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Synopsis-dnb
Educational Activities in Our Hospital
DEEP BRAIN STIMULATION
- It’s like a pacemaker for the brain. It involves putting an electrode in the brain and stimulating the brain using a battery which sits underneath the clavicle.
- Prior to the procedure Neuroimaging, Neurological and Psychological assessement to be done.
- It is a functional Stereotactic Surgery. There will be Electrophysiological exploration of targeted regions via test electrodes through 1. Microelectrode recordings (MER), 2. Macro/Macro stimulator.
- Electrode has 4 contacts on its distal end. The effects of stimulation from each combination of 2 contacts or monopolarly from each contact are assessed. It helps to determine best contact(s) to use to obtain optimal therapeutic benefit.
- DBS electrode stereotactically inserted with special rigid guide tube.
- Patient is awake and in the medication-“off” state after 12-hour withdrawal.
- Patient turns stimulator “on” and “off” by passing magnet over the skin overlying stimulator.
- Typical stimulator settings:
Voltage amplitude: 2-3 V, Pulse width: 90 μs, Stimulation frequency: 130-185 Hz
- Commonly takes 6 months to obtain the best settings.
- FDA Approval:
1997-ET, 2002-PD, 2003-Dystonia, 2009-OCD, 2018-Epilepsy.
- Inclusion Criteria for DBS in IPD:
a) Diagnosis of IPD, b) L-dopa responsiveness, c) L-dopa motor complications despite optimal management, d) Absence of dementia or active psychiatric illness
- Exclusion Criteria for DBS in IPD:
a) Atypical Parkinsonism b) No response to L-dopa c) PD Dementia d) Severe depression or psychosis.
- Expected outcome:
a) Symptoms responsive to DBS: Rigidity, Tremor, Bradykinesia, Drug induced dyskinesia.
b) Symptoms non responsive to DBS: Cognitive decline, hypophonia, postural instability, on state gait freezing, autonomic dysfunction.
- Indications and Targets:
INDICATIONS | TARGETS |
Idiopathic parkinson disease |
|
Primary Dystonia | Globus pallidus internus |
Essential Tremors | Ventral Intermediate Nucleus of thalamus |
OCD |
|
Epilepsy |
|
Complications:
Surgery related: Hemorrhage, Infection, Epilepsy, Air embolism.
Machinery related: Electrode breakage, skin erosions over Internal pulse generator or wirings.
Stimulation related: Psychiatric or cognitive malfunction and increased risk for suicides.
TAKE HOME MESSAGE:
DBS is like a pacemaker for the brain. DBS is preffered over pallidotomy or thalamotomy because of adjustibility and reversibility of DBS with lower complication rates. Its main indications are for the drug resistant movement disorders like IPD, Primary Dystonia, Epilepsy, Tardive syndrome, Essential tremor.
DR. METTA RANJINI MBBS, MD (General Medicine), DrNB Neurology Resident
MENINGITIS
Meningitis, a potentially life-threatening inflammation of the protective membranes covering the brain and spinal cord, remains a significant public health concern globally. In this lecture, we delve into the intricacies of this disease, aiming to provide a comprehensive understanding of its causes, symptoms, types, diagnosis, treatment, and prevention strategies.
The lecture begins by elucidating the etiology of meningitis, highlighting the diverse array of pathogens responsible for its occurrence, including bacteria, viruses, fungi, and, rarely, parasites. Through case studies and epidemiological data, attendees gain insights into the varied clinical manifestations of meningitis, ranging from fever, headache, and neck stiffness to more severe symptoms such as altered mental status, seizures and signs of meningitis like Kernig’s sign, Brudzinski’s neck sign and Brudzinski’s contralateral leg sign.
Emphasizing the critical role of early diagnosis in mitigating the morbidity and mortality associated with meningitis, the lecture explores the various diagnostic modalities available, including lumbar puncture, imaging studies, and laboratory tests. Special attention is paid to the challenges inherent in distinguishing between bacterial and viral meningitis, underscoring the need for judicious clinical assessment and prompt initiation of appropriate therapy with Empirical Treatment with ceftriaxone 2g I/V BD to reduce the mortality and treatment of TB that includes TB meningitis -12 months of ATT, TB Spine (Pott’s spine)-18 months of ATT.
Also they highlighted that CSF Sample should be collected in 4 tubes. 1st Sample goes to Biochemistry as due to risk of minor trauma during LP procedure. The initial tube may contain RBC, so generally it is not sent to pathlab for cell count. Furthermore, the lecture addresses the importance of supportive care measures in optimizing patient outcomes, including close monitoring of vital signs, hydration, and pain management.
In conclusion, this lecture serves as a testament to the multifaceted nature of meningitis, underscoring the imperative for comprehensive understanding, timely intervention, and concerted prevention efforts in tackling this formidable infectious disease threat.
DR. METTA RANJINI MBBS, MD (General Medicine), DrNB Neurology Resident
Cerebral Venous Sinus Thrombosis
Cerebral Venos Sinus Thrombosis(CVT) an important cause of stroke in
young adults (mean age 33y rs) and children.
Caused by complete or partial occlusion of the major cerebral venoussinuses(cerebral venous
sinusthrombosis) .
Three time more common in females.
Changes in blood stasis, vessel wall abnormalities and the composition of the blood (Virchow’striad) lead
to an imbalance between prothrombotic and fibrinolytic processes, progressive predisposing veins to
thrombosis.
Major causes
Dehydration
Infection – Ear,sinuses,mouth,face, neck
Coagulation disorders
Pregnancy, Puerperium,Usage ofOCP, Anaemia
CardiacCauses:ASD,VSD, PFO, Cardiomyopathies,Previous MI
Head trauma, Neurosurgery
Presentation
Headache,seizures, focal neurological deficits, isolated intracranial hypertension
For cavernoussinusthrombosis: Headache, ocular pain, chemosis, proptosis, cranial
nerve palsies (III, IV, VI, opthalmic division of V nerve), Fever (If there isinfective
etiology)
Radiological findings
MRI & MRV
CT & CTV
RADIOLOGICALSIGNS CORD SIGN, EMPTY DELTA SIGN, DENSE TRIANGLE SIGN
(1) CT and MRI images showing superior venous sinus thrombosis
(2) Site of infarction in relation to the thrombus formation in different venous system.
(3) Cord Sign
(A) NCCT Head sagittal, shows abnormal hyperattenuation in the superior sagittal sinus (arrow) and straight sinus (arrowhead).
(B) Sagittal T1MRI, Normal hypointense flow void is absent in the superior sagittal sinus (arrow).
(C) Sagittal Contrast enhanced T1MRI, Normal enhancement is absent in the occluded segment of the superior sagittal sinus (arrow) and straight sinus (arrowhead).
(D) Axial Contrast enhanced T1MRI, shows the “empty delta” sign (arrow) in the occluded segment of the superior sagittal sinus.
Prognostic scoreof CVT
Malignancy, Coma, DVT – 2 points each
Male sex, ICH – 1 point each
>3 – High risk, poor outcome
<3- Low risk, good outcome
Treatment
ESO recommendedlow- molecular-weight heparin as soon as possible after the diagnosis has been
established.
Itisfollowed by longer-termanticoagulation to prevent further venous thrombotic
events.
Duration of anticoagulants : 3 to 6 months for 1 episode of CVT + transient risk factors.
6 to 12 months for 1 episode of CVT + unknown cause. 2 or 3 episodes of CVT or 1 episode and a severe
prothrombotic condition : Lifelong
Dabigatran versus warfarin for 6 months (Re-SPECT CVT), there were no recurrent venous
thromboembolic eventsin either treatment group.
ESOguidelinesrecommend that endovascular treatment should only be considered in
patients with a high pretreatment risk of poor outcome.
Take home message
Cerebral venousthrombosisis a rare, potentially life threatening.
disease presenting in a variety of ways and to a variety of services.
Heparin is the mainstay of acute treatment.
Steroids are not recommended and are linked to poorer prognosis
in CVT. (But in Meningitis, Malignancy, Inflammatory conditions –
used).
Antiepileptic drugsshould not be given routinely as prophylaxis butshould
be initiated quickly if a seizure occurs.
Patients with rapid neurological deterioration because of impending herniation can benefit
from decompression with craniectomy
DR. METTA RANJINI MBBS, MD (General Medicine), DrNB Neurology Resident
APPROACH TO DELIRIUM IN EMERGENCY
DEFINITION:
Delirium is a clinical syndrome that usually develops in the elderly, it’s characterized by an alteration of attention, consciousness and cognition with reduced ability to focus sustain or shift attention.
MAJOR CAUSES:
-Acute neurological diseases. [Acute stroke, haemmorage , encephalitis)
-Metabolic derangement [ dyselectrolaemia, Hyperammanemia)
-Medication (sedative, hypnotics, narcotics, anticholenergic drugs, Steroids, withdrawal of alcohol or alchohol intoxication)
-Seizures [post-Ictal]
-Intercurrent illness. (infections, anemia, dehydration)
-Multiple comonbidry (DM, HTN, asthma)
PRESENTATION:
-It is characterized by acute disturbance of consciousness, change in cognition, fear, anxiety, depression, irritability, anger, euphonia, psychomotar disturbance.
Investigations
Full Biochemistry along with electrolytes and ABG.
TREATMENT:
- Acute correction of underlying cause of delirium
- Symptomatic treatment
- Haloperidol
- Quitiapine
- Dexmedetomodine
- Resperidone
TAKE HOME MESSAGE:
Delirium is a medical emergency which requires urgent care & Investigation to know the Cause & appropriate treatment.
DR. Asharab K. Tadavi (M.B.B.S, M.D Anesthesiology)
EPISTAXIS
Epistaxis, commonly known as nosebleed, is a frequent occurrence encountered in clinical practice, presenting a spectrum of challenges in its diagnosis and management. This lecture aims to demystify the intricacies of epistaxis, offering a comprehensive exploration of its etiology, risk factors, clinical presentation, diagnostic approach, therapeutic interventions, and preventive strategies.
The lecture unravels the delicate vascular architecture of the nasal cavity and the vulnerability of its mucosal lining to trauma, inflammation, and vascular abnormalities. Risk factors for epistaxis are scrutinized, with a focus on modifiable contributors such as environmental conditions, nasal trauma, coagulopathies, hypertension, and anticoagulant or antiplatelet therapy.
Clinical manifestations of epistaxis are explored in detail, encompassing the spectrum of severity from mild, self-limiting bleeds to recurrent or profuse hemorrhage necessitating urgent intervention. Through case studies, clinical vignettes and demo on how to nasal pack, attendees acquired proficiency in the systematic evaluation of epistaxis, including assessment of bleeding severity, localization of the bleeding source, and identification of associated symptoms or complications.
The lecture delves into the diagnostic workup for epistaxis, encompassing a range of modalities such as nasal endoscopy, imaging studies, and laboratory investigations aimed at identifying underlying causes and guiding therapeutic strategies. Special attention is paid to the role of Trotter’s method, hemostatic agents, nasal packing, cautery techniques, and surgical interventions in achieving hemostasis and preventing recurrence.
In conclusion, this lecture serves as a beacon of enlightenment amidst the challenges posed by epistaxis, empowering healthcare professionals with the knowledge, skills, and tools necessary to navigate the bleeding maze effectively.
DR. BHANU BHARDWAJ (M.B.B.S , M.S (ENT))
CARDIAC ARREST
Cardiac arrest stands as a sudden, life-threatening event that strikes without warning, challenging medical professionals and society as a whole. This lecture endeavors to unravel the complexities surrounding cardiac arrest, offering a multifaceted exploration encompassing its mechanisms, risk factors, clinical presentation, management strategies, and avenues for prevention.
Commencing with a profound understanding of the physiological underpinnings of cardiac arrest, the lecture navigates through the intricate interplay of electrical dysrhythmias, ischemia, and structural heart disease, which collectively precipitate this critical condition. By elucidating the cascade of events leading to the cessation of cardiac activity, attendees gain insights into the urgency and gravity of the situation.
Risk factors for cardiac arrest are scrutinized, with a focus on modifiable contributors such as hypertension, coronary artery disease, and lifestyle factors including smoking and physical inactivity.
The lecture delves into the nuances of advanced cardiac life support (ACLS) algorithms, training in basic life support (BLS), and access to automated external defibrillators (AEDs). Furthermore, attendees are apprised of emerging technologies and interventions on the horizon, poised to revolutionize the landscape of cardiac arrest management and prevention.
In summation, this lecture serves as a beacon of enlightenment amidst the darkness of cardiac arrest, empowering healthcare professionals with the knowledge, skills, and tools necessary to confront this formidable adversary head-on.
DR. AABID HUSAIN (M.B.B.S , MD, DM Cardiology)
ANTIPLATELETS
Whenever there is an injury to the blood vessel collagen and von willebrand’s factor activate platelets to secrete aggregants like TXA2, 5HT, adenosine diphosphate receptors. The aggregants then undergo adhesion to the vwF in subendothelial membrane.
Activation of glycoprotein IIb/IIIa in the platelets further promotes aggregation and binds aggregates to fibrinogen.
Exposed phospholipid from platelet surface promote thrombin formation in the coagulation pathway, which converts fibrinogen to fibrin to stablize the clot.
DOSAGE:
ASPIRIN: 81-325mg qd. CLOPIDOGREL: 300mg load, 75mg qd. PRASUGREL: 60mg load, 10mg qd. TICAGRELOR: 180mg load, 90mg bid. TICLOPIDINE: 250mg bid. DIPYRIDAMOLE: 75-100mg qid. CILASTAZOL: 100mg bid. ABCIXIMAB: Bolus: 0.25 mg/kg IV bolus, 10-60 minutes before the start of PCI, followed by infusion of 0.125 µg/kg/min (maximum 10 µg/min) is given for 12 hours. EPTIFIBATIDE: Bolus :180 mcg/kg IV immediately before the procedure followed by an infusion of 2 mcg/kg/min for up to 18-24 hours post-PCI. TIROFIBAN: Bolus :25 mcg/kg IV over 3 to 5minutes, followed by an infusion of 0.15 mcg/kg/min is administered for up to 18 hours.
Aspirin is category A drug in pregnancy. Clopidogrel, Prasugrel, Ticlopidine, Dipyridamole, Eptifibatide and Tirofiban are category B drugs. Ticagrelor, Abciximab and Cilastazole are category C drugs.
DAPT VS SAPT:
|
DAPT(DUAL ANTIPLATELET THERAPY): |
SAPT (SINGLE ANTIPLATELET THERAPY) |
|
ACS- upto 12 months, In high risk patients, duration prolonged |
DAPT is followed SAPT lifelong. |
|
AIS- a) In Intracranial large artery atherosclerosis with severe stenosis (70% to 99%) for 90 days. b) For small artery disease, extracranial large artery atherosclerosis (no revascularization) and c) Intracranial large artery atherosclerosis with stenosis 50% to 69%, or cryptogenic : If NIHSS score <5, For about 21 days. In TIA, if ABCD2 score > 4 for upto 21days. |
AIS- a) Large Infarcts –More than 1/3rd territory of MCA or ½ territory of PCA b) Infarct with hremorrhagic transformation. c) For small artery disease, extracranial large artery atherosclerosis (no revascularization) and Intracranial large artery atherosclerosis with stenosis 50% to 69%, or cryptogenic : If NIHSS score >5 In TIA, if ABCD2 score < 4. |
|
For CAS, Before and 30days after procedure |
For CEA |
|
Unstable angina |
Emergent surgeries should be done even if the patient is on DAPT. For elective surgeries: Aspirin can be continued.
Cangrelor has to be withheld 3 days before whereas clopidogrel before 5 days and prasugrel 7 days prior to the surgery.
Lumbar puncture can be carried out, if patient is aspirin alone. Clopidogrel and prasugrel withheld 5 to 7 days prior and ticlopidine 14 days prior to the LP.
SIDE EFFECTS:
- Bleedig, GI : Ulceration, Angioedema, Bronchospasm, Dermatological problems, Hepatotoxicity, Nausea and vomiting, Thrombocytopenia, Renal damage.
- Clopidogrel has Interaction with PPIs as both are metabolised by CYP3A4.
TAKE HOME MESSAGE:
Antiplatelets indicated in primary and secondary prevention of stroke, acute coronary syndrome, unstable angina, peripheral arterial disease.
DAPT used in ACS for 1 year, in AIS for 21 days to 90days and In TIA for 21days, if ABCD2> 4.
The administration of antiplatelet agents as an adjunctive therapy within 24 hours of intravenous fibrinolysis is not recommended.
Detection of an unruptured intracerebral aneurysm should not be regarded as a contraindication to antiplatelet therapy.
- Patient is on Aspirin
- No AF and no indication of anticoagulation
- Recurrent CVA
- Suspect for Aspirin resistance.
DR. METTA RANJINI MBBS, MD (General Medicine), DrNB Neurology Resident
ANTICOAGULANTS
Anticoagulants inhibit the coagulation pathway there by inhibiting the conversion of fibrinogen into fibrin.
Intrinsic pathway and extrinsic pathway plays role in coagulation.
CLASSIFICATION:
- Vitamin K Antagonists: Warfarin, Acenocoumarol, Dicoumarol.
- Heparins and Heparinoids: UFH, LMWH : Enoxaparin, Dalteparin, Fondaparinux, Tinzaparin, Idraparinux
- Direct Thrombin Inhibitors: Bivalrudin, Lepirudin, Desirudin, Argatroban, Dabigatran, Melagatran
- Direct factor Xa inhibitors/NOACs/DOACs: Apixaban, Edoxaban, Betrixaban, Rivaroxaban
- Warfarin acts by inhibiting Vitamin K epoxide reductase enzyme which inhibits activation of vitamin K which inhibit synthesis of clotting factors II,VII,IX,X from the liver.
- Heparin acts by increasing binding of antithrombin to factor X and II. Thereby inhibiting factor Xa and IIa.
- Heparin acts on factor Xa and IIa equally. Whereas LMWH acts on factor Xa>IIa and Fondaparinux acts on Xa.
- DOACs acts by inhibiting factor Xa.
INDICATIONS FOR ANTICOAGULATION:
- Prevention and Treatment of Deep Venous Thrombosis b) Treatment of Pulmonary Emboli c)
Prevention of stroke in patients with atrial fibrillation, artificial heart valves, established thrombosis (DVT, Cardiac) d) Ischaemic heart disease e) CVST f) During procedures such as Cardiac Catheterisation, Dialysis.
- PT needs to be monitored in Warfarin. Target INR: 2-3 and for valvular heart diseases: 2.5 to 3.5
- aPTT need to be monitored in Heparin. Target aPTT 1.5 to 2.5 times above baseline.
SIDE EFFECTS:
Bleeding, Purple glove syndrome in warfarin, Thrombocytopenia, Osteoporosis, Hypersensitivity.
Warfarin is not indicated in pregnancy as it causes fetal warfarin syndrome.
HIT is major complication of Heparin. Female, Long term use of heparin, UFH, Recent surgeries are major risk groups. HIT occurs with UFH > LMWH > Fondaparinux. Treatment of HIT: Withdraw heparin and initiate Lepirudin or Argatroban.
Features to consider for NOACs
- Faster onset , Shorter ½ life, Less drug-drug interactions, No need for monitoring with NOACs.
- CHADS2VA2Sc score assess the risk of stroke in patient’s with non valvular AF. Total score: 9, Score >/=2 indicated high risk.
- HASBLED score assess the 1 year risk of major bleeding in patients on anticoagulation for AF. Total score: 9, Score >/=3 indicated as high risk of bleeding and needed frequent follow ups.
- Oral anticoagulation therapy to prevent thromboembolism is recommended in AF, If CHADS2VA2Sc score is more than 3 in male and more than 2 in female. NOACs is recommended over warfarin in such patients.
PREFERRED ANTICOAGULANT:
A)Cancer- LMWH, Factor X inhibitors. B) Once daily oral dose: Rivaroxaban, Edoxaban, VKA. C)Liver disease and coagulopathy-LMWH. D)Renal disease and creatinine cl<30ml/min- VKA (DOACs and LMWH –C/I, However, some DOACs dosing can be renally adjusted although adjustment varies). E)CAD-VKA, Rivaroxaban, Apixaban, Edoxaban. F)Dyspepsia or H/O GI bleeding: VKA, Apixaban. G) Valvular heart disese:VKA.H)Thrombolytic therapy : UFH. I)Reversal agents needed: VKA, UFH, DOACs. J) Pregnancy or pregnancy risk: LMWH
REVERSAL AGENTS:
- Warfarin: Vitamin K & FFP
- Dabigatran: Idracizumab 2-2.5 gm bolus IV
- Factor Xa Inhibitors (Rivaroxaban & Apixaban): Andexenat alpha IV bolus and infusion (2Hrs)
- Heparin: Protamine sulphate 1mg per 100units of heparin.
- Aripazine, Ciraparantag (PER977): Under investigationto reverse effects of, is an investigational drug designed to reverse the effects of factor Xa inhibitors, dabigatran, and heparin (UNH and LMWH).
FOR ELECTIVE SURGERIES:
DRUG | STOPPED BEFORE SURGERY | RESTARTED AFTER SURGERY |
WARFARIN | 5 DAYS PRIOR | NEXT DAY IF LOW BLEEDING RISK SECOND DAY IF HIGH BLEEDING RISK |
NOACS | 1DAY PRIOR (FOR LOW RISK BLEEDING)
2 DAYS PRIOR (FOR HIGH RISK BLEEDING)
| NEXT DAY
SECOND DAY |
HEPARIN | 6 TO 12 HOURS PRIOR | 4 TO 6 HOURS |
LMWH | 24 HOURS PRIOR | 12 TO 24 HOURS |
TAKE HOME MESSAGE:
NOACs considered over Warfarin but in valvular heart diseases still warfarin is preffered.
Oral anticoagulation therapy to prevent thromboembolism is recommended in patient’s with AF, If CHADS2VA2Sc score is more than 3 in male and more than 2 in female.
DR. METTA RANJINI MBBS, MD (General Medicine), DrNB Neurology Resident
