satisfactory blockade.
Procedures usually needing anaesthesia
Spine fixation
Intrathecal baclofen infusion apparatus
Ant sacral root stimulators, phrenic nerve pacing.
Urological procedures
Limbs, ulcers.
Other procedures.
Nutrition
Owen McIntyre
DEFINITIONS
•Basal metabolic rate
•Amount of energy liberated by catabolism of food per unit time under standardized conditions, ie relaxed, room temp, 12-14 hours post-prandial
•Corrected for age, sex and surface area
•Normal adult male= 197 Kj/m2/hr; 40Kcal/m2/hr
DEFINITIONS
•Calorie
•1 calorie=energy reqired to heat 1gram of water by 1o C
•1 Cal=1Kcal
1 kg of water by 1o C
•1 kcal= 4.18 kjoules
•Joule
•SI unit of energy
•1 joule=energy expended in moving a resistive force of 1 newton a distance of 1 metre
DEFINITIONS
•Nitrogen Balance
•1 gram of nitrogen=6.2 grams of protein
=30 grams of muscle
•Normal losses=0.15-0.2g/kg/day
•ITU losses can be> 0.5g/kg/day
•Mainly in urinary urea
•Approx 4g/day in skin/hair/faeces
•Also: proteinuria, GIT fistula
•Measured by 24 hour urea collection with corrections for other losses
DEFINITIONS
•Malnutrition
•Multiple nutrient deficiencies
•Common in hospital patients
•Impaired healing
•Reduced immune system function
•Reduced muscle mass/poor mobility and weaning
•Anaemia
•Electrolyte disturbances
•Starvation
•Carbs- hepatic and muscle glycogen = 24-48 hrs
•Protein- from skeletal muscle = 10-12 days
•Fat- from adipose tissue = 20-25 days
DEFINITIONS
•Catabolism
•Form of accelerated starvation with glycogenolysis, lipolysis and proteolysis/gluconeogenisis
•Malnutrition is a predisposing factor
•Assoc with severe illness, sepsis, burns, trauma and stress response to surgery
Common mechanism: catabolic hormones
insulin resistance
increased metabolic rate
increased oxygen demand
NORMAL DAILY REQUIREMENTS
•Energy: 30- 40 kcal/kg
carbs= 50% (4kcal/g)
lipids= 35% (9kcal/g)
protein= 15% (4kcal/g)
•Water: 30- 40 ml/kg
1000ml of water for 1000kcal expended
•Nitrogen: 0.2 g/kg=1.5 g/kg
•Fat: 2 g/kg
•Glucose: 2 g/kg
NORMAL DAILY REQUIREMENTS
•Na+ 1mmol/kg
•K+ 1
•Cl- 1.5
•Mg+ 0.1-0.2
•Ca+ 0.1-0.2
•Phos 0.2-0.5
NUTRITIONAL ASSESSMENT
•Careful history and exam
•Objective tests
•Subjective global assessment
•Experimental
•All difficult in ITU setting
•Nutritional Risk Screening
•Impaired nutritional status
•Severity of disease
QUESTIONS?
•What routes are available for nutritional support?
•List the pros and cons for each route
•List the contraindications for each
•List the complications of each
ENTERAL FEEDS
•Polymeric
•Normal gut function
•Nitrogen source is protein
•Energy from triglycerides and glucose polymers
•Elemental
•GI failure,pancreatic insufficiency, often NJ
•Nitrogen from amino acids or oligopeptides
•Energy from short glucose polymers, no lipid
•Specialist, Disease specific
PARENTERAL FEEDS
•Nitrogen from L-amino acids
•Energy from glucose-50% lipid emulsion-50%
•Electrolytes
•Trace elements and minerals
•Bespoke
MONITORING
•Fluid balance, calorie intake, ?weight
•Urea and electrolytes, phosphate
•Blood glucose
•FBC
•LFTs, Ca and Mg
•Plasma triglycerides
FINAL POINTS
•Glutamine
•Significantly reduce mortality and ITU stay?
•Prevents gut atrophy, direct fuel for enterocytes and lymphoid tissue
•Conditionally essential in critical illness
•Re-feeding Syndrome
•Previously malnourished
•Low K+, Mg+, Phosphate
DEFINITIONS
•Basal metabolic rate
•Amount of energy liberated by catabolism of food per unit time under standardized conditions, ie relaxed, room temp, 12-14 hours post-prandial
•Corrected for age, sex and surface area
•Normal adult male= 197 Kj/m2/hr; 40Kcal/m2/hr
DEFINITIONS
•Calorie
•1 calorie=energy reqired to heat 1gram of water by 1o C
•1 Cal=1Kcal
1 kg of water by 1o C
•1 kcal= 4.18 kjoules
•Joule
•SI unit of energy
•1 joule=energy expended in moving a resistive force of 1 newton a distance of 1 metre
DEFINITIONS
•Nitrogen Balance
•1 gram of nitrogen=6.2 grams of protein
=30 grams of muscle
•Normal losses=0.15-0.2g/kg/day
•ITU losses can be> 0.5g/kg/day
•Mainly in urinary urea
•Approx 4g/day in skin/hair/faeces
•Also: proteinuria, GIT fistula
•Measured by 24 hour urea collection with corrections for other losses
DEFINITIONS
•Malnutrition
•Multiple nutrient deficiencies
•Common in hospital patients
•Impaired healing
•Reduced immune system function
•Reduced muscle mass/poor mobility and weaning
•Anaemia
•Electrolyte disturbances
•Starvation
•Carbs- hepatic and muscle glycogen = 24-48 hrs
•Protein- from skeletal muscle = 10-12 days
•Fat- from adipose tissue = 20-25 days
DEFINITIONS
•Catabolism
•Form of accelerated starvation with glycogenolysis, lipolysis and proteolysis/gluconeogenisis
•Malnutrition is a predisposing factor
•Assoc with severe illness, sepsis, burns, trauma and stress response to surgery
Common mechanism: catabolic hormones
insulin resistance
increased metabolic rate
increased oxygen demand
NORMAL DAILY REQUIREMENTS
•Energy: 30- 40 kcal/kg
carbs= 50% (4kcal/g)
lipids= 35% (9kcal/g)
protein= 15% (4kcal/g)
•Water: 30- 40 ml/kg
1000ml of water for 1000kcal expended
•Nitrogen: 0.2 g/kg=1.5 g/kg
•Fat: 2 g/kg
•Glucose: 2 g/kg
NORMAL DAILY REQUIREMENTS
•Na+ 1mmol/kg
•K+ 1
•Cl- 1.5
•Mg+ 0.1-0.2
•Ca+ 0.1-0.2
•Phos 0.2-0.5
NUTRITIONAL ASSESSMENT
•Careful history and exam
•Objective tests
•Subjective global assessment
•Experimental
•All difficult in ITU setting
•Nutritional Risk Screening
•Impaired nutritional status
•Severity of disease
QUESTIONS?
•What routes are available for nutritional support?
•List the pros and cons for each route
•List the contraindications for each
•List the complications of each
ENTERAL FEEDS
•Polymeric
•Normal gut function
•Nitrogen source is protein
•Energy from triglycerides and glucose polymers
•Elemental
•GI failure,pancreatic insufficiency, often NJ
•Nitrogen from amino acids or oligopeptides
•Energy from short glucose polymers, no lipid
•Specialist, Disease specific
PARENTERAL FEEDS
•Nitrogen from L-amino acids
•Energy from glucose-50% lipid emulsion-50%
•Electrolytes
•Trace elements and minerals
•Bespoke
MONITORING
•Fluid balance, calorie intake, ?weight
•Urea and electrolytes, phosphate
•Blood glucose
•FBC
•LFTs, Ca and Mg
•Plasma triglycerides
FINAL POINTS
•Glutamine
•Significantly reduce mortality and ITU stay?
•Prevents gut atrophy, direct fuel for enterocytes and lymphoid tissue
•Conditionally essential in critical illness
•Re-feeding Syndrome
•Previously malnourished
•Low K+, Mg+, Phosphate
Carbon Monoxide Poisoning
Andy Ketchin
History
•Mr MJ,
56 year old male.
•House fire mid morning. Patient unharmed.
•Found with GCS 4 in house 5pm same day.
•Evidence of aspiration. No evidence self harm.
Background
•PMHx No significant past.
•DHx No regular meds, or allergy.
•SHx Lives alone.
? Learning difficulties.
Unemployed.
Smoker, no alcohol.
On Examination
•A Soot Intubated
•B Reduced air entry right lower zone.
•C Hypotensive Normal ECG.
•D GCS 4 Normoglycaemic/thermic.
•E No burns/trauma.
Investigations
•U&E,CRP NAD
•FBC WCC 43, HB16.0
•ABG pH 7.26 pO2 7.9 pCO2 4.6 BE - 12.0
•Toxicology COHb 43.5% à 12.8%
•CXR Right lower zone diffuse opacity.
Problem List & Plan
CO Poisoning - Presentation
Mild – constitutional / viral symptoms.
Severe – seizures, syncope, coma myocardial ischaemia ventricular arrhythmias pulmonary oedema profound lactic acidosis
“Cherry red” insensitive
CO Poisoning - Pathophysiology
•Affinity COHb 240 : HbO2
•(Non smokers < color="#ff0000">DO = CO x CaO2
CaO2 = (k1 x Hb x SaO2) + (k2 x PaO2)
{k1 = 1.32, k2 = 0.23}
CO Poisoning - Management
Hyperbaric therapy:
•Reduced COHb t1/2
•PaO2 increased from 0.3 à 6.0 ml/dl.
Hyperbaric Therapy
Recommended:
•CO level > 40%
•CO level > 20% in pregnancy
•LOC
•Severe acidosis, pH <>
Considerations:
•Delay < 6 hr
•Logistics
•Concomitant cyanide poisoning
History
•Mr MJ,
56 year old male.
•House fire mid morning. Patient unharmed.
•Found with GCS 4 in house 5pm same day.
•Evidence of aspiration. No evidence self harm.
Background
•PMHx No significant past.
•DHx No regular meds, or allergy.
•SHx Lives alone.
? Learning difficulties.
Unemployed.
Smoker, no alcohol.
On Examination
•A Soot Intubated
•B Reduced air entry right lower zone.
•C Hypotensive Normal ECG.
•D GCS 4 Normoglycaemic/thermic.
•E No burns/trauma.
Investigations
•U&E,CRP NAD
•FBC WCC 43, HB16.0
•ABG pH 7.26 pO2 7.9 pCO2 4.6 BE - 12.0
•Toxicology COHb 43.5% à 12.8%
•CXR Right lower zone diffuse opacity.
Problem List & Plan
CO Poisoning - Presentation
Mild – constitutional / viral symptoms.
Severe – seizures, syncope, coma myocardial ischaemia ventricular arrhythmias pulmonary oedema profound lactic acidosis
“Cherry red” insensitive
CO Poisoning - Pathophysiology
•Affinity COHb 240 : HbO2
•(Non smokers < color="#ff0000">DO = CO x CaO2
CaO2 = (k1 x Hb x SaO2) + (k2 x PaO2)
{k1 = 1.32, k2 = 0.23}
CO Poisoning - Management
Hyperbaric therapy:
•Reduced COHb t1/2
•PaO2 increased from 0.3 à 6.0 ml/dl.
Hyperbaric Therapy
Recommended:
•CO level > 40%
•CO level > 20% in pregnancy
•LOC
•Severe acidosis, pH <>
Considerations:
•Delay < 6 hr
•Logistics
•Concomitant cyanide poisoning
Inhaled Anaesthetics
Jason Koerber
Definitions
Gas
A substance above its critical temperature.
Volatile
A substance in a gaseous state but below its critical temperature.
Definitions - Anaesthesia
“Anaesthesia” was first used by the Greek philosopher Dioscorides in the 1st century to describe the narcotic effect of the plant mandragora.
The word reappeared in the 1771 Encyclopaedia Britannica, where it was defined as “privation of the senses”.
After introduction of ether by Morton in 1846, Oliver Wendell Holmes coined the word to describe the new phenomenon that made surgical procedures possible.
Definitions - Anaesthesia 2
We measure the response to stimulation.
Does the patient move when their name is called?
Does the response to incision suggest conscious perception?
Does the heart of BP go up in response to surgical manipulation?
Does the patient remember events, conversations, or pain?
Regional or General?
Definitions - Anaesthesia 3
Anaesthetic agent: reversible.
General consists of the following components:UnconsciousnessAmnesiaAnalgesiaMuscle relaxation
Regional: blockade of pain transmission.
MAC
Measure of potency.
Minimum alveolar concentration at steady state that prevents reaction to a standard surgical stimulus (skin incision) in 50% of subjects at sea level.
Meyer-Overton hypothesis
Name the Anaesthetic Agent!
H H H H
H C C O C C H
H H H H
Diethyl ether
Ethanol and sulphuric acid.
Flammable/explosive.
High blood:gas and oil:gas coefficients.
10% metabolised to ethanol and aldehydes.
Nausea and vomiting.
Seizures can occur.
Increased salivation.
Increased gluconeogenesis
Name the Anaesthetic Agent!
F H F
H C O C C F
F Cl F
Isoflurane
Halogenated ethyl methyl ether.
Resp: dep, pungent, bronchodil.
CVS: dec SVR, tachy,
? coronary steal.
CNS: best balance of reduction cerebral consumption and minimal increase in cerebral blood flow.
Met: 0.2% (trifluroacetic acid, F-, CO)
Name the Anaesthetic Agent!
F F H
H C O C C F
F F Cl
Enflurane
Halogenated ethyl methyl ether.
Resp: most dep, non-irritant
CVS: dec SVR, tachy, heart not sensitized.
CNS: high conc in presence of hypocarbia produce 3Hz spike and wave pattern. Increase ICP.
Met: 2% (F-)
Name the Anaesthetic Agent!
Cl F
H C C F
Br F
Halothane
Halogenated hydrocarbonThymol 0.01% preservative.Dissolves into rubber.
Resp: dep, sweet, bronchodil.
CVS: dec SVR, brady, sensitizes to catecholamines.
CNS: increases cerebral blood flow more than other volatiles.
Met: 25% (trifluroacetic acid, Cl-, Br-, F-). Hepatitis?
Name the Anaesthetic Agent!
F H F
H C O C C F
F F F
Desflurane
Fluorinated ethyl methyl ether.Tec 6 vaporizer.
Resp: dep, pungent, coughing and breath holding.CVS: Similar to isoflurane but at conc above 1 MAC may produce stimulation.
CNS: increased cerebral blood flow
Met: 0.02% (Trifluroacetic acid)
Name the Anaesthetic Agent!
F CH3
H C O C H
H CH3
Sevofluorane
Polyfluorinated isopropyl methyl ether.Achiral - unlike other volatiles.
Resp: dep, pleasant odour bronchodilationCVS: dec SVR, HR unchanged, heart not sensitized.
CNS: increases cerebral blood flow. ? Post-op agitation in children
Met: 3.5% (F-), compound A
Name the Anaesthetic Agent!
H F Cl
H C O C C H
H F Cl
Methoxyflurane
Halogenated ethyl methyl ether.
BP 105 degrees.
Very soluble in blood.Blood:gas coefficient 13.MAC 0.2.
Fluoride ion caused renal failure.
Nitrous oxide (N2O)
lManufacture: heating ammonium nitrate to 250 degrees. May contain impurities NH3, N2, NO, NO2, HNO3. These are removed by scrubbers, water and caustic soda.
lBlue cylinders. Filling ratio.
lConcentration effect, second gas effect and diffusion hypoxia.
lResp: small fall in VT and increase in rate.
lCVS: mild direct cardiac depressant. Normally counterbalanced by central sympathetic stimulant effects.
lCNS: increases cerebral blood flow. Produces analgesia.
lToxicity.
Xeon
lInert, odourless gas.
lMakes up 0.0000087% of atmosphere.
lFastest onset.
lResp: increases VT and decreases rate.
lCVS: no effect on contractility but may cause small decrease in HR.
lCNS: increases cerebral blood flow. May be used to enhance CT images of brain.Produces analgesia.
lNot metabolised.
The bloody table!!
Definitions
Gas
A substance above its critical temperature.
Volatile
A substance in a gaseous state but below its critical temperature.
Definitions - Anaesthesia
“Anaesthesia” was first used by the Greek philosopher Dioscorides in the 1st century to describe the narcotic effect of the plant mandragora.
The word reappeared in the 1771 Encyclopaedia Britannica, where it was defined as “privation of the senses”.
After introduction of ether by Morton in 1846, Oliver Wendell Holmes coined the word to describe the new phenomenon that made surgical procedures possible.
Definitions - Anaesthesia 2
We measure the response to stimulation.
Does the patient move when their name is called?
Does the response to incision suggest conscious perception?
Does the heart of BP go up in response to surgical manipulation?
Does the patient remember events, conversations, or pain?
Regional or General?
Definitions - Anaesthesia 3
Anaesthetic agent: reversible.
General consists of the following components:UnconsciousnessAmnesiaAnalgesiaMuscle relaxation
Regional: blockade of pain transmission.
MAC
Measure of potency.
Minimum alveolar concentration at steady state that prevents reaction to a standard surgical stimulus (skin incision) in 50% of subjects at sea level.
Meyer-Overton hypothesis
Name the Anaesthetic Agent!
H H H H
H C C O C C H
H H H H
Diethyl ether
Ethanol and sulphuric acid.
Flammable/explosive.
High blood:gas and oil:gas coefficients.
10% metabolised to ethanol and aldehydes.
Nausea and vomiting.
Seizures can occur.
Increased salivation.
Increased gluconeogenesis
Name the Anaesthetic Agent!
F H F
H C O C C F
F Cl F
Isoflurane
Halogenated ethyl methyl ether.
Resp: dep, pungent, bronchodil.
CVS: dec SVR, tachy,
? coronary steal.
CNS: best balance of reduction cerebral consumption and minimal increase in cerebral blood flow.
Met: 0.2% (trifluroacetic acid, F-, CO)
Name the Anaesthetic Agent!
F F H
H C O C C F
F F Cl
Enflurane
Halogenated ethyl methyl ether.
Resp: most dep, non-irritant
CVS: dec SVR, tachy, heart not sensitized.
CNS: high conc in presence of hypocarbia produce 3Hz spike and wave pattern. Increase ICP.
Met: 2% (F-)
Name the Anaesthetic Agent!
Cl F
H C C F
Br F
Halothane
Halogenated hydrocarbonThymol 0.01% preservative.Dissolves into rubber.
Resp: dep, sweet, bronchodil.
CVS: dec SVR, brady, sensitizes to catecholamines.
CNS: increases cerebral blood flow more than other volatiles.
Met: 25% (trifluroacetic acid, Cl-, Br-, F-). Hepatitis?
Name the Anaesthetic Agent!
F H F
H C O C C F
F F F
Desflurane
Fluorinated ethyl methyl ether.Tec 6 vaporizer.
Resp: dep, pungent, coughing and breath holding.CVS: Similar to isoflurane but at conc above 1 MAC may produce stimulation.
CNS: increased cerebral blood flow
Met: 0.02% (Trifluroacetic acid)
Name the Anaesthetic Agent!
F CH3
H C O C H
H CH3
Sevofluorane
Polyfluorinated isopropyl methyl ether.Achiral - unlike other volatiles.
Resp: dep, pleasant odour bronchodilationCVS: dec SVR, HR unchanged, heart not sensitized.
CNS: increases cerebral blood flow. ? Post-op agitation in children
Met: 3.5% (F-), compound A
Name the Anaesthetic Agent!
H F Cl
H C O C C H
H F Cl
Methoxyflurane
Halogenated ethyl methyl ether.
BP 105 degrees.
Very soluble in blood.Blood:gas coefficient 13.MAC 0.2.
Fluoride ion caused renal failure.
Nitrous oxide (N2O)
lManufacture: heating ammonium nitrate to 250 degrees. May contain impurities NH3, N2, NO, NO2, HNO3. These are removed by scrubbers, water and caustic soda.
lBlue cylinders. Filling ratio.
lConcentration effect, second gas effect and diffusion hypoxia.
lResp: small fall in VT and increase in rate.
lCVS: mild direct cardiac depressant. Normally counterbalanced by central sympathetic stimulant effects.
lCNS: increases cerebral blood flow. Produces analgesia.
lToxicity.
Xeon
lInert, odourless gas.
lMakes up 0.0000087% of atmosphere.
lFastest onset.
lResp: increases VT and decreases rate.
lCVS: no effect on contractility but may cause small decrease in HR.
lCNS: increases cerebral blood flow. May be used to enhance CT images of brain.Produces analgesia.
lNot metabolised.
The bloody table!!
Obesity and anaesthesia
Obesity
BMI = mass (kg)/[height (m)]2
BMI>28 obese, BMI >35 morbidly obese
17% of UK population are obese
Associated with BP, IHD, NIDDM, peripheral vascular disease, gallstones, etc…
Pathophysiology
Obesity is associated with
Increase in absolute blood volume, but it’s low relative to body mass
Increase O2 consumption by metabolically active adipose tissue & work of supporting ms.
Reduced FRC in awake pt, and significantly decreased following induction
Rapid desaturation.
OSA
Obesity hypoventilation syndrome, causing loss of CO2 resp drive & hypoxia, polycythemia and pulmonary hypertension
Increase gastric volume, raised intra-abdominal pressure, and a higher incidence of hiatus hernia pose a significant risk of aspiration.
Insulin resistance may cause peri-operative diabetes.
Vd for drugs is altered due to a smaller proportion of TBW, greater proportion of adipose tissue,
Increase lean body mass, and
Increase blood volume and cardiac output.
Conduct of anaesthesia
Difficult intubation
IV access
Operating table
Thromboembolic events.
Premedication.
Ventilation
Positioning
Regional anaesthesia
Post op
Post op mortality is doubled
Mobilize as soon as possible
Pulmonary atalectasis is common
Early physiotherapy.
Nocturnal nasal CPAP
PCA more predictable than IM morphine
HDU care should be available
Obstructive Sleep Apnoea
At least 5% of morbidly obese patients will have OSA particularly if they have associated risk factors such as large collar size (over 16.5 inches), evening alcohol consumption and pharyngeal abnormalities.
The disease is cause by passive collapse of the pharyngeal airway during deeper planes of sleep, resulting in snoring and intermittent airway obstruction.
Resultant hypoxaemia and hypercapnia results in arousal and disruption of quality sleep thus causing the characteristic daytime somnolence.
Cont.
Pulmonary and systemic vasoconstriction, polycythaemia, right ventricular failure and cor pulmonale can all occur.
lIndeed the relative hypoventilation can cause a progressive desensitisation of the respiratory centres to hypercapnia with resultant Type II respiratory failure.
Formal diagnosis is by sleep studies and treatment includes removal of precipitants, weight loss and nocturnal CPAP.
BMI = mass (kg)/[height (m)]2
BMI>28 obese, BMI >35 morbidly obese
17% of UK population are obese
Associated with BP, IHD, NIDDM, peripheral vascular disease, gallstones, etc…
Pathophysiology
Obesity is associated with
Increase in absolute blood volume, but it’s low relative to body mass
Increase O2 consumption by metabolically active adipose tissue & work of supporting ms.
Reduced FRC in awake pt, and significantly decreased following induction
Rapid desaturation.
OSA
Obesity hypoventilation syndrome, causing loss of CO2 resp drive & hypoxia, polycythemia and pulmonary hypertension
Increase gastric volume, raised intra-abdominal pressure, and a higher incidence of hiatus hernia pose a significant risk of aspiration.
Insulin resistance may cause peri-operative diabetes.
Vd for drugs is altered due to a smaller proportion of TBW, greater proportion of adipose tissue,
Increase lean body mass, and
Increase blood volume and cardiac output.
Conduct of anaesthesia
Difficult intubation
IV access
Operating table
Thromboembolic events.
Premedication.
Ventilation
Positioning
Regional anaesthesia
Post op
Post op mortality is doubled
Mobilize as soon as possible
Pulmonary atalectasis is common
Early physiotherapy.
Nocturnal nasal CPAP
PCA more predictable than IM morphine
HDU care should be available
Obstructive Sleep Apnoea
At least 5% of morbidly obese patients will have OSA particularly if they have associated risk factors such as large collar size (over 16.5 inches), evening alcohol consumption and pharyngeal abnormalities.
The disease is cause by passive collapse of the pharyngeal airway during deeper planes of sleep, resulting in snoring and intermittent airway obstruction.
Resultant hypoxaemia and hypercapnia results in arousal and disruption of quality sleep thus causing the characteristic daytime somnolence.
Cont.
Pulmonary and systemic vasoconstriction, polycythaemia, right ventricular failure and cor pulmonale can all occur.
lIndeed the relative hypoventilation can cause a progressive desensitisation of the respiratory centres to hypercapnia with resultant Type II respiratory failure.
Formal diagnosis is by sleep studies and treatment includes removal of precipitants, weight loss and nocturnal CPAP.
LAMINAR FLOW
FLOW- the quantity of fluid i.e. gas or liquid passing a point in unit time.
F= Q/T
Where-
F- Mean flow
Q- Quantity (mass or volume)
T- Time.
LAMINAR FLOW
In Laminar flow-fluid moves in a smooth manner and there are no eddies or turbulence.
The flow is greatest at the centre, being about twice the mean flow.
As the side of the tube is approached the flow becomes slower, until it becomes zero at the wall.
In order to drive fluid thru the tube a pressure difference, must be present across the ends.
Laminar flow has got a CONICAL VELOCITY PROFILE.
HAGEN-POISEUILLE equation.
Laminar flow is not the only type of flow occurring in anaesthesia. App., breathing systems, airways and circulation.
Laminar flow may change to TURBULENT FLOW if a constriction is reached which results in the fluid velocity increasing.
Fluid no longer exists in smooth manner, but, swirls in eddies and the resistance is higher than for the same laminar flow.
Turbulent flow has a FLAT VELOCITY PROFILE.
Although bronchi and smaller air passages are smaller than the trachea, air flow thru them is slower so laminar flow is usual in the LOWER RESP. TRACT.
Laminar flow-VISCOSITY.
Turbulent flow-DENSITY.
ROTAMETER
Anaesthetists require a continuous of gas flows in the anaesthetic machine and this is provided by a VARIABLE ORIFICE FLOWMETER.
This is often referred to by the trade name ROTAMETER.
A BOBBIN is supp. In the middle of a glass or plastic tube which is tapered.
As the gas flow increases, the bobbin rises in the tube and the clearance round the bobbin increases.
In other words, there is a variable orifice around the bobbin which depends on the gas flow.
The pressure across the bobbin remains CONSTANT because it gives rise to a force which balances the force of gravity on the bobbin.
The increase in area of the annular orifice as the bobbin rises reduces the flow resistance at higher flows and so the pressure across the bobbin stays constant, despite the flow increase.
VENTURI PRINCIPLE
The entrainment of a fluid thru the side arm into an area of low pressure caused by a constriction in a tube is the basis of the venturi principle.
It is called the BERNOULLI EFFECT.
Some equipment may include a tube with a constriction in which the cross section gradually decreases and then increases –this is known as VENTURI.
This principle is employed in gas mixing devices, including fixed performance oxygen devices, suction equipment and scavenging equipment.
F= Q/T
Where-
F- Mean flow
Q- Quantity (mass or volume)
T- Time.
LAMINAR FLOW
In Laminar flow-fluid moves in a smooth manner and there are no eddies or turbulence.
The flow is greatest at the centre, being about twice the mean flow.
As the side of the tube is approached the flow becomes slower, until it becomes zero at the wall.
In order to drive fluid thru the tube a pressure difference, must be present across the ends.
Laminar flow has got a CONICAL VELOCITY PROFILE.
HAGEN-POISEUILLE equation.
Laminar flow is not the only type of flow occurring in anaesthesia. App., breathing systems, airways and circulation.
Laminar flow may change to TURBULENT FLOW if a constriction is reached which results in the fluid velocity increasing.
Fluid no longer exists in smooth manner, but, swirls in eddies and the resistance is higher than for the same laminar flow.
Turbulent flow has a FLAT VELOCITY PROFILE.
Although bronchi and smaller air passages are smaller than the trachea, air flow thru them is slower so laminar flow is usual in the LOWER RESP. TRACT.
Laminar flow-VISCOSITY.
Turbulent flow-DENSITY.
ROTAMETER
Anaesthetists require a continuous of gas flows in the anaesthetic machine and this is provided by a VARIABLE ORIFICE FLOWMETER.
This is often referred to by the trade name ROTAMETER.
A BOBBIN is supp. In the middle of a glass or plastic tube which is tapered.
As the gas flow increases, the bobbin rises in the tube and the clearance round the bobbin increases.
In other words, there is a variable orifice around the bobbin which depends on the gas flow.
The pressure across the bobbin remains CONSTANT because it gives rise to a force which balances the force of gravity on the bobbin.
The increase in area of the annular orifice as the bobbin rises reduces the flow resistance at higher flows and so the pressure across the bobbin stays constant, despite the flow increase.
VENTURI PRINCIPLE
The entrainment of a fluid thru the side arm into an area of low pressure caused by a constriction in a tube is the basis of the venturi principle.
It is called the BERNOULLI EFFECT.
Some equipment may include a tube with a constriction in which the cross section gradually decreases and then increases –this is known as VENTURI.
This principle is employed in gas mixing devices, including fixed performance oxygen devices, suction equipment and scavenging equipment.
PONV
Dr Owen McIntyre
Define PONV
•NAUSEA
•Sensation that precedes vomiting
•VOMITING
•Rapid expulsion of stomach contents through the mouth
•PONV
•Multifactorial
•Incidence in GA with volatile between 20-40%
(Anywhere between 10-90%)
•Early: within first 6 hours
•Late: within first 24 hours
Neural pathways mediating N+V?
•CTZ: medulla, floor of 4th ventricle, outside BBB
•Primary NT is Dopamine, D2 (+5HT3)
•Vestibular afferents
•Raised ICP via direct action
•Metabolic abnormalities; uraemia, hypernatraemia
• Drugs: opiates, volatiles, etomidate, neostigmine
sympathomimetics; ketamine, ephedrine
cytotoxics, cardiac glycosides, apomorphine
•Efferents to VC
Neural pathways mediating N+V?
•Vomiting Centre: medulla, same level as CTZ
inside BBB
•Primary NT is Acetylchloine, M3 (+H1, ?mu opioid)
•Cortical affferents, limbic, olfactory,visual
•Visceral afferents, gut and heart (X and symp)
•Occulovestibular afferents
•Efferent compose Vomiting reflex pathway
Neural pathways mediating N+V?
•Substance P
•Slow excitatory neurotransmitter
•Acting at Neurokinin-1 receptors
•Loads of NK-1 receptors at key sites in medulla
•Could be final common pathway
•Vofopitant
Describe the vomiting reflex
•Complex: central, peripheral and enteric NS
•Reflex is preceded by retrograde peristalsis
•Increased salivation
•Forceful inspiration, breath held mid-insp
•Raise hyoid and larynx; closes glottis and opens crico-oesophageal sphincter
•Elevation of soft palate closes nasopharynx
•Contraction of diaphragm, abdo muscles
•Opening of LOS and relaxation of oesophagus
What are the risk factors for PONV?
•Patient factors
•Female(2-4x)
•Past history of PONV(3x)
•History of motion sickness
•Non smoker
•Obesity
•Children
•Early ambulation
What are the risk factors for PONV?
•Anaesthetic factors
•Volatiles
•Opiates
•N2O
•Etomidate, Thiopentone
•Neostigmine
•Sympathomimetics
•Hypotension
•Hypoxia
•Bag-mask ventilation
How would you manage PONV?
•Assessment of risk
•Prevention
•Pre
•Peri
•Post-op
•Pharmacotherapy
•Multimodal, ‘Balanced anti-emetic therapy’
•Prophylaxis vs. treatment
•Others
•Acupuncture
Prevention
•Pre-operative
•Optimize fasting; clear fluid 2hours pre-op
•Pre-med; benzos, ?metoclopramide
•Peri-operative
•Regional anaesthesia
•Avoid volatiles and N2O in favour of Propofol TCI
•Avoid thio, etomidate, ketamine
•Avoid NMBAs and therefore neostigmine
•Avoid opioids if possible, alternate analgesia
•Generous fluid therapy
•Post-operative
•Adequate analgesia
Can you classify antiemetics?
•Mode of action or site of action
•Anti-dopaminergic(D2)
•Anti-histamines(H1)
•Anti-cholinergic(M3)
•Anti-serotinergic(5HT3)
•Others
•Corticosteroids
•Cannabinoids
•Propofol
What are the side effects of the anti-emetics you commonly use?
•Cyclizine
•Ondansetron
•Dexamethasone
•?Prochlorperazine
•?Others
Strategy for the management of PONV
•A Simplified Risk Score for Predicting Postoperative Nausea and Vomiting
–Apfel et al, Anesthesiology 1999 91:693-700
•4 patient risk factors were as accurate at predicting PONV as more complicated equations
Female
Past history of PONV or Motion Sickness
Non smoker
Post-op opiates
•No association with type or duration of surgery
Strategy for the management of PONV
•Number of Risk Factors Incidence of PONV
0 10%
1 21%
2 39%
3 61%
4 79%
•If 2+ present risk is high
•Modify anaesthetic technique
•?Prophylaxis
•Multimodal approach
Evidence for the management of PONV
•Too much information!!
•Cost effectiveness: Individual drugs
Prophylaxis vs Treatment
•Patient satisfaction
•NNT much better for high risk patients
•Single antiemetic: Ondansetron NNT 5-6
•Combination therapy significantly better than monotherapy with no increased SE (Ondan + dex /drop)
Evidence for the management of PONV
•Multimodal Approach
•Scuderi et al, Anaest Analg 2000; 91
•TIVA: Propofol and remifentanil
•No nitrous
•No NMBA
•Aggressive IV fluids(25ml/kg)
•3x prophylactic anti-emetics
•98% response rate
Define PONV
•NAUSEA
•Sensation that precedes vomiting
•VOMITING
•Rapid expulsion of stomach contents through the mouth
•PONV
•Multifactorial
•Incidence in GA with volatile between 20-40%
(Anywhere between 10-90%)
•Early: within first 6 hours
•Late: within first 24 hours
Neural pathways mediating N+V?
•CTZ: medulla, floor of 4th ventricle, outside BBB
•Primary NT is Dopamine, D2 (+5HT3)
•Vestibular afferents
•Raised ICP via direct action
•Metabolic abnormalities; uraemia, hypernatraemia
• Drugs: opiates, volatiles, etomidate, neostigmine
sympathomimetics; ketamine, ephedrine
cytotoxics, cardiac glycosides, apomorphine
•Efferents to VC
Neural pathways mediating N+V?
•Vomiting Centre: medulla, same level as CTZ
inside BBB
•Primary NT is Acetylchloine, M3 (+H1, ?mu opioid)
•Cortical affferents, limbic, olfactory,visual
•Visceral afferents, gut and heart (X and symp)
•Occulovestibular afferents
•Efferent compose Vomiting reflex pathway
Neural pathways mediating N+V?
•Substance P
•Slow excitatory neurotransmitter
•Acting at Neurokinin-1 receptors
•Loads of NK-1 receptors at key sites in medulla
•Could be final common pathway
•Vofopitant
Describe the vomiting reflex
•Complex: central, peripheral and enteric NS
•Reflex is preceded by retrograde peristalsis
•Increased salivation
•Forceful inspiration, breath held mid-insp
•Raise hyoid and larynx; closes glottis and opens crico-oesophageal sphincter
•Elevation of soft palate closes nasopharynx
•Contraction of diaphragm, abdo muscles
•Opening of LOS and relaxation of oesophagus
What are the risk factors for PONV?
•Patient factors
•Female(2-4x)
•Past history of PONV(3x)
•History of motion sickness
•Non smoker
•Obesity
•Children
•Early ambulation
What are the risk factors for PONV?
•Anaesthetic factors
•Volatiles
•Opiates
•N2O
•Etomidate, Thiopentone
•Neostigmine
•Sympathomimetics
•Hypotension
•Hypoxia
•Bag-mask ventilation
How would you manage PONV?
•Assessment of risk
•Prevention
•Pre
•Peri
•Post-op
•Pharmacotherapy
•Multimodal, ‘Balanced anti-emetic therapy’
•Prophylaxis vs. treatment
•Others
•Acupuncture
Prevention
•Pre-operative
•Optimize fasting; clear fluid 2hours pre-op
•Pre-med; benzos, ?metoclopramide
•Peri-operative
•Regional anaesthesia
•Avoid volatiles and N2O in favour of Propofol TCI
•Avoid thio, etomidate, ketamine
•Avoid NMBAs and therefore neostigmine
•Avoid opioids if possible, alternate analgesia
•Generous fluid therapy
•Post-operative
•Adequate analgesia
Can you classify antiemetics?
•Mode of action or site of action
•Anti-dopaminergic(D2)
•Anti-histamines(H1)
•Anti-cholinergic(M3)
•Anti-serotinergic(5HT3)
•Others
•Corticosteroids
•Cannabinoids
•Propofol
What are the side effects of the anti-emetics you commonly use?
•Cyclizine
•Ondansetron
•Dexamethasone
•?Prochlorperazine
•?Others
Strategy for the management of PONV
•A Simplified Risk Score for Predicting Postoperative Nausea and Vomiting
–Apfel et al, Anesthesiology 1999 91:693-700
•4 patient risk factors were as accurate at predicting PONV as more complicated equations
Female
Past history of PONV or Motion Sickness
Non smoker
Post-op opiates
•No association with type or duration of surgery
Strategy for the management of PONV
•Number of Risk Factors Incidence of PONV
0 10%
1 21%
2 39%
3 61%
4 79%
•If 2+ present risk is high
•Modify anaesthetic technique
•?Prophylaxis
•Multimodal approach
Evidence for the management of PONV
•Too much information!!
•Cost effectiveness: Individual drugs
Prophylaxis vs Treatment
•Patient satisfaction
•NNT much better for high risk patients
•Single antiemetic: Ondansetron NNT 5-6
•Combination therapy significantly better than monotherapy with no increased SE (Ondan + dex /drop)
Evidence for the management of PONV
•Multimodal Approach
•Scuderi et al, Anaest Analg 2000; 91
•TIVA: Propofol and remifentanil
•No nitrous
•No NMBA
•Aggressive IV fluids(25ml/kg)
•3x prophylactic anti-emetics
•98% response rate
Fluid Balance
Body Organization
Cells exist in “internal sea” of ECF
Composition – primordial oceans
ECF = Interstitial Fluid + Blood plasma
TBW = ECF + ICF
18% protein,7% mineral,15% fat
60% - WATER
Body Water
60% Total body weight
40% intracellular
20% extra cellular
Extracellular – 25% intravascular
- 75% interstitial
Body Water
70 kg normal adult
TBW = 42 l
ICF = 28 l
ECF = 14 l
Measurements – fluid vol.
Inject subs that stay in one comp.
Vd = amount injected/conc. of subs
Mix evenly through the comp.
No effect on the dist of H20
Must be unchanged
Easy to measure
Plasma Volume
Dyes bound to plasma proteins
Evans blue (t-1824)
Sr. Alb labeled with radioactive iodine
Average value = 3500ml(70kg adult)
Blood vol.
Hematocrit (Hct)- % of blood vol made up of cells
Total blood vol. = plasma volume x 100/100- Hct
Red cell volume = total blood vol.-plasma volume
ECF Volume
Difficult to measure
Limits of the space are ill defined
Transcellular fluids
Inulin
Mannitol and sucrose
20% of body weight
Interstitial fluid vol.
Cannot be measured directly
ECF VOL – Plasma vol.
ECF: ICF - infants & children>adults
ICF VOLUME
Cannot be measured directly
ICF = TBW – ECF
TBW – Deuterium oxide D2O
Tritium oxide and aminopyrine
Water content of lean body tissue – 71 to72 ml/100gm of tissue
Conc. Of Solutes - Units
Mole
Millimoles, micromoles
Molecular weight
Equivalents
Moles
Gram molecular weight of a substance
One mole = 6 x 1023 molecules
SI unit for amount of substance
Mol. Wt – ratio of mass of one molecule of a substance to the mass of 1/12 the mass of an atom of carbon-12
Dalton – unit of mass equal to 1/12 the mass of an atom of carbon-12
Equivalents
1 eq is 1 mol of an ionized substance divided by its valence.
Water
Small, highly diffusible, polar molecule
Solvent – hydrate proteins, sugars and other substances-
Dissolving properties
Thermal properties
Ionizes very slightly (pH 7.0)
Bulk Flow & Diffusion
Bulk flow –movement of the solution mass in the direction of hydrostatic pressure gradient
Diffusion – molecular movement down conc. Gradient
Disperse local accumulation of molecules if it is free to move
Osmotic Pressure
Fluid compartment – principal solute
Mainly restricted to that compartment
K+ ICF
Na+ ECF
Plasma proteins: intra vascular space
Osmotic pressure – total number of particles
Osmosis
Solution – stable mixture of solute & solvent
Solute– dispersed individual molecules
Solvent – liquid bulk
Solute mol. Occupy space
Water mol. Net movement by diffusion.
Osmosis
Water – diffuse from region of high solvent conc. to low conc.
The extent of tendency for solvent to move – measured by use of semi permeable membrane. -hydrostatic pressure to produce equal and opposite bulk flow
Sum of conc. of all solute particles
Oncotic Pressure
Plasma proteins – albumin, globulin
Large mol wt & size –unable to leave intravascular space
Pressure diff between plasma and interstitial fluids
Colloid osmotic pressure
Amounts to only 0.7 mosmol/kg water
Thank you
Cells exist in “internal sea” of ECF
Composition – primordial oceans
ECF = Interstitial Fluid + Blood plasma
TBW = ECF + ICF
18% protein,7% mineral,15% fat
60% - WATER
Body Water
60% Total body weight
40% intracellular
20% extra cellular
Extracellular – 25% intravascular
- 75% interstitial
Body Water
70 kg normal adult
TBW = 42 l
ICF = 28 l
ECF = 14 l
Measurements – fluid vol.
Inject subs that stay in one comp.
Vd = amount injected/conc. of subs
Mix evenly through the comp.
No effect on the dist of H20
Must be unchanged
Easy to measure
Plasma Volume
Dyes bound to plasma proteins
Evans blue (t-1824)
Sr. Alb labeled with radioactive iodine
Average value = 3500ml(70kg adult)
Blood vol.
Hematocrit (Hct)- % of blood vol made up of cells
Total blood vol. = plasma volume x 100/100- Hct
Red cell volume = total blood vol.-plasma volume
ECF Volume
Difficult to measure
Limits of the space are ill defined
Transcellular fluids
Inulin
Mannitol and sucrose
20% of body weight
Interstitial fluid vol.
Cannot be measured directly
ECF VOL – Plasma vol.
ECF: ICF - infants & children>adults
ICF VOLUME
Cannot be measured directly
ICF = TBW – ECF
TBW – Deuterium oxide D2O
Tritium oxide and aminopyrine
Water content of lean body tissue – 71 to72 ml/100gm of tissue
Conc. Of Solutes - Units
Mole
Millimoles, micromoles
Molecular weight
Equivalents
Moles
Gram molecular weight of a substance
One mole = 6 x 1023 molecules
SI unit for amount of substance
Mol. Wt – ratio of mass of one molecule of a substance to the mass of 1/12 the mass of an atom of carbon-12
Dalton – unit of mass equal to 1/12 the mass of an atom of carbon-12
Equivalents
1 eq is 1 mol of an ionized substance divided by its valence.
Water
Small, highly diffusible, polar molecule
Solvent – hydrate proteins, sugars and other substances-
Dissolving properties
Thermal properties
Ionizes very slightly (pH 7.0)
Bulk Flow & Diffusion
Bulk flow –movement of the solution mass in the direction of hydrostatic pressure gradient
Diffusion – molecular movement down conc. Gradient
Disperse local accumulation of molecules if it is free to move
Osmotic Pressure
Fluid compartment – principal solute
Mainly restricted to that compartment
K+ ICF
Na+ ECF
Plasma proteins: intra vascular space
Osmotic pressure – total number of particles
Osmosis
Solution – stable mixture of solute & solvent
Solute– dispersed individual molecules
Solvent – liquid bulk
Solute mol. Occupy space
Water mol. Net movement by diffusion.
Osmosis
Water – diffuse from region of high solvent conc. to low conc.
The extent of tendency for solvent to move – measured by use of semi permeable membrane. -hydrostatic pressure to produce equal and opposite bulk flow
Sum of conc. of all solute particles
Oncotic Pressure
Plasma proteins – albumin, globulin
Large mol wt & size –unable to leave intravascular space
Pressure diff between plasma and interstitial fluids
Colloid osmotic pressure
Amounts to only 0.7 mosmol/kg water
Thank you
Bronchoscopy & Inhaled Foreign Bodies
Bronchoscopy & Management of Inhaled Foreign Bodies
Objectives-
Anatomy of Tracheobronchial tree
General Indications & Contraindications
Discuss problems & Options for management
How to manage a patient with a foreign body in the airway
Tracheobronchial Anatomy
Airway generations 0-23
0 – Trachea
1-4 – Main Lobar & segmental
5-11 – Small Bronchi
12-16 – Bronchioles
17-19 – Respiratory bronchioles
20-22 – Alveolar ducts
23 – Alveolar sacs
Tracheobronchial Anatomy
Indications for bronchoscopy
Diagnostic
Initial diagnosis (Flexible > Rigid)
Staging of disease
Indications continued
Therapeutic
R/O Foreign Body
Stent Insertion
Diathermy Resection
Airway Management
Insertion of DLT
Contraindications
Absolute
Don't exist?
Relative
Anaesthetic Risk
Surgical Risk - Biopsy
Tracheal Stenosis – Flexible type
Potential problems
Shared airway
Ventilation & Oxygenation
Potential for awareness
Scavenging
Concurrent disease
Work up
As for pneumonectomy especially if pre thoracotomy
What are they?
Minimal pulmonary function test criteria
Pre op Pneumonectomy criteria
PAP with unilateral occlusion
< 25 mmHg rest
< 35 mmHg exercise
Anaesthetic technique
Method of choice
TCI (Propofol +/- Remifentanil) for all but the shortest procedures
Exceptions
Upper airway obstruction
Bronchopleural fistula
Ventilation
Venturi – Sanders Injector
Ventilating bronchoscope
High Frequency Jet ventilation
Questions?
Inhaled Foreign Bodies
Who?
Children < 3y.o.
Elderly
Debilitated
Drunks
What?
Anything small enough to enter the airway
Organic e.g. Peanuts
Inorganic e.g. Coin
Case Example 1
2 y.o child presents after having coughing fit, stridor and shortness of breath
What is your management?
Case example 2
77 y.o man with a 6 week history of persistent cough
What are the findings on CXR?
X-Ray Findings
CXR
Acute presentation- Ipsilateral Obstructive Emphysema on Expiratory film
Chronic presentation - Features of collapse / consolidation distal to the FB
Anaesthetic technique
Inhalational Vs Intravenous
Upper airway obstruction or not?
Post operatively
When to Extubate?
Monitor for complications
Laryngospasm, Bronchospasm & pneumothorax
Summary
Anatomy
Indications / Contraindications
Problems & Management options
Specific management of inhaled foreign body
Objectives-
Anatomy of Tracheobronchial tree
General Indications & Contraindications
Discuss problems & Options for management
How to manage a patient with a foreign body in the airway
Tracheobronchial Anatomy
Airway generations 0-23
0 – Trachea
1-4 – Main Lobar & segmental
5-11 – Small Bronchi
12-16 – Bronchioles
17-19 – Respiratory bronchioles
20-22 – Alveolar ducts
23 – Alveolar sacs
Tracheobronchial Anatomy
Indications for bronchoscopy
Diagnostic
Initial diagnosis (Flexible > Rigid)
Staging of disease
Indications continued
Therapeutic
R/O Foreign Body
Stent Insertion
Diathermy Resection
Airway Management
Insertion of DLT
Contraindications
Absolute
Don't exist?
Relative
Anaesthetic Risk
Surgical Risk - Biopsy
Tracheal Stenosis – Flexible type
Potential problems
Shared airway
Ventilation & Oxygenation
Potential for awareness
Scavenging
Concurrent disease
Work up
As for pneumonectomy especially if pre thoracotomy
What are they?
Minimal pulmonary function test criteria
Pre op Pneumonectomy criteria
PAP with unilateral occlusion
< 25 mmHg rest
< 35 mmHg exercise
Anaesthetic technique
Method of choice
TCI (Propofol +/- Remifentanil) for all but the shortest procedures
Exceptions
Upper airway obstruction
Bronchopleural fistula
Ventilation
Venturi – Sanders Injector
Ventilating bronchoscope
High Frequency Jet ventilation
Questions?
Inhaled Foreign Bodies
Who?
Children < 3y.o.
Elderly
Debilitated
Drunks
What?
Anything small enough to enter the airway
Organic e.g. Peanuts
Inorganic e.g. Coin
Case Example 1
2 y.o child presents after having coughing fit, stridor and shortness of breath
What is your management?
Case example 2
77 y.o man with a 6 week history of persistent cough
What are the findings on CXR?
X-Ray Findings
CXR
Acute presentation- Ipsilateral Obstructive Emphysema on Expiratory film
Chronic presentation - Features of collapse / consolidation distal to the FB
Anaesthetic technique
Inhalational Vs Intravenous
Upper airway obstruction or not?
Post operatively
When to Extubate?
Monitor for complications
Laryngospasm, Bronchospasm & pneumothorax
Summary
Anatomy
Indications / Contraindications
Problems & Management options
Specific management of inhaled foreign body
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