Benign or not benign
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This document presents a case of a 37-year-old male who experienced a sudden and severe headache while having sex. Imaging revealed a subarachnoid hemorrhage localized to the perimesencephalic cisterns. The document then discusses perimesencephalic subarachnoid hemorrhage, defining it as a benign and non-aneurysmal form of subarachnoid hemorrhage centered around the midbrain. It reviews the epidemiology, proposed etiologies involving venous anomalies, clinical features and good prognosis of perimesencephalic subarachnoid hemorrhage.
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Brugada syndrome
Brugada syndrome (BrS) is an inherited cardiac disorder,
characterised by a typical ECG pattern and an increased
risk of arrhythmias and sudden cardiac death (SCD).
BrS is a challenging entity, in regard to diagnosis as
well as arrhythmia risk prediction and management.
Nowadays, asymptomatic patients represent the majority
of newly diagnosed patients with BrS, and its incidence
is expected to rise due to (genetic) family screening.
Progress in our understanding of the genetic and
molecular pathophysiology is limited by the absence
of a true gold standard, with consensus on its clinical
definition changing over time. Nevertheless, novel
insights continue to arise from detailed and in-depth
studies, including the complex genetic and molecular
basis. This includes the increasingly recognised
relevance of an underlying structural substrate. Risk
stratification in patients with BrS remains challenging,
particularly in those who are asymptomatic, but recent
studies have demonstrated the potential usefulness
of risk scores to identify patients at high risk of
arrhythmia and SCD. Development and validation of
a model that incorporates clinical and genetic factors,
comorbidities, age and gender, and environmental
aspects may facilitate improved prediction of disease
expressivity and arrhythmia/SCD risk, and potentially
guide patient management and therapy. This review
provides an update of the diagnosis, pathophysiology
and management of BrS, and discusses its future
perspectives.
Sudden cardiac death in structurally normal hearts
Potential causes of sudden cardiac death without structural heart disease include long QT syndrome, short QT syndrome, catecholaminergic polymorphic ventricular tachycardia, Brugada syndrome, early repolarization syndrome, idiopathic ventricular fibrillation, commotio cordis, and familial sudden cardiac death. These conditions are often genetic and can result in fatal arrhythmias. Evaluation of survivors and families of victims is important to determine the cause and provide appropriate treatment such as an implantable cardioverter-defibrillator.
Bayes syndrome and atrial fibrillation and stroke
1) Advanced interatrial block (aIAB) is associated with delayed and retrograde activation of the left atrium due to impairment of the Bachmann's bundle, which connects the left and right atria. This conduction delay between atria is linked to a high risk of atrial arrhythmias like atypical atrial flutter or fibrillation.
2) aIAB can be diagnosed on electrocardiogram by a prolonged P wave over 120ms with biphasic morphology in leads II, III, and aVF, indicating retrograde left atrial activation. aIAB prevalence increases with age and is a risk factor for atrial fibrillation and stroke.
3) "Bayes syndrome" refers
Cerebral Venous Thrombosis
A 37-year-old male painter was admitted due to seizures and headache. CT scan showed multiple hemorrhagic infarcts in both brain hemispheres. Further imaging revealed superior sagittal sinus and bilateral transverse sinus thrombosis. The patient was started on anticoagulation therapy and made a good recovery.
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Endomyocardial fibrosis (EMF) is a disease that is characterized by fibrosis of the apical endocardium of the right ventricle (RV), left ventricle (LV), or both.
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The heart failure is associated with atrioventricular-valve regurgitation.
Endomyocardial fibrosis is a major cause of illness and death in areas where it is endemic, and in its severest form carries a very poor prognosis, with an estimated survival of 2 years after diagnosis.
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Brugada syndrome
Brugada syndrome (BrS) is an inherited cardiac disorder,
characterised by a typical ECG pattern and an increased
risk of arrhythmias and sudden cardiac death (SCD).
BrS is a challenging entity, in regard to diagnosis as
well as arrhythmia risk prediction and management.
Nowadays, asymptomatic patients represent the majority
of newly diagnosed patients with BrS, and its incidence
is expected to rise due to (genetic) family screening.
Progress in our understanding of the genetic and
molecular pathophysiology is limited by the absence
of a true gold standard, with consensus on its clinical
definition changing over time. Nevertheless, novel
insights continue to arise from detailed and in-depth
studies, including the complex genetic and molecular
basis. This includes the increasingly recognised
relevance of an underlying structural substrate. Risk
stratification in patients with BrS remains challenging,
particularly in those who are asymptomatic, but recent
studies have demonstrated the potential usefulness
of risk scores to identify patients at high risk of
arrhythmia and SCD. Development and validation of
a model that incorporates clinical and genetic factors,
comorbidities, age and gender, and environmental
aspects may facilitate improved prediction of disease
expressivity and arrhythmia/SCD risk, and potentially
guide patient management and therapy. This review
provides an update of the diagnosis, pathophysiology
and management of BrS, and discusses its future
perspectives.
Sudden cardiac death in structurally normal hearts
Potential causes of sudden cardiac death without structural heart disease include long QT syndrome, short QT syndrome, catecholaminergic polymorphic ventricular tachycardia, Brugada syndrome, early repolarization syndrome, idiopathic ventricular fibrillation, commotio cordis, and familial sudden cardiac death. These conditions are often genetic and can result in fatal arrhythmias. Evaluation of survivors and families of victims is important to determine the cause and provide appropriate treatment such as an implantable cardioverter-defibrillator.
Bayes syndrome and atrial fibrillation and stroke
1) Advanced interatrial block (aIAB) is associated with delayed and retrograde activation of the left atrium due to impairment of the Bachmann's bundle, which connects the left and right atria. This conduction delay between atria is linked to a high risk of atrial arrhythmias like atypical atrial flutter or fibrillation.
2) aIAB can be diagnosed on electrocardiogram by a prolonged P wave over 120ms with biphasic morphology in leads II, III, and aVF, indicating retrograde left atrial activation. aIAB prevalence increases with age and is a risk factor for atrial fibrillation and stroke.
3) "Bayes syndrome" refers
Cerebral Venous Thrombosis
A 37-year-old male painter was admitted due to seizures and headache. CT scan showed multiple hemorrhagic infarcts in both brain hemispheres. Further imaging revealed superior sagittal sinus and bilateral transverse sinus thrombosis. The patient was started on anticoagulation therapy and made a good recovery.
Images of Vascular Medicine Symposia - The CRUDEM Foundation
A 36-year-old male on ACE inhibitors presents with a sore throat and difficulty swallowing, likely experiencing uvular angioedema as a rare but potentially fatal side effect of ACE inhibitors. A 50-year-old woman presents with shortness of breath and fatigue, and her ECG demonstrates a malignant pericardial effusion. A 40-year-old male with a heart murmur presents with fever, weight loss, and chills, exhibiting signs of infective endocarditis.
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Endomyocardial fibrosis (EMF) is a disease that is characterized by fibrosis of the apical endocardium of the right ventricle (RV), left ventricle (LV), or both.
The clinical manifestations are largely related to the consequences of restrictive ventricular filling, including left and right sided heart failure.
The heart failure is associated with atrioventricular-valve regurgitation.
Endomyocardial fibrosis is a major cause of illness and death in areas where it is endemic, and in its severest form carries a very poor prognosis, with an estimated survival of 2 years after diagnosis.
TOF.pptx
Tetralogy of Fallot (TOF) is a congenital heart defect characterized by four anatomical features - ventricular septal defect, right ventricular outflow tract obstruction, overriding aorta, and right ventricular hypertrophy. It is the most common cyanotic heart defect in children beyond infancy. Patients typically present with cyanosis in infancy which worsens with activity due to right-to-left shunting through the ventricular septal defect. On examination, a systolic murmur may be heard due to the outflow tract obstruction. Without surgical repair, long-term outcomes are poor.
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This document presents a case report of a rare case of cardiac amyloidosis diagnosed by MRI. A 73-year-old man presented with dyspnea and was found to have hypertrophied ventricles and diastolic dysfunction on echocardiogram. CMR revealed increased wall thickness, dilated atria, reduced ejection fraction, and global subendocardial late gadolinium enhancement of the ventricles and atria, consistent with cardiac amyloidosis which was later confirmed by biopsy. The case report demonstrates how CMR can help diagnose cardiac amyloidosis in a non-invasive manner by detecting characteristic amyloid infiltration patterns earlier than other imaging modalities.
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- Takatsubo cardiomyopathy (TTC), also known as stress cardiomyopathy or broken heart syndrome, is a reversible form of heart failure caused by transient left ventricular dysfunction.
- It is typically triggered by periods of intense emotional or physical stress and is characterized by EKG changes and chest pain similar to a heart attack despite an absence of coronary artery blockages.
- The leading theories for its pathophysiology include high catecholamine levels from stress overwhelming the heart muscle or coronary microvascular dysfunction impairing blood flow. The heart regains normal function within weeks with supportive care.
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1) The document discusses hypertrophic cardiomyopathy (HCM), a disease where the heart muscle becomes abnormally thick. HCM is most commonly caused by mutations in genes encoding sarcomeric proteins.
2) The genetic basis of HCM involves mutations in genes like beta-myosin heavy chain that result in mutated sarcomeric proteins. Research aims to understand how these mutations initiate disease pathways.
3) New genomic technologies like genotyping arrays and next-generation sequencing can be used to diagnose cardiomyopathies by determining genotypes across many genetic sites or sequencing entire genomes.
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2) Biomarkers like troponins and BNP are often elevated in sepsis patients and correlated with severity of illness.
3) Mechanisms contributing to cardiac dysfunction include circulatory changes, autonomic dysregulation, metabolic and mitochondrial dysfunction, inflammation, and calcium trafficking issues.
4) Cytokines and nitric oxide are thought to
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The results showed:
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- Extensive diagnostic testing including blood tests, echocardiograms, vessel imaging found relevant abnormalities in 136 of 203 patients on angiography and detected the likely stroke cause in nearly 90% of patients.
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This document provides an overview of cardiac amyloidosis, including:
1. The most common forms that affect the heart are immunoglobulin-derived light chains and transthyretin.
2. Cardiac amyloidosis typically presents in the 5th to 7th decade with symptoms of severe heart failure such as exertional dyspnea and peripheral edema.
3. Investigations include ECG showing low voltage complexes, echocardiogram showing concentric left ventricular thickening, and cardiac MRI and tissue biopsy to detect amyloid deposits.
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Here are the key points from the case:
- A 75-year-old post-menopausal woman presented with pneumonia and chest pain
- In the last 24 hours she experienced dyspnea and sputum production
- This physical stressor of pneumonia could potentially trigger Takotsubo cardiomyopathy in this high-risk demographic
- Her symptoms of chest pain could represent Takotsubo cardiomyopathy mimicking an acute coronary syndrome
- Further workup would be needed to evaluate for potential left ventricular dysfunction and regional wall motion abnormalities consistent with Takotsubo cardiomyopathy versus other causes of her symptoms.
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Early repolarisation syndrome (2)
Early repolarization syndrome is defined by J-point elevation in the ECG. While prevalence is 1-9% depending on factors, the arrhythmic risk is generally low though higher for those with horizontal or downward sloping ST segments. The mechanism involves enhanced outward potassium currents leading to transmural voltage gradients. Genetic variants have been linked to severe cases. Clinical manifestations range from asymptomatic findings to cardiac arrest. Diagnosis requires exclusion of other causes in survivors of sudden cardiac death. Prognosis depends on location and morphology of early repolarization pattern. Therapies include beta-agonists and antiarrhythmic drugs while ICDs are for high-risk patients. Familial inheritance is seen though screening asymptomatic family
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This case report describes a 30-year old male who presented with chest discomfort and progressive breathlessness. An ECG showed ST elevation resembling a STEMI. However, cardiac enzymes were normal and there was incoherence between symptoms and ECG. Cardiac sarcoidosis was considered and confirmed through cardiac MRI, endomyocardial biopsy, and elevated serum ACE level. The patient was started on steroids and anti-arrhythmics, resulting in partial symptom remission. This case highlights that cardiac sarcoidosis can present with ST elevation on ECG and should be considered to avoid unnecessary fibrinolysis when there is discrepancy between presentation and test results.
Takotsubo cardiomyopathy Machanism
1) Takotsubo syndrome is a cardiac condition triggered by stressful events where the left ventricle temporarily takes on a distinctive "Takotsubo" shape.
2) It is thought to be caused by very high levels of stress hormones like adrenaline activating negative inotropic pathways in the heart through beta-2 adrenergic receptors, particularly in the left ventricular apex.
3) This leads to left ventricular dysfunction and heart failure symptoms, but the heart typically recovers its normal function within weeks as the stress response subsides. However, the full pathophysiology and long term effects are still being uncovered.
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Takasubo cardiomyopathy
- Takatsubo cardiomyopathy (TTC), also known as stress cardiomyopathy or broken heart syndrome, is a reversible form of heart failure caused by transient left ventricular dysfunction.
- It is typically triggered by periods of intense emotional or physical stress and is characterized by EKG changes and chest pain similar to a heart attack despite an absence of coronary artery blockages.
- The leading theories for its pathophysiology include high catecholamine levels from stress overwhelming the heart muscle or coronary microvascular dysfunction impairing blood flow. The heart regains normal function within weeks with supportive care.
Hypertrophic Cardiomyopathy
1) The document discusses hypertrophic cardiomyopathy (HCM), a disease where the heart muscle becomes abnormally thick. HCM is most commonly caused by mutations in genes encoding sarcomeric proteins.
2) The genetic basis of HCM involves mutations in genes like beta-myosin heavy chain that result in mutated sarcomeric proteins. Research aims to understand how these mutations initiate disease pathways.
3) New genomic technologies like genotyping arrays and next-generation sequencing can be used to diagnose cardiomyopathies by determining genotypes across many genetic sites or sequencing entire genomes.
Noncompaction Cardiomyopathy, NGUYEN TUAN VU, NGUYEN THI KIM SANG, DUONG PHI ...
A 33-year-old female patient presented with severe heart failure for one year and was previously diagnosed with dilated cardiomyopathy. She underwent cardiac imaging tests including echocardiography, ECG, and MSCT to rule out coronary artery disease. The echocardiography and MSCT revealed prominent trabeculations and a spongiform appearance of the left ventricle consistent with noncompaction cardiomyopathy. Noncompaction cardiomyopathy is a rare genetic heart condition characterized by excessive trabeculations and deep intratrabecular recesses in the left ventricle.
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The patient presented with altered sensorium, decreased movement in their right side, and deviation of their mouth to the left. Imaging showed a non-hemorrhagic infarct in the left fronto-parietal region consistent with a stroke. An echocardiogram found left ventricular non-compaction (LVNC), a mobile clot attached to the left ventricle, and normal systolic function. The final diagnosis was LVNC, stroke, hyperhomocysteinemia, and hyperlipidemia. LVNC is a rare heart condition where the left ventricle fails to compact during development, leaving prominent trabeculations. It can cause heart failure, arrhythmias, and thromboemb
Early repolrisation syndrome(ERS)
This document discusses early repolarization syndrome (ERS). [1] ERS is characterized by J point elevation in the inferior and/or lateral leads of an ECG. [2] It was first described in the 1930s and takes its name from increased repolarization seen in some heart conditions. [3] ERS has three subtypes based on location of J point elevation and risk of arrhythmias. The mechanism involves increased heterogeneity of ventricular repolarization. ERS has been associated with increased risk of fatal arrhythmias, especially when the pattern involves the inferior leads.
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ICN Victoria presents Dr Andrew Hilton, Intensivist at the Austin Hospital in Melbourne, talking on the use of Echocardiography to evaluate the septic heart. Recorded at our November 2014 ICN Victoria meeting.
Sepsis-Induced Cardiac Dysfunction
This document provides an overview of sepsis-induced cardiac dysfunction, specifically intrinsic myocardial depression. It discusses several key points:
1) Myocardial depression occurs in 40-50% of patients with septic shock and is associated with worse outcomes. Survivors have lower ejection fractions and higher end-diastolic volumes compared to non-survivors.
2) Biomarkers like troponins and BNP are often elevated in sepsis patients and correlated with severity of illness.
3) Mechanisms contributing to cardiac dysfunction include circulatory changes, autonomic dysregulation, metabolic and mitochondrial dysfunction, inflammation, and calcium trafficking issues.
4) Cytokines and nitric oxide are thought to
Acv en jovenes
This study reviewed data on 215 young adults aged 18-45 admitted with ischemic stroke or transient ischemic attack (TIA) to a university hospital stroke center between 2005-2010.
The results showed:
- High rates of traditional vascular risk factors like hypertension (20%), diabetes (11%), dyslipidemia (38%), and smoking (34%).
- Extensive diagnostic testing including blood tests, echocardiograms, vessel imaging found relevant abnormalities in 136 of 203 patients on angiography and detected the likely stroke cause in nearly 90% of patients.
- Common causes were cardioembolism (47%), including 17% with patent foramen ovale, and arterial lesions in the middle cerebral artery (23%),
Cardiac amyloidosis,Review.2017
This document provides an overview of cardiac amyloidosis, including:
1. The most common forms that affect the heart are immunoglobulin-derived light chains and transthyretin.
2. Cardiac amyloidosis typically presents in the 5th to 7th decade with symptoms of severe heart failure such as exertional dyspnea and peripheral edema.
3. Investigations include ECG showing low voltage complexes, echocardiogram showing concentric left ventricular thickening, and cardiac MRI and tissue biopsy to detect amyloid deposits.
Brugada Syndrome - Case Study
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Precise data regarding Brugada Syndrome with a Case Study for DGNM, B.Sc Nursing & M.Sc Nursing Students.
Takotsubo cardiomyopathy
Here are the key points from the case:
- A 75-year-old post-menopausal woman presented with pneumonia and chest pain
- In the last 24 hours she experienced dyspnea and sputum production
- This physical stressor of pneumonia could potentially trigger Takotsubo cardiomyopathy in this high-risk demographic
- Her symptoms of chest pain could represent Takotsubo cardiomyopathy mimicking an acute coronary syndrome
- Further workup would be needed to evaluate for potential left ventricular dysfunction and regional wall motion abnormalities consistent with Takotsubo cardiomyopathy versus other causes of her symptoms.
Cerebral Venous Thrombosis
Cerebral vein thrombosis is an important cause of stroke in young adults and children. It has a wide variety of clinical manifestations, making it difficult to diagnose. The document outlines the anatomy, risk factors, clinical presentation, diagnostic imaging, treatment, and prognosis of cerebral vein thrombosis. Early diagnosis and anticoagulant treatment are emphasized as crucial for optimal outcomes of this condition.
CARDIAC PATHOLOGY (MCQ QUESTIONS & ANSWERS)
ALL THE QUESTIONS ARE HAVING VERY STANDARD ANSWERS FROM THE STANDARD BOOKS)
REF : ROBBINS & COTRAN PATHOLOGIC BASIS OF DISEASE.
COMPREHENSIVE IMAGE BASED REVIEW OF PATHOLOGY BY SONI .
GARG & GUPTA PATHOLOGY REVIEW & GENETICS.
Early repolarisation syndrome (2)
Early repolarization syndrome is defined by J-point elevation in the ECG. While prevalence is 1-9% depending on factors, the arrhythmic risk is generally low though higher for those with horizontal or downward sloping ST segments. The mechanism involves enhanced outward potassium currents leading to transmural voltage gradients. Genetic variants have been linked to severe cases. Clinical manifestations range from asymptomatic findings to cardiac arrest. Diagnosis requires exclusion of other causes in survivors of sudden cardiac death. Prognosis depends on location and morphology of early repolarization pattern. Therapies include beta-agonists and antiarrhythmic drugs while ICDs are for high-risk patients. Familial inheritance is seen though screening asymptomatic family
Fibrinolysis in stemi a second thought- tip august 2016
This case report describes a 30-year old male who presented with chest discomfort and progressive breathlessness. An ECG showed ST elevation resembling a STEMI. However, cardiac enzymes were normal and there was incoherence between symptoms and ECG. Cardiac sarcoidosis was considered and confirmed through cardiac MRI, endomyocardial biopsy, and elevated serum ACE level. The patient was started on steroids and anti-arrhythmics, resulting in partial symptom remission. This case highlights that cardiac sarcoidosis can present with ST elevation on ECG and should be considered to avoid unnecessary fibrinolysis when there is discrepancy between presentation and test results.
Takotsubo cardiomyopathy Machanism
1) Takotsubo syndrome is a cardiac condition triggered by stressful events where the left ventricle temporarily takes on a distinctive "Takotsubo" shape.
2) It is thought to be caused by very high levels of stress hormones like adrenaline activating negative inotropic pathways in the heart through beta-2 adrenergic receptors, particularly in the left ventricular apex.
3) This leads to left ventricular dysfunction and heart failure symptoms, but the heart typically recovers its normal function within weeks as the stress response subsides. However, the full pathophysiology and long term effects are still being uncovered.
Alcohol and heart
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Left Ventricular Noncompaction Cardiomyopathy (LVNC) with Left Ventricular Ap...
This case report describes a 60-year-old man diagnosed with left ventricular non-compaction cardiomyopathy (LVNC) presenting with congestive heart failure. Echocardiography revealed prominent trabeculations in the left ventricle with blood flow in the intertrabecular recesses, and a ratio of non-compacted to compacted myocardium greater than 2:1, consistent with LVNC. A small thrombus was also present. The patient was treated medically and showed improvement. LVNC is a rare congenital heart condition characterized by excessive trabeculations in the left ventricle that can cause heart failure, arrhythmias, or thromboembolic events. Echocardiography is
The indian consensus guidance on stroke prevention in
This document provides guidance on the use of non-vitamin K oral anticoagulants (NOACs) for stroke prevention in atrial fibrillation in India. It discusses dose recommendations, monitoring, and treatment of overdose for NOACs. It also reviews stroke risk and bleeding risk assessment tools and compares the efficacy and safety of NOACs to warfarin. NOACs are preferable to warfarin due to fewer drug and food interactions and no required monitoring, though special considerations are needed for Asian populations who are at higher risk of bleeding on warfarin. The guidance aims to optimize practical use of NOACs in various clinical scenarios.
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CSF cisterns
1. The document discusses the anatomy and imaging features of cerebrospinal fluid (CSF) cisterns and spaces. It describes the locations and contents of various cisterns such as the interpeduncular, chiasmatic, crural, ambient and cerebellomedullary cisterns.
2. Imaging findings of different pathological conditions are presented, including benign external hydrocephalus, subdural hematoma, hydrocephalus, atrophy and periventricular leukomalacia. Key distinguishing features between these entities are highlighted.
3. An overview of CSF spaces is given, outlining the appearance of normal, atrophic and edematous/hydrocephalic states.
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This document summarizes a presentation on whether early surgery improves outcomes for patients with poor-grade aneurysmal subarachnoid haemorrhage compared to delayed surgery. No randomized controlled trials have evaluated this question directly. The presentation reviews several observational studies that found early surgery (within 24 hours) was associated with mortality rates around 30% and favorable outcome rates around 50% for poor-grade patients. While the evidence is limited, indirect comparisons across studies suggest early surgery may reduce risks of rebleeding compared to delayed surgery, though individual patient factors still need consideration.
subarachnoid hemorrhage
A 35-year-old male presented to the emergency room with a sudden severe headache and neck stiffness after pruning flowers in his garden. A CT scan confirmed that he had experienced a subarachnoid hemorrhage (SAH), which is a type of stroke caused by bleeding into the space between the brain and the thin tissues that cover the brain. The bleeding is often due to the rupture of an aneurysm or arteriovenous malformation in the brain. Treatment involves bed rest, controlling hypertension, steroids or diuretics to reduce brain swelling, calcium channel blockers to reduce mortality, and potentially clipping or coiling the aneurysm to prevent rebleeding if it is the cause.
Cns Sah 5th Class.
Subarachnoid haemorrhage (SAH) typically presents with a sudden, severe thunderclap headache accompanied by vomiting. 85% of SAH cases are caused by saccular aneurysms bulging from cerebral artery bifurcations. The immediate mortality of aneurysmal SAH is about 30% and survivors have around a 40% risk of re-bleeding within the first 4 weeks without treatment. Endovascular coiling or surgical clipping of the aneurysm reduces the risks of early and late re-bleeding.
Cerebral Aneursym & Subarachnoid Haemorrhage
Property of Prof Dr. Alif Kelaney, Department of NeuroSurgery Department, Faculty of Medicine. University of Zagazig
Akinetic mutism after subarachnoid haemorrhage
This document describes three cases of patients who developed akinetic mutism after suffering subarachnoid haemorrhages from ruptured cerebral aneurysms. Akinetic mutism is characterized by a lack of verbal and motor output despite preserved alertness. In the cases presented, MRI imaging showed bilateral ischemia of the medial frontal lobes in all three patients. The cingulate cortex, which was affected in these cases, plays an important role in motor function, vocalization, and emotions. While prognosis is variable, two of the three patients showed significant improvement in functioning over time despite initial severe symptoms of akinetic mutism.
Subarachnoid hemorrhage
This document provides an overview of subarachnoid hemorrhage (SAH). It defines SAH as blood entering the subarachnoid space, with the most common cause being the rupture of an intracranial aneurysm (65-80% of cases). The incidence is about 9-10 per 100,000 people per year. Clinical presentation includes a sudden, severe headache and may include decreased consciousness, neck stiffness, vomiting, and vision changes. Diagnosis is made through CT scan, MRI, lumbar puncture, and angiography. Multiple grading scales exist to classify SAH severity and predict outcomes, with the Hunt and Hess and World Federation of Neurosurgeons scales discussed in detail.
Subarachnoid haemorrhage assessment and investigation
1) The document summarizes a presentation on the assessment and investigation of subarachnoid haemorrhage (SAH).
2) It finds that modern CT scans have high accuracy in detecting SAH within 6 hours, but lumbar puncture remains important for cases presenting later.
3) The risk of serious side effects from lumbar puncture often outweigh its benefits, except for patients with pre-test probabilities of SAH between 2-7% based on their history and exam findings.
Subarachnoid haemorrhage
Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space between the brain's outermost layers. It is often caused by the rupture of an aneurysm, which is a bulge or weakening in the wall of a brain artery. Symptoms include a sudden and severe headache, decreased consciousness, vomiting, and neck stiffness. Diagnosis involves CT scan and lumbar puncture to detect blood. Treatment focuses on preventing rebleeding through aneurysm coiling or clipping, and managing complications like hydrocephalus, vasospasm, seizures, and hyponatremia. Prognosis depends on the severity of the initial bleed and development of complications.
CT of acute intracranial pathology
This document provides an overview of common CT findings in acute intracranial pathology, including trauma and stroke. Key points include:
- Extradural hematomas appear as biconvex lenses, while subdural hematomas are crescent shaped. Intraparenchymal hemorrhages can cause mass effect.
- Ischemic strokes appear as low density areas that obscure gray-white matter differentiation. Hemorrhagic strokes are centered in basal ganglia.
- Subarachnoid hemorrhage has a classic "five-pointed star" appearance around the circle of Willis. It can extend into ventricles and cause hydrocephalus.
- Vasogenic edema spares
SAH (Subarachnoid Haemorrhage)
This document provides information on subarachnoid haemorrhage (SAH), including relevant anatomy, etiology, pathophysiology, risk factors, clinical presentation, grading scales, diagnostic workup and findings, and management. The key points are:
- SAH is bleeding into the subarachnoid space between the arachnoid and pia mater layers, where blood vessels and CSF circulate.
- The most common cause is aneurysm rupture (80-85%), followed by non-aneurysmal haemorrhage (10%) and other less common causes.
- Clinical presentation includes thunderclap headache, reduced consciousness, meningism, seizures. Grading
SUBARACHNOID HEMORRHAGE
Subarachnoid hemorrhage occurs when there is bleeding into the subarachnoid space surrounding the brain. It is usually caused by the rupture of an intracranial aneurysm. Risk factors include age, family history, smoking, and hypertension. Patients often present with a sudden and severe headache described as "the worst headache of my life". Diagnosis is typically made through CT scan or lumbar puncture. Treatment involves securing the aneurysm through clipping or coiling to prevent rebleeding, as well as managing complications such as cerebral vasospasm, seizures, and hydrocephalus.
Subarachnoid haemorrhage
The document provides information on subarachnoid haemorrhage (SAH), including:
- SAH is a neurological emergency caused by bleeding in the subarachnoid space, usually due to a ruptured saccular aneurysm.
- Clinical manifestations include the sudden onset of the worst headache of one's life, neck stiffness, vomiting, focal neurological deficits, and loss of consciousness.
- Investigations include non-contrast CT scan, which identifies the location and extent of subarachnoid blood in 95% of cases within 72 hours, and cerebral angiography to locate the aneurysm.
Imaging of Non-traumatic Intracranial Hemorrhage
This document discusses the evaluation and diagnosis of non-traumatic intracranial hemorrhage using head CT. It provides information on scan techniques for non-contrast, contrast-enhanced, CTA and CTV scans. It describes when to stop at a non-contrast CT, when IV contrast or additional imaging such as CTA, CTV or MRI is needed based on the location and appearance of the hemorrhage. The document also discusses the appearance, diagnosis and differentials of various types of hemorrhages such as SAH, SDH, IPH, and multi-compartment ICH.
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Subarachnoid haemorrhage assessment and investigation
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CEREBRAL VENOUS THROMBOSIS
Cerebral venous thrombosis (CVT) is an uncommon type of stroke caused by a blood clot in the brain's venous sinuses or veins. It has a significant morbidity. Common presentations include headache, seizures, and long-lasting neurological deficits. Diagnosis is made through imaging studies like MRI and MRV. Treatment involves management of increased intracranial pressure, seizures, and anticoagulation with heparin or thrombolytics to prevent extension of clots. Prognosis depends on factors like impaired consciousness, underlying cause and location of clots. Most patients recover without sequelae, but mortality can be high if left untreated.
Stroke, assessments , fibrolysis therapy
This document provides information about strokes, including:
- Strokes occur when the blood supply to the brain is interrupted, causing neurological deficits. The two main types are ischemic (85%) and hemorrhagic (15%).
- Risk factors include hypertension, diabetes, high cholesterol, smoking, obesity, and prior cardiovascular disease.
- Diagnosis involves history, physical exam, blood tests, CT/MRI scans. CT scans are used to distinguish between ischemic and hemorrhagic strokes.
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Aortic Dissection
The document describes a case of a 46-year-old male who presented with sudden onset chest and back pain that progressed to weakness in his lower extremities. Imaging revealed an aortic dissection involving the ascending aorta and descending aorta. He underwent surgery to replace the dissected ascending aorta but later developed multiple complications and died. The document also reviews the classification, presentation, risk factors, diagnosis and management of aortic dissections.
Aortic regurgitation
The document discusses the anatomy, causes, diagnosis, and management of aortic regurgitation (AR). It provides details on the location of the aortic valve, variants such as bicuspid aortic valve, and common causes of AR including rheumatic heart disease. Physical exam findings, echocardiography parameters, and indications for surgery to replace the aortic valve are summarized. Medical management including vasodilator therapy to reduce afterload is also reviewed.
QPR-Stroke
This document discusses the pathology of stroke and includes several case studies. It covers topics such as the types, etiology, pathogenesis, clinical features and complications of stroke. It also discusses transient ischemic attacks, hypertension and its complications and pathologies, arterial malformations, global ischemia, and venous infarcts. Microscopic features of infarction at various time points are also addressed.
Reversible cerebral vasoconstriction syndrome
RCVS is usually a benign cerebral vascular dysregulation induced clinico-radiological syndrome presents typically with recurrent thunderclap headache with or without ischemic/hemorrhagic stroke or cerebral edema with vasoconstriction. Various risk factors are responsible for this syndrome.
Vasc Demlecture
Vascular dementia has been recognized since the 17th century, but was more clearly defined in the late 19th/early 20th centuries. It results from vascular brain injuries including strokes and small vessel disease. Diagnostic criteria have evolved, with NINDS-AIREN currently most widely used. Pathogenesis involves reduced blood flow and oxidative stress damaging blood vessels and brain tissue. Imaging plays a key role, with MRI best showing lesions and white matter hyperintensities. Higher blood pressure is a risk factor, and controlling vascular risk factors may help prevent cognitive decline.
simultaneous anterolateral medullary infarct
This case report describes an unusual case of a 31-year-old male who presented with symptoms of Wallenberg syndrome due to simultaneous bilateral infarction of the anterolateral medulla. Extensive evaluation did not reveal a clear cause of the stroke. MRI showed subacute infarcts in the anterolateral aspect of the medulla bilaterally. CT angiogram showed a hypoplastic left vertebral artery but no significant stenosis. Investigations ruled out conditions like vasculitis, vascular malformations, and cardiac abnormalities. The patient was diagnosed with cryptogenic stroke and made a near complete recovery with treatment. This case highlights the importance of thorough evaluation for young patients presenting with stroke to identify potentially treatable causes.
Syncope A Case Presentation Edited
Jackie, a 54-year-old woman with a history of seizure disorder, presents with recurrent syncope. She has experienced 3 episodes in the past 8 months where she loses consciousness for about 5 minutes upon waking. Tests show sinus bradycardia on ECG and pauses of up to 2.7 seconds on Holter monitor, suggesting possible sick sinus syndrome. Based on risk factors including abnormal ECG, she has a 1% risk of mortality within one year. Further monitoring is needed to determine the cause and appropriate treatment.
Aortic dissection
This document presents the case of a 52-year-old male who presented with sudden onset severe back pain. Examination and tests revealed type B aortic dissection with possible acute kidney injury and polycystic kidney disease. The patient was managed medically but required endovascular intervention which was delayed, and he collapsed on the fourth day after referral. A review of literature discusses aortic dissection including causes, classification, clinical manifestations, physical findings, and management considerations.
Clinical conundrum in Perioperative Evaluation
Perioperative evaluation of difficult clinical scenarios which prompted to delay of surgery:
- Undiagnosed aortic regurgitation
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Stroke, etc. 082808.ppt
This document summarizes a lecture on stroke, subarachnoid hemorrhage, and hypothermia for cardiac arrest. It provides key facts about stroke including that about 780,000 Americans suffer strokes each year, strokes kill nearly 150,000 people annually making it the third leading cause of death, and stroke costs the US about $63 billion per year in medical costs and disability. It reviews definitions of stroke and transient ischemic attack. It also discusses risk factors for ischemic and hemorrhagic strokes. The remainder of the document involves a case study of a patient presenting with right-sided weakness and speech difficulties and the physician's examination and evaluation of the patient to determine if this is indeed a stroke and next steps in
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The document summarizes a lecture on stroke, subarachnoid hemorrhage, and hypothermia for cardiac arrest. It provides quick facts about stroke in the US, including prevalence, mortality rates, and costs. It defines stroke and outlines risk factors for ischemic and hemorrhagic stroke. It also discusses evaluation and management of acute stroke, including use of the NIH Stroke Scale and eligibility criteria for thrombolysis with t-PA within 3 hours of symptom onset.
Sub arachanoid heamorrhage
A 60-year-old male presented to the emergency department with the worst headache of his life along with nausea and vomiting. Subarachnoid hemorrhage (SAH) occurs when blood enters the subarachnoid space surrounding the brain. The most common cause is a ruptured brain aneurysm. Initial management included a CT scan, which has high sensitivity in detecting SAH, control of blood pressure to reduce risk of rebleeding, administration of nimodipine to prevent vasospasm, and neurosurgical consultation. The patient was admitted to the ICU for monitoring and treatment of potential complications of SAH such as rebleeding, vasospasm, hydrocephalus, and seizures.
Imaging in stroke
This document discusses stroke, including its types, causes, pathophysiology, imaging findings, and clinical features. It provides the following key points:
1. Stroke is caused by ischemia or hemorrhage in the brain. The main types are cerebral infarction (80%), intracerebral hemorrhage (15%), and subarachnoid hemorrhage (5%).
2. Imaging plays an important role in assessing the parenchyma, vessels, perfusion, and penumbra to guide therapy and predict outcomes. Techniques include CT, MRI, CT/MR perfusion, and angiography.
3. CT findings evolve over time from hyperacute to chronic stages. Early signs include
Subarachnoid hemorrhage
This document provides an overview of subarachnoid hemorrhage (SAH). It discusses the anatomy and histology of cerebral vasculature, epidemiology of SAH including risk factors and causes, classification of cerebral aneurysms, grading scales for SAH severity, clinical presentation, investigations including imaging and lumbar puncture, and laboratory tests. The epidemiology section notes that SAH accounts for 1-6% of strokes, has a high case fatality rate of up to 51%, and is most commonly caused by rupture of a cerebral aneurysm. Clinical presentation involves sudden, severe headache as the most common symptom along with possible neurological deficits, while investigations include noncontrast CT, CTA, MRI, lumbar puncture,
Stroke
This document discusses types of stroke, risk factors, statistics, recurrent strokes, ABCs of stroke support, stroke scales, interventions, drug therapy including fibrinolytics, CT scans, and ischemic versus hemorrhagic strokes. It covers the main types of stroke as hemorrhagic (15% of cases) and ischemic (85% of cases due to blood clots), risk factors like atrial fibrillation, statistics on prevalence and recurrence rates, and the stroke chain of survival steps for rapid diagnosis and treatment.
STROKE ENFERMEDAD CEREBROVASCULAR
This document provides information about stroke, including:
1. Stroke is the sudden onset of neurological deficit due to vascular infarction of brain tissue, confirmed by neuroimaging. The two main types are ischemic (80%) and hemorrhagic (20%).
2. Risk factors for ischemic stroke include atherosclerosis, atrial fibrillation, smoking, hypertension, diabetes, and heart disease. Evaluation includes CT, MRI, ECG, and NIH stroke scale.
3. Early signs of ischemia on CT within 6 hours include hypoattenuation of over 1/3 of the MCA territory, loss of gray-white differentiation, and hyperattenuation of vessels. The ASPECTS score quantifies the
NSG 6420_Grand_Round 2_Amougou_Yves
800,000 Americans have a stroke each year, making it the fifth leading cause of death. Strokes occur when blood flow to the brain is interrupted, either by a blockage (ischemic stroke) or bleeding (hemorrhagic stroke). AJ, a 52-year-old man with risk factors of hypertension, diabetes, and hyperlipidemia, arrived at the emergency room after his speech became slurred and he lost function in his right side, symptoms of an ischemic stroke. A CT scan confirmed he had an acute ischemic cerebrovascular accident affecting the left side of his brain. He received tPA treatment within 3 hours and was admitted for further rehabilitation and management of risk factors to prevent future strokes.
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Benign or not benign
- 1. “BENIGN OR NOT BENIGN”PERIMESENCEPHALIC SUBARACHNOID HAEMORRHAGE CASE PRESENTATION Andrew F. Alalade ST3 Neurosurgery
- 2. History 37 year old male Sudden-onset occipital headache while having sex Described it as the “worse headache” he ever had Later became generalised Had milder episodes in the two weeks prior to presentation Associated neck stiffness/pain
- 3. No photophobia Transient episode of amnesia after sudden onset headache Not a known hypertensive Examination GCS – 15/15. No neurological deficit Kerning's/ Brudzinki’s signs – negative FSH Does not smoke or drink alcohol. No family history of intracranial bleeds
- 4. Investigations Bloods – FBC, U&E, CRP, Clotting All parameters within normal limits CT Brain CT Angiography
- 6. Differential Diagnoses Subarachnoid haemorrhage - Aneurysmal SAH - Perimesencephalic SAH Orgasmic cephalgia Call-Fleming Syndrome (Idiopathic RCVS)
- 7. CT Brain
- 8. Subarachnoid haemorrhage Traumatic Spontaneous - Aneurysmal 80 – 85% - Arteriovenous malformations (AVMs) 4% - Perimesencephalic 10% - Others: Tumours, anticoagulant therapy, dissection etc.
- 9. ACOM aneurysm MCA aneurysm PCOM aneurysm
- 10. “When persons in good health are suddenly seized with pains in the head, and straightway are laid down speechless and breathe with stretor, they die in seven days”Described a headache due to “immoderate venery”Hippocrates 460 – 370BC Aphorisms on Apoplexy
- 11. Perimesencephalic SAH Introduction Definition Anatomy Epidemiology Clinical features Complications
- 12. It’s all in the name
- 13. History Cerebral angiography – discovered by Egas Moniz in 1927 Term (PNSAH) first coined in 1985 by J. Van Gijn et al
- 14. Definition A benign form of non-aneurysmal, angiographic and MRI –ve SAH with The epicentre of the haemorrhage is anterior to the midbrain or pons (with or without extension to the ambient cisterns) The haemorrhage might occupy the basal(but not the distal) part of the Sylvian fissure and part (but not all) of the interhemispheric fissure A sediment of ventricular blood (but not frank IV blood)
- 15. Cisterns
- 16. Epidemiology Age range 3 – 70 years (mean 50 years) 52 – 59% are male 20 – 68% of cases of angiogram-negative SAH (beware of timing of CT, adequacy of angiography and the definition of PNSAH) True incidence is more in the range of 50 – 75%
- 17. Aetiology Papers on primitive venous defects/micro-aneurysms
- 19. Type B: Normal discontinuous. There is discontinuous venous drainage, anterior to the uncal vein and posterior to the Vein of Galen.
- 20. Type C: Primitive variant. Drainage mainly into veins other than the Vein of Galen. Some authors have suggested that anatomical variations in BVR are frequent more prevalent in patients with perimesencephalic non-aneurysmal haemorrhage.
- 21. Distal basilar perforator artery aneurysm: case report. Ghogawala Z, Schumacher JM, Ogilvy CS Neurosurgery 1996; 39:393 – 396 Surgical treatment of a basilar artery aneurysm not accessible to endovascular treatment. Hamel W, Grzyska U, Westphal M, Kehler U. Acta Neurochirurgica (Wien) 2005; 147: 1283 – 1286 Distal aneurysms of basilar perforating and circumferential arteries. Report of three cases. Sanchez-Mejia RO, Lawton MT. Journal of Neurosurgery 2007, 107: 654 -9 Life expectancy after perimesencephalic subarachnoid haemorrhage. Greebe P, Rinkel GJ. Stroke 2007; 38:1222-4
- 22. Posterior cerebral artery dissecting aneurysm: another cause of perimesencephalic pattern of subarachnoid haemorrhage P. P. Lobo, J. Campos, L. Neto, P. Canhao J Neurol Neurosurg Psychiatry doi:10.1136/jnnp.2009.198531 Aneurysmal and microaneurysmal "angiogram-negative" subarachnoid haemorrhage. Tatter SB, Crowell RM, Ogilvy CS. Neurosurgery. 1995 Jul;37(1):48-55. Straight sinus Stenosis as a proposed cause of perimesencephalic non-aneurysmal haemorrhage Amjad Shad, Thomas J. Rourke, Ali Hamidian Jahromi and Alexander L. Green Journal of Clinical Neuroscience Vol. 15, Issue 7, July 2008; 839-841
- 23. Types Pre-Truncal PNSAH (anterior to the truncus cerebri) Schievink and Wijdicks 1997 Quadrigeminal PNSAH (in the quadrigeminal cistern) Quadrigeminal variant of perimesencephalic nonaneurysmal subarachnoid haemorrhage. Schwartz TH, Mayer SA. Neurosurgery. 2000 Mar;46(3):584-8.
- 24. Clinical features Clinical picture very similar to classic SAH Headache can be sudden-onset but develops in minutes (rather than seconds) Less frequently hypertensive (3 – 20%) No seizures/significant reduction in consciousness In 1/3rd of the patients, strenuous activities immediately precede the onset of symptoms (a proportion similar to that found in aneurysmal haemorrhage) van Gijn et al., 1985a; Linn et al., 1998. Angiographic negative
- 25. Complications Hydrocephalus – up to 15%, rarely requires shunting Angiographic vasospasm (rare) Clinical vasospasm (extremely rare) Hyponatriemia Overall prognosis is excellent
- 26. Other causes of angiographic negative SAH
- 27. Angiographic negative, and then positive
- 28. THANK YOU