sudar hosp

Dear IMACGP Team
Tuticorin
25.10.2020
Warm Greetings,


Family Doctors are the Backbone of Healthcare Delivery system of any Nation more so for a
Developing Nation like India. Strengthening Primary care is the need of the Home. Universal Health

coverage is built on Primary care only.


To strengthen Primary care, Indian Medical Association formed IMA college of General Practitioners
in the year 1963.


IMACGP grew strategically in strength & created good number of Qualified Family Physicians in our

Country. In 2007 IMACGP Head Quarters was shifted to Chennai for further Growth.


To educate the actively practicing Family Physicians, IMACGP created a blended learning system on
virtual class room with IMA evarsity, which is the hall mark of Academic Growth of IMACGP. Many

Family Physicians of India got updated their knowledge & skills Through “ IMA Evarsity”


I am happy to learn IMACGP is coming out a E Journal during the Digital GPICON 2020.


When Dr.PC Bhatla was the founder Dean, he brought out a CME Booklet and when I took over as
Dean published, Family Medicine India


Today is Digital Era & I am confident Digital IMACGP Journal will connect the Primary care
Physicians of India and also South Asia Region.


Wishing IMACGP a Continued Growth towards UHC.








Best Wishes

Prof.Dr.Arulrhaj
Past National President, IMA National President API
Past Dean, IMACGP Past Commonwealth President CMA, UK

To


Dr. Hiranmay Adhikari

Dean, IMA College of GP

HQ Chennai


I am elated to applaud and congratulate the team of officers of our IMA
college of General practitioner under your headship and the dynamic
stewardship of Dr.Yasodha ,for the pain taken to lead our much awaited

National conference amidst the Corona Pandemic.

I was confident of your poignant passion and unquenchable hunger for
quintessence of unity and persuasiveness in upbringing the bliss and ecstasy of
our wing and delighted to greet you for your mighty accomplishment on this

blessed day.

The rejuvenating, invigorating and revivifying 2019-20 led with sally forth
and overhaul of incredulous sardine hiccoughs due to corona by your salmon

shine virtues, along with the vigilant headful of past leaders was a year to be
reminisced as a scintillating pageant ,and symbiosing unity in every bit of events
and meet, flamboyantly the family convenes .


The tone of expectations on your tenure was attire to soprano and I am
happy today with your team of adept, proficient teammates and rock-solid
handholding of all of us as elders you have made a golden era in the conquering
epitomes of the annals of our IMA CGP. The unique achievement of creating the

State faculty unit in Manipur, Publishing the Journal of CME by Assam IMA,
enhancement of membership in North east and your unique interactive Zonal
meets are praiseworthy jewels on your crown.


I fully endorse and appreciate our loving and affectionate secretary for
her immaculate perfection, blissful personal interactions with members, and
homely atmosphere stemmed by her affectionate gesticulations in the college,


Sustain the umbilical cord with state HQ and National HQ and ensure
every one of us feel happy.

Yours in IMA service

Dear Dr. Yesodha,




I am glad to know that you are organizing the virtual National

Conference of IMA CGP on 8th November 2020. Despite all odds

and difficulties created by COVID 19, you and your dynamic team

continuously organized several scienti c programs throughout the

pandemic.





I congratulate your team for the same and wish you all the best.
I


During my one year tenure as a Dean of IMA CGP we together

worked hard to spread the activities of CGP in northern states,

where the branches are not very active. I am very hopeful that

coming teams will also concentrate on the same. There is also a

r requirement to strengthen the research atmosphere among the

general practitioners, which we had a plan but couldn’t start

during my tenure. Hopefully it can also be taken up further.




Best wishes

COVID-19 IN CHILDRENS AND TEENS

Age Group:- Kids and teens (0-18 years) are less prone to disease. They become
asymptomatic carrier. There is less severing an fatality in this pandemic age group.
Usually kids and Teens are rare infective but certain under medical condition the illness may
be severe in nature.
Medical Conditions:-
 Asthma or chronic lung disease.  Weak immunity due to same medical
 Diabetes. conditions.
 Genetic, neurological or metabolic conditions.  Medical complexity.
 Heart disease since birth.  Obesity.
Symptoms:-
 Fever (100.4°F or higher).  Nausea or vomiting.
 Cough, sore throat.  Stomachache.
 Nasal congestion or running nose.  Tiredness, Headache
 Loss of taste or smell.  Muscle or body aches.
 Sore throat.  Poor appetite or poor feeding, especially in
 Shortness of breath or difficulty in breathing. babies under 1 year.
 Diarrhea.
Treatment plan:-
(A) If your child is asymptomatic but positive. Then you cure at home with rest. Take proper
consultation with your doctor and take care of (him/her).
 If you keep child at home.
(then)
 Keep other people, pets in the house away from your child.
 Try to have only one person care for the sick child.
 Provide them separate washroom.
 If the child is above 2 years, provide then mask (but don’t leave there alone).
 Use proper sanitization of doors, knobs & floor.
 Wash hands atleast for 20 sec.
(B) Some kids are having symptoms caused by inflammation through out the body, sometime after
several weak they were infected with virus called.
MULTI SYSTEM – INFLAMMATORY – SYNDROME
(In childhood) (MIS-C)
 Fever, belly pain.
 Vomiting, diarrhea
 Neck pain, rash, red eyes.
 Swollen hands, feats
 Swollen lymph nodes.
In this condition for better care they will shift to I.C.U. or special care in hospitals.
Prevention
As we all know prevention is always better than cure:-
 Wash hands
 Cover cough and sneezes.
 Avoid contact with other people those who are sick.
 Make sure kids get all recommended vaccinations like flue, measles etc.


Dr. Ravindra Singh Bhadhoria
M.B.B.S., D.C.H.
Secretary- IMACGP (U.P.)
E-mail: [email protected]

IMAGING IN COVID-19



DR.G.M.Vignesh Krishna.,MD.RD.,

Consultant Radiologist
Indian Scan, Chennai


INTRODUCTION TO COVID-19
 The official name of the illness is COVID-19 (a shortening of COronaVIrus Disease-

2019) and it is caused by the "severe acute respiratory syndrome coronavirus 2"

(SARS-CoV-2).
 WHO announced COVID-19 outbreak as a pandemic on 11 March 2020.
 As of October 2020, the number of confirmed case of COVID-19 globally is nearly 40

million affecting almost every territory and the number of deaths from COVID-19
exceeds 1.1 million globally.

 COVID-19 can either be symptomatic or asymptomatic. Symptoms can be systemic
and/or limited to respiratory system. Common symptoms are fever, anosmia, cough,

fatigue, sputum production and shortness of breath.
 Some also experience mild gastrointestinal or cardiovascular symptoms, although

these are less common.

RADIOLOGICAL FEATURES OF COVID-19

 Chest X-Rays are of less diagnostic value in initial stages, whereas CT findings may be
present even before the onset of symptom.

 Chest X-Ray may show diffuse bilateral coalescent opacities in the intermediate to

advanced stages of the disease.
 The characteristic patterns of COVID-19 on CT imaging are ground glass opacification
(GGO), airspace opacities, crazy paving pattern, vascular dilatation, traction

bronchiectasis and subpleural bands.
 The involvement is predominantly bilateral, peripheral distribution and multilobar

(more than one lobe).
 In majority of the affected patients, involvement of multiple lobes, particularly the

lower lobes with a peripheral or posterior distribution (or both) were reported.
 Bilateral lung involvement with a consolidative pattern is reported in patients with

moderate-severe symptoms and a predominantly ground-glass pattern is reported in
patients with mild symptoms.

Mild Moderate Severe


 Although chest CT has demonstrated high sensitivity along with RT-PCR testing for
COVID-19 diagnosis, it may not reveal distinct patterns for COVID-19 in all cases. This
can make it hard to distinguish COVID-19 from other causes of viral pneumonia.

For example, Influenza and COVID-19 both demonstrate GGO and consolidation on
chest CT.

 These imaging features also closely resemble those of MERS and SARS but bilateral
lung involvement on initial imaging is more likely to be seen with COVID-19.

 Pleural effusion, pleural thickening, pericardial effusion, lymphadenopathy,
cavitation, CT halo sign, and pneumothorax were less common.

 The severity of the lung involvement on the CT correlates with the severity of the
disease/symptoms.
 Visual assessment - the severity on CT can be estimated by gross visual assessment.

 Severity score - another method is by scoring the percentages of each of the five

lobes that is involved from 0-5. The total CT score is the sum of the individual lobar
scores and can range from 0 (no involvement) to 25 (maximum involvement). Another
variation of this scoring is based on individual segmental involvement (maximum 40).

 Few reports have however stated that in about 15% of individuals, initial imaging
might show normal findings, so a normal chest imaging does not exclude the

infection.
 In some cases with an initial false-negative reverse transcription polymerase chain

reaction (RT-PCR) screening test, CT findings have proven to be diagnostic.
 A combination of chest CT and repeat laboratory testing may be beneficial for COVID-

19 diagnosis in the setting of strong clinical suspicion, including individuals showing
typical clinical manifestations and those with a history of exposure.

UPDATE ANSWERING THE QUIZ




1. HbA1c measurement may be affected by all the following EXCEPT

a) Iron deficiency anaemia

b) Haemolytic anaemia

c) Insulin administration prior to the test

d) Sickle cell anaemia

e) Massive haemorrhage
2. Regarding calcium channel blockers, all are true except..

a) LV Function should be assessed periodically.

b) Diltiazm is contra indicated in LV Dysfunction.

c) Better to combine DHP CCB with Beta blockers

d) Short acting Nifidipine is good in emergencies.


3. The differential diagnosis of fever with thrombocytopenia include all the following
except
a) Septicemia with DIC
b) Dengue
c) Bacterial endocarditic
d) Scrub Typhus
e) Leptospirosis

4. Which of the following viral infections can cause cirrhosis?

a) Hepatitis A
b) Hepatitis B
c) Hepatitis C
d) Hepatitis E


5. Acute Viral Hepatitis E is diagnosed by which of the following?
a) Anti HEV IgG
b) Anti HBcTotal
c) Anti HBs
d) Anti HEV IgM

6. What are tests to be sent when a HBsAg positive person comes with jaundice?
a) HBV DNA viral load
b) Anti Hbc Total
c) Anti HBc IgM
d) HBeAg
e) Anti HEV IgM


7. Which of the following tests indicate acute viral hepatitis B?

a) HBV DNA viral load
b) Anti Hbc Total
c) Anti HBc IgM
d) HBeAg
e) Anti HEV IgM


8. 40 /m ,Asymptomatic ,comes with a positive AntiHBS result? What are the
possibilities?

a) Vaccinated for Hepatitis B
b) Cleared previous infection with HBsAg in the past
c) Active infection with Hepatitis B

Epilepsy care in India





Introduction

Epilepsy, a neurological disorder, is associated with significantly adverse cognitive, psychological,
and social consequences. A major share of the global health burden of epilepsy (80%) is borne by the
1
developing world. A meta-analysis showed that the median lifetime epilepsy prevalence in
developed countries was 5.8 per 1,000, as compared to 15.4 per 1,000 for rural and 10.3 for urban
2
studies in developing countries. The burden of epilepsy in India has been projected to be more than
3
10 million persons. However, there will be a deviation in the estimates from the actual burden
owing to the higher burden of untreated epilepsy, especially in rural areas. Epilepsy is under-
reported as subjects fail to seek medical attention, perhaps due to stigma, beliefs, and negative
public attitudes about the causes and consequences of epilepsy and limited access to health
services. In the milieu of an epilepsy treatment gap owing to the cost of antiepileptic drug
treatment, neurologists face the problem of treatment discontinuation. Conventional antiepileptic
drugs (AED) are apparently a cost-effective option for the initial treatment of epilepsy.



Challenges related to epilepsy in India

In India, managing people with epilepsy is a herculean task considering the impact of epilepsy on the
triad of patient, family/caretaker, and the healthcare provider. Overcoming issues associated with
each component of the triad is important for achieving treatment goals and reducing the overall
burden of epilepsy.

Issues in practice

Neurologists face a set of issues in delivering accurate diagnosis and appropriate treatment to
people with epilepsy.
1
• Limited availability of video/electroencephalogram (EEG) monitoring and sophisticated
neuroimaging
• Neurologist to patient ratio is low and therefore time given for each patient is less
• Wide prevalence of risk factors for nonepileptic seizures (alcoholism, unemployment,
depression, political instability, and domestic and social violence)
• Improper description of the signs and symptoms during a seizure
• Cost and availability of antiepileptic medication
• Suboptimal seizure control due to improper dosing of AEDs
• Side effects of AEDs
• Lack of facilities for therapeutic monitoring of drug serum levels

Social stigma
Epilepsy is associated with a social stigma that is deeply rooted in society and within the individual at
4
three different levels (internalized, interpersonal, and institutional).
• Internalized stigma relates to the negative attitude that develops within the person with
epilepsy. It reflects his thoughts, beliefs, and fear of being different from others.

• Interpersonal stigma arises when the person with epilepsy interacts with and reacts to the
other people in society. Compared to the general population, more than one-fifth of people
with epilepsy have personality problems.
• Institutional stigma represents the collective stand taken against all people with epilepsy,
which brings forth legal implications. In most countries, people with epilepsy have
restrictions in driving a vehicle.

Most often people with epilepsy are deprived of education, job opportunities, marriage, and a social
life. Owing to the unpredictable nature of epilepsy, it is viewed as a supernatural ailment caused by
5
evil spirits. Many commonly held supernatural beliefs and the adverse outcomes of such beliefs
1,3
contribute to the morbidity and mortality of epilepsy.
Economic impact of epilepsy
Epilepsy is a life-long problem. Epilepsy causes significant socioeconomic burden at individual,
family, health services, and societal levels. No direct data are available confirming the economic
impact of epilepsy. However, the treatment cost of epilepsy is classified as either tangible or
3
intangible (Box 1). Thomas et al, reported the direct and the indirect costs of treatment as 27.1 and
6
72.9% of the total cost, respectively.
Box 1. Treatment cost
Tangible costs Intangible costs
Direct costs Indirect costs
Cost of: Costs attributed to: Cost attributed to:
• Hospitalization • Loss of time and • Pain
• Treatment productivity • Mental suffering
• Medicines • Income lost by family • Social stigma
• Homecare members
• Ancillary services • Foregone leisure time

Treatment gap

Despite the availability of newer and better antiepileptic drugs, neurologists observe a significant
gap in the treatment of epliepsy. The epilepsy treatment gap refers to the proportion of people with
7
epilepsy who require treatment but do not receive it. The treatment gap in epilepsy results due to
status epilepticus, death,
stigma, loss of quality of life,
Figure 1. Reasons for drug discontinuation
and social alienation. There is a
100
dramatic global disparity in the 90
90
care for epilepsy between high- 80
and low-income countries, and 70
between rural and urban 60
settings. In India, treatment People with epilepsy (%) 50
gaps ranged from 22% in an 40
urban middle-income 30 21 20 21
population to 90% in a sample 20 10
10
7
of rural villages. The main
0
causes of the epilepsy Treatment cost Unemployment Frustration Lack of Marital
treatment gap are availability, medicines disharmony

accessibility, affordability, and awareness of treatment. In India, treatment cost (non-affordability) is
8
the leading reason for the epilepsy treatment gap (Figure 1). Therefore, it is important to ensure
that the treatment plan is simple and cost-effective.



Conventional AEDs are cost-effective for initial monotherapy
The global burden of epilepsy could be reduced by 36% if 80% of the epilepsy population were
9
treated with cost-effective AEDs. As found by a study, there are no significant differences in
treatment benefits, but newer AEDs are more expensive as monotherapy for newly diagnosed
10
patients with partial seizures than conventional AEDs. Conventional first-line AEDs are phenytoin,
phenobarbitone, carbamazepine, and valproate. Among them, phenytoin and phenobarbitone are
more cost-effective than carbamazepine and valproate. The most efficient strategy for reducing the
11
burden of epilepsy in developing regions is the use of phenobarbitone or phenytoin. Indian
guidelines recommend monotherapy with conventional AEDs for initial treatment; and other AEDs
as monotherapy or a combination if the subject is non-responsive to initial treatment. Compared to
the newer AEDs, the side-effect profiles of older conventional AEDs are well-established.

Phenytoin: A cost-effective option
Phenytoin is commonly used for all age groups and all seizure types except generalized absence and
1
myoclonic seizures and spasms. Phenytoin carries a relatively lower risk of respiratory or cerebral
depression and does not cause tachyphylaxis. It has a prolonged action. However, the
pharmacokinetic profile of the drug mandates therapeutic drug monitoring. Usually patients achieve
total control of seizure at lower doses itself. Subjects tolerate the drug well in the long term and
12
rarely need to change the medication.
A meta-analysis found no significant differences in efficacy between phenytoin and phenobarbitone,
but people with epilepsy were more compliant with phenytoin than phenobarbitone; perhaps owing
to the high rate of adverse effects with phenobarbitone. The time to treatment withdrawal was in
13
favour of phenytoin (hazard ratio of 1.62 (1.23 to 2.14). The relative advantage of phenytoin over
other AEDs is attributed to its lower cost, lower withdrawal rates, and comparable efficacy with
other conventional AEDs. 11,13–15 Phenytoin is safe for use in elderly people with comorbid
16
conditions. Hence, phenytoin can be an ideal AED in a setting like India, where the high cost of
epilepsy treatment causes a substantial treatment gap..


Summary

Epilepsy is a neurological disorder that has serious implications to both the patients and their
caretakers. Diagnosing and treating patients with epilepsy are a challenge to neurologists in the
limited framework of the available medical care and facilities. People with epilepsy are discriminated
in all walks of life, which causes serious repercussions to themselves and their families. Being a life-
long problem, epilepsy causes a significant socioeconomic burden at individual, family, health
services, and societal levels. Also, the epilepsy treatment gap is a significant problem that can result
in status epilepticus, death, stigma, loss of quality of life, and social alienation. In India, high
treatment cost is the main contributing factor to the epilepsy treatment gap. Conventional first-line
AEDs (phenytoin, phenobarbitone, carbamazepine, and valproate) are more cost-effective than
newer AEDs. Indian guidelines recommend monotherapy with conventional AEDs for initial

treatment, and other AEDs as monotherapy or combination if the subject is non-responsive to initial
treatment. Therefore, the most efficient strategy for reducing the burden of epilepsy in developing
regions is the use of phenobarbitone or phenytoin.

References
1. World Federation of Neurology .Epilepsy: Global issues for the practicing neurologist. Available from
http://www.wfneurology.org/cache/downloads/dgyqpc1861skokcgo8kwgg4ww/wfn_demos_epileps
y.pdf Accessed on: June 2, 2014.
2. Ngugi AK, Bottomley C, Kleinschmidt I, et al. Estimation of the burden of active and life-time epilepsy:
A meta-analytic approach. Epilepsia. 2010;51(5):883–90.
3. Tripathi M, Jain DC, M. Devi G, et al. Need for a national epilepsy control program. Ann Indian Acad
Neurol. 2012;15(2):89–93.
4. Jacoby A, Austin JK. Social stigma for adults and children with epilepsy. Epilepsia. 2007;48 Suppl 9:6-9.
5. Lim YJ, Chan SY, Ko Y. Stigma and health-related quality of life in Asian adults with epilepsy. Epilepsy
Res. 2009 Dec;87(2-3):107–19.
6. Thomas SV, Sarma PS, Alexander M, et al. Economic burden of epilepsy in India. Epilepsia.
2001;42:1052–60.
7. Meyer A-C, Dua T, Ma J, et al. Global disparities in the epilepsy treatment gap: A systematic review.
Bull World Health Organ. 2010;88:260–266.
8. Mani KS, Rangan G, Srinivas HV, et al. The Yelandur study: A community-based approach to epilepsy in
rural South India--epidemiological aspects. Seizure. 1998 Aug; 7(4):281–8. Cross reference: Tripathi
M, Jain DC, M. Devi G, et al. Need for a national epilepsy control program. Ann Indian Acad Neurol.
2012;15(2):89–93.
9. Neligana A, Sander JW. The treatment gap in epilepsy: A global perspective. Epileptology.
2013;1(1):28–30.
10. Wilby J, Kainth A, Hawkins N, et al. Clinical effectiveness, tolerability and cost-effectiveness of newer
drugs for epilepsy in adults: A systematic review and economic evaluation. Health Technol Assess.
2005 Apr;9(15):1–157, iii–iv.
11. Chisholm D; WHO-CHOICE. Cost-effectiveness of first-line antiepileptic drug treatments in the
developing world: A population-level analysis. Epilepsia. 2005 May;46(5):751–9.
rd
12. Shorvon SD. Handbook of epilepsy treatment. 3 Edition. November 2010, Wiley-Blackwell:UK.
13. Nolan SJ, Tudur Smith C, Pulman J, Marson AG. Phenobarbitone versus phenytoin monotherapy for
partial onset seizures and generalised onset tonic-clonic seizures. Cochrane Database of Systematic
Reviews 2013, Issue 1. Art. No.: CD002217. DOI: 0.1002/14651858.CD002217.pub2.
14. Nolan SJ, Marson AG, Pulman J, et al. Phenytoin versus valproate monotherapy for partial onset
seizures and generalised onset tonic-clonic seizures. Cochrane Database Syst Rev. 2013 Aug
23;8:CD001769. doi: 10.1002/14651858.CD001769.pub2
15. Nolan SJ, Muller M, Tudur Smith C, et al. Oxcarbazepine versus phenytoin monotherapy for epilepsy.
Cochrane Database Syst Rev. 2013 May 31;5:CD003615. doi: 10.1002/14651858.CD003615.pub3.
16. MK Roy, Das D. Indian guidelines on epilepsy. Available from
http://www.apiindia.org/medicine_update_2013/chap116.pdf Accessed on June 3 2014

Clinical acuity: Gastroscopy


Melena and fainting in an elderly

patient with CAD





A 66-year-old man presented to the clinic with chief complaints of giddiness, fainting, and black
colored stool. His medical history revealed that he had coronary artery disease (CAD) and that he
was taking aspirin.



What is the clinical diagnosis?
Melena, history of CAD, and low-dose acetyl salicyclic acid (LDASA) prescription is indicative of
gastrointestinal (GI) bleeding.

Further probes into medical history, physical examination, laboratory tests, and in some cases,
nasogastric lavage will give vital clues.

• Watch for vital signs and other indicators of shock or hypovolemia (eg, tachycardia,
tachypnea, pallor, diaphoresis, oliguria, confusion) and anemia (eg, pallor, diaphoresis).
• Abdominal examination might reveal tenderness and pain in the abdomen.
• A digital rectal examination is necessary to examine for stool color, masses, and fissures.
• Melena is mostly related to upper GI bleed (100 to 200 mL), but can occur as a result of
bleeding from the small bowel or right colon.
• A positive fecal occult blood test and low hemoglobin level are indicative of blood loss.
Hematochezia (passage of gross blood from the rectum) is indicative of lower GI bleeding or
vigorous upper GI bleeding with rapid transit of blood through the intestines.


Gastroscopy or endoscopy aids in assessing the severity and
Figure 1. Endoscopy of the upper
source of bleeding in the GI tract. Additional information on gastrointestinal tract
chronic abuse of nonsteroidal anti-inflammatory drugs
(NSAIDs) is vital.

What were the gastroscopic findings??
The endoscopy showed large prepyloric ulcers with bleeding.


For all suspected cases of upper gastrointestinal bleeding,
esophagogastroduodenoscopy is the routine diagnostic tool.
Colonoscopy is indicated for acute lower gastrointestinal
bleeding.
What treatment should be prescribed?

Endoscopic sclerotherapy is a well-established treatment for
bleeding GI varices.

Crafoord and Frenckner pioneered the concept of sclerotherapy in 1939. Endoscopic sclerotherapy
accomplishes vascular obliteration by the injection of a sclerosing agent. Injection sclerotherapy is a
low-cost, effective, and safe procedure. This procedure can be carried out in most clinical settings.



Discussion
LDASA (low-dose aspirin), as antiplatelet therapy, is the mainstay of secondary prevention following
1
2
myocardial infarction (MI) or stroke. LDASA reduces the risk of MI by about 25%–30%. LDASA
2
prevents 4 MIs per 1,000 persons treated per year. Aspirin has been associated with GI injuries,
1
especially peptic ulcer bleeding. LDASA increases the risk for gastroduodenal ulcer by 2- to 4-folds.
Occurrence of upper GI symptoms negatively affect patients’ adherence to daily LDASA. One-fourth
3
of the patients fail to adhere to LDASA therapy on the same day of occurrence of GI symptoms.
Nevertheless, discontinuation of aspirin may precipitate cardiovascular and cerebrovascular events.
Upper GI bleeding associated with antiplatelet therapy can be reduced by suppressing gastric acid
production. Therefore, in patients with high risk for peptic ulcers, adverse GI symptoms can be
prevented by a co-prescription of antisecretory agents such as proton pump inhibitors (PPIs) or
4
histamine H2 receptor antagonists (H2RA). Suppression of acid production promotes healing of
peptic ulcer and mucosal erosions and stabilizes the thrombi. Observational data suggest PPIs may
be more effective than H2RAs in preventing upper GI bleeding. The ACCF/ACG/AHA 2010 Expert
Consensus (American College of Cardiology Foundation [ACCF], the American College of

Gastroenterology [ACG], and the American Heart Association [AHA]) recommends the use of
PPIs: 4

 To reduce GI bleeding among patients with a history of upper GI bleeding

 In patients with multiple risk factors for GI bleeding who require antiplatelet therapy


PPIs demonstrated: 4

 A 50% reduction in baseline antiplatelet therapy related gastroduodenal bleeding risk

 Absolute risk reduction of GI bleeding of 2.8% per year among patients with ≥3 risk factors
for GI bleeding

Esomeprazole, a PPI, was effective in preventing and resolving patient-reported upper GI symptoms
5
in LDASA users who were at increased GI risk. Treatment with esomeprazole (20 or 40 mg for 26
weeks) significantly reduced the cumulative proportion of patients developing peptic ulcers.
Incidence of peptic ulcer were 1.5%, 1.1%, and 7.4% respectively for esomeprazole 20 mg, 40 mg,
and placebo. 5

Patients with GI bleeding are at increased of recurrent bleeding. PPIs, by virtue of their gastric acid
inhibition, improve therapeutic outcomes after endoscopic treatment of ulcers. Initiation of PPIs
6
after endoscopic diagnosis of peptic ulcer bleeding significantly reduces the risk of re-bleeding. In a
study, addition of PPI to combination injection sclerotherapy decreased the rate of recurrent
bleeding, reduced the need for surgery and transfusion, and shortened the hospital stay for patients
7
with stigmata of recent hemorrhage. The strategy of giving oral PPIs, both before and after
endoscopy, with endoscopic hemostatic therapy is proven to be cost-effective. 6

References
1. Cayla G1, Collet JP, Silvain J, et al. Prevalence and clinical impact of upper gastrointestinal symptoms in subjects
treated with low dose aspirin: The UGLA survey. Int J Cardiol. 2012 Apr 5;156(1):69–75.
2. 2. Hernández-Díaz S Rodríguez LAG. Cardioprotective aspirin users and their excess risk of upper gastrointestinal
complications. BMC Medicine. 2006, 4:22 doi:10.1186/1741-7015-4-22.
3. Pratt S, Thompson VJ, Elkin EP. The impact of upper gastrointestinal symptoms on nonadherence to, and
discontinuation of, low-dose acetylsalicylic acid in patients with cardiovascular risk. Am J Cardiovasc Drugs.
2010;10(5):281–88.
4. ACCF/ACG/AHA 2010 Expert Consensus Document on the Concomitant Use of Proton Pump Inhibitors and
Thienopyridines: A Focused Update of the ACCF/ACG/AHA2008 Expert Consensus Document on Reducing the
Gastrointestinal Risks of Antiplatelet Therapy and NSAID Use. JACC. 2010;56(24):2051–66.
5. Scheiman JM1, Devereaux PJ, Herlitz J, et al. Prevention of peptic ulcers with esomeprazole in patients at risk of
ulcer development treated with low-dose acetylsalicylic acid: a randomised, controlled trial (OBERON). Heart.
2011;97(10):797–802.
6. Leontiadis GI, Sreedharan A, Dorward S, et al. Systematic reviews of the clinical effectiveness and cost-
effectiveness of proton pump inhibitors in acute upper gastrointestinal bleeding. Health Technol Assess. 2007
Dec;11(51):iii-iv, 1–164.
7. Javid G1, Masoodi I, Zargar SA, et al. Omeprazole as adjuvant therapy to endoscopic combination injection
sclerotherapy for treating bleeding peptic ulcer. Am J Med. 2001;111(4):280–4.

Clinical journey


CHB as a cause of giddiness





Case


A 56-year-old diabetic patient complained of giddiness. Her blood pressure (BP) readings and random
blood glucose levels were within normal limits. A cardiovascular examination, including ECG, was
performed.

What condition does the ECG suggest?

rd
Answer: 3 degree heart block or complete heart block (CHB)















What treatment should be suggested

for such cases?

Answer: Temporary transvenous pacemaker



What does the post treatment ECG
suggest?

Answer: Post-procedure ECG shows pacemaker rhythm.



















Lesson: Etiology for neurology lies in cardiology

Case discussion


Identifying the cause of giddiness

Giddiness, dizziness, and a feeling of lightheadedness are nonspecific terms that could have a variety of
pathophysiologic processes. Hence identifying the cause of giddiness is important (Figure 1).

A routine blood work-up is performed to rule out the possibility of hypoglycemia and other causes of
giddiness. Negative history of vertigo, disequilibrium, or psychiatric symptoms suggests a possible
cardiovascular cause of giddiness. Electrocardiography (ECG), as a part of the cardiac work-up, aids in
confirming the cardiovascular etiology of giddiness. The ECG shows asynchronous atrial and ventricular
activity, ie no relationship between P wave and QRS complexes, thereby suggesting heart block. In
patients with heart block, due to the absence of escape rhythm, ventricular asystole occurs. These ECG
1
findings with a ventricular rate of less than 45 is indicative of complete heart block (CHB).




































Figure 1. Clinical work-up of diagnosing the cause of giddiness



CHB


Signs and symptoms

Signs and symptoms of CHB vary based on the degree of the heart block. It manifests as fainting,
2,3
dizziness or lightheadedness, fatigue (tiredness), dyspnea, and chest pain.

Diagnosis and treatment of CHB


CHB can be easily detected by a simple test: ECG. On an ECG, the P waves occur at a faster rate, and are
2
not co-ordinated with the QRS waves. CHB is the end-point of either Mobitz I (due to progressive
fatigue of atrioventricular [AV] nodal cells) or Mobitz II AV block (due to sudden onset of complete
4
conduction failure throughout the His-Purkinje system). In some CHB cases, ventricular escape rhythm
1,2
is sufficient to keep up the ventricular rate and prevent hemodynamic collapse; and the ventricular
2
rate is slower than the normal heart rate and is not synchronous with atrial contractions. Whereas in
some cases CHB can cause ventricular standstill leading to syncope (if self-terminating) or sudden
cardiac arrest and is fatal; hence CHB often requires emergency treatment with a temporary
2,4
pacemaker. Temporary pacemaker placing is done in cases where a permanent pacemaker is not
5
available. It is indicated in the treatment of bradycardia and heart blocks. The suggested long-term
treatment would be the placement of a long-term pacemaker..
2,4
Differential diagnosis
CHB can be confused with:
4

• Severe second degree heart block (high grade AV block) with a very slow ventricular rate, but
4
some evidence of occasional AV conduction.
• AV dissociation: Independent asynchronous atrial and ventricular rhythms due to other causes:
o Interference-dissociation occurs due to the presence of a ventricular rhythm such as
4
accelerated idioventricular rhythm (AIVR) or ventricular tachycardia (VT).
o Isorhythmic atrioventricular dissociation occurs when atrial and ventricular rates are
similar. However AV conduction is impeded when impulses from the sino-atrial node
(SAN) and an escape pacemaker cancel each other when they enter the AV node
1,4
simultaneously.
AV dissociation may be transient or sustained. CHB by itself can cause AV dissociation; however,
1
the terms are not synonymous.

References

1. Abedin Z, Conner R. ECG Interpretation: The self-assessment approach. Blackwell Futura. ISBN 978-1-
4051-6749-9.
2. National Institute of Health. National Heart, Lung, and Blood Institute. What Is heart block? Available at:
www.nhlbi.nih.gov/health/health-topics/topics/hb/. Accessed on May 24, 2014.
3. National Health Service Choices. Heart block. Available at www.nhs.uk Accessed on May 24, 2014.
4. AV block: 3rd degree (complete heart block). Complete (3rd degree) heart block - Life in the FastLane ECG
library. Available at http://lifeinthefastlane.com/ecg-library/basics/complete-heart-block/ . Accessed on
May 20, 2014.
5. Sovari AA. Transvenous cardiac pacing. Available at: http://emedicine.medscape.com/article/80659-
overview#aw2aab6b2b2 Accessed on May, 26 2014.

ECG 1


“ ECG of concealment”


This is the routine ECG of 84-year-old female.













































1.Describe all ECG changes

2.Why is this clue?


3.What are practical implications?




ECG CHANGES:


This ECG shows normal sinus rhythm, Right Bundle Branch Block

(RBBB) with Left Atrial Fascicular Block (LAFB) with upper limit of PR
interval. There are no typical secondary ST T changes of RBBB, and

they are replaced by primary horizontal ST segment and symmetrical

T inversion.

THE CLUE:


1. The V1 shows evidence of RBBB. But the RBBB is not typical.

The initial R in V1 is tall and Broad and almost equal to Terminal

R wave. The secondary ST T changes are replaced by primary ST

T changes. In uncomplicated RBBB this initial r wave is small
and sharp because it is due to septal activation occurring from

left to right. This initial R wave is tall and broad if it is

accompanied by Posterior Wall MI (PWMI). It is often difficult

to diagnose PWMI in the presence of RBBB as both of these

conditions produce Tall R in V1. The following points may help;
in uncomplicated PWMI there is tall R in V1 without QRS

widening. In uncomplicated RBBB, QRS is wide and initial r is

small and sharp. When both RBBB and PWMI coexist, there is

significant change in initial R wave in V1 which becomes Tall

and broad and secondary ST changes disappear (Fig 66A).
This is the first concealment of PWMI by RBBB, in this ECG.
















Fig. 66A


2.Now we shift our focus to limb leads. In RBBB, these is terminal S in
Lead I due to the terminal vector going towards right and away from

Lead I. But here there is no terminal S wave in this ECG and because
of widening of QRS, L I looks like LBBB. So here RBBB in chest leads

Masquerades as LBBB in limb leads due to absence of terminal S,

which is due to the dominant LAFB where terminal vector is going to
superior and left. So, this Masquerading Bundle Branch Block

(MBBB). Here RBBB is concealed in limb leads by dominant LAFB. So

this is second concealment.


3.The LAFB is also not typical here. The uncomplicated LAFB, shows
initial sharp r wave in L II, L III, avF due to the initial vector coming

towards inferior leads and terminal S wave due to dominant terminal

vectors which is going up and left,away from inferior leads.But in
IWMI there is initial Q. So,there is difficulty in diagnosing IWMI in the

presence of LAFB and vice versa. In this ECG, the initial r in inferior

leads is replaced by slurring of initial portion of QRS which is called
initial incident (Fig 66B). This occurs because of associated IWMI

involving only anterior portion of inferior wall (This is already
discussed). So here IWMI is concealed by LAFB. This is the third

concealment.




















Fig. 66B




4.In anterior chest leads, the ST T changes are not typical of
secondary changes because the ST segment is horizontal and

there is symmetrical T inversion. So it is likely these ST T changes

are most often mistaken for secondary ST T changes due to RBBB
and IHD may be missed. So here RBBB is concealing IHD. This is

fourth concealment.

As this ECG has all these features, the clue is given as “ECG of

Concealment”

PRACTICAL IMPLICATION:

So, if one is not familiar with above changes, inferior wall and

posterior wall infarction are likely to be missed and not treated. In

addition, MBBB usually has poor prognosis as it is most often
accompanied by LV dysfunction and further advanced conduction

system disorders, especially when associated with upper limit of

PR interval.

ECG 2


“Similar but not Same yet Saves Spending”


ECG of 60 y female; Guess her complaints apart from ECG

interpretation.

1.Describe ECG changes


1. Why is this clue and what is the complaint?

2. What are practical implications?
ECG CHANGES


ECG shows basic bradycardia with right bundle branch block (RBBB) with qR
pattern and Left Anterior Fascicular Block (LAFB). PR interval is normal and

fixed. There is Atrio Ventricular association. There seems to be ‘P’ in the ST
segment of all beats. There is horizontal ST with splayed deep T inversion, the

QTc is prolonged. The presence of S wave in V1 indicates RBBB is dominant.
The absence of initial r in V1 and initial q in V5,V6 suggest probable old septal
MI.


CLUES AND COMPLAINTS:


“Similar but not same” :


1. The regular P wave in ST segment in all beats looks similar to 2:1 AV
Block. So, in the presence of bifascicular block (RBBB+LAFB) it looks
similar to Trifascicular block. But, P wave in ST segment(P’) looks

different from sinus P especially in V2 (Fig.67A). In addition to this, sinus
P to P’ interval is shorter than P’ to sinus P interval indicating the P in ST

segment (P’) is premature. As the p wave in ST segment (P’)has different
configuration and prematurity, it is likely to be Atrial Premature

Depolarisation (APD) in bigeminy) rather than blocked sinus P. So, this P-
P’ sequence is similar to 2:1 AVB but not the same.

Fig 67 A: The P in ST segment (P’) is different from the previous P and P-
P’ interval is short in this expanded V2.


2. The deep T inversion is similar to ischemic deep inversion (Flat ST,

symmetrical T inversion). But here T wave inversion broad and splayed
with prolonged QTc. In the presence of conduction disturbance

(Bifascicular block), there deep broad T inversion indicates recent stokes
Adam Attack which is called “Stoffwechsel syndrome”. So here T

inversion is similar to CAD but not same.
3. The qR in V1 is similar to RVH and RAE. But here the QRS is wide and it is

accompanied by loss of initial q in V5V6. There is no right axis deviation.
So qR pattern in RBBB is due to loss of initial septal q due to old ASMI.

The qR in V1 is similar to RVH, RAE but not the same.
4. In the presence of bi or trifascicular block, the broad splayed T inversion
with prolonged QTc indicates recent SA attack. So, this patient needs

early permanent pacemaker implantation with this ECG itself without
undergoing any costly investigation such as EP studies. So, this ECG has

saved the spending of the patient.
5. The complaint is likely to be syncopal attack because of these typical T

changes.
Because of these findings, the clue of “Similar but not Same yet Saves

Spending” is given.

PRACTICAL IMPLICATION


The immediate Permanent Pacemaker Implantation is needed in this patient,

from this ECG itself. If the APD is misdiagnosed as 2:1 AV Block, administration
of cardiac stimulants will further aggravate atrial arrhythmias. If the T wave
inversion is misdiagnosed as CAD, the investigations and management will be

going in a completely wrong direction.

ANSWERS TO QUIZ





1. Insulin administration prior to the test

2. Short acting Nifidipine is good in emergencies.

3. Bacterial endocarditic

4. Hepatitis B and C


5. Anti HEV IgM

6. All of the above

7. Anti HBc IgM

8. 1&2