The document summarizes a clinical case of a 22-year-old female patient diagnosed with myasthenia gravis and hypothyroidism. She was admitted with worsening symptoms including diplopia, slurred speech, limb weakness, and difficulty swallowing. Her condition deteriorated and she experienced a myasthenic crisis requiring intubation and treatment including plasmapheresis, intravenous immunoglobulin, and medications. Her status was monitored daily with notes from physicians and treatment adjustments. After several plasmapheresis sessions and medication changes, her condition gradually improved.
GEMC: Myasthenia Gravis (Case of the Week): Resident TrainingOpen.Michigan
This is a lecture by Dr. Chris Oppong from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC: Myasthenia Gravis (Case of the Week): Resident TrainingOpen.Michigan
This is a lecture by Dr. Chris Oppong from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This powerpoint is a case presentation, that explains the case of ADCHF, with comorbidities, comprising HTN, CAD and DLP.
A summary on the recent advancements in HF management, along with justification of therapy provided, has been elucidated.
A note on home remedies and counselling tips has also been provided.
This powerpoint is a case presentation, that explains the case of ADCHF, with comorbidities, comprising HTN, CAD and DLP.
A summary on the recent advancements in HF management, along with justification of therapy provided, has been elucidated.
A note on home remedies and counselling tips has also been provided.
The Subjective, Objective, Assessment and Plan (SOAP).the assessment will identify what the drug related/induced problem is likely to be and the reasoning/evidence behind it. This will include etiology and risk factors, assessments of the need for therapy, current therapy, and therapy options.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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.
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
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
2. Patient details
Name - Shubhangi Sheshrao Deshbhartar
Age / Sex – 22yrs / F
Reg no – 1226958
Diagnosis – Myasthenia gravis with
hypothyroidism
3. S/B AP ↓ ENT 2 on 23/07/2016
Chief complaints
Dysphagia
Findings
Oral cavity – WNL
Indirect laryngoscopy -
WNL
k/c/o myasthenia gravis
on medication since 1
year
Advise
Physician opinion
4. S/B Physician ↓ 2 on 23/07/2016
Referred from ENT
Chief complaints
k/c/o myasthenia gravis with
hypothyroidism since 2 year
Diplopia since 1 ½ year
Slurring speech since 1 ½
month
Weakness of both upper &
lower limb since 1 ½ month
Difficulty in deglutition with
regurgitation since 8 days
O/E
P – 80 bpm
BP – 100/60 mm of Hg
S/E
RS & CVS – WNL
CNS – Conscious Oriented
Motor system
Nutrition – average
Power – 5/5
Hand grip – 60%
DTR 2+
Plantar – b/l flexor
5. S/B Physician ↓ 6 on 23/07/2016
No h/o ptosis
Tab thyroxine 100µg
Tab azaron ( azathioprine )50mg OD
Tab omnacortil (Prednisolone)5 mg OD
Advice
Please admit patient in Female Medicine Ward
6. S/B Lecturer / AP on 23/07/2016 at
2 pm
GC – Moderate
Afebrile
P- 78bpm
RS – Clear
Vitals – Stable
Advice
Plasmapheresis
Nephro call
Same treatment was
continued on 24/07/2016
Treatment
1 point DNS
Inj neostigmine 0.5mg BD
Inj atropine 0.6mg before
neostigmine
Tab omnacortil (Prednisolone)
5mg OD
Tab thyroxine 100µg OD
↑↑Tab azaron (azathioprine)
150mg OD
7. S/B Registrar/ SP ↓ med 6 on
25/07/2016
Nasal twang - ++ ,Opthalmoplegia
GC – moderate
Afebrile
P – 90bpm
HS – normal
RS – clear
P/A – soft
Investigation
Hb – 7.6gm/dL
TLC – 4000 cells/ mm3
Platelet – 298000/mm3
Treatment
1 point DNS
Inj neostigmine 0.5mg BD
Inj atropine 0.6mg before neostigmine
↑↑ Tab omnacortil (prednisolone) 40mg
OD
Tab thyroxine 100µg OD
Tab azaron (azathioprine)150mg OD
Tab distinon (pyridostigmine) 60mg BD
Diagnosis - Myasthenia gravis with
exacerbation
8. S/B Lecturer ↓ nephrology on
25/07/2016
Kindly send patient for plasmapheresis
Right sided double lumen HD catheter inserted
Advice
HIV - negative
HBsAg – negative
B+ve
Anti HCV
Arrange 5 FFP
Plasma filter
Dialysis tubing
9. S/B Registrar ↓ med 6 on
26/07/2016
GC – moderate
Afebrile
P – 78 bpm
BP – 110/70mm of Hg
RS – NAD
HS – Normal
CNS – NAD
Treatment
1 point DNS
Inj neostigmine 0.5mg BD
Inj atropine 0.6mg before
neostigmine
Tab omnacortil (prednisolone)
40mg OD
Tab thyroxine 100µg OD
Tab azaron (azathioprine) 150mg
OD
Tab distinon (pyridostigmine) 60mg
BD
10. 26/07/2016 at 11am –
Plasmapheresis - 1
↓ All Aseptic Precautions
double lumen Double Lumen
Catheter inserted ↓ local
anaesthesia procedure
uneventful
Patient had hypotension during
Plasmapheresis
1.5 litre plasma removed
5 unit FFP + 1 litre NS infused
Advice
Inj monocef (ceftriaxone) 1
gm iv BD
Arrange 5 unit of Fresh
Frozen Plasma for next
session on 28/07/2016
X ray chest PA view
11. S/B Reg ↓ med 6 / SP ↓ 6 on
27/07/2016
GC – moderate
Afebrile
P – 78 bpm
BP – 110/70mm of Hg
RS – NAD
HS – Normal
CNS – NAD
Treatment
1 point DNS
↑↑ Inj neostigmine 0.5mg TDS
Inj atropine 0.6mg before
neostigmine
Tab omnacortil 40mg OD
Tab thyroxine 100µg OD
Tab azaron 150mg OD
Tab shelcal 500mg BD
Tab distinon 60mg BD
13. S/B Lecturer ↓ Nephrology
28/07/2016 at 3.45 pm
While shifting patient c/o
discomfort
P – 150 bpm irregular
SpO2 – 94%
Inj Lasix 20mg iv stat
Inj hydrocortisone 100mg iv
stat
Drop in SpO2 to 70%
Hence AMBU bag ventilation
done
SpO2 – 98 % achieved
Bipap connected SpO2 – 98%
maintained
Semiconscious
?? Myasthenia Crisis
Advice
Shift to Intensive Cardiac Care
Uunit & Continue bipap
Urgent Ca++, CBC , PT/INR,
ABG
14. Transfer out notes to ICCU on
28/07/ 2016
C/O myasthenia gravis with exacerbation
Treatment
1 point DNS
Inj neostigmine 0.5mg TDS
Inj atropine 0.6mg before neostigmine
Tab omnacortil (prednisolone) 40mg OD
Tab thyroxine 100µg OD
Tab azaron (azathioprine) 150mg OD
Inj monocef 1 gm BD
Tab shelcal 500mg OD
15. Receiving notes in ICU
28/07/2016
P – 136bpm
BP – 90/ 60 mm of Hg
SpO2 – 100%
Chest – clear
Dyspnoeic
Sr Ca++ - 10.2
Sr Na+ - 142meq/L
Sr K+ - 2.8 meq/ L
Sr Mg++ - 3.8 meq /L
Treatment
2 point NS fast
Inj neostigmine 0.5mg TDS
Inj atropine 0.6mg before neostigmine
Inj monocef 1gm iv BD
Tab omnacortil 40mg OD
Tab thyroxine 100µg OD
Tab azaron 150mg OD
Tab shelcal 500mg BD
Tab distinon 60mg BD
Inj KCl 40meq in 1 point NS over 8hrs
16. S/B Reg ↓ med 6 on 29/07/2016
at 8 AM
GC – moderate
Afebrile
P – 86 bpm
BP – 100/70 mm of Hg
U/O – 800ml
RS – NAD
HS – Normal
CNS – NAD
P /A – soft
Treatment
Inj neostigmine 0.5mg TDS
Inj atropine 0.6mg before neostigmine
D5 Tab omnacortil 40mg OD
Tab thyroxine 100µg OD
Tab azaron 150mg OD
Tab shelcal 500mg BD
Tab distinon 60mg BD
D3 Inj monocef 1gm iv BD
pH – 7.4
HCO3- - 22
PCO2 - 25
17. S/B Senior Physician ↓ 6 on
29/07/2016 at 10.40AM
P – 90bpm
Opthalmoplegia ++
No Cyanosis
Chest – Clear
Mild improvement in
deglutition
Treatment
Inj neostigmine 0.5mg SOS
↑↑ Tab pyridostigmine 60mg
TDS
W/H omnacortil
(prednisolone)
D1/3 - Inj methyl
prednisolone 500mg OD
Rest ct all
18. Intubation notes 29/07/2016
↓ All aseptic precautions patient was
intubated with ET tube size 7.5 mm AE
b/l equal fixed put on ventilatory
support SpO2 - 92%
Procedure - uneventful
19. S/B Registrar ↓ ICU 29/07/2016 at
6PM
GC – poor
Unconcious
On ventilatory support
HS – normal
Chest – clear
SpO2 – 92%
Sr T3 – 490 IU
Sr T4 – 18 IU
TSH – 0.01IU
Advice
W/H Tab Thyroxine 100µg
Rest ct all
20. S/B MO / Registrar /SP↓ ICCU at
30/07/2016 at 8 AM
GC – moderate
Afebrile
P – 86 bpm
Chest – clear
BP – 110/70mm of Hg
U/O – 650ml
RS – NAD
HS – Normal
CNS – NAD
P/A – soft non tender
Treatment
D1 Inj levofloxacin 500mg OD
D4 Inj monocef 1gm iv BD
D2/3 Inj methyl prednisolone 500mg OD
Tab azaron (azathioprine)150mg OD
Inj neostigmine 0.5mg TDS
Inj atropine 0.6mg before neostigmine
Tab pyridostigmine 60mg OD
Tab shelcal 500mg BD
21. S/B Lecturer nephrology at
30/07/2016
c/o myasthenia gravis in
myasthenic crisis
Intubated yesterday in
view of poor respiratory
efforts
P – 80 bpm
BP - 110/70 mm of Hg
B/L AEBE
Concious oriented / moves
limb on command
Advice
Plasmapheresis today
Arrange 5 @ FFP
Send patient with accompanying
resident doctors by12.30PM
High risk plasmapheresis
explained to relatives
Sr Ca+ -9.8mg/dL
Sr Mg+ -1.97mg/dL
Sr Na+ -137mEq/L
Sr K+ - 2.6mEq/L
22. S/B SP ↓ 6 at 30/07/2016 at 2 PM
GC- not stable on ventilator
Conscious afebrile
P – 78 bpm
B/L Clear
HS – normal
Treatment
↑↑Tab pyridostigmine 60 mg QID
Rest ct all
Investigation
Sr urea -14mg/dL
Sr creat – 0.7mg/dL
T protein – 5.3gm%
T Bilirubin – 0.7mg%
ALP - 44 IU/L
SGOT – 40 IU/L
SGPT – 13 IU/L
23. S/B Lecturer ↓ Nephrology on
30/07/2016 - Plasmapheresis - 3
c/o myasthenia gravis currently in
crisis on ventilatory support
plasmapheresis 3rd today
No spontaneous breathing on
Intermittent Positive Pressure
Ventilation
Advice
2 litre exchange
5 FFP
2 @ RL
1 @ NS
Inj calcium gluconate 10 cc post
plasmapheresis
Post plasmapheresis – there was
spontaneous trigerring on
ventilator
Advice
PT/INR , Sr electrolytes
Tensilon (edrophonium challenge
test)
Plan for IVIg
Would offer plasamapheresis on
Monday with 5@ FFP &
accompanying medicine resident
@ 10 AM
24. S/B Registrar ↓ ICCU / SP ↓ 2 on
31/07/2016 at 8 AM
Patient on ventilator
GC – moderate
Afebrile
P – 82 bpm
BP – 120/80 mm of Hg
U/O – 1200ml
RS – clear
P/A – soft non tender
CVS – S1S2
CNS – conscious oriented
Treatment
D2 inj levofloxacin 500mg OD
D5 inj monocef 1gm BD
D3/3 inj methylprednisolone 500mg OD
Tab azoran 150mg OD
Inj pyridostigmine 60 mg QID
Inj neostigmine 0.5mg im SOS
Inj atropine 0.6mg SOS before inj
neostigmine
Tab shelcal 1 BD
PT/INR - 13/1.11
25. S/B registrar ↓ ICCU / SP ↓ 6 on
1/08/2016 at 8 AM
GC – not stable
Afebrile
P – 80 bpm
BP – 130/90 mm of Hg
U/O – 500ml
RS – clear
P/A – soft non tender
CVS – S1S2
CNS – NAD
SpO2 – 100%
Treatment
↓↓Inj pyridostigmine 60 mg
TDS
D3 inj levofloxacin 500mg OD
D6 inj monocef 1gm BD
Inj neostigmine 0.5mg im SOS
Inj atropine 2cc BD
Tab shelcal 1 BD
Tab azoran 150mg OD
26. Transfer notes 11PM at
01/08/2016
Here by transferring out this patient from ward 24 to
nephrology for plasmapheresis c/o myasthenia gravis with crisis
Treatment
Inj pyridostigmine 60 mg TDS
Inj neostigmine 0.5mg im SOS
Inj atropine 0.6mg SOS before inj neostigmine
D3 inj levofloxacin 500mg OD
D6 inj monocef 1gm BD
Tab azoran 150mg OD
27. S/B Lecturer ↓ Nephrology on
01/08/2016 Plasmapheresis - 4
c/o myasthenia gravis with crisis
BP – 120/ 80 mm of Hg
Advice
Plasmapheresis today
2 litre volume exchange
5 point FFP
2 point NS
2 point RL
Inj calcium gluconate …post plasma pheresis
28. S/B Registrar ↓ ICCU / SP ↓ 2 on
02/08/2016 at 8 AM
GC – not stable
Afebrile
P – 86 bpm
BP – 120/80 mm of Hg
U/O – 2000ml
SpO2 – 99%
RS – clear
CVS – S1S2
CNS – conscious oriented
Proximal muscle weakness +
Opthalmoplegia +
Treatment
Inj pyridostigmine 60 mg TDS
Inj neostigmine 0.5mg im SOS
Inj atropine 0.6mg SOS
before inj neostigmine
Inj rantac 50mg BD
D4 inj levofloxacin 500mg OD
D7 inj monocef 1gm BD
Tab shelcal 1 BD
Tab azoran 150mg OD
29. S/B SP ↓ 6/ SP ICCU at
02/08/2016 at 10 AM
GC – moderate
Conscious
Afebrile
P – 80bpm
Wt – 48 × 2 = 96gm
Advice
Plasmapheresis
Free T3 , T4 , TSH
Endocrinologist call
CVTS call
Treatment
Ct all
Inj IVIg 20gm/day × 5 days
-last day 15gm
30. 03/08/2016
To CVTS surgeon,
Sir /madam ,
kindly evaluate this patient c/o hypothyroidism with
myasthenia gravis with thymoma patient is not improving on
plasmapheresis . Kindly advice regarding thymectomy
Thanking you
S/B by Dr Ashish
Advice
Thymectomy only after GC – improves
31. S/B registrar ↓ ICCU / SP ↓ 6 on
03/08/2016 at 8 AM
Patient on ventilator
GC – not stable
Ventilatory support
Afebrile
P – 90 bpm
BP – 110/70 mm of Hg
RS – clear
P/A – soft non tender
CVS – S1S2
CNS – conscious oriented
Treatment
Inj pyridostigmine 60 mg TDS
Inj neostigmine 0.5mg im SOS
Inj atropine 0.6mg SOS before inj
neostigmine
D4 inj levofloxacin 500mg OD
D9 inj monocef 1gm BD
Tab shelcal 1 BD
Tab azoran 150mg OD
Plasmapheresis
Nephrologist reference
32. S/B Lecturer ↓ nephrology – 03/08/2016
Plasmapheresis – 5
C/O myasthenia gravis with crisis received 4 plasmapheresis
Advice
Send patient accompanying medicine resident with 5 @
Fresh Frozen Plasma
Plasma removal – 2 L
Replace with 5 Fresh Frozen Plasma
2 @ RL
33. S/B Registrar ↓ ICCU / SP ↓ 6 on
04/08/2016 at 8 AM
GC – not stable
Afebrile
P – 82 bpm
BP – 120/90 mm of Hg
SpO2 – 100% on Ventilatory
support
U/O – 1600ml
RS – clear
P/A – soft non tender
CVS – S1S2
CNS – conscious oriented
Treatment
Inj pyridostigmine 60 mg TDS
Inj neostigmine 0.5mg im SOS
Inj atropine 0.6mg SOS
before inj neostigmine
D5 inj levofloxacin 500mg OD
D10 inj monocef 1gm BD
Tab shelcal 1 BD
Tab azoran 150mg OD
Plasmapheresis
34. 04/08/2016 Recovery Room
To
MO/ Registrar
Anaesthesia on call
kindly call over to evaluate this patient a c/o
myasthenia gravis on ventilation not maintaining
saturation on A/C mode and opine expertise management
Thanking you
35. S/B Anaesthetist on 04/08/2016
C/O myasthenia gravis
Conscious oriented
Afebrile
P – 83 bpm
BP – 120/70 mm of Hg
RS – clear
CVS – S1S2
SpO2- 96%
Ventilation
Mode – NC/AC
RR - 16 cycles/min
Positive End Expiratory Pressure - 5
TN – 360
FiO2 -100%
Advice
Propped up
Ct ventilatory support
Ct all
36. S/B Registrar ↓ ICCU / SP ↓ 6 on
04/08/2016 at 8 AM
GC – not stable
Afebrile
P – 95 bpm
BP – 130/70 mm of Hg
SpO2 – 100% on Ventilatory
support
U/O – 1300ml
RS – clear
P/A – soft non tender
CVS – S1S2
CNS – conscious oriented
Treatment
Inj pyridostigmine 60 mg TDS
Inj neostigmine 0.5mg im SOS
Inj atropine 0.5cc before inj
neostigmine
D6 inj levofloxacin 500mg OD
D11 inj monocef 1gm BD
Tab shelcal 1 BD
Tab azoran 150mg OD
Tracheostomy tommorrow
37. 04/08/2016 at 1 AM
To ,
Medical officer / registrar
Anaesthesia on call,
kindly call over to evaluate this patient a c/o
myasthenia gravis on ventilation not maintaining
saturation on A/C mode and opine expertise management
thanks
38. 04/08/2016 at 1.05 AM S/B
Anaesthesiologist Registrar
A case of myasthenia gravis
Ventilation
Mode VC/AC
Rate – 16 cpm
PEEP – 5
T n – 360
FiO2 – 100%
O/E
Conscious oriented
Afebrile
P – 83 bpm
BP – 120/70 mm of Hg
CVS - NAD
SpO2 – 96%
Advice
Propped up
Ct all
39. Treatment on 05/08/2016 ,
06/08/2016 , 07/08/2016
08/08/2016 , same as on
04/08/2016
ENT reference was done on
06/08/2016 and
tracheostomy was done on
06/08/2016 under LA and
under all aseptic precautions
RT feeding was started on
08/08/2016 and diet
reference was done on same
day
40. S/B Registrar ↓ ICCU / SP ↓ 6 on
09/08/2016 at 8 AM
GC – moderate
Afebrile
P – 95 bpm
BP – 130/70 mm of Hg
SpO2 – 100% on Ventilatory
support
U/O – 1000ml
RS – clear
P/A – soft non tender
CVS – S1S2
CNS – conscious oriented
Treatment
D1 Inj piptaz 4.5 gm TDS
Inj pyridostigmine 80 mg QID
D10 inj levofloxacin 500mg OD
Inj neostigmine 0.5mg im SOS
Inj atropine 0.6cc before inj neostigmine
D11 inj monocef 1gm BD
Tab shelcal 1 BD
Tab azoran 150mg OD
IVF – 2 point NS
Inj pantop 40mg OD
Inj emset 4 mg TDS
41. 09/08/2016 AT 9.30 AM S/B
Senior Physician ↓ 6
GC – moderate
Afebrile
P – 90 bpm
Chest – clear
Tracheostomy tube in situ
P/A – soft
Treatment
Inj Amino drip OD
Protein powder
Inj wymesone (dexamethasone) 4 mg
8hrly
Tab Azoran 150mg OD
D2 Inj piptaz 4.5 gm TDS
D10 Inj levofloxacin 500mg OD
Tab pyridostigmine 60mg TDS
Inj emset 4 mg TDS
42. 10/08/2016 to
18/08/2016
Treatment was same
as on 09/08/2016
Except
12/08/2016 tracheal culture & sensitivity
pseudomonas grown
R – amikacin , aztreonam , cefepime ,
ceftazidime , gentamicin , imipenem ,
piperacillin
S – polymyxin B
Day 17 Inj Levofloxacin was stopped on
16/08/2016
17/08/2016 bladder clamping and bladder
wash started tracheostomy dressing
changed
43. S/B Neurologist on 18/08/2016
25yrs /F
Patient diagnosed case of myasthenia
gravis { AChR antibody - +ve}
h/o diplopia / weakness of all 4 limbs
since 1year
O/E
Pt intubated on mechanical ventilation
SIMV mode with SpO2- 96%
Occular movements are normal
Neck weakness - +
Power – grade 4 in all 4 limbs
DTR – 2+
Plantar – b/l ↓
Pt received plasmapheresis 5
cycles
Received IVIg 5 days (2gm/kg)
Patient improving according history
Advice
Ct tab pyridostigmine 60mg TDS
Ct tab dexamethasone 4mg TDS
Ct tab azoran 150mg OD
Can be considered for repeat IVIg
after 1month if relapse occurs or
difficulty to wean situation
44. S/B Registrar ↓ ICCU / SP ↓ 6 on
19/08/2016 at 8 AM
GC – moderate
Afebrile
P – 80 bpm
BP – 130/80 mm of Hg
SpO2 – 98% on Ventilatory
support
U/O – 800ml
RS – clear
P/A – soft non tender
CVS – S1S2
CNS – conscious oriented
Treatment
Amino drip alternate day
D11 Inj piptaz 4.5 gm TDS
Inj wymesone 4mg TDS
Inj atropine 0.6cc BD
Tab pyridostigmine 60 mg TDS
Tab azoran 150mg OD
Inj pantop 40mg OD
45. 20/08/2016 same as on
19/08/2016
21/08/2016 same as on
20/08/2016
22/08/2016 ,
23/08/2016 same as on
21/08/2016
Augmentin was started
and piptaz was stopped on
20/08/2016
Nebulisation with
mucomix was added on
21/08/2016
46. Patient was discharged on 16/09/2016
on following medicines
Tab levofloxacin 0.5gm BD
Tab predmet 16 mg TDS
Tab distinus (pyridostigmine) 60mg TDS
Tab azoran 150mg BD
Protein biscuits
Follow up after 15 days for work up of thymectomy
49. Myasthenia Gravis
Neuromuscular disorder characterized by weakness and
fatigability of skeletal muscles
Underlying defect - ↓ in number of available acetylcholine
receptors (AChRs) at neuromuscular junctions due to an
antibody-mediated autoimmune attack
Myasthenic crisis - Severe weakness of bulbar (innervated
by cranial nerves) and/or Respiratory muscles, enough to
cause inability to maintain adequate ventilation and/or
permeability of upper airways, causing respiratory failure
that requires artificial airway or ventilator support
52. Rationality
Anticholinesterase medication
Inj neostigmine 0.5mg BD
Tab /Inj pyridostigmine 60 mg TDS
Use – rational
Improve muscle contraction - Ach released from
prejunctional endings to accumulate and act on
receptors over a larger area, as well as by directly
depolarizing endplate
Whether combination can be used is not given in any
text book
54. Corticosteroids /
Immunosuppresion
Inj methyl prednisolone 15- 25mg /day in single dose
to avoid side effects
Use – Rational
Inhibit production of Nicotinic Receptor (NR)-
antibodies & may ↑ synthesis of NRs
Dose ↑ stepwise - by 5 mg/d at 2- to 3-day intervals →
marked Clinical improvement or dose of 50 - 60 mg/d
reached
This dose maintained for 1 - 3months
Alternate-day regimen over course of 1 -3 months
Goal is to ↓ dose on off day to zero or to minimal level
55. Rationality
Tab azathioprine 50mg OD
Use – Rational
Previously most commonly used immunosuppressive
agent because of its
Relative safety
Long track record
Therapeutic effect may add to glucocorticoids
effect &/or allow glucocorticoid dose to ↓
56. Rationality
Plasmapheresis
Use – rational
Plasma contains pathogenic antibodies, is
mechanically separated from blood cells
Course of 5 exchanges (3 - 4 L per exchange) -
Over 10 to 14 day period
Advantages in Our set up – Comparatively
inexpensive to IVIg but requires expertise
57. Rationality
Intravenous immunoglobulins
Use – rational
Advantage
Doesn’t require special equipment & Large-bore venous
access
Ease of administration
Disadvantage – expensive
Usual dose is 2 g/kg - over 5 days (400 mg/kg per
day)
58. Rationality
Antibiotics
Inj ceftriaxone 1gm iv BD
Inj levofloxacin 0.5gm iv BD
Inj piperacillin tazobactum 4.5 gm TDS
Cap amoxicillin clavulunate 625mg BD
Use – rational
Most common cause of crisis is intercurrent
infection
59. Rationality
Tab thyroxine 100µg OD
Use – rational
Hypothyroidism
Inj KCl 10-20meq/hr
Use – rational
To treat hypokalemia
Inj calcium gluconate 90mg iv over 10 min post plasma pheresis
Use – rational
To treat hypocalcemia associated with plasmapheresis
60. Not rational
Prednisolone dose on admission should have been
increased
Brand names were used
Respiratory secretions – culture and sensitivity was
done late
Instead of ceftriaxone they could have used
ceftazidime and cefoperazone
61. Not rational
Culture and sensitivity of drugs given was not
done
Urine & blood culture & sensitivity was not
done
At some places doses and route of
administration were missing
63. Management of myasthenic crisis
exacerbation of weakness sufficient to endanger life (usually
consists of respiratory failure caused by diaphragmatic &
intercostal muscle weakness)
Crisis rarely occurs in properly managed patients
Intensive care units staffed with teams experienced in the
management of MG, respiratory insufficiency, infectious disease,
fluid & electrolyte therapy
Deterioration could be due to excessive anticholinesterase
medication (cholinergic crisis) - best excluded by temporarily
stopping anticholinesterase drugs
64. most common cause of crisis is intercurrent infection
This should be treated immediately, because the mechanical and
immu-nologic defenses of the patient can be assumed to be
compromised.
The myasthenic patient with fever & early infection should be
treated like other immunocompromised patients.
Early & effective antibiotic therapy, respiratory assistance
(preferably noninvasive, using bilevel positive airway pressure), &
pulmonary physiotherapy are essentials of the treatment program
As discussed above plasmapheresis or IVIg is frequently helpful
in hastening recovery