Malignant hyperthermia is a pharmacogenetic disorder triggered by volatile anesthetic gases and succinylcholine. It results in an abnormal rise in intracellular calcium in genetically susceptible individuals which leads to rapid increases in body temperature, muscle rigidity, and metabolic acidosis that can be fatal if not treated promptly. The key features of malignant hyperthermia include inappropriate tachycardia, arrhythmias, acidosis, hypercarbia, muscle breakdown and a rapid rise in temperature. Treatment involves immediately terminating the triggering agents, active cooling, hyperventilation with 100% oxygen, administration of dantrolene to reduce calcium levels in the muscle, and treating complications like acidosis and hyperkalemia
Malignant hyperthermia (MH) is a disease that causes a fast rise in body temperature and severe muscle contractions when someone with the MH gets general anesthesia. MH is passed down through families. Hyperthermia means high body temperature.
Malignant hyperthermia (MH) is a disease that causes a fast rise in body temperature and severe muscle contractions when someone with the MH gets general anesthesia. MH is passed down through families. Hyperthermia means high body temperature.
A patient with pacemaker presents a complex challenge to the attending anaesthesiologist. The mode of management will be according to the type of pacemaker implanted. This presentation discusses in brief the peri-operative consideration in a patient with pacemaker.
Malignant Hyperthermia - Essential Charactistics:
>An inherited disorder of skeletal muscle triggered in susceptibles (human or animal) in most instances by inhalation agents and/or succinylcholine, resulting in hypermetabolism, skeletal muscle damage, hyperthermia, and death if untreated.
>Underlying physiologic mechanism – abnormal handling of intracellular calcium levels.
Neuromuscular monitoring, also known as train of four monitoring, is a technique used during recovery from the application of general anesthesia to objectively determine how well a patient's muscles are able to function. It involves the application of electrical stimulation to nerves and recording of muscle response using, for example, an acceleromyograph. Neuromuscular monitoring is typically used when neuromuscular-blocking drugs have been part of the general anesthesia and the doctor wishes to avoid postoperative residual curarization (PORC) in the patient, that is, the residual paralysis of muscles stemming from these drugs.
A patient with pacemaker presents a complex challenge to the attending anaesthesiologist. The mode of management will be according to the type of pacemaker implanted. This presentation discusses in brief the peri-operative consideration in a patient with pacemaker.
Malignant Hyperthermia - Essential Charactistics:
>An inherited disorder of skeletal muscle triggered in susceptibles (human or animal) in most instances by inhalation agents and/or succinylcholine, resulting in hypermetabolism, skeletal muscle damage, hyperthermia, and death if untreated.
>Underlying physiologic mechanism – abnormal handling of intracellular calcium levels.
Neuromuscular monitoring, also known as train of four monitoring, is a technique used during recovery from the application of general anesthesia to objectively determine how well a patient's muscles are able to function. It involves the application of electrical stimulation to nerves and recording of muscle response using, for example, an acceleromyograph. Neuromuscular monitoring is typically used when neuromuscular-blocking drugs have been part of the general anesthesia and the doctor wishes to avoid postoperative residual curarization (PORC) in the patient, that is, the residual paralysis of muscles stemming from these drugs.
Dr Neerav Goyal discusses the various aspects of acute liver failure that includes the criteria, pre transplant issues, critical care management, overall survival.
Malignant hyperthermia is a potentially fatal hyperdynamic response due to pharmacogenetic abnormalities. This ppt gives a brief description of pathology and pharmacotherapy of malignant hyperthermia.
Common Transfusion Reactions by Randal Covin, MD, FCAPbloodbankhawaii
Lorem ipsum dolor sit amet, voluptaria percipitur has eu. Nibh iriure nostrud ei mea. Vel dicta voluptua convenire ei, id pro libris viderer. Pri et legendos atomorum, vel eu noster probatus menandri. Omnes possim ut eam, sed ea labore maiorum.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
2. Introduction
Malignant Hyperthermia
Pharmaco-genetic disorder
In Genetically Susceptible.
On exposure
Volatile inhalational agents & Sch.
Abnormal ↑↑ intracellular Ca²⁺
Rapid ↑
Body Temperature: Hyperthermia
Skeletal muscle activity
Rhabdomyolysis and metabolic acidosis
→ Death
Malignant
3. HISTORY
• Ist case reported ~ 1960: Australia
• Danbourough And Lovell
– 21 year/M → malleolar # fixation
– George Locher (Wisconsin) and Beverly Britt (Toronto)
• Familial disorder
• Central loss of temperature control
– Disorder of skeletal muscle metabolism
• 1966: Wilson et al
• Ist coined the term “malignant hyperthermia”
• 2001: Punj et al (IRCH): Ist case of MH in India
History of 10 anesthesia
related deaths in the family
4. PATHOPHYSIOLOGY
• NORMAL PHYSIOLOGY
• STORE OPERATED CALCIUM ENTRY
1.Motor neuron
releases Ach
2.Ach binds to Ach
receptors -opens Na⁺
channels & generates APs
3. AP reaches T
tubule
4. Voltage Sensor
DHPR receptors
activated
5.Ca²⁺ is released from SER
via Ryanodine receptor.
(3isoforms: Cardiac, Skeletal,
Brain). Biphasic response to
Ca ²⁺ & Inhibited by Mg²⁺
6. Ca²⁺ binds to
Troponin and
promotes actin-
myosin interaction
7. SERCA pumps propel Ca²⁺ back
to the SR & cause relaxation when
Ca²⁺ is <10 -7 M and require ATP
5. PATHOPHYSIOLOGY
Abn Excitation contraction Coupling
1.Motor neuron
releases Ach
2.Ach binds to Ach
receptors & opens
Na⁺ channels &
generates APs
3. AP is propagated
to the T tubule
4. Voltage Sensor
DHPR receptors
activated
5.Ca ² ⁺ is released
from SER via
Ryanodine
rececptors
6. Ca ² ⁺ then binds
to Troponin
facilitates actin-
myosin complex
7. SERCA propel Ca²⁺ back to SR &
causes relaxation when Ca²⁺ is
<10 -7 M and require ATP
6. PATHOPHYSIOLOGY
• Calcium releasing Unit (CRU)
– Key unit of Excitation
Contraction Coupling
– Includes Ryanodine
• Central component of CRU
• Interacts with Ca²⁺ V1.1 and
other proteins
• Homer 1, calstabin, triadin,
junctin, junctophilin etc.
– Predominantly affected by MH
mutations
7. PATHOPHYSIOLOGY
MH Mutations: AD with Variable Penetrance
↑ sensitivity
•Inhalational anesthetics
•Caffeine
•4-chloro-m-cresol
• K⁺
↓ inhibition
•Ca²⁺ >10-5 M
•Mg²⁺
MOST COMMON
•RyR1 (50-70%): Chr. 19q
•DHPR : CACNA1s (Chr. 1)
•Calsequestrin
INHERITANCE
CAN VARY
9. • Indications
– Individuals with “MH susceptible” contracture test
• Identify the mutation involved
– Can be offered as first line test if “hyperthermic
reaction under anesthesia”
– Ist degree relatives of an index case
• Risk of transmission: 50%
– Family member of a person +ve mutation test
– Contracture test
• Not available
• Refusal by patient
GENETICS AND DNA TESTING
10. GENETICS AND DNA TESTING
DNA testing
Involves testing for Ryr1 and CACNA1s
Universal application is not possible
A negative test has to be confirmed with Contracture tests
Misses MH due to mutation of other genes
Many mutations are not expressed.
Can’t rule out MH susceptibility completely
11. CONTRACTURE TEST
• Gold standard
– Sensitivity & Specificity
• >90%
– Detects abnormal muscle response to Halothane
and caffeine.
– Requires
• Muscle Harvesting: Quadriceps(MC),Rectus abdominus.
– Specimen Length: 15-25 mm, Thickness: 2-3 mm and Weight
100-150 mg (max 2-4gm).
– Local infiltration or femoral and lat. Femoral cut. nerve block.
– Weight>30 Kg and age > 4 years
It is 99 % sensitive and specific.
BUT
1. Inter laboratory variability.
2. Averages are recorded
3. Accuracy of caffeine and
halothane concentrations.
12. CONTRACTURE TEST
• Indications
– History of hyperthermic reaction under GA
– Negative Genetic analysis in a suspected
case
– Recurrent Rhabdomyolysis
• Record Contracture
– Caffeine > 2mmol/l and halothane
>2%(IVCT)/3% (CHCT)
• Localized contracture test
– Microdialysis based
– Infusion of caffiene or halothane into
muscle
– Acid base changes in muscle
+ve test: Contracture > 0.2 G
Caffeine conc.<2mmol/L
halothane conc. <2%
13. CONTRACTURE TEST
IVCT
• Used in Europe
• Both Incremental Halothane
(0.5-3%) and Incremental
caffeine 0.5 -32 m mol/l are
used (2X increments).
• MH equivocal → MHs/MHc
CHCT
• Used In USA
• Halothane is used at fixed 3
% and incremental caffeine
in 2X increments.
• MH susceptibleIF RESULT IS POSITIVE FOR EITHER CAFFEINE OR HALOTHANE
14. CONTRACTURE TEST
MH Susceptible
Positive response
to both halothane
and caffeine
MH Equivocal
Positive response
to either Caffeine
or halothane
MH Normal
Contracture less than 2 g
at Caffeine >3mmol/L or
Halothane>2%.
MH Susceptible
Positive response to both halothane
and caffeine
MHc: Positive response to Caffeine
MHH:Positive response to halothane.
MH Normal
Contracture less than 2 g
at Caffeine >3mmol/L or
Halothane>2%.
15. Porcine
stress
syndrome
Exertional
Rhabdom-
yolysis
Non
anesthetic
MH
Myopathy
↑↑ CPK
NON ANESTHETIC MH
Animal model of Human MH
AR : Inbreeding
Homozygous for RyR
MH like syndrome with
stressors:
Endogenous & exogenous
stressor
Assoc. with Recurrent
Exertional Heat stroke also
•All MH suspectible
•King Denbourough syndrome.
Abn facies with prox. Myopathy
•Central Core disease
CPK may be normal.
+ve IVCT
•Evan’s myopathy
Awake MH
•MH in the absence of classical triggers
•Coexistent 2nd mutation
• Higher susceptibility to exogenous trigger
•Extreme Physical activity in hot
surroundings
•Infectious fever
16. NON ANESTHETIC MH
Genetic
• Combined
myopathy with
RyR mutation.
• Variable
penetrance.
Diagnosis
• Dilemma
• Unknown
mutations
• CHCT/IVCT
• Poor Sensitivity &
Specificity.
• Diagnosis with
different
triggers/new tests.
Avoid
• Heat exposure
• Physical activity
in Hot
environment.
• Febrile illness:
Early t/t: Rapid
Cooling
• Prophlaxis:
Dantrolene
• Counseling to
parents.NOT AUTOSOMAL
DOMINANT
Heat,Oxidative stress
Non invasive : P31 MRI
At Risk of MH
Hypertrophy
Muscle Hypotonia
Spasm
Opthalmoplegia .
18. MH: Clinical presentation
• INCIDNCE
– WORLD : 1: 10,000 – 1:220,000.
– JAPAN : 1:60,000 →1:73,000.
– INDIA: Under reported 16- 17 cases
Mortality:
Intially: 70%.
With Dantrolene: 1.4-5%
19. Clinical Presentations
• Males> females
• MC in young age, muscular
• ENT/DENTAL/SQUINT
• Most Rapid onset halothane + Sch
• MH can occur
– Previously Uneventful anesthesia exposure
MAC requirement is highest in young age
Exposed to higher dose.
Fulminant MH
Immediate onset
Rapid Course
Insidious MH
Delayed Onset.
Can present even
in Recovery Room
TYPES
20. PATHOGENESIS
Trigger
Susceptibility
Absent inhibitory
factors
Persistent Ca2+Release
From the SR→
Sustained Muscle
Contracture
↑Skeletal Muscle metabolic
activity
Hypercarbia
Tachypnea.
Metabolic acidosis(↑lactate)
↑ O2 consumption
Fall in SpO2
Fall in SvO2.
↑ed sympathetic
activity
Tachycardia
Arrhythmia
Sweating
Generalized Muscle
Rigidity
Elevated Temp.
Muscle break down
Cyanosis
Rhabdomyolyisis
HyperKalemia
VT/VF
DIC
21. CLINICAL FEATURES
•1. HYPERCARBIA IS ALSO EARLIEST SIGN
OF MH
•2. MASSTER SPASM CAN EVEN PRECEDE
HYPERCARBIA BUT PRESENT ONLY IN 27%.
22. CLINICAL FEATURES
• EARLY SIGNS
1. Inappropriately
elevated CO2
production
(↑EtCO2, ↑RR).
2. ↑O2 Consumption
3. Mixed Metabolic
and Respiratory
acidosis
4. Profuse Sweating.
5. Mottling of skin.
1.Inappropriate
tachycardia
2.Cardiac
arrhythmias
(Ventricular ectopics
&Bigemini).
3.Unstabele arterial
Pressure.
1.Masster Spasm
with Sch.
2. Generalized
Muscle rigidity
METABOLIC CARDIOVASCULAR MUSCLE
TEMPERATURE
CAHANGES ARE LATE
SIGNS
23. CLINICAL FEATURES
1. Rapid rise in Core
body temperature.
2. Severe Cardiac
arrhythmias.
3. Cardiac arrest.
PHYSICAL
1. HyperKalemia.
2. Grossly elevated
CPK.
3. Grossly elevated
Blood Myoglobin.
4. Dark Colored urine
5. D.I.C.
LABORATORY
•Rapid rise in Temperature and high Temperature
correlate with Mortality .
•Core Temperature monitoring shows mortality
benefit as time to administer Dantrolene is
shortened.
• No benefit of skin Temperature monitoring.
24. • Generalized Muscle Rigidity - 15
(R/o Hypothermia & Immediate awakening from GA)
• Masseter spasm after Sch - 15
Rigidity
• ↑ CK after anesthesia with Sch(>20,000). - 15
• ↑CK after anesthesia w/o Sch(>10,000). - 15
• Myoglobinuria (>60mcg/ml) - 15
• Serum myoglobin > 170mcg/ml -15
• Serum K+ >6.0 meq/L(r/o renal failure.) -15
Muscle
Breakdown
• EtCO2> 55 or Art. CO2> 60 with Controlled ventilation
-15
• EtCO2> 60 or Art. CO2> 65 with Spont. Ventilation -15
• Inappropriate HyperCarbia. -15
• Inappropriate tachypnea - 10
Respiratory
Acidosis
Clinical Score
• Larach Score (1994)
25. Clinical Score
• Larach Score (1994)
• Inappropriate rapid rise in temperature- 15
• Inappropriately raised temperature >38.8◦ C in periop
period- 10
Rise in
Temperature
• Inappropriate sinus tachycardia -3
• VT or VF- 3
Cardiac
Involvement
• +ve Family H/O in 1st degree relative. - 15
• +ve Family H/O in other relatives.- 5
Family History
• BE>-8meq/L -10
• pH<7.25.- 10
• +ve Family H/O with +ve anesthetic History of MH.( exclude ↑
CPK).-5
• +ve Family H/O with ↑ CPK -10
Other Indicators
Grading (only the Highest Score of a Process)
SCORE
1. 0
2. 3-9
3. 10-19
4. 20-34
5 35-49
6. 50+
MH RANK
1
2
3
4
5
6
Likelihood
Almost never
Unlikely
Some what Less than likely
Somewhat more likely
Very likely
Certain
26. Differential diagnosis for a
“GREAT MIMIC”
• Anaphylactic reaction
• Diabetic coma
• Drug toxicity or abuse
• Equipment malfunction with increased carbon dioxide (CO2)
• Exercise hyperthermia
• Hyperthyroidism
• Hypoventilation or low fresh gas flow
• Increased ETCO2 from laparoscopicsurgery
• Insufficient anesthesia or analgesia (or both)
• Intracranial free blood
• Malignant neuroleptic syndrome
• Muscular (Duchenne and Becker) dystrophies/Myotonias
• Pheochromocytoma
• Rhabdomyolysis
• Sepsis
27. TREATMENT
IMMEDIATELY
Declare emergency and call for Help.
Inform surgeons
Termination of Surgery
Stop all Inhalational agents
Switch to Non Trigger anesthesia
Hyperventilation with flow 10 L
100% O2
Disconnect circuit.
Inform1800-MHHYPER Monitoring
•ECG, NIBP, EtCO2
•Wide bore IV
•Consider CVP, Arterial early
• Investigation
K+, CPK, ABG, Myoglobin,
Blood sugar
29. TREATMENT
Hyperthermia
2-3 L of ice cold
saline(4 Celsius)
Surface cooling,
cold sheets, ice
packs in axilla and
groin
Temperature<38
Celsius.
Acidosis
Hyperventilate
→normocapnia
Soda Bicarb.
HyperKalemia
50 ml 50 % D WITH 50
UNITS INSULIN.
10 ML 10% CALCIUM
GLUCONATE
DIALYSIS
ARRYTHMIAS
Amiodarone 3mg/kg
B blocker if Persistent
Urine output
Hyper hydration
Furosemide 1-2mg/kg
Mannitol 1g/kg.
Observe for at least 24 hours in ICU.
Recrudescence risk is 50%
32. Masseter Spasm
• Usually seen after Sch
• Jaw muscle Rigidity with whole body flaccidity > 2min.
– MH susceptibility: 30%.
– Higher risk→ Jaw + whole Body rigidity
• “Jaws of steel”
– Most severe variant
– Ventilation and Intubation might not be possible.
– Stop surgery
• Surgery
– Controversial in others
– To proceed or to stop
Slow Tonic fibers in Jaw muscle
Grading
Grade 1: Jaw stiffness only
Grade 2: Jaw stiffness
interfering with intubation
Grade 3: Jaws of Steel
34. ANESTHESIA MH SUSCEPTIBLITY
• Avoid trigger agents
• Flush the circuit with 10 L O2.
• Use Charcoal filter in anesthesia machine
• TIVA
• Regional anesthesia.
• Xenon (Case Report)
35.
36. PATHOPHYSIOLOGY
• SERCA pumps
– Propel Ca ² ⁺ back to the SR
– Relaxation
• Ca ² ⁺ is <10 -7 M
– Requires ATP
• Ryanodine
– SR Ca ² ⁺ release channel
– 3 isoforms
• Cardiac, Skeletal, Brain
– Biphasic response to Ca ²⁺
– Mg²⁺
37. GENETICS AND DNA TESTING
• Malignant Hyperthermia
– Pharamacogenetic syndrome.
– Ryanodine mutations 50-80%
• Chr. 19q
• Associated with Myopathies
– Central core disease, Evans Myopathy.
• Vary