The document discusses various neurological and neuromuscular diseases relevant to anaesthesia including epilepsy, multiple sclerosis, Guillain-Barre syndrome, poliomyelitis, and cerebral palsy. It covers the pathophysiology, clinical features, diagnostic criteria, and anaesthetic considerations for managing patients with these conditions. Key points discussed include preoperative assessment and planning, choice of anaesthetic agents to avoid exacerbating symptoms, special monitoring needs, and postoperative care considerations.
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.
The transversus abdominis plane, more commonly referred to as the TAP block,
Places local anesthetic in the lateral abdominal wall in a plane between the internal oblique and the transversus abdominis muscles.
Here, the local anesthetic block can block many of the abdominal nerves as they pass to the abdominal structures.
Guillain Barre’ syndrome(GBS) and Anesthesia considerationTenzin yoezer
Patients with GBS need special care when coming to the surgery. They have a high risk of aspiration, airway compromise, autonomic instability, altered response to NMBs. It is the duty of the anesthesia providers to recognize those problems and minimize the complications.
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.
The transversus abdominis plane, more commonly referred to as the TAP block,
Places local anesthetic in the lateral abdominal wall in a plane between the internal oblique and the transversus abdominis muscles.
Here, the local anesthetic block can block many of the abdominal nerves as they pass to the abdominal structures.
Guillain Barre’ syndrome(GBS) and Anesthesia considerationTenzin yoezer
Patients with GBS need special care when coming to the surgery. They have a high risk of aspiration, airway compromise, autonomic instability, altered response to NMBs. It is the duty of the anesthesia providers to recognize those problems and minimize the complications.
In this slideshow, we covered most of neuromuscular disorders which might face you in medicine in general and in pediatrics in particular.
We hope if you find this slideshow helpful for your seeking of this subject.
Cheers,
Disorders of the neuromuscular junction include Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Botulism, Tetanus, Strychnine intoxication, Organophosphates poisoning and neuromyotonia. Pharmacology of the NMJ is also reviewed in brief.
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.
The advent of plasma exchange and intravenous immunoglobulins has dramatically improved the prognosis of patients with GBS. Despite this fact, mortality and morbidity rates remain unacceptably high. Until better therapies are developed, the appropriate utilization of immune-modulating therapy and careful attention to supportive care issues will help to minimize these unfavorable outcomes
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
3. SEIZURE DISORDER
• Seizure is caused by
transient , paroxysmal,
and synchronised
discharge of group of
neurons in brain.
• Epilepsy is defined as
recurrent unprovoked
seizures.
Partial
• simple
• complex
Generalised
• Tonic
• Clonic
• GTCS
• myoclonic
• Abscence
4. MECHANISM OF ACTION OF AEDs
• Increase GABA activity
Increased frequency of Cl channel opening :
– Benzodiazepines (binds to BZ2 receptors);
– Tiagabine (prevents reuptake);
– Gabapentin (prevents reuptake).
Increased mean Cl channel opening duration : Barbiturates.
• Blocks GABA transaminase (blocking GABA catabolism within the
neuron) : Vigabatrin.
• Glutamate antagonist : Topiramate (at AMPA receptor).
• Reduction of inward voltage-gated positive currents
– Phenytoin (Na+ channel);
– Carbamazepine (Na+ channel);
– Ethosuximide (Ca2+ channel).
• Increased outward voltage-gated positive currents
– Sodium valproate (K+ channel);
– Pleotropic sites of action: Sodium valproate (1, 2, 3 and 4)*;
lamotrigine (2 and 3)*; topiramate (1, 2, and 3)
5. EFFECTS OF ANTIEPILEPTICS ON
ANAESTHETIC DRUGS
DRUG INTERACTION DUE TO ALTERED METABOLISM
ENZYME INDUCERS
• PHENYTOIN VALPROATE
• CARBAMAZEPINE>> OXCARBAZEPINE
• PHENOBARBITONE
• PRIMIDONE
• TOPIRAMATE
ENZYME INHIBITORS
DRUG INTERCTIONS RELATED TO PROTEIN BINDING
PHENYTOIN VALPROATE CARBAMAZEPINE
7. • NEUROMUSCULAR :
– None of the neuromuscular blocking agents appear to
have any pro-convulsant or anticonvulsant effects
– LAUDANOSINE: metabolite of atracurium, induce seizure
activity esp in hepatic failure
• LOCAL ANAESTHETIC: generalized convulsions at higher
doses, resulting from an accidental i.v. administration or rapid
systemic absorption from a highly vascular area.
• ANTIEMETICS: avoid dopamine antagonist like
metaclopramide
8. • Preoperative assessement:
– History ( manifestation , severity and control of disease)
– Medications( drugs and dosage)
– Investigations ( hemogram, LFT, KFT, serum electrolyte)
• Avoid prolonged disruption of AEDs
• Avail intravenous forms of AEDs in OT.
• Avoid prolonged fasting.
• Careful selection of anaesthetic drugs.
• Avoid hyperventilation.
9.
10. MULTIPLE SCLEROSIS
• Autoimmune destruction of myelin
sheath within CNS nerve
conduction failure
• Females, 20-40 years & >60 years.
• Etiology : unknown
• Diagnosis based on combination of
clinical and laboratory tests
• Treatement :
– combinations of
immunosuppression modalities.
IFN, Glatiramer, Mitoxantrone,
Natalizumab, Cladribine,
Fingolimod
– Corticosteroids for acute phase
– Dantrolene, Diazepam, Baclofen,
Carbamazepine for muscle spasm,
chronic pain, seizures & dysthesia
11. MS: ANAESTHETIC CONCERNS
• Preoperative assessement includes details of symptoms and
neurological examination.
• Surgery and anaesthesia may aggravate MS.
• Continue immunosuppressive medications in perioperative
period.
• Minimize changes in homeostasis( fluid / temperature).
• Intravenous induction and inhaled anaesthetic safe.
• Careful cardiovascular monitoring .
• Avoid Sch. Nondepolarising NM blockers safe.
• REGIONAL anaesthesia: EPIDURALS in low dose safe but
SPINAL anaesthesia aggravate symptoms.
• Need of Post operative ventilation???
12. • DRUG INTERACTIONS:
– Cardiotoxicity from immunosupressants
– Altered response to ms relaxants.
– Baclofen increases sensitivity to nondepolarising MR.
– Anticonvulsants produce resistance to nondepolarising
MR.
13. GULLAINE BARRE SYNDROME
• GBS is an acute frequently severe and fulminant radiculopathy
• With the marked decline in the incidence of polio, Guillain-Barré
syndrome is now the most common cause of acute flaccid paralysis
in healthy people
• Autoimmune in nature
• Incidence : one case per million per month.
• Males are at higher risk( 1.5 times)
• Adults more frequently affected than children
• The main modalities of therapy for Guillain-Barré syndrome include
– Plasmapheresis
– Administration of intravenous immune globulin
14. SUBTYPES OF GBS
SUBTYPE FEATURES ELECTRODIAGNOSIS PATHOLOGY
Acute inflammatory
Demyelinatimg
polyneuropathy
(AIDP)
ADULTS> CHILDREN
RAPID RECOVERY
ANTI GM1
ANTIBODIES
DEMYELINATING First attack on
schwann cell
surface( myelin
damage) secondary
axonal damage
Acute motor axonal
neuropathy(AMAN)
Children and young
adults, may be
seasonal, rapid
recovery anti-GD1a
antibodies
AXONAL 1st attack at motor
nodes of ranvier.
Extent of damage
highly variable
Acute motor
sensory axonal
neuropthy(AMSAN)
Adults, uncommon,
slow recovery
AXONAL Same as AMAN but
sensory fibres also
affected
Miller fisher
syndrome
Adults and children,
uncommon, triad of
areflexia , ataxia
and
ophthalmoplegiaG
Q-1b antibodies
DEMYELINATING Resembles AIDP
15. DIAGNOSTIC CRITERIA
• PROGRESSIVE WEAKNESS OF 2 OR MORE LIMBS
DUE TO NEUROPATHY
• AREFLEXIA
• DISEASE COURSE <4 WEEKS
• EXCLUSION OF OYHER CAUSES ( VASCULITIS,
TOXINS, BOTULISM, DIPTHERIA PORPHYRIA etc.
REQUIRED
CRITERIA
• Symmetric weakness
• Mild sensory involvement
• Cranial nerve involvement
• Abscence of fever
• Typical csf profile
• Electrophysiological evidence of
demyelination.
SUPPORTIVE
CRITERIA
16. GULLAINE BARRE SYNDROME
• There is risk for autonomic dysfunction, respiratory failure,
and aspiration.
• Great care should be taken to maintain circulatory stability,
including adequate cardiac preload and afterload.
• Exaggerated responses to indirect-acting vasopressors.
• Careful hemodynamic monitoring.
• Regional anaesthesia is not contraindicated.
• Succinylcholine should not be used (risk of hyperkalemia).
• A non-depolarizing muscle relaxant with minimal circulatory
effects, such as cisatracurium or vecuronium, may be used if
needed.
• Noxious stimulation, such as direct laryngoscopy, can cause
exaggerated increases in blood pressure.
• Compensatory cardiovascular responses may be absent to
changes in posture, blood loss, or positive airway pressure
may be absent.
17. POLIOMYELITIS
• Poliomyelitis is caused by an enterovirus that initially infect
the reticuloendothelial system.
• After being eliminated from our country, clinician will see
patients with postpolio sequelae much more commonly than
those with acute polio.
• Postpolio sequelae manifest as fatigue, skeletal muscle
weakness, joint pain, cold intolerance, dysphagia, and sleep
and breathing problems.
20. • DIAGNOSIS : Virus
recovery from throat
washing, stool culture,
blood culture, and CSF
culture. Viral studies in
stool specimens are
essential for the diagnosis
of poliomyelitis.
• CSF examinantion :
pleocytosis/ Raised csf
proteins
• TREATEMENT: supportive
21. ANAESTHETIC CONCERNS
• Sensitivity to the sedative effects of anesthetics.
• Delayed awakening from general anesthesia.
• Sensitivity to nondepolarizing muscle relaxants.
• Careful positioning.
• Postoperative shivering may be profound, since these
individuals are very sensitive to cold.
• Postoperative pain perception may be abnormal.
• Outpatient surgery may not be appropriate for many
postpolio patients since they are at increased risk of
complications.
22. CEREBRAL PALSY
• Originates from a non-progressive neurological insult sustained
perinatally or before 2 yrs of age.
• Predominantly affects the motor system, and the resultant spasticity
and hypertonicity are progressive.
• Infants generally have very low birth weight.
• Spastic: Lesion in cerebrum. Includes quadriplegia, diplegia,
hemiplegia.
• Dyskinetic: Lesion in basal ganglia.
• Ataxic: Lesion in cerebellum includes tremor, loss of balance, and
speech.
• Mixed: Includes spasticity and athetoid movements.
23.
24.
25. Cerebral palsy – preoperative
• Gastroesophageal Reflux: Impaired ability to handle
pharyngeal secretions, Increased salivation: Recurrent
pneumonia (chronic aspiration and inability to cough).
• Reactive airway disease is common.
• Neurological:Seizures are present in roughly 30% -
anticonvulsants.
• Musculo-skeletal:Poor nutrition, contractures, fragile bones
etc.
26. Peri-operative management
• Premedication includes sedatives, antiacids , anticonvulsants,
anticholinergics and anti emetics.
• Vascular access may be difficult.
• Careful positioning.
• Latex allergy has been reported.
• Lower M.A.C., sensitivity to inhalational agents.
• Temperature: risk of Hypothermia (↓ body fat, ↓ temp
regulation.
• Excessive secretions and or a history of gastro-oesophageal reflux
is a concern.
• ET size selection should be based on their age as this usually
provides the most appropriate fit.
27. • Resistance to non-depolarising muscle relaxants
• Elevated pain threshold, decreased central pain perception
• Emergence from anaesthesia may be delayed :
Hypothermia, Residual volatile anaesthetic agents
• Irritability on emergence from anaesthesia is common : Pain,
Urinary retention, Unfamiliar environment etc.
30. Occluded artery Clinical features
Anterior cerebral artery Contralateral leg weakness
Middle cerebral artery Contralateral hemiparesis and
hemisensory deficit (face and arm
more than leg)
Aphasia (dominant hemisphere)
Contralateral visual field defect
Posterior cerebral
artery
Contralateral visual field defect
Contralateral hemiparesis
Penetrating arteries Contralateral hemiparesis
Contralateral hemisensory deficits
Basilar artery Oculomotor deficits and/or ataxia
with crossed sensory and motor
deficits
Vertebral artery Lower cranial nerve deficits and/or
ataxia with crossed sensory deficits
31.
32. ANAESTHETIC CONSIDERATION:
• Careful preoperative assessment, examination &
evaluation including drug history, precipitating events.
• Antihypertensive medication to be continued till the
time of operation.
• Thromboprophylaxis is advisable unless contraindicated.
• Pressor and depressor agents may be used to treat
unwanted changes in blood pressure during induction.
• Intravenous fluid replacement should be proactive rather
than reactive.
• Inducing agents with minimal hemodynamic effects ( esp
BP) prefered.
• Avoid hyperventilation.
• Examine the patient early in the postoperative period.
33. MOTOR NEURON DISEASE
• Degeneration of upper and/or
lower motor neurons i.e.
Amyotrophic Lateral Sclerosis
• Muscular weakness and
atrophy.
• Steady, asymmetric
progression.
• Sensory systems, voluntary eye
movements, and urinary
sphincters are spared.
34. AMYOTROPHIC LATERAL SCLEROSIS
ANAESTHETIC CONCERN
• Increased Sensitivity to NDMRs
– Reduction in choline acetyltransferase (involved in
synthesis of ACh) occurs secondary to degeneration of
anterior horn cells.
• Avoid Sux
– Hyperkalemic response in degenerating muscles.
• GA documented to cause ventilatory depression post-
operatively, even without use of muscle relaxants
– Respiratory complications are common and a major cause
for concern.
• Regional anaesthesia to be avoided in pts with motor
neuron disease, including ALS, for the fear of exacerbating the
disease
35. ALZHEIMER'S DISEASE
• Most common cause of Dementia in old age patients .
• Autosomal dominant mode.
• Diffuse amyloid rich senile plaques & neurofibrillary tangles-
hallmark findings.
• C/f: cognitive impairment such as dementia, apraxia, aphasia,
agnosia.
• Drug therapy includes Cholinesterase inhibitors- rivastigmine,
Donepezil, tacrine, Galantamine.
36. Anaesthetic consideration
• Monitored & Regional anaesthesia- challenging options.
• Shorter acting sedative-hypnotic drugs.
• Cautious use of anticholinergics- glycopyrrolate>> atropine.
• Cautious use of Muscle relaxants- prolonged action of Sch &
relative resistance to NDMR.
37. PARKINSON'S DISEASE
• Neurodegenerative disorder in the elderly patients causing
loss of Dopaminergic neurons in basal ganglia.
• Dopamine deficiency causes activaion of GABA neurons
resulting in cortical inhibition.
• C/f : tremors,abnormal gait & posture,dyskinesia.
• Increase in glutamate neurotransmission causes increased
cholinergic activity- sialorrhoea,seborrhoea,bladder
dysfunction,dysphagia.
• Lewy bodies-hallmark finding.
39. ANAESTHETIC CONCERNS
• Preop thorough assessment of neurological disabilities & medications.
• Continue antiparkinsonian medication till the day of surgery,
apomorphine- s/c or i/v intraoperatively.
• Premedication- prone for aspiration pnuemonitis.
– avoid metoclopramide, droperidol ,phenothiazines.
• Opioid- acute dystonias,chest wall rigidity.
• Ketamine-controversial??
• Autonomic dysfunction chr. by orthostatic hypotension.
• Cautious use of volatile anaesthetics.
• DRUG INTERCTIONS: reaction with meperidine in pt recieving
selegelline, risk of Neurolept malignant syndrome.
• Post op care: need for respiratory support ,hallucinations & mental
confusion.
40.
41. DRUG COMMENT
INTRAVENOUS INDUCING AGENTS
PROPOFOL
THIOPENTONE
ETOMIDATE
AVOID FOR STEREOTACTIC PROCEDURES
SAFE
SAFE
VOLATILE ANAESTHETIC
HALOTHANE
ISOFLURANE
SEVOFLURANE
DESFLURANE
Possible arrhythmias
Probably safe
Probably safe
Probably safe
NEUROMUSCULAR BLOCKING AGENTS
DEPOLARISING
NONDEPOLARISING
Possible hyperkalemia
Probably safe
ANALGESICS
MORPHINE
PETHIDINE
FENTANYL
ALFENTANYL
Possible muscle rigidity
Avoid in patients on selegiline
Possible muscle rigidity
Possible dystonic reactions
42. NEUROLEPTIC MALIGNANT
SYNDROME
• Result from relative lack of dopamine:
– dopamine receptor blockade.
– inadequate dopamine production.
• Supporting evidence:
– Neuroleptic drugs block dopamine receptors.
– Occurs with other dopamine blocking drugs.
– Occurs on sudden withdrawal of antiparkinsonian therapy.
– Responds to dopamine agonists.
• Essential evidence:
– Recent or current therapy with dopamine blocking drug
• Neuroleptic (ANTIDOPAMINERGIC)
• other drug eg metoclopramide
– recently stopped a dopamine agonist eg L-dopa.
43. PATHOPHYSIOLOGY
BLOCKADE OF DOPAMINERGIC FIBRES IN CENTRAL NERVOUS SYSTEM
CORPUS STRIATUM
MUSCLE RIGIDITY AND CONTRACTION
THERMOREGULATORY CENTRES IN
PREOPTIC NUCLEI OF ANTERIOR
HYPOTHALAMUS
PYREXIA
NIGROSTRIATAL & MESOCORTICAL
SYSTEM
MENTAL STATUS CHANGES
SPINAL CORD
AUTONOMIC DISTURBANCES
44. HYPERTHERMIA
Oral temperature >
38°C (100.4°F) in the
absence of another
known cause
EXTRAPYRAMIDAL
EFFECTS(>2)
Choreiform movements
Cogwheel rigidity
Dyskinesia
Dysphagia
Festinating gait
Lead pipe muscle rigidity
Oculogyric crisis
Opisthotonous
Sialorrhoea
Trismus
AUTONOMIC
DYSFUNCTION(>2)
Hypertension (diastolic
blood pressure at least 20
mm Hg
above baseline)
Incontinence
Prominent diaphoresis
Tachycardia (heart rate at
least 30 bpm above
baseline)
Tachypnoea (respiration >
25 breaths/min)
DIAGNOSTIC CRITERIA
45. MANAGEMENT
• Discontinuation of the offending neuroleptic agent
• ABC, FLUID RESUSCUTATION
• Cooling measures
• Pharmacotherapy
Bromocriptine
1. 2.5 mg q8h up to 5 mg q4h
2. continue for 7–10 days after resolution then taper over 1–2 weeks (except depot
preparations)
Dantrolene
1. 2–3 mg/kg
2. extreme rigidity, very high fever (> 40oC), unable to tolerate oral treatment
Benzodiazepines
1. to control agitation/delirium
ECT
1. refractory to adequate trial of dopamine agonist/supportive care
2. after resolution of acute features
1. remain catatonic or
2. develop ECT-responsive psychotic features
3. suspected acute lethal catatonia
46. MYASTHENIA GRAVIS
• Myasthenia gravis is caused by autoimmune disruption of
postsynaptic acetylcholine receptors at the neuromuscular
junction.
• Hallmarks are weakness and rapid exhaustion of voluntary
skeletal muscles.
• Muscle strength characteristically improves with rest,
deteriorates rapidly with exertion.
• Laryngeal and pharyngeal muscle weakness may lead to
aspiration, problems clearing secretions, difficulty chewing.
• Disease course marked by exacerbations and remissions :
– Infection, stress, surgery, pregnancy have unpredictable
effects, but often cause exacerbations.
– Antibiotics can aggravate weakness.
47. • Diseases considered AI in origin often coexist
– Decreased thyroid function
– RA
– SLE
– Pernicious Anemia
• Clinical Classification OSSERMAN’S GRADING
– Class 1: ocular symptoms only
– Class 1A: ocular symptoms with EMG evidence of
peripheral muscle involvement
– Class 2A: mild generalized symptoms
– Class 2B: more severe and rapidly progressive symptoms
– Class 3: acute and severe bulbar symptoms
– Class 4: late in the course of disease with severe bulbar
symptoms and marked generalized weakness
50. TYPE ETIOLOGY ONSET SEX COURSE THYMUS
NEONATAL Passage of ab
from myasthenic
mothers across
placenta
Neonatal Both Transient Normal
CONGENITAL Congenital end
plate pathology
Genetic
autosomal
recessive pattern
0-2 years M>F Nonfluctuating
compatible with
long survival
normal
JUVENILLE Autoimmune 2-20 years F > m Slowly progressive Hyperplasia
ADULT Autoimmune 20-40
years
F > m Maximum severity Hyperplasia
within 3-5
years
ELDERLY Autoimmune >40 years M > F Rapid progressive
High mortality
Thymoma
51. Therapy - Myasthenia Gravis
• Immunosuppressants: Steroids , Azathioprine,Cyclosporine
• Plasmapheresis, iv immunoglobulin
– Acute exacerbations, i.e. in immediate post-operative
period if anticholinesterases have been withheld and
symptoms are severe
– Plasmapheresis + IVIG for 5 days -> rapid improvement,
may last for weeks
• Thymectomy
• Anticholinesterase drugs
– Pyridostigmine, po duration of 2-4 hours
– Excessive administration -> Cholinergic Crisis
• SLUDGE: Salivation, lacrimation, urination, defecation, +
miosis + bradycardia + bronchospasm
• Profound weakness: due to excess Ach at NMJ ->
persistent depolarization
52. CHOLINERGIC CRISIS VS MUSCARINIC CRISIS
MUSCARINIC CRISIS CHOLINERGIC CRISIS
An exacerbation of the myasthenic
symptoms caused by
undermedication
with anticholinesterases
an acute exacerbation of muscleweakness
caused by
overmedication
with cholinergic anticholinesterase drugs
Generalised muscle weakness
Pupils - miosis
TENSILON TEST : improvement in
symptoms
Muscle weakness + parasympathomimetic
effects
Pupils – mydriasis
Further deterioration
Atropine + supportive Neostigmine + supportive
53.
54.
55. ANAESTHETIC CONCERNS
• Plasmapheresis depletes plasma
esterase levels, thus prolonging the
effect of drugs eliminated by these
enzyme systems (suxamethonium,
mivacurium, ester-linked local
anaesthetics).
• Sch may have an altered effect and
patients may be resistant to
depolarization due to reduced
receptor activity, requiring increased
dose. This, in conjunction with
treatment-induced plasma esterase
deficiency, leads to an increased risk of
non-depolarizing (Phase II) block.
56. PREOPERATIVE ASSESSEMENT:
• Assess the degree of weakness and the duration of
symptoms.
• Any degree of bulbar palsy is predictive of the need for both
intra- and postoperative airway protection.
• Perform lung function tests—FVC <50% predicted (or <2.9
litres) or those who have coexisting respiratory disease are
more likely to require postoperative ventilation.
• Take a full drug history and determine the effect of a missed
dose of anticholinesterase on the patient.
• Continue anticholinesterase therapy.
• Premedication should be minimal.
• Facilities for postoperative ventilation should be available.
57. PERIOPERATIVE CONSIDERATION:
• Sch may be used if indicated—doses of 1.5 mg/kg are usually
effective.
• If doubt exists as to the difficulty of intubation, awake
techniques may be useful.
• If sch is used, do not use any neuromuscular blockade drug
until muscle activity has returned and no fade is present.
• Non-depolarizing drugs should be used sparingly
• Use reduced doses of relaxant (10% normal) under nerve
stimulator control.
• Use of rocuronium & reversal with sugammadex is
alternative.
• Reversal of neuromuscular blocking drugs should be
achievable with standard doses of neostigmine.
• Careful Extubation.
58. DRUGS INTERACTIONS
NONDEPOLARIZING NM BLOCKERS INCREASED SENSTIVITY
SUCCINYLCHOLINE RESISTANCE TO BLOCKADE AND DELAYED
ONSET
INHALATIONAL AGENTS REDUCE NEUROMUSCULAR
TRANSMISSION
INTRAVEINOUS AGENTS NO EFFECT
LOCAL ANESTTHETICS PROLONGED ACTION AND INCREASED
TOXICITY OF ESTER LINKED AGENTS WITH
ANTICHOLINESTERASE THERAPY &
PLASMAPHERESIS
ANTIBIOTICS NEUROMUSCULAR BLOCKADE INCREASES
WITH AMINOGLYCOSIDES,
ERYTHROMYCIN etc.
59. MYASTHENIA SYNDROME
LAMBERT EATON MYASTHENIC
SYNDROME
• Proximal muscle weakness associated with cancer (most often
small cell carcinoma of the lung).
• Due to a reduction in the release of acetylcholine
(prejunctional failure).
• It is not reversed by anticholinesterase therapy and muscle
weakness is improved by exercise.
• Associated with dys-autonomia .
• Sensitive to both depolarizing and non-depolarizing
neuromuscular agents.
60. MYASTHENIC SYNDROME MYASTHENIA GRAVIS
Manifestations Proximal limb weakness
Strength improves with exercise
Muscle pain common
Reflexes -/ decreased
Extraocular, bulbar and facial
muscle weakness
Fatigue with exercise
Muscle pain uncommon
Reflexes normal
Gender Male>female female >male
Coexisting
pathology
Small cell carcinoma Thymoma
Response to
muscle
relaxant
Sensitive to scholine &
nondepolarising agents
Poor response to
anticholinesterase
Resistant to scholine
Sensitive to nondepolarising
agents
Good response to
anticholinesterase
62. MYOTONIC DYSTROPHY
• Most common muscle
dystrophy in ADULTS
• Characterized by persistent
contractures of skeletal
muscles after voluntary
contraction or following
electrical stimulation
• Abnormality in the
intracellular ATP system that
fails to return calcium to the
sarcoplasmic reticulum
• SWAN NECK / HATCHET
FACE
63. ASSSOCIATED ORGAN DYSFUNCTION
• Cardiac Involvement
– Mitral valve prolapse – 20% of individuals
– Deterioration of the His-Purkinje system lead to arrhythmias
• 1st degree AV block very common
• Pulmonary Pathology
– Restrictive lung disease
– Impaired responses to hypoxia and hypercarbia
• Cataracts( CHRISTMAS TREE ) very common
• GI abnormalities
– Gastric atony
– Intestinal hyper-motility
– Pharyngeal muscle weakness with impaired airway protection
– Cholelithiasis
64. ANAESTHETIC CONCERNS
• Eventually develop extremely compromised respiratory
function.
– Pulmonary Aspiration, Pneumonia
– Chronic Alveolar hypoventilation because of impaired
neuromuscular function -> chronic hypercapnoea.
– Decreased FRC, VC, MIP.
• Avoid premedication with sedatives – very sensitive to
respiratory depressant effects of narcotics and
benzodiazepines.
• Avoid Etomidate.
– May cause myoclonus and precipitate contractures.
• Avoid Sux.
– Produces an exaggerated contracture.
• Susceptible to MH.
65. • Avoid Anticholinesterases – may precipitate contracture by
increasing ACh available at NMJ.
• Keep room warm – shivering may lead to contractures.
• Exaggerated effects of myocardial depression from inhaled
agents- even Asymptomatic pts have some degree of
cardiomyopathy.
• Anesthesia and surgery could theoretically aggravate co-
existing cardiac conduction blockade by increasing vagal tone.
or causing transient hypoxia of the conduction system.
• Pregnancy:
– Exacerbation of symptoms is likely.
– Uterine atony and retained placental often complicate
vaginal delivery.
67. DUCHENNE’S AND BECKERS
MUSCULAR DYSTROPHY
• X linked recessive disorder
• Most common muscle
dystrophy seen in
children(& most severe)
• Males> females,
• Affects Dystrophin gene
(present in skeletal , smooth
& cardiac muscle)
• DIAGNOSIS : CPK levels &
muscle biopsy &
electrodiagnostic testing
68.
69.
70. ASSOCIATED COMORBIDITIES
• MENTAL RETARDATION
• RESPIRATORY INSUFFICIENCY:
– Most common cause of death in DMD.
– Early involvement of expiratory muscles with sparing of
diaphragm.
– Scoliosis ( with every 10* of scoliosis FVC decreases by
4%).
– Ineffective cough retained secretions leading to
infection.
• CARDIAC INVOLVEMENT:
– DCM in early course.
– Systolic dysfunction in later phase of disease.
– MR due to papillary muscle dysfunction.
71. ANAESTHETIC CONSIDERATION
• Perioperative complications disproportionate to severity of
disease.
• Preoperative cardiology and pulmonary assessement.
• Increased risk of aspiration , premedication with prokinetics
and anti emetics.
• Premedication with antisialogogue.
• Careful intravenous induction of anaesthesia with balanced
opioid/ induction agent.
• Masseter spasm may be seen.
72. • Potent inhalational anaesthetics should be carefully used
due to risk of myocardial depression. Hence TIVA preferred.
• Sch should be avoided.
• Non-depolarizing neuromuscular blockers are safe. Nerve
stimulator monitoring should be used.
• Malignant hyperpyrexia has been associated with muscular
dystrophy.
• Respiratory depressant effects of all anaesthetic drugs are
enhanced and postoperative respiratory function should be
monitored carefully.
• Some may need prolonged ventilatory support.
• Regional analgesia is safer than GA.
73. CHANNELOPATHIES
Disturbance in the transfer of ions across the sarcolemma.
1) Familial periodic paralysis
– Hyperkalemic Periodic Paralysis.
– Hypokalemic Periodic Paralysis
2) Ligand Gated Calcium Channelopathy
Malignant Hyperthermia
74. MALIGNANT HYPERTHERMIA
• It is a pharmacogenetic clinical syndrome that in its classic
form occurs during anesthesia with a triggering agents with
rapidly increasing body temperature (by as much as 1°C/5
min) and extreme acidosis
• TRIGGERING AGENTS
– DEPOLARISING MUSCLE RELAXANTS, the only currently
used of which is succinylcholine.
– INHALATION AGENTS ether, halothane, enflurane,
isoflurane, desflurane, sevoflurane.
75. Two classic clinical manifestations of fulminant MH syndrome :
– Rigidity after induction with thiopental and succinylcholine
but successful intubation, followed rapidly by the
symptoms .
– Normal response to induction of anesthesia and
uneventful anesthetic course until onset of the following
symptoms:
• Unexplained sinus tachycardia or ventricular
arrhythmias, or both.
• Tachypnea if spontaneous ventilation is present.
• Unexplained decrease in O2 saturation (because of a
decrease in venous O2 saturation).
• Increased in end-tidal PCO2 with adequate ventilation
(and in most cases unchanged ventilation).
• Unexpected metabolic and respiratory acidosis.
• Central venous desaturation.
• Increase in body temperature above 38.8°C with no
obvious cause.
76. MALIGNANT HYPERTHERMIA
MORE SPECIFIC SIGNS
• Generalised muscle
rigidity
• Rapidly unexplained
increase in end tidal CO2
• Rapidly developing fever
• Increased serum creatine
phosphate
• Cola coloured urine
LESS SPECIFIC SIGNS
• Tachycardia
• Tachypnoea
• Arrhythmias
• Hypertension /
hypotension
• Metabolic acidosis
• Hyperkalemia
• Coagulopathy
• Cyanosis
77. Criteria Used in the Malignant
Hyperthermia Scale Clinical Grading
• Process I: Muscle rigidity
– Generalized rigidity
– Masseter rigidity
• Process II: Myonecrosis
– Elevated CK >20,000 (after
succinylcholine administration)
– Elevated CK >10,000 (without
exposure to succinylcholine)
– Cola-colored urine
– Myoglobin in urine >60 µg/L
– Blood/plasma/serum K+ >6
mEg/ml
15
15
15
15
10
5
3
78. • Process III: Respiratory acidosis
– PetCO2 >55 with controlled ventilation
– PaCO2 >60 with controlled ventilation
– PetCO2 >60 with spontaneous
ventilation
– Inappropriate hypercarbia
– Inappropriate tachypnoea
• Process IV: Temperature increase
– Rapid increase in temperature 15
– Inappropriate temperature >38.8°C in
perioperative period
• Process V: Cardiac involvement
– Inappropriate tachycardia
– Ventricular tachycardia or fibrillation
15
15
15
15
10
15
10
3
3
81. TREATMENT
• Discontinue all anesthetic agents and hyperventilate with 100%
oxygen.
• Administer dantrolene (2.5 mg/kg intravenously) to a total dose of
10 mg/kg IV every 5 to 10 minutes until symptoms subside.
• Correct the metabolic acidosis with frequent monitoring of blood
gases and Ph.
• Control fever by administering iced fluids, cooling the body surface,
cooling body cavities with sterile iced fluids. Cooling should be
halted at 38°C to 39°C to prevent inadvertent hypothermia
• Monitor urinary output and establish diuresis to protect the kidney
from probable myoglobinuria.
• Further therapy is guided by blood gases, electrolytes,
temperature, arrhythmia, muscle tone, and urinary output.
• Treatment of hyperkalemia with glucose and insulin should be slow.
The most effective way to lower serum potassium is reversal of MH
by effective doses of dantrolene.
• Analyze coagulation studies (e.g., international normalized ratio,
platelet count, prothrombin time, fibrinogen, fibrin split or
degradation products).
82. PREVENTION IN SUSCEPTIBLE
PATIENTS
• Screening with CAFFEINE CONTRACTURE TEST on muscle
biopsy- gold standard test.
• Avoid use of triggering agents.
• Prefer anaethetic workstation without prior use of inhaled
agents.
• Or, anaesthetic machines may be purged wih activated
charcoal.(Drain, remove, or disable anaesthetic vaporizers,
and changing tubing and CO2 absorbent and flowing oxygen at
10 L/min for 10 minutes or longer. )
• Dantrolene need not be given preoperatively .
83. Familial periodic paralysis
HYPERKALEMIC :
• Early onset, sometimes in infancy (autosomal dominant).
• Periodic paralysis with brief episodes of flaccid
weakness that resolve spontaneously
• Respiratory and cranial muscles are typically spared
• Genetic mutation that affects sodium channels causes
sustained sodium currents which don’t allow the
formation of action potentials during these brief attacks.
• ECG signs of hyperkalemia, also ectopic beats or
paroxysmal.
• Preo-perative management consists of potassium-free
dextrose-containing solutions.
• Avoid cold, hyperkalaemia and carbohydrate depletion
• Succinylcholine is contra-indicated
84. HYPOKALEMIC
• Most common type, onset during adolescence.
• Results from a mutation in a calcium channel.
• Attacks can be severe, resulting in respiratory compromise and
cardiac disturbances.
• Triggers are strenuous exercise, high carbohydrate intake, lowserum
potassium, mental stress, cold, trauma and infection.
• Maintain normal serum potassium, glucose and acid bases Status
peri-operatively.
• Adequate premedication needed to avoid stress.
• Maintain normothermia.
• Avoid overeating the day before surgery.
• Avoid intravenous fluids with dextrose and sodium .
85. METABOLIC & MITOCHONDRIAL
MYOPATHIES
• Heterogeneous group of disorders is now the commonest cause of
muscle weakness in children with an incidence of 1 in 4000
• Electron transport chain (ETC) function results in decreased ATP
production,and an increased production of free radicals.The acidosis
and excess free radicals further damage the mitochondria
• Mitochondrial DNA mutations include:-
– MELAS: mitochondrial encephalopathy, lactate acidosis
– MERRF: myoclonic epilepsy with red fibres syndrome
• The severest forms can present in the neonatal period with profound
weakness, liver and renal failure, and substantial neurological
impairment
86. • In acid maltase deficiency-severe respiratory deficiency,recurrent
aspiration pneumonia and pulmonary arterial hyper-tension might
occur
• In lipid storage deficiencies, patients are susceptible to hypo-
glycaemia, acidosis, general muscle weakness, rhabdomyolysis, and
progressive cardiac insufficiency
• Patients have exaggerated metabolic responses to prolongedfasting,
fever and illness.
• The patient is typically a floppy infant, a poor feeder with small
stature, displays developmental delay, is hypotonic or
hypoglycaemic, with or without positive family history.ECG and Echo
might reveal cardiomyopathy or conduction deficits, and ventricular
dilatation can compress the airway.
87. Anesthetic Considerations
• Evaluate pre-operative cardiac and respiratory status. Total AV
block requires pacing
• Evaluate metabolic status: glucose, lactate, liver enzymes and
serum creatinine. Overnight fasting can cause hypoglycaemia,
dehydration and mild metabolic acidosis
• Maintain intravenous infusion containing glucose and electrolyte
pre-operatively, avoid lactate-containing fluids
• Increased sensitivity to sedatives, barbiturates, and propofol.
• Variable sensitivity to nondepolarising muscle relaxants. Avoid
succinylcholine.
• Inhalation or total intravenous anaesthesia.
• Propofol may have an adverse effect on fatty acid oxidation and
impair mitochondrial respiratory chain function, and therefore put
patients with mitochondrial disorders and carnitine deficiency
syndromes at risk for a clinical scenario similar to propofol infusion
syndrome (PRIS).
88. • Alternative intravenous anaesthetics that are under
investigation include ketamine, etomidate, and
dexmedetomidine.
• Many clinicians now consider sevoflurane as the agent of choice
in these patients, how ever some respiratory chain disorders are
more sensitive to inhaled agents and require lower MAC.
• Adequate Pain management as the response to pain may
heighten the risk of lactic acidosis from depletion of energy
stores and increased oxygen demand.
• Prevent hypothermia.