ºÝºÝߣshows by User: ManivelramKannan / http://www.slideshare.net/images/logo.gif ºÝºÝߣshows by User: ManivelramKannan / Thu, 10 Nov 2022 17:39:19 GMT ºÝºÝߣShare feed for ºÝºÝߣshows by User: ManivelramKannan Leptospirosis Protocol for NABH accredition /slideshow/leptospirosis-protocol-for-nabh-accredition/254115940 leptospirosis-221110173919-adf8628e
Leptospirosis Protocol for NABH accredition - prepared for Institute of Internal Medicine, Madras Medical College.]]>
Leptospirosis Protocol for NABH accredition - prepared for Institute of Internal Medicine, Madras Medical College.]]> Thu, 10 Nov 2022 17:39:19 GMT /slideshow/leptospirosis-protocol-for-nabh-accredition/254115940 ManivelramKannan@slideshare.net(ManivelramKannan) Leptospirosis Protocol for NABH accredition ManivelramKannan Leptospirosis Protocol for NABH accredition - prepared for Institute of Internal Medicine, Madras Medical College. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/leptospirosis-221110173919-adf8628e-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Leptospirosis Protocol for NABH accredition - prepared for Institute of Internal Medicine, Madras Medical College.
Leptospirosis Protocol for NABH accredition from Manievelraaman Kannan
]]> 79 0 https://cdn.slidesharecdn.com/ss_thumbnails/leptospirosis-221110173919-adf8628e-thumbnail.jpg?width=120&height=120&fit=bounds document Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Manievelraaman's APPROACH TO NEUROLOGICAL WEAKNESS /slideshow/manievelraamans-approach-to-neurological-weakness/254114941 manievelraamansapproachtoneurologicalweakness-221110171836-6441fcfe
Manievelraaman's APPROACH TO NEUROLOGICAL WEAKNESS. PPT used for PG symposium of M.D. General Medicine Post-Graduates]]>
Manievelraaman's APPROACH TO NEUROLOGICAL WEAKNESS. PPT used for PG symposium of M.D. General Medicine Post-Graduates]]> Thu, 10 Nov 2022 17:18:36 GMT /slideshow/manievelraamans-approach-to-neurological-weakness/254114941 ManivelramKannan@slideshare.net(ManivelramKannan) Manievelraaman's APPROACH TO NEUROLOGICAL WEAKNESS ManivelramKannan Manievelraaman's APPROACH TO NEUROLOGICAL WEAKNESS. PPT used for PG symposium of M.D. General Medicine Post-Graduates <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/manievelraamansapproachtoneurologicalweakness-221110171836-6441fcfe-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Manievelraaman&#39;s APPROACH TO NEUROLOGICAL WEAKNESS. PPT used for PG symposium of M.D. General Medicine Post-Graduates
Manievelraaman's APPROACH TO NEUROLOGICAL WEAKNESS from Manievelraaman Kannan
]]> 977 0 https://cdn.slidesharecdn.com/ss_thumbnails/manievelraamansapproachtoneurologicalweakness-221110171836-6441fcfe-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Parkinson Plus Syndrome - Multiple System Atrophy: Case Report /slideshow/parkinson-plus-syndrome-multiple-system-atrophy-case-report/254114834 cmcmacmsa-221110170433-dda4afe3
Parkinson Plus Syndrome - Multiple System Atrophy: Case Report. Poster used in CMC MAC 2021. ABSTRACT A 61yr/Male, K/C/O T2DM & Parkinson’s disease(PD) on T.Metformin and T.Syndopa for 3 years, presented to us with complaints of unsteadiness of gait, dysarthria, bilateral upper limb tremor. These symptoms started gradually and has been there for last 3 years and it is progressive. Initially, it started as inability to write and difficulty in mixing food due to tremulousness of both hands which worsens with activity. Then it progressed to slurred speech and then to gait unsteadiness. Patient also has urinary incontinence for last 2 years. Patient’s symptoms are more in severity for last 6 months. On examination, patient was having orthostatic hypotension, cogwheel rigidity on bilateral wrist movement and pendular knee jerks. All cerebellar signs were present bilaterally including finger nose test abnormality, past pointing, dysdiadochokinesia, heel shin test abnormality, gross truncal ataxia, wide based gait, impaired tandem walking, gaze evoked nystagmus, scanning speech. Presence of cerebellar signs, autonomic disturbances, poor response to syndopa, rapid progression, lack of resting tremor at presentation, symmetrical involvement, early speech and gait involvement - are usually NOT seen in PD. So, evaluated further. MRI Brain T2 showed classical cruciform hyperintensity in pons (Hot cross bun sign) & diffuse cerebellar atrophy. Hence the diagnosis MULTIPLE SYSTEM ATROPHY (MSA-C) - Shy Drager Syndrome. This shows the importance of identifying atypical features in PD.]]>
Parkinson Plus Syndrome - Multiple System Atrophy: Case Report. Poster used in CMC MAC 2021. ABSTRACT A 61yr/Male, K/C/O T2DM & Parkinson’s disease(PD) on T.Metformin and T.Syndopa for 3 years, presented to us with complaints of unsteadiness of gait, dysarthria, bilateral upper limb tremor. These symptoms started gradually and has been there for last 3 years and it is progressive. Initially, it started as inability to write and difficulty in mixing food due to tremulousness of both hands which worsens with activity. Then it progressed to slurred speech and then to gait unsteadiness. Patient also has urinary incontinence for last 2 years. Patient’s symptoms are more in severity for last 6 months. On examination, patient was having orthostatic hypotension, cogwheel rigidity on bilateral wrist movement and pendular knee jerks. All cerebellar signs were present bilaterally including finger nose test abnormality, past pointing, dysdiadochokinesia, heel shin test abnormality, gross truncal ataxia, wide based gait, impaired tandem walking, gaze evoked nystagmus, scanning speech. Presence of cerebellar signs, autonomic disturbances, poor response to syndopa, rapid progression, lack of resting tremor at presentation, symmetrical involvement, early speech and gait involvement - are usually NOT seen in PD. So, evaluated further. MRI Brain T2 showed classical cruciform hyperintensity in pons (Hot cross bun sign) & diffuse cerebellar atrophy. Hence the diagnosis MULTIPLE SYSTEM ATROPHY (MSA-C) - Shy Drager Syndrome. This shows the importance of identifying atypical features in PD.]]> Thu, 10 Nov 2022 17:04:33 GMT /slideshow/parkinson-plus-syndrome-multiple-system-atrophy-case-report/254114834 ManivelramKannan@slideshare.net(ManivelramKannan) Parkinson Plus Syndrome - Multiple System Atrophy: Case Report ManivelramKannan Parkinson Plus Syndrome - Multiple System Atrophy: Case Report. Poster used in CMC MAC 2021. ABSTRACT A 61yr/Male, K/C/O T2DM & Parkinson’s disease(PD) on T.Metformin and T.Syndopa for 3 years, presented to us with complaints of unsteadiness of gait, dysarthria, bilateral upper limb tremor. These symptoms started gradually and has been there for last 3 years and it is progressive. Initially, it started as inability to write and difficulty in mixing food due to tremulousness of both hands which worsens with activity. Then it progressed to slurred speech and then to gait unsteadiness. Patient also has urinary incontinence for last 2 years. Patient’s symptoms are more in severity for last 6 months. On examination, patient was having orthostatic hypotension, cogwheel rigidity on bilateral wrist movement and pendular knee jerks. All cerebellar signs were present bilaterally including finger nose test abnormality, past pointing, dysdiadochokinesia, heel shin test abnormality, gross truncal ataxia, wide based gait, impaired tandem walking, gaze evoked nystagmus, scanning speech. Presence of cerebellar signs, autonomic disturbances, poor response to syndopa, rapid progression, lack of resting tremor at presentation, symmetrical involvement, early speech and gait involvement - are usually NOT seen in PD. So, evaluated further. MRI Brain T2 showed classical cruciform hyperintensity in pons (Hot cross bun sign) & diffuse cerebellar atrophy. Hence the diagnosis MULTIPLE SYSTEM ATROPHY (MSA-C) - Shy Drager Syndrome. This shows the importance of identifying atypical features in PD. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/cmcmacmsa-221110170433-dda4afe3-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Parkinson Plus Syndrome - Multiple System Atrophy: Case Report. Poster used in CMC MAC 2021. ABSTRACT A 61yr/Male, K/C/O T2DM &amp; Parkinson’s disease(PD) on T.Metformin and T.Syndopa for 3 years, presented to us with complaints of unsteadiness of gait, dysarthria, bilateral upper limb tremor. These symptoms started gradually and has been there for last 3 years and it is progressive. Initially, it started as inability to write and difficulty in mixing food due to tremulousness of both hands which worsens with activity. Then it progressed to slurred speech and then to gait unsteadiness. Patient also has urinary incontinence for last 2 years. Patient’s symptoms are more in severity for last 6 months. On examination, patient was having orthostatic hypotension, cogwheel rigidity on bilateral wrist movement and pendular knee jerks. All cerebellar signs were present bilaterally including finger nose test abnormality, past pointing, dysdiadochokinesia, heel shin test abnormality, gross truncal ataxia, wide based gait, impaired tandem walking, gaze evoked nystagmus, scanning speech. Presence of cerebellar signs, autonomic disturbances, poor response to syndopa, rapid progression, lack of resting tremor at presentation, symmetrical involvement, early speech and gait involvement - are usually NOT seen in PD. So, evaluated further. MRI Brain T2 showed classical cruciform hyperintensity in pons (Hot cross bun sign) &amp; diffuse cerebellar atrophy. Hence the diagnosis MULTIPLE SYSTEM ATROPHY (MSA-C) - Shy Drager Syndrome. This shows the importance of identifying atypical features in PD.
Parkinson Plus Syndrome - Multiple System Atrophy: Case Report from Manievelraaman Kannan
]]> 190 0 https://cdn.slidesharecdn.com/ss_thumbnails/cmcmacmsa-221110170433-dda4afe3-thumbnail.jpg?width=120&height=120&fit=bounds document Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Allergy Induced Acute Coronary Syndrome - Kounis Syndrome /slideshow/allergy-induced-acute-coronary-syndrome-kounis-syndrome/254114780 cmcmackounis-221110165827-cdb695c1
Allergy Induced Acute Coronary Syndrome - Kounis Syndrome: Case Report. Poster used in CMC MAC 2021. OBJECTIVE: To discuss a rare occurrence of allergic reaction to NSAID causing Myocardial Infarction. BACKGROUND: A 21-year-old obese female with no other comorbidities was referred to us with history of chest pain, generalized urticarial rashes and itch suddenly following Inj.IM Diclofenac, which was given for heel pain relief. She was hemodynamically stable, but tachypneic, orthopneic and was having bilateral basal crepitations. ECG revealed significant ST depression & T inversion in II,III,aVF and V2-V6 and ST elevation in aVR. CXR showed pulmonary edema. Diagnosed as ACS following anaphylaxis and loading dose was given along with IM adrenaline, antihistamines, and steroids. Echo revealed global hypokinesia of LV. Cardiac enzymes were elevated. Meanwhile, she had a prompt relief of chestpain, but dyspnea worsened and warranted NIV support. Repeat ECG revealed regression of ST changes correlating with chest pain relief. After 2 days of NIV, patient’s dyspnea improved and weaned from NIV. CAG revealed normal epicardial coronaries. Serial cardiac enzyme levels showed falling trend and ECG was completely normal with no significant ST-T changes. Pre-discharge, repeat echo showed persistence of global hypokinesia. 2weeks later, repeat echo showed dramatic improvement with normal LV systolic function suggesting recovery from myocardial stunning. RESULTS: This qualifies for the diagnosis of MINOCA (Myocardial Infarction with No Obstructive Coronary Arteries). In the setting of allergic trigger, vasospasm or coronary hypersensitivity is the underlying mechanism- described as KOUNIS SYNDROME. CONCLUSION: ECG changes and chest discomforts that occur in allergic reactions are not always secondary to distributive/anaphylactic shock. Sometimes heart could be the primarily affected organ by the allergic reaction as in this case. Although <200cases reported globally until 2017, it’s suspected to be frequently overlooked, hence likely to be more prevalent. ]]>
Allergy Induced Acute Coronary Syndrome - Kounis Syndrome: Case Report. Poster used in CMC MAC 2021. OBJECTIVE: To discuss a rare occurrence of allergic reaction to NSAID causing Myocardial Infarction. BACKGROUND: A 21-year-old obese female with no other comorbidities was referred to us with history of chest pain, generalized urticarial rashes and itch suddenly following Inj.IM Diclofenac, which was given for heel pain relief. She was hemodynamically stable, but tachypneic, orthopneic and was having bilateral basal crepitations. ECG revealed significant ST depression & T inversion in II,III,aVF and V2-V6 and ST elevation in aVR. CXR showed pulmonary edema. Diagnosed as ACS following anaphylaxis and loading dose was given along with IM adrenaline, antihistamines, and steroids. Echo revealed global hypokinesia of LV. Cardiac enzymes were elevated. Meanwhile, she had a prompt relief of chestpain, but dyspnea worsened and warranted NIV support. Repeat ECG revealed regression of ST changes correlating with chest pain relief. After 2 days of NIV, patient’s dyspnea improved and weaned from NIV. CAG revealed normal epicardial coronaries. Serial cardiac enzyme levels showed falling trend and ECG was completely normal with no significant ST-T changes. Pre-discharge, repeat echo showed persistence of global hypokinesia. 2weeks later, repeat echo showed dramatic improvement with normal LV systolic function suggesting recovery from myocardial stunning. RESULTS: This qualifies for the diagnosis of MINOCA (Myocardial Infarction with No Obstructive Coronary Arteries). In the setting of allergic trigger, vasospasm or coronary hypersensitivity is the underlying mechanism- described as KOUNIS SYNDROME. CONCLUSION: ECG changes and chest discomforts that occur in allergic reactions are not always secondary to distributive/anaphylactic shock. Sometimes heart could be the primarily affected organ by the allergic reaction as in this case. Although <200cases reported globally until 2017, it’s suspected to be frequently overlooked, hence likely to be more prevalent. ]]> Thu, 10 Nov 2022 16:58:27 GMT /slideshow/allergy-induced-acute-coronary-syndrome-kounis-syndrome/254114780 ManivelramKannan@slideshare.net(ManivelramKannan) Allergy Induced Acute Coronary Syndrome - Kounis Syndrome ManivelramKannan Allergy Induced Acute Coronary Syndrome - Kounis Syndrome: Case Report. Poster used in CMC MAC 2021. OBJECTIVE: To discuss a rare occurrence of allergic reaction to NSAID causing Myocardial Infarction. BACKGROUND: A 21-year-old obese female with no other comorbidities was referred to us with history of chest pain, generalized urticarial rashes and itch suddenly following Inj.IM Diclofenac, which was given for heel pain relief. She was hemodynamically stable, but tachypneic, orthopneic and was having bilateral basal crepitations. ECG revealed significant ST depression & T inversion in II,III,aVF and V2-V6 and ST elevation in aVR. CXR showed pulmonary edema. Diagnosed as ACS following anaphylaxis and loading dose was given along with IM adrenaline, antihistamines, and steroids. Echo revealed global hypokinesia of LV. Cardiac enzymes were elevated. Meanwhile, she had a prompt relief of chestpain, but dyspnea worsened and warranted NIV support. Repeat ECG revealed regression of ST changes correlating with chest pain relief. After 2 days of NIV, patient’s dyspnea improved and weaned from NIV. CAG revealed normal epicardial coronaries. Serial cardiac enzyme levels showed falling trend and ECG was completely normal with no significant ST-T changes. Pre-discharge, repeat echo showed persistence of global hypokinesia. 2weeks later, repeat echo showed dramatic improvement with normal LV systolic function suggesting recovery from myocardial stunning. RESULTS: This qualifies for the diagnosis of MINOCA (Myocardial Infarction with No Obstructive Coronary Arteries). In the setting of allergic trigger, vasospasm or coronary hypersensitivity is the underlying mechanism- described as KOUNIS SYNDROME. CONCLUSION: ECG changes and chest discomforts that occur in allergic reactions are not always secondary to distributive/anaphylactic shock. Sometimes heart could be the primarily affected organ by the allergic reaction as in this case. Although <200cases reported globally until 2017, it’s suspected to be frequently overlooked, hence likely to be more prevalent. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/cmcmackounis-221110165827-cdb695c1-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Allergy Induced Acute Coronary Syndrome - Kounis Syndrome: Case Report. Poster used in CMC MAC 2021. OBJECTIVE: To discuss a rare occurrence of allergic reaction to NSAID causing Myocardial Infarction. BACKGROUND: A 21-year-old obese female with no other comorbidities was referred to us with history of chest pain, generalized urticarial rashes and itch suddenly following Inj.IM Diclofenac, which was given for heel pain relief. She was hemodynamically stable, but tachypneic, orthopneic and was having bilateral basal crepitations. ECG revealed significant ST depression &amp; T inversion in II,III,aVF and V2-V6 and ST elevation in aVR. CXR showed pulmonary edema. Diagnosed as ACS following anaphylaxis and loading dose was given along with IM adrenaline, antihistamines, and steroids. Echo revealed global hypokinesia of LV. Cardiac enzymes were elevated. Meanwhile, she had a prompt relief of chestpain, but dyspnea worsened and warranted NIV support. Repeat ECG revealed regression of ST changes correlating with chest pain relief. After 2 days of NIV, patient’s dyspnea improved and weaned from NIV. CAG revealed normal epicardial coronaries. Serial cardiac enzyme levels showed falling trend and ECG was completely normal with no significant ST-T changes. Pre-discharge, repeat echo showed persistence of global hypokinesia. 2weeks later, repeat echo showed dramatic improvement with normal LV systolic function suggesting recovery from myocardial stunning. RESULTS: This qualifies for the diagnosis of MINOCA (Myocardial Infarction with No Obstructive Coronary Arteries). In the setting of allergic trigger, vasospasm or coronary hypersensitivity is the underlying mechanism- described as KOUNIS SYNDROME. CONCLUSION: ECG changes and chest discomforts that occur in allergic reactions are not always secondary to distributive/anaphylactic shock. Sometimes heart could be the primarily affected organ by the allergic reaction as in this case. Although &lt;200cases reported globally until 2017, it’s suspected to be frequently overlooked, hence likely to be more prevalent.
Allergy Induced Acute Coronary Syndrome - Kounis Syndrome from Manievelraaman Kannan
]]> 137 0 https://cdn.slidesharecdn.com/ss_thumbnails/cmcmackounis-221110165827-cdb695c1-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Brugada Syndrome - A Cardiac Channelopathy: Case Report /slideshow/brugada-syndrome-a-cardiac-channelopathy-case-report/254114655 cmcmacbrugada-221110164545-737fbf80
Case Report: Brugada Syndrome - A Cardiac Channelopathy. Poster used for presentation in CMC MAC 2021. OBJECTIVE: To discuss an interesting case of Brugada syndrome presenting as seizures. BACKGROUND: A 25-year-old well-informed male presented to us with complaints of seizure on day 3 of an acute febrile illness. He was conscious, oriented, GCS15/15 and system examinations were unremarkable. He had a similar history of seizure during fever 1 year back and was started on anti-epileptics since then and was treated with empirical antibiotics and CSF analysis, MRI brain with seizure protocol and EEG were completely normal during that episode. As described by patient, both episodes were very similar and was like darkening of visual field followed by LOC and bystanders witnessed few jerks involving both sides of body followed by regaining consciousness. This raised suspicion for syncope and ECG revealed RBBB-rSR’ pattern and saddleback STE in V1-V3(type2-brugada pattern-not diagnostic on its own). But on probing, patient revealed SCD in his father at age 42. RESULTS: Echo revealed structurally normal heart. Expert opinion sought and flecainide challenge test revealed the classical type1 brugada pattern (diagnostic) with coved STE and T inversion in V1-V3 clinching the diagnosis of BRUGADA SYNDROME. Genetic testing for channelopathy was unremarkable. Type 1 Brugada pattern (on provocative testing) along with syncopal event and family history strongly warranted AICD insertion and patient opted for subcutaneous ICD. 6 months later, ICD interrogation revealed occurrence of 1 episode of NSVT, which fell below the ICD intervention threshold. CONCLUSION: Brugada syndrome is a rare cardiac channelopathy with high risk of SCD in the absence of intervention. Events during fever and family history are very classical. It has male preponderance and more seen in Southeast Asia. All cases of suspected syncopal attacks warrant a thorough search for ECG markers of SCD. ]]>
Case Report: Brugada Syndrome - A Cardiac Channelopathy. Poster used for presentation in CMC MAC 2021. OBJECTIVE: To discuss an interesting case of Brugada syndrome presenting as seizures. BACKGROUND: A 25-year-old well-informed male presented to us with complaints of seizure on day 3 of an acute febrile illness. He was conscious, oriented, GCS15/15 and system examinations were unremarkable. He had a similar history of seizure during fever 1 year back and was started on anti-epileptics since then and was treated with empirical antibiotics and CSF analysis, MRI brain with seizure protocol and EEG were completely normal during that episode. As described by patient, both episodes were very similar and was like darkening of visual field followed by LOC and bystanders witnessed few jerks involving both sides of body followed by regaining consciousness. This raised suspicion for syncope and ECG revealed RBBB-rSR’ pattern and saddleback STE in V1-V3(type2-brugada pattern-not diagnostic on its own). But on probing, patient revealed SCD in his father at age 42. RESULTS: Echo revealed structurally normal heart. Expert opinion sought and flecainide challenge test revealed the classical type1 brugada pattern (diagnostic) with coved STE and T inversion in V1-V3 clinching the diagnosis of BRUGADA SYNDROME. Genetic testing for channelopathy was unremarkable. Type 1 Brugada pattern (on provocative testing) along with syncopal event and family history strongly warranted AICD insertion and patient opted for subcutaneous ICD. 6 months later, ICD interrogation revealed occurrence of 1 episode of NSVT, which fell below the ICD intervention threshold. CONCLUSION: Brugada syndrome is a rare cardiac channelopathy with high risk of SCD in the absence of intervention. Events during fever and family history are very classical. It has male preponderance and more seen in Southeast Asia. All cases of suspected syncopal attacks warrant a thorough search for ECG markers of SCD. ]]> Thu, 10 Nov 2022 16:45:45 GMT /slideshow/brugada-syndrome-a-cardiac-channelopathy-case-report/254114655 ManivelramKannan@slideshare.net(ManivelramKannan) Brugada Syndrome - A Cardiac Channelopathy: Case Report ManivelramKannan Case Report: Brugada Syndrome - A Cardiac Channelopathy. Poster used for presentation in CMC MAC 2021. OBJECTIVE: To discuss an interesting case of Brugada syndrome presenting as seizures. BACKGROUND: A 25-year-old well-informed male presented to us with complaints of seizure on day 3 of an acute febrile illness. He was conscious, oriented, GCS15/15 and system examinations were unremarkable. He had a similar history of seizure during fever 1 year back and was started on anti-epileptics since then and was treated with empirical antibiotics and CSF analysis, MRI brain with seizure protocol and EEG were completely normal during that episode. As described by patient, both episodes were very similar and was like darkening of visual field followed by LOC and bystanders witnessed few jerks involving both sides of body followed by regaining consciousness. This raised suspicion for syncope and ECG revealed RBBB-rSR’ pattern and saddleback STE in V1-V3(type2-brugada pattern-not diagnostic on its own). But on probing, patient revealed SCD in his father at age 42. RESULTS: Echo revealed structurally normal heart. Expert opinion sought and flecainide challenge test revealed the classical type1 brugada pattern (diagnostic) with coved STE and T inversion in V1-V3 clinching the diagnosis of BRUGADA SYNDROME. Genetic testing for channelopathy was unremarkable. Type 1 Brugada pattern (on provocative testing) along with syncopal event and family history strongly warranted AICD insertion and patient opted for subcutaneous ICD. 6 months later, ICD interrogation revealed occurrence of 1 episode of NSVT, which fell below the ICD intervention threshold. CONCLUSION: Brugada syndrome is a rare cardiac channelopathy with high risk of SCD in the absence of intervention. Events during fever and family history are very classical. It has male preponderance and more seen in Southeast Asia. All cases of suspected syncopal attacks warrant a thorough search for ECG markers of SCD. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/cmcmacbrugada-221110164545-737fbf80-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Case Report: Brugada Syndrome - A Cardiac Channelopathy. Poster used for presentation in CMC MAC 2021. OBJECTIVE: To discuss an interesting case of Brugada syndrome presenting as seizures. BACKGROUND: A 25-year-old well-informed male presented to us with complaints of seizure on day 3 of an acute febrile illness. He was conscious, oriented, GCS15/15 and system examinations were unremarkable. He had a similar history of seizure during fever 1 year back and was started on anti-epileptics since then and was treated with empirical antibiotics and CSF analysis, MRI brain with seizure protocol and EEG were completely normal during that episode. As described by patient, both episodes were very similar and was like darkening of visual field followed by LOC and bystanders witnessed few jerks involving both sides of body followed by regaining consciousness. This raised suspicion for syncope and ECG revealed RBBB-rSR’ pattern and saddleback STE in V1-V3(type2-brugada pattern-not diagnostic on its own). But on probing, patient revealed SCD in his father at age 42. RESULTS: Echo revealed structurally normal heart. Expert opinion sought and flecainide challenge test revealed the classical type1 brugada pattern (diagnostic) with coved STE and T inversion in V1-V3 clinching the diagnosis of BRUGADA SYNDROME. Genetic testing for channelopathy was unremarkable. Type 1 Brugada pattern (on provocative testing) along with syncopal event and family history strongly warranted AICD insertion and patient opted for subcutaneous ICD. 6 months later, ICD interrogation revealed occurrence of 1 episode of NSVT, which fell below the ICD intervention threshold. CONCLUSION: Brugada syndrome is a rare cardiac channelopathy with high risk of SCD in the absence of intervention. Events during fever and family history are very classical. It has male preponderance and more seen in Southeast Asia. All cases of suspected syncopal attacks warrant a thorough search for ECG markers of SCD.
Brugada Syndrome - A Cardiac Channelopathy: Case Report from Manievelraaman Kannan
]]> 73 0 https://cdn.slidesharecdn.com/ss_thumbnails/cmcmacbrugada-221110164545-737fbf80-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Allergy Induced Myocardial Infarction - Kounis Syndrome / Coronary Hypersensitivity Disorder / Vasospastic Angina /slideshow/allergy-induced-myocardial-infarction-kounis-syndrome-coronary-hypersensitivity-disorder-vasospastic-angina/254114461 tapiconepaperpresentation-221110162330-9638f9ee
Case Presentation PPT - For TAPICON 2021 Case Report: Allergy Induced Myocardial Infarction - Kounis Syndrome / Coronary Hypersensitivity Disorder / Vasospastic Angina. Abstract A young female with no coronary risk factors presented to us with history of chest pain, generalized urticarial rashes and itch suddenly following Inj.IM Diclofenac, which was given for heel pain relief. She was hemodynamically stable, but tachypneic, orthopneic with bilateral basal crepitations. ECG showed significant ST depression & T inversion in II,III,aVF and V2-V6 and ST elevation in aVR. CXR showed pulmonary edema. Echo revealed global hypokinesia of LV. Cardiac enzymes were elevated. Treated for acute coronary syndrome (ACS) and her pain got relieved. CAG showed normal epicardial coronaries. Repeat ECG showed regression of ST changes correlating with chest pain relief and enzymes were also falling. Pre-discharge, ECG normalised but echo showed persistence of global hypokinesia. Two weeks later, repeat echo showed dramatic improvement with normal LV systolic function suggesting recovery from myocardial stunning. This qualifies for the diagnosis of MINOCA (Myocardial Infarction with No Obstructive Coronary Arteries). In the setting of allergic trigger, vasospasm or coronary hypersensitivity is the underlying mechanism - described as KOUNIS SYNDROME. ECG changes and chest discomforts that occur in allergic reactions are NOT ALWAYS SECONDARY to distributive/anaphylactic shock. Sometimes heart could be the primarily affected organ by the allergic reaction. It is frequently overlooked and its timely recognition and appropriate intervention will improve the outcome.]]>
Case Presentation PPT - For TAPICON 2021 Case Report: Allergy Induced Myocardial Infarction - Kounis Syndrome / Coronary Hypersensitivity Disorder / Vasospastic Angina. Abstract A young female with no coronary risk factors presented to us with history of chest pain, generalized urticarial rashes and itch suddenly following Inj.IM Diclofenac, which was given for heel pain relief. She was hemodynamically stable, but tachypneic, orthopneic with bilateral basal crepitations. ECG showed significant ST depression & T inversion in II,III,aVF and V2-V6 and ST elevation in aVR. CXR showed pulmonary edema. Echo revealed global hypokinesia of LV. Cardiac enzymes were elevated. Treated for acute coronary syndrome (ACS) and her pain got relieved. CAG showed normal epicardial coronaries. Repeat ECG showed regression of ST changes correlating with chest pain relief and enzymes were also falling. Pre-discharge, ECG normalised but echo showed persistence of global hypokinesia. Two weeks later, repeat echo showed dramatic improvement with normal LV systolic function suggesting recovery from myocardial stunning. This qualifies for the diagnosis of MINOCA (Myocardial Infarction with No Obstructive Coronary Arteries). In the setting of allergic trigger, vasospasm or coronary hypersensitivity is the underlying mechanism - described as KOUNIS SYNDROME. ECG changes and chest discomforts that occur in allergic reactions are NOT ALWAYS SECONDARY to distributive/anaphylactic shock. Sometimes heart could be the primarily affected organ by the allergic reaction. It is frequently overlooked and its timely recognition and appropriate intervention will improve the outcome.]]> Thu, 10 Nov 2022 16:23:30 GMT /slideshow/allergy-induced-myocardial-infarction-kounis-syndrome-coronary-hypersensitivity-disorder-vasospastic-angina/254114461 ManivelramKannan@slideshare.net(ManivelramKannan) Allergy Induced Myocardial Infarction - Kounis Syndrome / Coronary Hypersensitivity Disorder / Vasospastic Angina ManivelramKannan Case Presentation PPT - For TAPICON 2021 Case Report: Allergy Induced Myocardial Infarction - Kounis Syndrome / Coronary Hypersensitivity Disorder / Vasospastic Angina. Abstract A young female with no coronary risk factors presented to us with history of chest pain, generalized urticarial rashes and itch suddenly following Inj.IM Diclofenac, which was given for heel pain relief. She was hemodynamically stable, but tachypneic, orthopneic with bilateral basal crepitations. ECG showed significant ST depression & T inversion in II,III,aVF and V2-V6 and ST elevation in aVR. CXR showed pulmonary edema. Echo revealed global hypokinesia of LV. Cardiac enzymes were elevated. Treated for acute coronary syndrome (ACS) and her pain got relieved. CAG showed normal epicardial coronaries. Repeat ECG showed regression of ST changes correlating with chest pain relief and enzymes were also falling. Pre-discharge, ECG normalised but echo showed persistence of global hypokinesia. Two weeks later, repeat echo showed dramatic improvement with normal LV systolic function suggesting recovery from myocardial stunning. This qualifies for the diagnosis of MINOCA (Myocardial Infarction with No Obstructive Coronary Arteries). In the setting of allergic trigger, vasospasm or coronary hypersensitivity is the underlying mechanism - described as KOUNIS SYNDROME. ECG changes and chest discomforts that occur in allergic reactions are NOT ALWAYS SECONDARY to distributive/anaphylactic shock. Sometimes heart could be the primarily affected organ by the allergic reaction. It is frequently overlooked and its timely recognition and appropriate intervention will improve the outcome. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/tapiconepaperpresentation-221110162330-9638f9ee-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Case Presentation PPT - For TAPICON 2021 Case Report: Allergy Induced Myocardial Infarction - Kounis Syndrome / Coronary Hypersensitivity Disorder / Vasospastic Angina. Abstract A young female with no coronary risk factors presented to us with history of chest pain, generalized urticarial rashes and itch suddenly following Inj.IM Diclofenac, which was given for heel pain relief. She was hemodynamically stable, but tachypneic, orthopneic with bilateral basal crepitations. ECG showed significant ST depression &amp; T inversion in II,III,aVF and V2-V6 and ST elevation in aVR. CXR showed pulmonary edema. Echo revealed global hypokinesia of LV. Cardiac enzymes were elevated. Treated for acute coronary syndrome (ACS) and her pain got relieved. CAG showed normal epicardial coronaries. Repeat ECG showed regression of ST changes correlating with chest pain relief and enzymes were also falling. Pre-discharge, ECG normalised but echo showed persistence of global hypokinesia. Two weeks later, repeat echo showed dramatic improvement with normal LV systolic function suggesting recovery from myocardial stunning. This qualifies for the diagnosis of MINOCA (Myocardial Infarction with No Obstructive Coronary Arteries). In the setting of allergic trigger, vasospasm or coronary hypersensitivity is the underlying mechanism - described as KOUNIS SYNDROME. ECG changes and chest discomforts that occur in allergic reactions are NOT ALWAYS SECONDARY to distributive/anaphylactic shock. Sometimes heart could be the primarily affected organ by the allergic reaction. It is frequently overlooked and its timely recognition and appropriate intervention will improve the outcome.
Allergy Induced Myocardial Infarction - Kounis Syndrome / Coronary Hypersensitivity Disorder / Vasospastic Angina from Manievelraaman Kannan
]]> 204 0 https://cdn.slidesharecdn.com/ss_thumbnails/tapiconepaperpresentation-221110162330-9638f9ee-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 TB Myeloradiculopathy /slideshow/tb-myeloradiculopathy/249896316 generalclinicsjuly2021-210731101349
A case of Acute onset areflexic flaccid paraparesis with paresthesia with bladder involvement]]>
A case of Acute onset areflexic flaccid paraparesis with paresthesia with bladder involvement]]> Sat, 31 Jul 2021 10:13:49 GMT /slideshow/tb-myeloradiculopathy/249896316 ManivelramKannan@slideshare.net(ManivelramKannan) TB Myeloradiculopathy ManivelramKannan A case of Acute onset areflexic flaccid paraparesis with paresthesia with bladder involvement <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/generalclinicsjuly2021-210731101349-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> A case of Acute onset areflexic flaccid paraparesis with paresthesia with bladder involvement
TB Myeloradiculopathy from Manievelraaman Kannan
]]> 258 0 https://cdn.slidesharecdn.com/ss_thumbnails/generalclinicsjuly2021-210731101349-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 COLLOID CYST OF BRAIN / CNS SPACE OCCUPYING LESIONS - BENIGN /ManivelramKannan/colloid-cyst-image-of-the-week-247703499 imageoftheweekcolloidcyst-210504111915
ALL HYPERDENSITIES IN CT BRAIN ARE NOT BLEEDS. THIS IS COLLOID CYST OF BRAIN - IDENTIFIED BY TYPICAL HISTORY AND APPROPRIATE LOCATION OF CYST]]>
ALL HYPERDENSITIES IN CT BRAIN ARE NOT BLEEDS. THIS IS COLLOID CYST OF BRAIN - IDENTIFIED BY TYPICAL HISTORY AND APPROPRIATE LOCATION OF CYST]]> Tue, 04 May 2021 11:19:15 GMT /ManivelramKannan/colloid-cyst-image-of-the-week-247703499 ManivelramKannan@slideshare.net(ManivelramKannan) COLLOID CYST OF BRAIN / CNS SPACE OCCUPYING LESIONS - BENIGN ManivelramKannan ALL HYPERDENSITIES IN CT BRAIN ARE NOT BLEEDS. THIS IS COLLOID CYST OF BRAIN - IDENTIFIED BY TYPICAL HISTORY AND APPROPRIATE LOCATION OF CYST <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/imageoftheweekcolloidcyst-210504111915-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> ALL HYPERDENSITIES IN CT BRAIN ARE NOT BLEEDS. THIS IS COLLOID CYST OF BRAIN - IDENTIFIED BY TYPICAL HISTORY AND APPROPRIATE LOCATION OF CYST
COLLOID CYST OF BRAIN / CNS SPACE OCCUPYING LESIONS - BENIGN from Manievelraaman Kannan
]]> 91 0 https://cdn.slidesharecdn.com/ss_thumbnails/imageoftheweekcolloidcyst-210504111915-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Allergic Acute Coronary Syndrome - KOUNIS SYNDROME /slideshow/allergic-acute-coronary-syndrome-kounis-syndrome/247703165 allergicacsbymanievelraaman-210504111127
CASE REPORT OF A YOUNG OTHERWISE HEALTHY FEMALE WHO DEVELOPED ACUTE CORONARY SYNDROME (ACS) FOLLOWING DICLOFENAC INJECTION]]>
CASE REPORT OF A YOUNG OTHERWISE HEALTHY FEMALE WHO DEVELOPED ACUTE CORONARY SYNDROME (ACS) FOLLOWING DICLOFENAC INJECTION]]> Tue, 04 May 2021 11:11:27 GMT /slideshow/allergic-acute-coronary-syndrome-kounis-syndrome/247703165 ManivelramKannan@slideshare.net(ManivelramKannan) Allergic Acute Coronary Syndrome - KOUNIS SYNDROME ManivelramKannan CASE REPORT OF A YOUNG OTHERWISE HEALTHY FEMALE WHO DEVELOPED ACUTE CORONARY SYNDROME (ACS) FOLLOWING DICLOFENAC INJECTION <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/allergicacsbymanievelraaman-210504111127-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> CASE REPORT OF A YOUNG OTHERWISE HEALTHY FEMALE WHO DEVELOPED ACUTE CORONARY SYNDROME (ACS) FOLLOWING DICLOFENAC INJECTION
Allergic Acute Coronary Syndrome - KOUNIS SYNDROME from Manievelraaman Kannan
]]> 542 0 https://cdn.slidesharecdn.com/ss_thumbnails/allergicacsbymanievelraaman-210504111127-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Abnormal Uterine Bleeding (AUB) -Etiopathogenesis /slideshow/abnormal-uterine-bleeding-aub-etiopathogenesis/82061316 abnormaluterinebleeding-etiopathogenesis-171114171640
A brief note on WHAT causes AUB and WHY it does so.]]>
A brief note on WHAT causes AUB and WHY it does so.]]> Tue, 14 Nov 2017 17:16:40 GMT /slideshow/abnormal-uterine-bleeding-aub-etiopathogenesis/82061316 ManivelramKannan@slideshare.net(ManivelramKannan) Abnormal Uterine Bleeding (AUB) -Etiopathogenesis ManivelramKannan A brief note on WHAT causes AUB and WHY it does so. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/abnormaluterinebleeding-etiopathogenesis-171114171640-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> A brief note on WHAT causes AUB and WHY it does so.
Abnormal Uterine Bleeding (AUB) -Etiopathogenesis from Manievelraaman Kannan
]]> 5409 3 https://cdn.slidesharecdn.com/ss_thumbnails/abnormaluterinebleeding-etiopathogenesis-171114171640-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Small Intestine TB (Tuberculosis) /slideshow/small-intestine-tb-tuberculosis/82060667 smallintestinetb-171114170729
A quick overview on Intestinal Tuberculosis (TB)]]>
A quick overview on Intestinal Tuberculosis (TB)]]> Tue, 14 Nov 2017 17:07:29 GMT /slideshow/small-intestine-tb-tuberculosis/82060667 ManivelramKannan@slideshare.net(ManivelramKannan) Small Intestine TB (Tuberculosis) ManivelramKannan A quick overview on Intestinal Tuberculosis (TB) <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/smallintestinetb-171114170729-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> A quick overview on Intestinal Tuberculosis (TB)
Small Intestine TB (Tuberculosis) from Manievelraaman Kannan
]]> 12801 4 https://cdn.slidesharecdn.com/ss_thumbnails/smallintestinetb-171114170729-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 https://cdn.slidesharecdn.com/profile-photo-ManivelramKannan-48x48.jpg?cb=1718730411 MBBS, M.D.General Medicine - Madras Medical College https://cdn.slidesharecdn.com/ss_thumbnails/leptospirosis-221110173919-adf8628e-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/leptospirosis-protocol-for-nabh-accredition/254115940 Leptospirosis Protocol... https://cdn.slidesharecdn.com/ss_thumbnails/manievelraamansapproachtoneurologicalweakness-221110171836-6441fcfe-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/manievelraamans-approach-to-neurological-weakness/254114941 Manievelraaman&#39;s APPRO... https://cdn.slidesharecdn.com/ss_thumbnails/cmcmacmsa-221110170433-dda4afe3-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/parkinson-plus-syndrome-multiple-system-atrophy-case-report/254114834 Parkinson Plus Syndrom...