Edward Fohrman shares some valuable insight into the postanesthesia recovery process.
For information about Edward and his work, visit EdwardFohrman.com
The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena.
The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena.
This is a lecture by Dr. Pamela Fry from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
Anesthetic Management of a Patient with Peripartum Cardiomyopathy for LUCSMd Rabiul Alam
Peripartum cardiomyopathy is one of the leading causes of death in obstetric patients since it is usually diagnosed incidentally. Echocardiogram remains the mainstay to diagnose it. Many of the peripheral hospitals are deficient of echocardiogram facilities, so there are possibilities to send the patient to OR without diagnosis. To manage such a case and bring out the success depends on quick detection of the problems & immediate medical intervention after confirming the diagnosis. Obviously, any surgical intervention requires lot of clinical experiences of the whole team, particularly the anesthesiologists.
David Collins gives an excellent lecture on Toxicology at the Sydney Intensive Care Network meeting for the Intensive Care Network (www.intensivecarenetwork.com). The podcast to go with this can be found on iTunes (Oli Flower's ICU Podcasts) or on www.intensivecarenetwork.com
This is a lecture by Dr. Pamela Fry from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
Anesthetic Management of a Patient with Peripartum Cardiomyopathy for LUCSMd Rabiul Alam
Peripartum cardiomyopathy is one of the leading causes of death in obstetric patients since it is usually diagnosed incidentally. Echocardiogram remains the mainstay to diagnose it. Many of the peripheral hospitals are deficient of echocardiogram facilities, so there are possibilities to send the patient to OR without diagnosis. To manage such a case and bring out the success depends on quick detection of the problems & immediate medical intervention after confirming the diagnosis. Obviously, any surgical intervention requires lot of clinical experiences of the whole team, particularly the anesthesiologists.
David Collins gives an excellent lecture on Toxicology at the Sydney Intensive Care Network meeting for the Intensive Care Network (www.intensivecarenetwork.com). The podcast to go with this can be found on iTunes (Oli Flower's ICU Podcasts) or on www.intensivecarenetwork.com
Cardiology 1.3. Syncope - by Dr. Farjad IkramFarjad Ikram
Introduction to one of the more challenging symptoms to investigate. Syncope is transient loss of consciousness with loss of postural tone due to diffuse hypoperfusion of cerebral cortex, followed by rapid, complete and spontaneous recovery.
Template design credits - http://www.slidescarnival.com
Edward Fohrman | Anesthesia for Pituitary SurgeryEdward Fohrman
Edward Fohrman shares his lecture slides on anesthesia for pituitary surgery. Edward founded Fohrman Anesthesia Services & Consulting in 2010.
Read more at EdwardFohrman.com.
Edward Fohrman | Anesthetic Considerations for Intracranial TumorsEdward Fohrman
Read Edward Fohrman's thoughts on Anesthetic considerations for intracranial tumors. Edward is the Founder and CEO of Fohrman Anesthesia.
Read more at EdwardFohrman.com
Edward Fohrman | Neuroanesthesia in NeurotraumaEdward Fohrman
Edward Fohrman, anesthesiologist extraordinaire, describes how to use neuroanesthesia when it comes to neurotrauma in this presentation for one of his lectures.
Visited EdwardFohrman.com for more information!
Edward Fohrman | Introduction to NeuroanesthesiaEdward Fohrman
Edward Fohrman MD is an experienced anesthesiologist who runs Fohrman Anesthesiology. Here he shares his thoughts about neuroanesthesia.
Visit EdwardFohrman.com for more.
Edward Fohrman | Anesthetic Considerations for Carotid EndarterectomyEdward Fohrman
Edward Fohrman, an experienced anesthesiologist in CA, discusses some considerations to take into consideration when it comes to carotid endarterectomy and anesthesia.
Edward Fohrman | Anesthetic Considerations in Vascular Neurosurgery Edward Fohrman
Edward Fohrman discusses what to take into consideration during vascular neurosurgery. Dr. Fohrman is the CEO of Fohrman Anesthesia Services & Consulting, Inc., which he founded in 2010.
Visit EdwardFohrman.com for more.
Edward Fohrman | Neuroanesthesia for Cerebral Arteriovenous MalformationsEdward Fohrman
Edward Fohrman shares his presentation about Neuroanesthesia for Cerebral Arteriovenous Malformations.
Visit EdwardFohrman.com for more information about Edward and his industry insights.
India Clinical Trials Market: Industry Size and Growth Trends [2030] Analyzed...Kumar Satyam
According to TechSci Research report, "India Clinical Trials Market- By Region, Competition, Forecast & Opportunities, 2030F," the India Clinical Trials Market was valued at USD 2.05 billion in 2024 and is projected to grow at a compound annual growth rate (CAGR) of 8.64% through 2030. The market is driven by a variety of factors, making India an attractive destination for pharmaceutical companies and researchers. India's vast and diverse patient population, cost-effective operational environment, and a large pool of skilled medical professionals contribute significantly to the market's growth. Additionally, increasing government support in streamlining regulations and the growing prevalence of lifestyle diseases further propel the clinical trials market.
Growing Prevalence of Lifestyle Diseases
The rising incidence of lifestyle diseases such as diabetes, cardiovascular diseases, and cancer is a major trend driving the clinical trials market in India. These conditions necessitate the development and testing of new treatment methods, creating a robust demand for clinical trials. The increasing burden of these diseases highlights the need for innovative therapies and underscores the importance of India as a key player in global clinical research.
Health Education on prevention of hypertensionRadhika kulvi
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Global launch of the Healthy Ageing and Prevention Index 2nd wave – alongside...ILC- UK
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Alongside the 77th World Health Assembly in Geneva on 28 May 2024, we launched the second version of our Index, allowing us to track progress and give new insights into what needs to be done to keep populations healthier for longer.
The speakers included:
Professor Orazio Schillaci, Minister of Health, Italy
Dr Hans Groth, Chairman of the Board, World Demographic & Ageing Forum
Professor Ilona Kickbusch, Founder and Chair, Global Health Centre, Geneva Graduate Institute and co-chair, World Health Summit Council
Dr Natasha Azzopardi Muscat, Director, Country Health Policies and Systems Division, World Health Organisation EURO
Dr Marta Lomazzi, Executive Manager, World Federation of Public Health Associations
Dr Shyam Bishen, Head, Centre for Health and Healthcare and Member of the Executive Committee, World Economic Forum
Dr Karin Tegmark Wisell, Director General, Public Health Agency of Sweden
How many patients does case series should have In comparison to case reports.pdfpubrica101
Pubrica’s team of researchers and writers create scientific and medical research articles, which may be important resources for authors and practitioners. Pubrica medical writers assist you in creating and revising the introduction by alerting the reader to gaps in the chosen study subject. Our professionals understand the order in which the hypothesis topic is followed by the broad subject, the issue, and the backdrop.
https://pubrica.com/academy/case-study-or-series/how-many-patients-does-case-series-should-have-in-comparison-to-case-reports/
ICH Guidelines for Pharmacovigilance.pdfNEHA GUPTA
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Collaborations and Partnerships
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Expansion of Diagnostic Chains
The expansion of diagnostic chains is a driving force behind the growing demand for diagnostic lab services. Diagnostic chains often establish multiple laboratories and diagnostic centers in various cities and regions, including urban and rural areas. This expanded network makes diagnostic services more accessible to a larger portion of the population, addressing healthcare disparities and reaching underserved populations. The presence of diagnostic chain facilities in multiple locations within a city or region provides convenience for patients, reducing travel time and effort. A broader network of labs often leads to reduced waiting times for appointments and sample collection, ensuring that patients receive timely and efficient diagnostic services.
Rising Prevalence of Chronic Diseases
The increasing prevalence of chronic diseases is a significant driver for the demand for diagnostic lab services. Chronic conditions such as diabetes, cardiovascular diseases, and cancer require regular monitoring and diagnostic testing for effective management. The rise in chronic diseases necessitates the use of advanced diagnostic tools and technologies, driving the growth of the diagnostic labs market. Additionally, early diagnosis and timely intervention are crucial for managing chronic diseases, further boosting the demand for diagnostic lab services.
Navigating Women's Health: Understanding Prenatal Care and Beyond
Edward Fohrman | Postanesthesia Recovery
1. Edward B. Fohrman M.D
Assistant Professor, Department of Anesthesiology
Northwestern University, Feinberg School of Medicine
POSTANESTHESIA RECOVERY
2. CASE
▪ 55 y.o. male s/p robotic prostatectomy
otherwise uneventful…
▪ Surgery is over
▪ Volatile agent is off
▪ Reversal given
▪ HOW DO U KNOW WHEN PT. IS READY FOR
EXTUBATION???
3. EXTUBATION CRITERIA?
▪ PaO2/FiO2 > 300
▪ PaCO2 < 50 mmHg
▪ Vd/Vt < 0.6
▪ RR < 35
▪ Vt > 5 ml/kg
▪ NIF > (-20 mm H20)
▪ TOF ratio > 0.9
▪ Clinical Strength (5 sec head lift)
▪ Mental Status c/w ability to maintain airway
▪ No Airway Edema/Vocal cord paralysis or other cause of airway
obstruction
▪ Hemodynamic Stability
4. When to transfer to PACU?
▪ ABC’s
▪ Patent or secure airway
▪ Adequate Oxygenation & Ventilation
▪ Hemodynamically stable
5. O2 During Transport?
1) <93% after extubated in OR
2) Unconscious
3) Age > 60
4) Wgt > 100 kg
5) Pulmonary disease
6) Difficult airway
7) OSA
8) Surgery: Abd., Thoracic, Neuro, Cardiac, ENT
9) N2O (avoid diffusion hypoxia)
10) SpO2 < 93% upon arrival to PACU
Probably NOT necessary in LOW RISK patient
population…
“Favor using O2 in anyone who’s physiology would
be negatively affected by even a brief hypoxemic
episode”
6. How much O2 R U giving?
Each liter of Nasal Cannula O2 increases
FiO2 by 3 - 4%
(Starting from room air 21%)
Nasal cannula does not suppress
respiratory drive even in COPD
It is impossible to deliver more than 40%
FiO2 with N.C. due to limitations in flow
dynamics
*DELIVERY OF 100% O2 can only be
achieved with INTUBATION!!!
Short of this, the highest O2 delivery can
be achieved with a high flow, 10L
“Nonrebreather” Face mask ≈ 90% FiO2
Miller’s Anesthesia 6th Ed. 2005
7. Admission to the PACU
▪ Patient’s name & age
▪ Surgical procedure/Anes type
▪ Coexisting medical probs
▪ Allergies
▪ Fluids: EBL, IVF, UOP
▪ Anes/Surgical complications
▪ (difficult airway?)
▪ Special requests: meds, labs, x-rays
▪ Lines/Location (a-line, iv’s, epidural)
9. Case
▪ 52 y.o. male s/p C4-6 ACDF brought to
PACU after extubation
▪ 20 min later to inform u patient is
tachypneic with SpO2 91
▪ DDX?
▪ What else do you want to know?
▪ What’s your next move???
10. Case
▪ 8 y.o. male s/p inguinal hernia repair brought to PACU
after deep extubation
▪ The patient suddenly bucks and begins to desaturate
rapidly…DDX? Treatment?
▪ What is Stage 2 anesthesia and why is it significant?
▪ How do you know when a patient is in stage 2
anesthesia?
11. Upper Airway Obstruction
▪ Loss of pharyngeal muscle tone
▪ Obstructive Sleep Apnea (OSA)
▪ Laryngospasm
▪ Deep extubation? / Tx?
▪ Airway edema
▪ ↑IVF, ↑EBL, ↑Duration, Prone position
▪ Surgery of tongue, pharynx, neck, thyroid, CEA
▪ CUFF TEST
▪ Neck hematoma
▪ Monitor airway patency during transport –
(Look, Listen, Feel)
12. Residual Neuromuscular Blockade
▪ Assessment of adequate reversal?
▪ TOF, DBS, Clinical sx
▪ What factors increase risk of residual block?
▪ Drugs – Volatiles, local, Antiarrhythmics, Antibiotics, Corticosteroids,
CCB’s, Dantrolene, Lasix, BCP’s
▪ Metabolic Physiologic states - ↑Mg, ↓Ca, Hypothermia, acidosis, liver/
renal failure, Myasthenia Gravis, Extremes of age
▪ Prolonged Depolarizing block
▪ Atypical pseudocholinesterase, Phase II block, Pregnancy, Echothiophate
(irreversible), Edro, Neo, Pyrido (reversible)
13. Classification of NMB’s
Depolarizing
▪ Succinylcholine
Nondepolarizing
➢ Short Acting
➢Mivacurium
➢Rapacuronium
➢ Intermediate Acting
➢Rocuronium
➢Vecuronium
➢Cisatracurium
➢Atracurium
➢ Long Acting
➢Pancuronium
14. Case
▪ You just “deep” extubated your patient to avoid
bucking on the tube after an otoplasty. As you are
moving the patient to the gurney, the patient
bucks and coughs and begins to turn blue.
▪ More good news…your IV was inadvertantly pulled
out during the move and is now dripping on the O.R.
floor…
▪ What’s the problem and how are you going to save
the day?
15. Succinylcholine
• 2 Ach molecules linked by methyl groups
• Agonist action binds the alpha subunit and leads to muscle contraction and
refractory period
• Depolarizing block also called Phase I block
• Intubating dose: 1-1.5mg/kg (ED95 = 0.3mg/kg)
• Onset 30-60 secs and duration 5-10 minutes
• Defasciculating dose of nondepolarizer
• (5-10% of ED95 2-4 min prior) must increase sux dose by 70%
•Repeated doses > 3-5mg/kg >>> Phase II block
•Serum potassium (K+) by 0.5 to 1 mEq/L
• EJnAchR’s increase K+ ???
16. Why Sux is unique?
▪ The only Depolarizing blocker used
clinically today
▪ Most rapid onset of any other NMB
▪ Most rapid recovery/offset of any NMB
▪ Most significant degree of vocal cord
paralysis/BEST intubating conditions
▪ Only NMB with rapid effects when given
I.M. in cases of no IV access…IM dose?
17. Each of the following patients requires
urgent intubation…what do they all
have in common???
75 y.o. male s/p ischemic CVA 3 weeks ago with
residual left hemiparesis
21 y.o. female PMH - MVA 4 years ago with
incomplete T4 level – urosepsis/pneumonia and
SpO2 89%
18 y.o. male s/p GSW to head, in barb coma w/
vecuronium gtt x 7 days who was inadvertantly
extubated by the RN…
18. Sux: Adverse side effects
▪ Hyperkalemia!!!
▪ Note: 1mg/kg Sux does NOT increase ICP (Kovarik et al.
Anesthesia&Analgesia, 1994;78:469-73
▪ Myoglobuinuria – Malignant Hyperthermia (MH)
▪ Cardiac dysrhythmias (esp. 2nd dose!)
▪ Sinus brady, Jct brady, Sinus arrest
▪ Fasciculations
▪ Myalgia (especially in outpatients)
▪ Increased intraocular pressure (not more than bucking)
▪ Increased intragastric pressure
▪ Trismus - Masseter muscle rigidity common in peds (4%)
▪ Associated with subsequent development of MH
22. ▪ 22 y.o. 70 kg. male without significant
PMH/PSH undergoes a RSI for acute
appendicitis. 10 min after 1mg/kg of sux,
the patient receives a 30mg dose of ROC.
▪ The case goes well and the surgeon begins
skin closure.
▪ TOF reveals that the patient still has no
twitches 1 hour after the last dose of
ROC….WHY?
CASE
23. Atypical Cholinesterase
▪ Check TOF after sux, (before NDNMB)
▪ Dx after a patient has a prolonged response to
sux or mivacurium (>1hour)
▪ Dibucaine Number
▪ Dibucaine – amide local anesthetic
▪ Inhibits normal enzyme by 80%
▪ Inhibits abnormal enzyme by only 20%
24. Variants of Plasma Cholinesterase and Duration of action of
Succinylcholine
Variants of Plasma
Cholinesterase Incidence
Dibucaine Number
(% Inhibition of
enzyme activity)
Duration of
succinylcholine
induced
neuromuscular
blockade (min)
Homozygous
Typical
Normal 70-80 5-10
Heterozygous 1 in 480 50-60 20
Homozygous
Atypical
1 in 3200 20-30 60-180
Stoelting & Miller, Basics of Anesthesia. 2007
28. Arterial Hypoxemia
3. Shunt V/Q = 0 (Absolute shunt)
▪ perfusion without ventilation
▪ PTX, bronchial intubation/single lung ventilation, R>L
cardiac shunt, ARDS/sepsis, liver failure, AVM, atelectasis,
pneumonia/mucous plugging, pulmonary contusion,
bronchospasm, CHF
▪ Shunted blood is NOT exposed to alveoli, thus O2
unresponsive for shunt > 30%
▪ Shunt fraction = Qs/Qt = CcO2-CaO2/CcO2-CvO2
▪ 2 sources of normal shunt: Bronchial arteries and
thebesian veins. (Normally 2-5%)
29. Arterial Hypoxemia
4. V/Q Mismatch V/Q = ∞
Dead space: ventilation without perfusion V/Q>1
i.e. Pulmonary Embolus
V/Q matching optimally should be 1:1
Hypoxic Pulmonary Vasoconstriction (HPV)
5. Diffusion defects
Advanced pulmonary disease, pulmonary edema, ARDS
6. ↑Venous Admixture
(Low cardiac output states)
O2 Delivery = O2 content x Cardiac Output
O2 Content = 1.34 x Hgb x SaO2 + (PaO2 x 0.003)
Decreased CO, ↑ O2 consumption, Anemia,
Hgb dysfct.
30. Shunt – Response to O2
▪ Increasing FiO2 from room
air to 100% results in a
large increase in PaO2
when the shunt fraction is
small; however,
oxygen will have
little effect on PaO2
in patients with a
large shunt fraction
Miller’s Anesthesia 6th Edition, 2005
31. Case
▪ 38 y.o. female s/p scoliosis repair is
brought to the ICU intubated.
▪ You note SpO2 of 89% and absent BS on
the Left chest
▪ You ask for a stat CXR for line placement
(left SCV cordis)
▪ What’s your next move???
33. Reintubation in PACU?
▪ PaO2/FiO2 ratio < 300
▪ Respiratory rate > 35 breaths/minute
▪ Tidal Volume Vt < 5 cc/kg
▪ Vital capacity <15ml/kg (adults) <10ml/kg (peds)
▪ Negative inspiratory force of < -20 mmHg
▪ PaO2 < 70 mmHg on 40% FiO2
▪ PaCO2 > 55-60 mmHg (except chronic CO2 retainers i.e.COPD)
▪ Alveolar-arterial (A-a) gradient > 350 mmHg on 100% FiO2
▪ Dead Space (VD/VT) > 0.6
▪ Hemodynamic instability?
▪ WHAT DOES THE PATIENT LOOK LIKE???
34. Case
▪ 68 y.o. male s/p RLL Lobectomy under GA,
Thoracic epidural, Dbl lumen ETT, now
extubated to PACU
▪ BP 70/40, HR 120, SpO2 93%
▪ DDX?
▪ What’s your next move???
35. HYPOTENSION
BP = CO x SVR
CO = SV x HR SVR = MAP- CVP
CO
Preload
Afterload
Cardiac Contractility
36. Hypotension
▪ ↓Intravascular Volume (Preload)
▪ (PCWP<5-10mmHg) with normal CI (2.5-4.0)
▪Bleeding!
▪Bleeding!!
▪Bleeding!!!
▪3rd Spacing
▪Insensible losses
41. Cardiac issues in PACU
▪ Risk factors for CAD
▪ Smoking
▪ HTN
▪ Hypercholesterolemia
▪ Diabetes Mellitus
▪ Obesity
▪ Physical Inactivity
▪ Family History
▪ (1st order relative prior to age 55)
Identify patients at risk!
42. ECG ∆’s in PACU
▪ Low Risk Patient ?
▪ Age < 45
▪ No known Cardiac History
▪ Only 1 Cardiac Risk Factor
▪ Post op ST ∆’s = MI? Usually NOT
▪ Usually benign and do not require more than routine PACU observation
unless associated dysrhythmia and/or hemodynamic instability
DON’T DO A MILLION $ Work UP!!!
43. ECG ∆’s (High Risk)
▪ Who is High Risk?
▪ Post op ST and T ∆’s may be significant even in the absence
of typical sx
▪ 12 lead ECG (vs. preop ECG)
▪ Serial Troponin-I (cTni), CBC, Chem, ABG
▪ O2, NTP/NTG, Beta Blockade
▪ If BP unstable
▪ consider re-intubation/echo/PA catheter/Inotropes
▪ Notify primary service/ discuss your concerns
▪ Cardiology consult/ follow-up
▪ Disposition – Tele, ICU, floor?
45. Case
▪ 44 y.o. male patient s/p appy
▪ 5 minutes after giving report, the patient’s HR
is 40…
▪ What else do you want to know?
▪ What are you going to do?
46. Atrial Dysrhythmias
▪ Noncardiac Surgery (10%)
▪ Cardiothoracic Surgery (25-30%)
▪ Associated with longer hospital stay and higher
mortality
▪ Electrical Cardioversion vs. ctrl Ventricular response
– CCB, β-Blockade, Amiodarone
▪ Vagal maneuvers, adenosine to distinguish between
SVT and A-fib/flutter
47. Ventricular Dysrhythmias
▪ PVC’s, Ventricular Bigeminy are common, but
rarely degenerate into V-tach
▪ PVC’s may just reflect ↑ sympathetic stim.
(hypercapnia, intubation)
▪ Multifocal PVC’s vs. Unifocal PVC’s?
▪ Consider ABG, CBC, Chem, cTni if suspect
myocardial ischemia – Torsades, QT
prolongation?
▪ Electrical Cardioversion vs. Amiodarone
48. Case
▪ 81 y.o. male s/p Right Hip Pinning under
GA, now extubated to PACU
▪ Mr. Cartman is confused…
▪ DDX?
▪ What’s your next move?
49. Delirium
▪ An acute change in cognition or
disturbance of consciousness that
cannot be attributed to a
preexisting medical condition ,
substance intoxication, or
medication.
▪ 10% Incidence: > 50 y.o.
undergoing elective surgery up to
POD #5
▪ Higher incidence (30%) after Hip
ORIF and Bilateral TKR
50. Risk Factors: Post-Op Delirium
▪ Advanced age
▪ Preoperative cognitive impairment
▪ Decreased functional status
▪ ETOH abuse
▪ History of delirium
51. Management of Post-Op Delirium
▪ Vitals!
▪ Patient Safety
▪ Restraints
▪ Physical ( soft restraint/full restraint)
▪ Chemical (Versed, Physostigmine, Antipsychotics
(Haldol)
▪ Even if it means Reintubation!
▪ Work-UP Etiology…
53. Case
▪ 49 y.o. male s/p ex-lap for perforated
diverticulitis under GA, now extubated to
PACU
▪ Patient has no urine output from the
foley
▪ DDX?
▪ What’s your next move?
54. Oliguria
▪ Most commonly “pre-renal” from depletion of intravascular
volume
▪ Usually responds to a 500-1000ml bolus
▪ Check Hct to rule out surgical bleeding
▪ d/w surgeon/?check bladder pressure to rule out intra-
abdominal htn
▪ Intra-abdominal Pressure > 30cm H2O can impair renal
perfusion
▪ Value of fractional excretion of sodium (FeNa) is limited in the
PACU and confounded by diuretics
▪ In cases where the patient’s volume status and/or cardiac
function is in question (MI, CHF, SIRS), consider placing a PA
Catheter/or obtaining an echocardiogram
55. Renal Dysfunction
▪ Oliguria (<0.5 ml/kg/hr)
▪ Preop vs. Intraop vs. Postop
▪ Usually multifactorial (i.e. Preexisting
CRI confounded by an intraoperative
insult)
▪ Focus on “treatable causes” in PACU
Classification
• Prerenal
• Renal
• Postrenal
59. Body Temperature & Shivering
▪ Postoperative shivering
▪ Incidence: 5%→65%
▪ Mechanism
▪ Hypothermia- thermoregulatory center
▪ Normothermia- more rapid recovery of spinal cord function,
uninhibited spinal reflexes→ clonic activity
▪ Treatment
▪ Identification of hypothermia by core body temp
▪ Forced air warmers
▪ Opioids, Clonidine, Meperidine (most effective)
60. Body Temperature & Shivering
▪ Clinical Effects
▪ Increases O2 consumption and CO2 production
▪ Increased CO, HR and BP
▪ Inhibition of platelet function, coagulation factor activity
and drug metabolism
▪ Exacerbates postoperative bleeding, prolongs neuromuscular
blockade, and may delay awakening
▪ Prolonged PACU stay
▪ Long Term: increased incidence of myocardial ischemia/
infarction, delayed wound healing, increased perioperative
mortality
62. PONV RISK
▪ High Risk Patients
▪ Female
▪ History of Motion
sickness/PONV
▪ Nonsmoker
▪ Intra/Postoperative
opioids
▪ Peds
▪ Other Risk Factors
▪ Obesity
▪ Anxiety
▪ Gastroparesis/ Gastric
distension
▪ GERD
▪ Dehydration
▪ Type of Surgery (eye muscle,
middle ear, laparoscopic,
Breast, Plastics)
▪ Anesthetic Drugs (Volatile
0-2hrs, N2O, NMB Reversal?)
Consensus Guidelines for Managing PONV, Anesth & Analg 7/2003
63. PONV
▪ For every 30 minutes of inhalational
anesthesia, there is a 60% increase in PONV
risk…
Consensus Guidelines for Managing PONV, Anesth & Analg 7/2003
64. PONV
▪ Serotonin (5-HT3) Antagonists (Ondansetron)
▪ Effective when given 30min before end of case
▪ Corticosteroids (Dexamethasone)
▪ Replaced droperidol for 1st line prophylaxis, unknown
mechanism (reduce prostaglandins)
▪ Anticholinergics (Scopolamine)
▪ Antihistamines (Hydroxyzine)
▪ Prokinetic (Promethazine)
▪ Butyrophenones (Droperidol)
▪ Very effective, FDA Warning 6/2001, 6 hour monitoring for
cardiac dysrhythmia (torsades de pointes)
66. Bleeding Abnormalities
Test Normal Value Abnormality
Platelet Count >150,000 cells/mm3 Dilutional, DIC
Bleeding Time 3-10 min Platelet-inhibiting Rx
Prothrombin Time 12-14 sec DIC, Vit K Def, Liver Dz,
Coumadin
Partial Thromboplastin Time 25-35 sec Factor V and VIII Def,
Heparin, Heophilia
Fibrinogen 200-400 mg/dL DIC
Fibrin Split Products <4 µg/ml DIC
TEG N/A Platelet and clotting factor
deficiencies
Platelet Fct Assay N/A Plt Adhesion & Aggregation
67. Case
▪ You are the PACU resident of the week
and the RN calls re:
▪“My patient in slot 12 isn’t
waking up!”
▪ What else do you want to know?
▪ DDX?
68. Delayed Awakening
▪ Possible explanations…
▪ Pharmacological
▪ Residual Drug Effect (Opioids, BDZ, anticholinergics)
***Most frequent cause
▪ Chemical (Metabolic)
▪ Hypoxemia, Hypercarbia, Hypoglycemia, Electrolyte
abnormalities
▪ Physical
▪ Hypothermia (Temp < 33°C), Air Embolism
▪ Neurologic
▪ Increased ICP, Sz/Postictal, Hysteria?