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.
Intro to Hypoxic pulmonary vasoconstriction Arun Shetty
Hypoxic pulmonary vasoconstriction, a seldom heard phenomenon but very effective physiologic property which helps lungs utilise ventilation to the maximum
Intro to Hypoxic pulmonary vasoconstriction Arun Shetty
Hypoxic pulmonary vasoconstriction, a seldom heard phenomenon but very effective physiologic property which helps lungs utilise ventilation to the maximum
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.
Scalp block is simple and easy to perform. It has the advantages of minimizing cardiovascular effects and decreasing intraoperative analgesia requirements.
New GCS, the GCS-P was adopted in 2018 by the same person who proposed GCS. It gives better prognosticate outcomes compared to GCS.
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.
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.
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.
Scalp block is simple and easy to perform. It has the advantages of minimizing cardiovascular effects and decreasing intraoperative analgesia requirements.
New GCS, the GCS-P was adopted in 2018 by the same person who proposed GCS. It gives better prognosticate outcomes compared to GCS.
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.
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 Abdullah Ansari
PG-2 (Medicine)
AMU ALIGARH
A general approach to periodic paralysis....
(including hypokalemic periodic paralysis and thyrotoxic periodic paralysis, and other “Channelopathies” or “Membranopathies)
Pathophysiology
Epidemiology
Primary or familial periodic paralysis
Secondary periodic paralysis
Conventional classification of periodic paralysis
Classification of primary periodic paralysis based on ion-channel abnormalities
Clinical approach to a case of periodic paralysis
History of muscle weakness
Age of onset
Family history
Timing
Intensity
History of administration of certain drugs
Clinical examination
Differential Diagnosis
Laboratory investigations
Serum K+
CPK and serum myoglobin
ECG
EMG
Nerve conduction studies
Provocative Testing
Muscle biopsy
Treatment
Prognosis
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
learn about excellent case article published in NEJM regarding celiac disease,its rare presentation and approach for the same along with discussion ..we should always think about this rare presentations
GBS is an autoimmune disorder that is thought to be a postinfectious polyneuropathy, involving mainly motor but also sensory and sometimes autonomic nerves.
This syndrome affects people of all ages and is not hereditary.
Most patients in the U.S and Europe have a demyelinating neuropathy, but primarily axonal degeneration is apparent in some forms of GBS, seen mainly in China, Mexico, Bangladesh, and Japan.
Clinical Manifestations
The onset of weakness usually follows a nonspecific GI or respiratory infection by ~ 10 days.
The original infection might have caused only GI (especially C. jejuni, but also H.pylori ), respiratory tract (especially M.pneumoniae ), or systemic (Zika virus) symptoms.
Consumption of undercooked poultry , unpasteurized milk, and contaminated water are the main sources of GI infections.
West Nile virus also can mimic GBS, but more often causes a motor neuron disease similar to poliomyelitis.
GBS may follow administration of vaccines against rabies , influenza, and conjugated meningococcal vaccine, particularly serogroup C.
Other infectious precursors of GBS include mononucleosis, Lyme disease, CMV, and the Zika virus
Initial symptoms include numbness and paresthesia, followed by weakness.
Radicular back pain and myalgia are common in the initial stages ; affected children can be very irritable.
Weakness usually begins in the lower extremities and progressively involves the trunk, the upper limbs, and finally the bulbar muscles, but weakness is sometimes proximally prominent.
Extraocular muscle involvement is rare, but many patients develop facial weakness.
In most patients, weakness is essentially symmetric.
Weakness progresses over days or weeks, the clinical nadir occurring in < 4 wk.
~ 60% of children lose the ability to walk at some point in their illness; a small proportion progress to flaccid tetraplegia.
The maximal severity of weakness is reached by 4 wk after onset.
GBS and MFS and their subtypes form a continuum of discrete and overlapping syndromes.
The pattern of weakness for each subtype is as follows:
Classic GBS, tetraparesis with or without motor cranial nerve involvement;
Paraparetic GBS, lower limbs;
pharyngeal-cervical-brachial weakness, bulbar, neck, and upper limbs; bifacial weakness with paresthesias,
Facial; MFS, external ophthalmoplegia
Bickerstaff brainstem encephalitis, external ophthalmoplegia.
Facial weakness and motor cranial nerve involvement are more frequent in demyelinating-type classic GBS (AIDP) than in axonal-type GBS (acute motor axonal neuropathy).
In MFS , there is ataxia, and in its CNS subtype, Bickerstaff brainstem encephalitis, there is additional hypersomnolence
DDX
SPINAL CORD LESIONS
Acute transverse myelitis
Epidural abscess
Tumors
Poliomyelitis
Enteroviruses
Acute flaccid myelitis
Hopkins syndrome
Vascular malformations
Anesthesia consideration in intestinal obstruction is gastric aspiration, rapid sequence induction, electrolyte and acid base disorder, hydration, AKI and hemodynamic status.
Hypothyroidism and hyperthyroidism have significant clinical effects. Both should be optimized. Anesthesia providers should be able to diagnose and manage.
Blood pressure optimization is important in pheochromocytoma patients before going to surgery. It is important for the anesthesia providers to diagnose, optimize and manage those patients..
Anesthetic management in Diabetic mellitusTenzin yoezer
Diabetic is a systemic disease. Preoperative assessment includes blood sugar control, involvement of systems, and types of medication. Intraoperative and postoperative management is also vital.
Describes coronary blood supply anatomy, myocardial oxygen demand and supply, and basic anesthesia consideration (history taking, special investigation, and optimization)
It is a rare but potentially catastrophic event that is associated with high mortality. The reported incidence of ICA varies considerably across studies.
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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
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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.
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.
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
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
2. History
• 52 yr old female, previously well with history of chronic alcohol abuse
presented with bilateral lower limb weakness and pain for 3 days.
• Limb weakness was progressive and on 4th day onwards became bed
bound
• 1 week prior to limb weakness had self limiting loose stool
• While in P/ling hospital developed seizure(type of seizure not
mentioned)
• Referred to JDWNRH for further mx
• While in ER developed two episodes of seizure and didn’t gain
consciousness
3. History
• Was intubated and kept in AICU
• O/E – mild icteric
• Other examination were unremarkable except
• Limb examination:
• Both UL and LL power – grade 2
• Tone – flaccid
• Reflex – not mentioned
• Initial lab reports at P/ling:
• WBC- 18 LFT - normal
• Neu – 86% RFT - normal
• Hb – 12 USG - normal
• Plt – 324 CXR - NAD
5. • All the vitals stable throughout the illness
• CT brain: atrophy with mild ventricular dilatation
• ECG - sinus rhythm
• ESR – 40
• CSF studies – no cells, protein -137.8 mg/dL
• Neurophysiological studies – report not available
6. • On 14th day of illness IVIg was initiated after consulting
neurologist(HVO): for 5 days
• IVIg 400 mg
• IV drip 20 mL/hr x 1 hr
• 40 mL/hr x 1hr
• 60 mL/hr x 1 hr
• 80 mL/hr x 1 hr
7. • While in the ward developed 4th degree sacral bed sore.
• Brought in OT for W/D
• Face mask with TIVA:
• Inj Midazolam 2mg
• Inj Fentanyl 50 mcg
• Inj Propofol 100 + 20 mg
8. Final diagnosis
• Acute inflammatory demyelinating polyradiculopathy
• Complex partial seizure
• Grade IV seizure
10. Introduction
• First described in 1859
• Acute inflammatory demyelinating peripheral polyneuropathy usually
secondary to immunologic response to viral or bacterial infection
(usually respiratory or GI )
• Ascending progressive muscle weakness, autonomic dysfunction and
areflexia
• It causes significant morbidity requiring long hospital stay and
significant period of rehabilitation
• Approximately 10-15% require long term residual disability assistance
11. Epidemiology
• Worldwide incidence is 1.1 – 1.8 cases per 100,000/year
• M> F
• Bimodal age incidence:
• peak in young adults and elderly
• > 50 yrs : incidence rises to 3.3 cases per 100,000/year
• Strong association(70%) with precedent respiratory and GI origin
infection
• There is weak association between GBS and vaccination
12. Clinical features
• Symptoms :
• Weakness and sensory disturbances in LL- pain, numbness,
parasthesia
• Progressive ascending motor weakness
• Respiratory mucles weakness and respiratory failure
• Facial nerve paralysis
• Bulbar weakness(involvement of CIX-CXII)- difficulty in
swallowing,chewing, slurring of speech, chokking on liquids
• Opthalmoplegia
13. Clinical features
• Signs:
• Flaccid areflexic paralysis
• Muscle wasting
• Autonomic dysfunction
• Arrhythmias
• Swing in BP
• Urinary retention
• Paralytic ileus
• Hyperhidrosis
14. GBS subtypes
• 1) Acute inflammatory demyelinating polyradiculoneuropathy(AIDP)
• 2) Acute motor axonal neuropathy(AMAN)
• 3) Acute motor and sensory axonal neuropathy(AMSAN)
• 4) Miller Fisher syndrome(MFS)
• 5) chronic inflammatory demyelinating polyradiculopathy(CIDP)
15. Acute inflammatory demyelinating
polyradiculoneuropathy(AIDP)
• Most common form – 85 – 90%
• Symmetrical ascending motor weakness with hypo- or areflexia
• Underlying pathological process is inflammation and destruction of
the myelin sheaths surrounding peripheral nerve axons by activated
macrophages
• Slowing and blockage of conduction
• Muscle weakness
• Severe cases develop secondary axonal damage
16. Acute motor axonal neuropathy(AMAN)
• More common in Japan and China
• Young people
• Summer months
• Association with Campylobacter jejuni
• C/F similar to AIDP but tendon reflexes may be preserved
• Electrophysiological test distinguish from other variants – selective
motor nerve and axonal involvement
• Binding of antibodies to ganglioside antigen on the axon
• Macrophages invasion, inflammation and axonal damage
17. Acute motor and sensory axonal neuropathy(AMSAN)
• Both motor and sensory fibers involved
• Severe
• Associated with prolonged or even partial recovery
• C/F are similar to AMAN but also involves sensory
symptoms
• Pathology – antibody mediated axonal damage
18. Miller Fisher syndrome
• Presents with ataxia, areflexia and ophthalmoplegia
• 25% may develop limb weakness
• Electrophysiological studies – sensory conduction failure
• Antiganglioside antibodies to GQ1b are found in 90% of pt and are
associated with opthalmoplegia
• Pathological – demyelination of nerve roots
21. Investigation
• Antiganglioside and antibodies
• Anti-GM1 – positive in 25% ( worse outcome)
• Ant-GD1a – associated with AMAN subtype
• Ant-GQ1b – Miller-Fisher syndrome
• Infection screen:
• Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, herpes
simplex virus, Mycoplasma pneumoniae, HIV
22. Investigation
• Radiological
• CT – to exclude other causes of symptoms and evidence of raised ICP
• MRI – may show selective anterior spinal nerve root enhancement
with gadolinium
• Excludes cervical nerve impingement
• Lumbar puncture
• Protein – raised(may be normal in first 2 weeks)
• Cell count and glucose - normal
23. Investigations
• Nerve conduction studies
• Findings depend on subtype of GBS
• Majority show demyelinating pattern
• Some show axonal loss with little or no demyelination
• Respiratory function tests
• Reduced vital capacity, max inspiratory and expiratory pressure
• ABG – progressive respiratory failure
25. Diagnostic criteria for GBS, from stoelting
• Features required for diagnosis
• Progressive b/l weakness in arms and legs
• Areflexia
• Features strogy supporting the
diagnosis
• Progression of symptoms over 2-4 wks
• Symmetry of symptoms
• Mild sensory symptoms and signs
• Cranial nerve involvement(esp b/l facial
nerve weakness)
• Decrease nerve conduction velocity
• ANS dysfunction
• No fever at onset
• Elevated conc of protien in CSF with cell
counts < 10/mm3
• Spontaneous recovery starting 2-4 wks
after progression halts
• Features making diagnosis likely
• Definite sensory level
• Marked persistent bowel and bladder
dysfunction
• > 50 white cells/mm3 in CSF
27. Supportive care
• Airway and respiratory
• Around 30% require ventilatory support
• Deterioration of respiratory function may be rapid
• Vital capacity provides information of about respiratory sufficiency
• Max inspiratory and expiratory pressure provide information about
power of respective group of respiratory muscles
• Both test can be difficult to interpret in pts with bulbar
weakness(difficulty in forming a seal around the mouth)
28. Airway and respiratory
• ABG – evidence of respiratory failure
• Desaturation can be late sign
• Clinical indication for intubation and ventilation are:
• Vital capacity of <1L or <15 mL/kg
• Max inspiratory pressure of < 30 cmH20
• Max expiratory pressure of < 40 cm H20
• Bulbar involvement with inability to cough, swallow and protect the airway
• Evidence of respiratory failure on ABG and autonomic instability
• Tracheostomy should be considered if prolonged respiratory support
is needed
29. Cardiovascular
• Autonomic dysfunction in 70% - life threatening
• ECG, BP and fluid balance
• Most common arrhythmia – sinus tachycardia
• Other arrhythmias – atrial and ventricular tachycardia, prolonged QT interval,
AV block, asystole
• BP fluctuates- severe HTN and hypotension
• Orthostatic hypotension is common
• Care should be taken when treating extremes of BP with vasoactive agents as
pt may be particularly sensitive to their effects(upregulation of post synapting
response)
• Intubated patient with autonomic dysfunction may develop instability after
tracheal suction
30. Gastrointestinal
• Good nutrition is important particularly for those with bulbar
weakness, sedated and mechanically ventilated
• Dietician recommendation
• Pt with autonomic dysfunction – paralytic ileus
• (prokinetic agents – metoclopramide, erythromycin)
31. Neurological
• Neuropathic -50%
• NSAIDs in combination with opioids
• May add adjunctive such as anticonvulsants(Gabapentin
or carbemazepine), Tricyclic antidepressant
32. Venous thromboembolism prophylaxis
• High risk for DVT and PE
• LMWH in combination with pneumatic compression device or
anti-embolism stocking recommended until pt can walk
34. Rehabilitation
• 40% pt needs
• Careful attention should be paid to limb positioning and posture as
limb weakness can lead to nerve compression and palsies, pressure
sore and contracture
• Extensive input from physiotherapists and occupational therapist is
essential to provide tailored strengthening exercise and support
• Patient may also suffer from persistent fatigue- responsive to exercise
programme
35. Immunomodulatory
• IV immunoglobulin (IVIg)-15 mlL/kg
• Its effect is comparable to plasma exchange
• Most effective if administered within 2 weeks of the onset of
symptoms
• Advantages over plasma exchange:
• Widely available
• Less labour intensive
• Less side effect
• Indication: muscle weakness and respiratory depression
36. • IVIg contains donor IgG antibodies – reduces severity of autoimmune
inflammation in GBS by blocking Fc receptors
• Prevents antibody mediated cell destruction
• Alters complement activation
• Contraindication to IVIg:
• Previous anaphylactic reaction to IVIg and IgA deficiency
• Side effects of IVIg: nausea, headache, dermatological
disorders(erythroderma), fluid overload, deranged LFT, venous
thromboembolus, ARF, anaphylaxis
• No evidence of repeated treatment beneficial
37. Plasma exchange
• Aim – to remove antibodies associated with underlying autoimmune
response
• Accelerates recovery
• Improvements have been demonstrated in regaining muscle strength,
ability to walk, reduce duration of ventilator
• More beneficial if commenced within week of the onset of symptoms
• But can be beneficial upto 30 days after onset of illness
• Indication – same as IVIg
• CI: coagulopathy, overwhelming sepsis, hemodynamic instability and shock
• Side effects: nausea, vomiting, diarrhea, fever, coagulopathy,
immunosuppression, hypoglycemia
39. Prognosis
• Most recover fully
• 15% may suffer persistent disability
• 10% are unable to walk unaided at 1 yr
• Recurrence in 2-5%
• Mortality – 2-12%
• Common death – venous thromboembolism, pneumonitis,
arrhythmias and complication related to dysautonomia
40. Marker of poor prognosis
• Age > 40
• Rapid onset of symptoms
• Severe weakness esp if mechanical ventilation is required or marked
upper limb weakness
• Associated with precedent diarrheal illness or campylo bacter
infection
• Evidence of axonal damage on electrophysiological studies
• Lack of treatment with either plasma exchange or IVIg
42. Anesthesia consideration
• Aspiration risk due to to bulbar dysfunction
• Perioperative respiratory insufficiency due to muscle weakness
(anticipate need for postoperative ventilation)
• Autonomic dysfunction with possible hemodynamic instability
& autonomic hyperreflexia type reactions:
• Arrhythmias, cardiac arrest
• Physical stimulation can precipitate hypertension & tachycardia
• Altered response to neuromuscular blocking drugs (NMBs):
• Succinylcholine contraindicated due to hyperkalemia risk
• NdMR (nondepolarizing muscle relaxant) sensitivity
• ↑ risk of venous thromboembolism
43. Anesthesia consideration
• Goals:
• Minimize aspiration risk-consider prophylaxis, RSI
• Maximize respiratory function – avoid NMBs or reduced dose of NdMR and
full reversal, secretions, pain mx)
• Maintain hemodynamic stability
• Conflicts:
• RSI vs avoid succinylcholine
• Hemodynamic stability
• Neurological deficits and regional techniques
44. Pregnancy consideration
• Uterine tone is maintained – can deliver vaginally
• IUGR and oligohyramniosis – LSCS
• Extent of disease guides for GA/RA- no prospective randomized trial
• Document pre-existing deficits
• If GA chosen: avoid sux, minimal or avoid NdMR
• RA – safely used even in the presence of autonomic
dysfunction(Brooks et al) with SA and EA (Alici et al)
45. Reference
• GUILLAIN-BARRÉ SYNDROME ANAESTHESIA TUTORIAL OF THE WEEK 238
29th August 2011 Dr Sonya Daniel ST3, Southampton General Hospital, UK
Dr Richard Green( anesthesia tutorial week)
• https://www.anesthesiaconsiderations.com/guillain-barre-syndrome-
considerations
• The choice of anesthesia for cesarean section in patients with Guillain
Barre Syndrome – The dilemma continues Suman Arora ,NeeruSahni,
Latha Y
• Stoelting anesthesia and co-existing disease 7th edition p321-322
Sabrasez breath holding test: • Ask the patient to take a full but not too deep breath & hold it as long as possible. >25 SEC.-NORMAL Cardiopulmonary Reserve (CPR) 15-25 SEC- LIMITED CPR <15 SEC- VERY POOR CPR
2) Single breath count: After deep breath, hold it and start counting till the next breath. N- 30-40 COUNT Indicates vital capacity
3) SCHNEIDER’S MATCH BLOWING TEST: MEASURES Maximum Breathing Capacity. Ask to blow a match stick from a distance of 6” (15 cms) with- Mouth wide open Chin rested/supported No purse lipping No head movement No air movement in the room Mouth and match at the same level. Can not blow out a match MBC < 60 L/min FEV1 < 1.6L Able to blow out a match MBC > 60 L/min FEV1 > 1.6L MODIFIED MATCH TEST: DISTANCE MBC 9” >150 L/MIN. 6” >60 L/MIN. 3” > 40 L/MIN.
4) COUGH TEST: DEEP BREATH F/BY COUGH ABILITY TO COUGH STRENGTH EFFECTIVENESS INADEQUATE COUGH IF: FVC<20 ML/KG FEV1 < 15 ML/KG PEFR < 200 L/MIN. VC ~ 3 TIMES TV FOR EFFECTIVE COUGH. A wet productive cough / self propagated paraoxysms of coughing – patient susceptible for pulmonary Complication.
Initial tratment is facemask then CPAP. With CPAP the vital capacity and max inspiratory and expiratory pressure is known, if inadequate intubation