This document provides information about subarachnoid hemorrhage (SAH):
- SAH is bleeding into the subarachnoid space, which occurs in 5% of strokes and is usually caused by a ruptured aneurysm.
- Presenting symptoms include a sudden, severe headache and signs of meningeal irritation. Investigations include CT, LP, CTA/MRA to identify the source of bleeding.
- Treatment focuses on stabilizing the patient, securing the aneurysm via coiling or clipping, and preventing/treating complications like rebleeding, hydrocephalus, seizures, and delayed cerebral ischemia.
- Complications are managed through measures like strict blood
The document summarizes subarachnoid hemorrhage (SAH). The most common cause is a ruptured cerebral aneurysm. Clinical presentation includes sudden, severe headache and loss of consciousness. Diagnosis is made using non-contrast CT or lumbar puncture. Treatment involves securing the aneurysm with coiling or clipping, managing rebleeding risk with blood pressure control, and treating complications like hydrocephalus. Outcomes depend on factors like disease severity, treatment at high-volume centers, and management of neurological complications including rebleeding, hydrocephalus, and seizures.
Subarachnoid Hemorrhage (SAH) is a type of stroke caused by bleeding into the subarachnoid space surrounding the brain. The leading cause is a ruptured aneurysm, which accounts for 75% of cases. SAH presents with an extremely severe headache, neck stiffness, nausea, and sometimes decreased consciousness. Diagnosis is confirmed through CT scan or lumbar puncture. Treatment focuses on controlling blood pressure, preventing rebleeding, and reducing complications like hydrocephalus and cerebral vasospasm.
This document provides an overview of neuromyelitis optica spectrum disorders (NMOSD). It discusses the epidemiology, clinical features, diagnostic criteria, investigations, neuroimaging findings, and treatments for NMOSD. Key points include that NMOSD predominantly affects the optic nerves and spinal cord, is strongly associated with antibodies against the aquaporin-4 protein, and treatments involve high-dose steroids, plasma exchange, or intravenous immunoglobulins for acute exacerbations. The diagnostic criteria were revised in 2015 to incorporate aquaporin-4 antibody testing and distinguish NMOSD from multiple sclerosis.
This document provides an overview of approaches to diagnosing leukodystrophies. It begins by defining leukodystrophies and differentiating them from other white matter disorders. Clinical features that suggest a leukodystrophy are described. A 3-step MRI approach is outlined involving identifying symmetric white matter involvement, patterns of involvement, and distinctive features. Common leukodystrophies in adults are discussed in detail including clinical presentation, genetics, imaging findings, and diagnostic testing. The document emphasizes a systematic approach to diagnosis utilizing clinical features, imaging, and ancillary tests.
NeuroMyelitis Optica Spectrum Disorder (NMOSD) is an inflammatory disorder of the central nervous system characterized by demyelination and damage of the optic nerves and spinal cord. It was previously considered a variant of multiple sclerosis but is now recognized as a distinct condition mediated by autoantibodies against aquaporin-4. NMOSD can present with optic neuritis causing vision loss or transverse myelitis with varying degrees of weakness and sensory loss. Brain involvement is also seen in around half of patients. The disease predominantly affects women and typically involves recurrent, severe attacks with varying recovery. Diagnosis involves identifying clinical features, MRI imaging, and serologic testing for aquaporin-4 antibodies.
1. The document discusses cerebral venous thrombosis (CVT), providing statistics on incidence and demographics.
2. It describes the most commonly thrombosed venous structures as being the superior sagittal sinus, lateral sinus, and straight sinus.
3. Imaging findings of CVT include direct visualization of clot, absence of flow voids, empty delta sign on contrast-enhanced CT or MR, and venous infarction patterns like bilateral parasagittal lesions.
Intracerebral hemorhage Diagnosis and managementRamesh Babu
About ICH - Diagnosis and management, Discussed the clinical presentation, evaluation, radiological features and management including recent guidelines
The document summarizes subarachnoid hemorrhage (SAH). The most common cause is a ruptured cerebral aneurysm. Clinical presentation includes sudden, severe headache and loss of consciousness. Diagnosis is made using non-contrast CT or lumbar puncture. Treatment involves securing the aneurysm with coiling or clipping, managing rebleeding risk with blood pressure control, and treating complications like hydrocephalus. Outcomes depend on factors like disease severity, treatment at high-volume centers, and management of neurological complications including rebleeding, hydrocephalus, and seizures.
Subarachnoid Hemorrhage (SAH) is a type of stroke caused by bleeding into the subarachnoid space surrounding the brain. The leading cause is a ruptured aneurysm, which accounts for 75% of cases. SAH presents with an extremely severe headache, neck stiffness, nausea, and sometimes decreased consciousness. Diagnosis is confirmed through CT scan or lumbar puncture. Treatment focuses on controlling blood pressure, preventing rebleeding, and reducing complications like hydrocephalus and cerebral vasospasm.
This document provides an overview of neuromyelitis optica spectrum disorders (NMOSD). It discusses the epidemiology, clinical features, diagnostic criteria, investigations, neuroimaging findings, and treatments for NMOSD. Key points include that NMOSD predominantly affects the optic nerves and spinal cord, is strongly associated with antibodies against the aquaporin-4 protein, and treatments involve high-dose steroids, plasma exchange, or intravenous immunoglobulins for acute exacerbations. The diagnostic criteria were revised in 2015 to incorporate aquaporin-4 antibody testing and distinguish NMOSD from multiple sclerosis.
This document provides an overview of approaches to diagnosing leukodystrophies. It begins by defining leukodystrophies and differentiating them from other white matter disorders. Clinical features that suggest a leukodystrophy are described. A 3-step MRI approach is outlined involving identifying symmetric white matter involvement, patterns of involvement, and distinctive features. Common leukodystrophies in adults are discussed in detail including clinical presentation, genetics, imaging findings, and diagnostic testing. The document emphasizes a systematic approach to diagnosis utilizing clinical features, imaging, and ancillary tests.
NeuroMyelitis Optica Spectrum Disorder (NMOSD) is an inflammatory disorder of the central nervous system characterized by demyelination and damage of the optic nerves and spinal cord. It was previously considered a variant of multiple sclerosis but is now recognized as a distinct condition mediated by autoantibodies against aquaporin-4. NMOSD can present with optic neuritis causing vision loss or transverse myelitis with varying degrees of weakness and sensory loss. Brain involvement is also seen in around half of patients. The disease predominantly affects women and typically involves recurrent, severe attacks with varying recovery. Diagnosis involves identifying clinical features, MRI imaging, and serologic testing for aquaporin-4 antibodies.
1. The document discusses cerebral venous thrombosis (CVT), providing statistics on incidence and demographics.
2. It describes the most commonly thrombosed venous structures as being the superior sagittal sinus, lateral sinus, and straight sinus.
3. Imaging findings of CVT include direct visualization of clot, absence of flow voids, empty delta sign on contrast-enhanced CT or MR, and venous infarction patterns like bilateral parasagittal lesions.
Intracerebral hemorhage Diagnosis and managementRamesh Babu
About ICH - Diagnosis and management, Discussed the clinical presentation, evaluation, radiological features and management including recent guidelines
Subarachnoid hemorrhage is a neurological emergency caused by sudden bleeding into the subarachnoid space, often presenting with a thunderclap headache. It is usually caused by the rupture of an intracranial aneurysm. The case fatality rate of aneurysmal SAH is 30-70% on average. Survivors often have major disability, with 60% never regaining their pre-hemorrhage quality of life. Diagnosis involves CT, LP, CTA and conventional angiography to detect the source of bleeding. Complications include rebleeding, hydrocephalus, vasospasm and hyponatremia. Aggressive treatment is aimed at securing the aneurysm to prevent re
1) Normal pressure hydrocephalus (NPH) is characterized by abnormal gait, urinary incontinence, and dementia. It is most common in the elderly and can be caused by conditions like subarachnoid hemorrhage.
2) Diagnosis involves evaluating symptoms, imaging tests showing disproportionate ventricle enlargement, and tests like lumbar puncture to check CSF pressure and flow.
3) Treatment usually involves surgically placing a CSF shunt if symptoms improve with temporary drainage, with benefits seen in 50-61% of cases but also a high risk of complications.
Tuberous sclerosis is a genetic disorder characterized by the growth of noncancerous tumors in multiple organs like the skin, brain, kidneys, and heart. It is caused by mutations in either the TSC1 or TSC2 genes. The signs and symptoms vary between people but can include skin abnormalities like hypomelanotic macules, facial angiofibromas, and shagreen patches. Neurological effects include seizures, developmental delays, and noncancerous brain tumors like subependymal nodules and subependymal giant cell astrocytomas. It has an autosomal dominant inheritance pattern and affects approximately 1 in 6,000 newborns. While there is no cure, treatment focuses
- Transcranial Doppler (TCD) ultrasonography uses 2MHz probes to visualize intracranial vasculature non-invasively and measure blood flow velocities. It was introduced in 1982 and can monitor the middle cerebral artery, anterior cerebral artery, internal carotid artery, and other vessels.
- TCD is useful for evaluating stroke, cerebral vasospasm, intracranial stenosis, emboli, aneurysms, and raised intracranial pressure. It has good correlation with angiography and can detect stenosis with high sensitivity and specificity. Hemodynamic changes and collateral flow patterns can also be assessed.
- Monitoring emboli with TCD has helped identify the
1) Cerebral venous thrombosis (CVT) is an uncommon form of stroke caused by thrombosis of cerebral veins and dural sinuses. It presents with highly variable clinical features including headache, seizures, focal neurological deficits, and altered mental status.
2) Risk factors for CVT include inherited and acquired thrombophilias, pregnancy, oral contraceptive use, and various systemic diseases. Diagnosis is made using neuroimaging techniques like MRI, MRV, and CT venography.
3) Treatment involves anticoagulation with heparin or warfarin for 3-12 months depending on risk factors. Outcomes are generally good with around 80% of patients making a complete or near-complete recovery, but mortality
Dr. Shubham Garg discusses neuromyelitis optica (NMO), an autoimmune condition where antibodies attack aquaporin-4 in the central nervous system. NMO predominantly affects women and has a median age of onset of 32-41 years. Key clinical features include transverse myelitis, typically longitudinally extensive, and severe optic neuritis. Treatment involves high-dose steroids for acute attacks and immunosuppressants like azathioprine to reduce relapse rates. Prognosis is generally worse than multiple sclerosis due to risk of cumulative disability, though relapse rates can be lowered with appropriate treatment.
1) The document discusses wheat pill (aluminum phosphide) poisoning, which produces phosphine gas that is toxic and can be fatal in small doses.
2) Phosphine gas causes multiple organ damage by inhibiting cytochrome oxidase and damaging cell membranes. It can cause cardiac arrest, pulmonary edema, liver failure and death.
3) Management of wheat pill poisoning involves gastric lavage with potassium permanganate or oils, magnesium and calcium supplementation, IV fluids, ventilation, inotropes, antiarrhythmics and supportive care over 48-72 hours given the high mortality risk despite treatment.
This document provides an overview of Moyamoya disease. It defines Moyamoya disease as a progressive stenosis of the intracranial arteries, typically the internal carotid arteries and proximal middle and anterior cerebral arteries, accompanied by a compensatory network of collaterals at the brain's base. The cause is unknown but genetic factors are believed to play a role. Clinically, it can present with transient ischemic attacks, strokes, or hemorrhage. Diagnosis is based on neuroimaging findings on MRI, MRA, CTA or DSA showing the characteristic vascular changes. Treatment involves medical management as well as surgical revascularization procedures. Prognosis depends on the extent of vascular involvement and collateral formation.
neuromyelitis optica spectrum disorder Dr. Musa AtarzadehMusa Atazadeh
1. The document discusses the diagnosis and diagnostic criteria for Neuromyelitis Optica Spectrum Disorder (NMOSD) according to the 2015 AAN criteria.
2. The diagnosis involves assessing for core clinical characteristics, compatible neuroimaging findings, and testing for AQP4-IgG antibodies.
3. Certain clinical presentations and neuroimaging patterns can raise red flags and suggest alternative diagnoses rather than NMOSD. Repeating AQP4-IgG testing over time or in the CSF may also be considered in some cases.
This document provides information about idiopathic intracranial hypertension (IIH), including its symptoms, pathophysiology, risk factors, diagnosis, and treatment. IIH is characterized by increased intracranial pressure without a tumor or other identifiable cause. Common symptoms include headache, nausea, visual disturbances, and papilledema. The main risk factors are obesity, particularly in women of childbearing age. The cause is unknown but may involve increased cerebrospinal fluid production or impaired cerebral venous drainage. Diagnosis involves evaluating signs and symptoms of increased intracranial pressure and ruling out other potential causes through imaging and lumbar puncture.
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
This document discusses Posterior Reversible Encephalopathy Syndrome (PRES). It begins with the historical background of the condition. PRES is characterized by reversible subcortical vasogenic brain edema that presents with neurological symptoms like seizures, headaches, and visual disturbances. It is often associated with issues like hypertension, renal failure, cytotoxic drugs, and preeclampsia. Brain imaging typically shows edema in the parieto-occipital regions that is usually reversible. The pathophysiology involves endothelial injury from abrupt blood pressure changes that causes breakdown of the blood-brain barrier and brain edema. PRES has diverse clinical manifestations and comorbid conditions that can trigger it. Diagnosis involves clinical context and supportive brain imaging findings.
This document discusses normal pressure hydrocephalus (NPH), a potentially reversible cause of significant morbidities. NPH is characterized by a triad of gait disturbance, urinary incontinence, and dementia. It can be idiopathic or secondary to other conditions like subarachnoid hemorrhage. Diagnosis involves imaging showing enlarged ventricles without cortical atrophy, along with improvement of symptoms after CSF drainage. Shunting procedures may benefit those without severe white matter lesions or dementia, but have high complication rates. The prognosis for NPH is generally poor.
This document discusses moyamoya disease, a progressive cerebral angiopathy characterized by stenosis of the internal carotid artery and development of collateral vessels appearing as a "puff of smoke". It is more common in East Asia and presents with ischemic or hemorrhagic strokes. Diagnosis is made through angiography showing the characteristic findings. Treatment involves surgical revascularization for symptomatic patients to prevent further strokes.
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.
This document discusses aneurysmal subarachnoid hemorrhage (SAH), including its causes, diagnosis, treatment, and complications. The most common cause is rupture of a cerebral aneurysm, which accounts for 80-85% of cases. Diagnosis involves CT scan and lumbar puncture to detect blood. Angiography is used to identify the aneurysm's location. Early securing of the aneurysm via coiling or clipping can prevent rebleeding and improve outcomes, which are also impacted by age, neurological grade, amount of bleeding, vasospasm severity and other factors. Complications include rebleeding, vasospasm, hydrocephalus, seizures, and medical issues.
1. A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by focal brain or retinal ischemia, with symptoms typically lasting less than one hour without evidence of acute infarction.
2. The risk of stroke is highest in the first few days after a TIA, with about a 10% risk of stroke in the first week and 15% risk within the first 90 days.
3. Evaluation of patients with suspected TIA involves detailed history, neurological exam, prognostic testing like the ABCD2 score, and investigations including blood tests, brain and vascular imaging to identify the cause and risk of future stroke.
This document discusses acute ischemic stroke interventions. It provides details on:
- The typical size and duration of untreated ischemic strokes
- How many neurons and synapses are lost each hour and minute of untreated stroke
- Guidelines for emergency evaluation, diagnosis, and imaging of acute ischemic strokes
- Details on different imaging techniques like CT, MRI, CTA, and perfusion imaging
- Guidelines and recommendations for intravenous thrombolysis with rtPA within 3-4.5 hours of stroke onset.
This document summarizes pseudotumor cerebri (PTC), also known as idiopathic intracranial hypertension (IIH). It describes a case of a 39-year-old obese female with PTC symptoms including headaches, visual issues, and papilledema. PTC is characterized by increased intracranial pressure without a tumor. Treatment involves weight loss, medications like acetazolamide, surgical procedures like optic nerve sheath fenestration or shunt placement, and managing any underlying causes. Complications can include permanent vision loss if not properly treated.
1. A 50-year-old female smoker with hypertension presented with sudden severe headache and brief loss of consciousness at work. She was found to have subarachnoid hemorrhage.
2. Subarachnoid hemorrhage is a neurological emergency caused by bleeding into the subarachnoid space, usually from a ruptured berry aneurysm. It requires rapid diagnosis and treatment to prevent rebleeding, vasospasm, and other complications.
3. Diagnostic tests included a non-contrast CT, which was positive, as well as a CTA and lumbar puncture to confirm the diagnosis and identify the source of bleeding. The patient was treated supportively in the ICU to control
Subarachnoid haemorrhage (SAH) is a neurological emergency caused by bleeding into the subarachnoid space surrounding the brain. The most common cause is a ruptured saccular aneurysm. Patients typically experience a sudden severe headache and may experience loss of consciousness or focal neurological deficits. Diagnosis is confirmed through CT scan or lumbar puncture. Treatment focuses on securing the aneurysm through surgical clipping or endovascular coiling, managing vasospasm, and preventing rebleeding. Outcomes depend on the severity of the initial bleed and development of complications.
Subarachnoid hemorrhage is a neurological emergency caused by sudden bleeding into the subarachnoid space, often presenting with a thunderclap headache. It is usually caused by the rupture of an intracranial aneurysm. The case fatality rate of aneurysmal SAH is 30-70% on average. Survivors often have major disability, with 60% never regaining their pre-hemorrhage quality of life. Diagnosis involves CT, LP, CTA and conventional angiography to detect the source of bleeding. Complications include rebleeding, hydrocephalus, vasospasm and hyponatremia. Aggressive treatment is aimed at securing the aneurysm to prevent re
1) Normal pressure hydrocephalus (NPH) is characterized by abnormal gait, urinary incontinence, and dementia. It is most common in the elderly and can be caused by conditions like subarachnoid hemorrhage.
2) Diagnosis involves evaluating symptoms, imaging tests showing disproportionate ventricle enlargement, and tests like lumbar puncture to check CSF pressure and flow.
3) Treatment usually involves surgically placing a CSF shunt if symptoms improve with temporary drainage, with benefits seen in 50-61% of cases but also a high risk of complications.
Tuberous sclerosis is a genetic disorder characterized by the growth of noncancerous tumors in multiple organs like the skin, brain, kidneys, and heart. It is caused by mutations in either the TSC1 or TSC2 genes. The signs and symptoms vary between people but can include skin abnormalities like hypomelanotic macules, facial angiofibromas, and shagreen patches. Neurological effects include seizures, developmental delays, and noncancerous brain tumors like subependymal nodules and subependymal giant cell astrocytomas. It has an autosomal dominant inheritance pattern and affects approximately 1 in 6,000 newborns. While there is no cure, treatment focuses
- Transcranial Doppler (TCD) ultrasonography uses 2MHz probes to visualize intracranial vasculature non-invasively and measure blood flow velocities. It was introduced in 1982 and can monitor the middle cerebral artery, anterior cerebral artery, internal carotid artery, and other vessels.
- TCD is useful for evaluating stroke, cerebral vasospasm, intracranial stenosis, emboli, aneurysms, and raised intracranial pressure. It has good correlation with angiography and can detect stenosis with high sensitivity and specificity. Hemodynamic changes and collateral flow patterns can also be assessed.
- Monitoring emboli with TCD has helped identify the
1) Cerebral venous thrombosis (CVT) is an uncommon form of stroke caused by thrombosis of cerebral veins and dural sinuses. It presents with highly variable clinical features including headache, seizures, focal neurological deficits, and altered mental status.
2) Risk factors for CVT include inherited and acquired thrombophilias, pregnancy, oral contraceptive use, and various systemic diseases. Diagnosis is made using neuroimaging techniques like MRI, MRV, and CT venography.
3) Treatment involves anticoagulation with heparin or warfarin for 3-12 months depending on risk factors. Outcomes are generally good with around 80% of patients making a complete or near-complete recovery, but mortality
Dr. Shubham Garg discusses neuromyelitis optica (NMO), an autoimmune condition where antibodies attack aquaporin-4 in the central nervous system. NMO predominantly affects women and has a median age of onset of 32-41 years. Key clinical features include transverse myelitis, typically longitudinally extensive, and severe optic neuritis. Treatment involves high-dose steroids for acute attacks and immunosuppressants like azathioprine to reduce relapse rates. Prognosis is generally worse than multiple sclerosis due to risk of cumulative disability, though relapse rates can be lowered with appropriate treatment.
1) The document discusses wheat pill (aluminum phosphide) poisoning, which produces phosphine gas that is toxic and can be fatal in small doses.
2) Phosphine gas causes multiple organ damage by inhibiting cytochrome oxidase and damaging cell membranes. It can cause cardiac arrest, pulmonary edema, liver failure and death.
3) Management of wheat pill poisoning involves gastric lavage with potassium permanganate or oils, magnesium and calcium supplementation, IV fluids, ventilation, inotropes, antiarrhythmics and supportive care over 48-72 hours given the high mortality risk despite treatment.
This document provides an overview of Moyamoya disease. It defines Moyamoya disease as a progressive stenosis of the intracranial arteries, typically the internal carotid arteries and proximal middle and anterior cerebral arteries, accompanied by a compensatory network of collaterals at the brain's base. The cause is unknown but genetic factors are believed to play a role. Clinically, it can present with transient ischemic attacks, strokes, or hemorrhage. Diagnosis is based on neuroimaging findings on MRI, MRA, CTA or DSA showing the characteristic vascular changes. Treatment involves medical management as well as surgical revascularization procedures. Prognosis depends on the extent of vascular involvement and collateral formation.
neuromyelitis optica spectrum disorder Dr. Musa AtarzadehMusa Atazadeh
1. The document discusses the diagnosis and diagnostic criteria for Neuromyelitis Optica Spectrum Disorder (NMOSD) according to the 2015 AAN criteria.
2. The diagnosis involves assessing for core clinical characteristics, compatible neuroimaging findings, and testing for AQP4-IgG antibodies.
3. Certain clinical presentations and neuroimaging patterns can raise red flags and suggest alternative diagnoses rather than NMOSD. Repeating AQP4-IgG testing over time or in the CSF may also be considered in some cases.
This document provides information about idiopathic intracranial hypertension (IIH), including its symptoms, pathophysiology, risk factors, diagnosis, and treatment. IIH is characterized by increased intracranial pressure without a tumor or other identifiable cause. Common symptoms include headache, nausea, visual disturbances, and papilledema. The main risk factors are obesity, particularly in women of childbearing age. The cause is unknown but may involve increased cerebrospinal fluid production or impaired cerebral venous drainage. Diagnosis involves evaluating signs and symptoms of increased intracranial pressure and ruling out other potential causes through imaging and lumbar puncture.
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
This document discusses Posterior Reversible Encephalopathy Syndrome (PRES). It begins with the historical background of the condition. PRES is characterized by reversible subcortical vasogenic brain edema that presents with neurological symptoms like seizures, headaches, and visual disturbances. It is often associated with issues like hypertension, renal failure, cytotoxic drugs, and preeclampsia. Brain imaging typically shows edema in the parieto-occipital regions that is usually reversible. The pathophysiology involves endothelial injury from abrupt blood pressure changes that causes breakdown of the blood-brain barrier and brain edema. PRES has diverse clinical manifestations and comorbid conditions that can trigger it. Diagnosis involves clinical context and supportive brain imaging findings.
This document discusses normal pressure hydrocephalus (NPH), a potentially reversible cause of significant morbidities. NPH is characterized by a triad of gait disturbance, urinary incontinence, and dementia. It can be idiopathic or secondary to other conditions like subarachnoid hemorrhage. Diagnosis involves imaging showing enlarged ventricles without cortical atrophy, along with improvement of symptoms after CSF drainage. Shunting procedures may benefit those without severe white matter lesions or dementia, but have high complication rates. The prognosis for NPH is generally poor.
This document discusses moyamoya disease, a progressive cerebral angiopathy characterized by stenosis of the internal carotid artery and development of collateral vessels appearing as a "puff of smoke". It is more common in East Asia and presents with ischemic or hemorrhagic strokes. Diagnosis is made through angiography showing the characteristic findings. Treatment involves surgical revascularization for symptomatic patients to prevent further strokes.
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.
This document discusses aneurysmal subarachnoid hemorrhage (SAH), including its causes, diagnosis, treatment, and complications. The most common cause is rupture of a cerebral aneurysm, which accounts for 80-85% of cases. Diagnosis involves CT scan and lumbar puncture to detect blood. Angiography is used to identify the aneurysm's location. Early securing of the aneurysm via coiling or clipping can prevent rebleeding and improve outcomes, which are also impacted by age, neurological grade, amount of bleeding, vasospasm severity and other factors. Complications include rebleeding, vasospasm, hydrocephalus, seizures, and medical issues.
1. A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by focal brain or retinal ischemia, with symptoms typically lasting less than one hour without evidence of acute infarction.
2. The risk of stroke is highest in the first few days after a TIA, with about a 10% risk of stroke in the first week and 15% risk within the first 90 days.
3. Evaluation of patients with suspected TIA involves detailed history, neurological exam, prognostic testing like the ABCD2 score, and investigations including blood tests, brain and vascular imaging to identify the cause and risk of future stroke.
This document discusses acute ischemic stroke interventions. It provides details on:
- The typical size and duration of untreated ischemic strokes
- How many neurons and synapses are lost each hour and minute of untreated stroke
- Guidelines for emergency evaluation, diagnosis, and imaging of acute ischemic strokes
- Details on different imaging techniques like CT, MRI, CTA, and perfusion imaging
- Guidelines and recommendations for intravenous thrombolysis with rtPA within 3-4.5 hours of stroke onset.
This document summarizes pseudotumor cerebri (PTC), also known as idiopathic intracranial hypertension (IIH). It describes a case of a 39-year-old obese female with PTC symptoms including headaches, visual issues, and papilledema. PTC is characterized by increased intracranial pressure without a tumor. Treatment involves weight loss, medications like acetazolamide, surgical procedures like optic nerve sheath fenestration or shunt placement, and managing any underlying causes. Complications can include permanent vision loss if not properly treated.
1. A 50-year-old female smoker with hypertension presented with sudden severe headache and brief loss of consciousness at work. She was found to have subarachnoid hemorrhage.
2. Subarachnoid hemorrhage is a neurological emergency caused by bleeding into the subarachnoid space, usually from a ruptured berry aneurysm. It requires rapid diagnosis and treatment to prevent rebleeding, vasospasm, and other complications.
3. Diagnostic tests included a non-contrast CT, which was positive, as well as a CTA and lumbar puncture to confirm the diagnosis and identify the source of bleeding. The patient was treated supportively in the ICU to control
Subarachnoid haemorrhage (SAH) is a neurological emergency caused by bleeding into the subarachnoid space surrounding the brain. The most common cause is a ruptured saccular aneurysm. Patients typically experience a sudden severe headache and may experience loss of consciousness or focal neurological deficits. Diagnosis is confirmed through CT scan or lumbar puncture. Treatment focuses on securing the aneurysm through surgical clipping or endovascular coiling, managing vasospasm, and preventing rebleeding. Outcomes depend on the severity of the initial bleed and development of complications.
Non traumatic Subarachnoid hemorrhage (SAH)Milan Silwal
The document discusses imaging of non-traumatic subarachnoid hemorrhage (SAH). The most common cause of SAH is the rupture of a saccular aneurysm, usually located in the circle of Willis. CT and MRI are used to diagnose and locate SAH, while CT angiography, MR angiography, and conventional angiography can identify aneurysms. Complications of SAH like hydrocephalus and cerebral ischemia are also discussed. Perimesencephalic and convexal SAH represent patterns of non-aneurysmal SAH with different etiologies and prognoses.
Diagnosing Subarachnoid Haemorrhage in Neuro Critical CareSMACC Conference
Join the debate between Bill Knight and Fernanda Bellolio as they go head-to-head, discussing diagnosing subarachnoid haemorrhage in neuro critical care headache. Should you rely on CT and lumbar puncture or, CT followed by CT angiogram.
Why should you care?
Acute headache accounts for 4% of all visits to the emergency departments. These patients will often describe the “Worst headache of life” – a phrase which can ring the alarm bells in the clincian’s mind. 88% of these will be from benign causes including migraine, tension and cluster. However 10% will have a subarachnoid haemorrhage, of which the vast majority are caused by an aneurysm.
These are frequently missed - up to 51% of the time in all settings and 6% of the time in the emergency department. It is in face one of the largest sources of US litigation claims and settlements.
So – what is the best way to diagnosis subarachnoid haemorrhage?
Bill asserts that the lumbar puncture (LP) following the CT is the way to go. He stresses that the “miss rate” needs to be 0% for subarachnoid haemorrhage. He argues that with the combination of CT and LP the sensitivity for subarachnoid haemorrhage is 100%
Fernanda on the other hand is a big proponent of using the combination of CT followed by CT angiogram (CTA). She discusses the very low incidence of subarachnoid haemorrhade and takes this into account when calculating the pre- and post-test probability for her patients. She argues that if the pre-test probability is higher for a patient, then a CTA can be utilised.
Bill Knight and Fernanda Bellolio present a compelling case for both sides when identifying the best way to diagnose subarachnoid haemorrhage in neuro critical care headache.
The document discusses the anesthetic management of patients undergoing treatment for cerebral aneurysms, including definitions, epidemiology, presentation, diagnosis, management of vasospasm, intracranial pressure, pre-operative assessment and testing, and radiological procedures such as coiling of aneurysms. Precise management of hemodynamics, fluid balance, and respiratory status is important due to the risks of re-bleeding, cerebral ischemia, and impaired autoregulation in these patients.
This patient presented with left-sided weakness and slurred speech. CT scan was normal. After tPA infusion, her blood pressure was elevated. The appropriate next step is to administer nicardipine to lower her blood pressure and prevent intracerebral hemorrhage.
This patient is being followed up after an ischemic stroke. Testing shows a left pontine infarct. The appropriate secondary prevention is to substitute clopidogrel for aspirin given his history of peripheral artery disease.
This patient presented with headache and papilledema. MRI was normal. Magnetic resonance venography is the best next test to evaluate for dural sinus venous thrombosis given her risk factors.
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.
Subarachnoid haemorrhage occurs when there is bleeding into the subarachnoid space between the membranes surrounding the brain. The most common cause is rupture of a berry aneurysm. Patients typically experience a sudden and severe headache, vomiting, and may lose consciousness. Complications include rebleeding, hydrocephalus, cerebral vasospasm leading to ischemia, and hyponatremia. Prompt diagnosis and treatment are important to prevent neurological deficits and reduce mortality.
A 35-year-old man presented to the emergency department with neck pain, dizziness and confusion after yanking a fishing rod the previous day. Imaging revealed a left internal carotid artery dissection with an ischemic stroke in the left frontal region. He was started on dual antiplatelet therapy and speech therapy. A follow up after 3 months showed modified Rankin score of 0-1, indicating minimal or no symptoms. Cervico-cephalic artery dissections occur when there is a tear in the artery wall, allowing blood to dissect into the wall and cause a hematoma. They typically present with neck pain, headaches, strokes, or Horner's syndrome. Diagnosis is made using CTA, MRA
1. Intracranial aneurysms are abnormal dilations of arteries in the brain that can rupture and cause subarachnoid hemorrhage (SAH).
2. Common types include saccular, fusiform, and dissecting aneurysms, which often form at artery branch points due to hemodynamic stress.
3. Clinical features of SAH include a sudden, severe headache and other signs of meningismus. Diagnosis involves CT, LP, and cerebral angiography.
Brain aneurysms are weakened bulges in the wall of an artery in the brain that can rupture and cause bleeding. Risk factors include hypertension, smoking, family history, and genetic conditions. A rupture causes a thunderclap headache and may lead to meningismus. Diagnosis is with CT, MRI, or lumbar puncture. Treatment depends on aneurysm size and location, and involves clipping or coiling to repair the bulge. Ruptured aneurysms have high mortality risks, especially from rebleeding, vasospasm, and hydrocephalus. Strict blood pressure control and monitoring are important after treatment to prevent further bleeding.
1. Subarachnoid hemorrhage is most commonly caused by trauma or the rupture of an intracranial aneurysm.
2. Symptoms of aneurysmal subarachnoid hemorrhage include a sudden, severe headache and cranial nerve palsies.
3. CT and CTA are effective imaging modalities for detecting aneurysms and evaluating the location and extent of subarachnoid hemorrhage. Management involves treating the underlying cause, usually by clipping or coiling the aneurysm, to prevent rebleeding and complications.
This document discusses diagnostic imaging for acute ischemic stroke. It provides details on the use of non-contrast CT, MRI, CT angiography and MR angiography to evaluate patients with suspected stroke. CT is widely available but MRI, especially diffusion-weighted imaging, can detect small or recent strokes better. Ultrasound is used to screen for carotid artery stenosis and can classify severity based on blood flow velocities. Digital subtraction angiography remains the gold standard but is more invasive. The pathophysiology of cerebral infarction over time correlates to changing imaging appearances on CT and MRI.
This document provides an overview of cerebrovascular diseases for medical students. It covers anatomy of the intracranial cerebrovascular system, common acute stroke presentations based on arterial distribution, features suggestive of brainstem stroke, watershed areas vulnerable to hypoperfusion, stroke risk factors, types of strokes, stroke epidemiology, case examples, acute stroke treatment options including thrombolytics, management of blood pressure, stroke workup, secondary stroke prevention, post-stroke care, and intracranial hemorrhage. Key points include differences between transient ischemic attack and stroke, use of the NIH stroke scale to determine severity, eligibility criteria for thrombolysis with tPA, and management of cerebral venous sinus thrombosis.
This document discusses subarachnoid hemorrhage (SAH), which occurs when there is bleeding into the space between the brain and the thin tissues that cover the brain. The most common cause of SAH is the rupture of an intracranial aneurysm, which affects around 25,000-30,000 people in the US each year. The initial mortality rate is around 45% and over half of survivors are left with major neurological deficits. Diagnosis involves CT scans, lumbar puncture, and angiography. Treatment focuses on surgical clipping or coiling of the aneurysm as well as managing complications like vasospasm, hydrocephalus, and rebleeding through medical therapy.
This document discusses the surgical management of intracranial aneurysms. It begins by defining a cerebral aneurysm as a bulging, weakened area in the wall of an artery in the brain. It then discusses factors that can cause aneurysms like smoking, hypertension, and family history. The document covers types of aneurysms like ruptured vs unruptured, symptoms of subarachnoid hemorrhage, grading scales for severity, risks of rebleeding, hydrocephalus, and vasospasm. It concludes by noting that unruptured intracranial aneurysms can be incidental findings or detected as they grow and cause compression of brain structures.
Subarachnoid hemorrhage occurs when blood leaks into the subarachnoid space surrounding the brain. The most common cause is a ruptured intracranial aneurysm. Patients present with a sudden, severe headache and may experience nausea, vomiting, neck stiffness, loss of consciousness or neurological deficits. CT scans can detect bleeding in the first 12 hours, while lumbar puncture detects blood in the cerebrospinal fluid if CT is negative. Treatment involves stabilizing the patient, detecting and treating the aneurysm with clipping or coiling, and managing complications like vasospasm, delayed cerebral ischemia, hyponatremia, fever and rebleeding.
An intracranial aneurysm is a weak spot on a blood vessel in the brain that bulges outward. They are most common in certain blood vessels like the anterior communicating artery. Unruptured aneurysms are often incidental findings and have a low annual rupture risk of around 1%. However, ruptured aneurysms cause a subarachnoid hemorrhage, which has high mortality. Treatment options include microsurgical clipping or endovascular coiling to block blood flow to the aneurysm. The timing of treatment depends on the patient's condition and aneurysm factors. Neuroprotective techniques during surgery aim to reduce brain injury from temporary ischemia.
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.
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2. Introduction
Bleeding into the subarachnoid space (space between the pia &
arachnoid meningeal layers where blood vessels lie & CSF
flows.)
3. Introduction
Less common than other types of stroke only 5%
Affects about 6/100000 population
Women more common
Usually presents before 65 yrs
Most commonly occurs between 40- 60 yrs
6. Causes of Non Traumatic SAH
• Ruptured berry aneurysm 85%
• Non aneurysmal or perimesencephalic haemorrhage-10%
• Rupture AVM
• Vertebral Artery Dissection
7. Aneurysm
• About 2% of adults harbor intracranial aneurysm.
• Ruptured, Unruptured
• Saccular,Mycotic,Fusiform,globular,Gaint,Diffuse
• Most common locations are-
Anterior Circulation
Terminal ICA
Bifurcation of MCA
Top of the Basilar artery
8. Aneurysm
• Size- 2mm to 3cm
• Average size- 7.5mm
• Those which rupture are usually 10mm or more but smaller ones can
also get ruptured
10. What causes the aneurysms to form?
• Defects in the media of the arteries
• Defects are thought to expand as a result of hydrostatic pressure from
pulsatile blood flow and blood turbulence, which is greatest at the
arterial bifurcations
• Other theory says it is initiated by focal destruction of internal elastic
membrane caused by hemodynamic forced acting at bifurcations &
branching of arteries. As a result of local weakness in vessel wall
intima bulges out covered only by adventetia
11. Clinical Feature
Sudden severe thunderclap headache
Often occipital
Last for hours or even days
Vomiting
Antecedents –
Physical exertion
Straining
Sexual excitement
Loss of conciousness at onset
16. • High resolution non-contrast CT detect SAH in almost 95% cases in
first 3 days
• Blood appears high density in subarachnoid space
• After 5-7 days sensitivity decreases sharply
• Also assesses ventricular size, infarct, hemorrhage
• May predict aneurysm location based on pattern of blood
• Anterior interhemispheric fissure- Acom
• One sylvian fissure- Ipsilateral MCA or Pcom
• Prepontine or peduncular cistern- Basilar top or SCA
CT Scan
19. CT Scan contd..
Fisher grading for SAH on CT:
• Grade 1 - No subarachnoid blood seen on CT scan
• Grade 2 - Diffuse or vertical layers of SAH less than 1 mm thick
• Grade 3 - Diffuse clot and/or vertical layer greater than 1 mm
thick
• Grade 4 - Intracerebral or intraventricular clot with diffuse or no
subarachnoid blood
20. Lumbar Puncture
• Usually done when CT is negative but strong clinical suspicion
• Opening pressure: elevated
• Non-clotting bloody fluids not clearing with sequential tubes
• Xanthochromia
• Yellowish coloration of CSF supernatent
• Almost 100% sensitive after 12 hours, 40% at 4 weeks
• Spectrophotometry is more sensitive than visual inspection
• False negative: Jaundice, very high CSF protein
22. MRI
• Not sensitive in first 24-48 hours due to less methemoglobin
• Better after 4-7 days for subacute hemorrhage
• FLAIR & proton density images may be as sensitive as CT in acute
stage
• FLAIR, DWI, GRE, proton density sequences may help diagnosis in the
second week when CT are being negative
23. A. GRE MRI after 10 days of SAH shows blood in left Sylvian fissure
B. DSA shows a small aneurysm in left MCA bifurcation
24. Angiophraphy
• CTA may detect aneurysm in 97% cases
• MRA is 92% sensitive, 97% specific
• For decision of type of repair, DSA is indicated
• Sensitivity is less for aneurysm less than 3mm size
• 10-15% SAH are angio-negative (perimesencephalic SAH)
• Repeat angiogram may be needed 2-3 weeks later
27. Treatment
Historical concept:
• Strict BP control
• Fluid restriction
• Conservative approach & delay in specific management
This approach was associated with high mortality & morbidity due to
complications of hypovolemia, hypotension & rebleeding
28. Treatment
• Initial stabilization & monitoring
• Endovascular coiling or Surgical clipping
• Prevention & treatment of complications
29.
30. Treatment contd..
• Pt should be admitted in Neuro-ICU
• Initial stabilization: Assess airway, breathing, circulation
• Endotracheal intubation is indicated if the pt is in coma, depressed
consciousness or unable to protect airway
• Monitoring:
• Cardiac monitoring
• Pulse oximetry
• Arterial BP monitoring
• Urine output via catheter
31. • The focus in the first few minutes to hours after SAH, until the patient
can undergo treatment of the ruptured aneurysm, should be directed
toward the prevention of rebleeding.
• This life-threatening complication, with a mortality rate of 20% to 60%,
has its highest rate (8%to 23%) within the first 72 hours after SAH, with
the majority of rebleeding (50% to 90%) occurring within the first 6
hours
32. HUNT AND HESS SCALE
Grade 0: Asymptomatic
Grade 1: Mild headache and mild nuchal rigidity, no neurological
deficit
Grade 2: Moderate to severe headache but no neurological deficit
other than cranial nerve palsy
Grade 3: Drowsy, confused, or mild focal deficit
Grade 4: Stupor, moderate to severe hemiparesis, and early
decerebrate posturing
Grade 5: Deep comatose, decerebrate posturing
33. WORLD FEDERATION OF NEUROLOGICAL SURGEONS
(WFNS) SCALE
Glasgow coma scale Motor deficit
Grade 0 15 Absent
Grade 1 15 Present
Grade 2 13–14 Absent
Grade 3 13–14 Present
Grade 4 7–12 Present or absent
Grade 5 3–6 Present or absent
34. Blood Pressure Management
• Early management is important to prevent rebleeding & to maintain
cerebral perfusion pressure
• Start antihypertensive agent if SBP>160 or MBP>130 mmHg
• Target BP: SBP no more than 140 mmHg unless vasospasm
• i.v. beta blocker labetalol, if no contra-indication, is the first choice
because it has short half-life, is easily titratable & do not raise ICP
• Nitroglycerine & nitroprusside raise ICP
• ACE inhibitors are delayed acting
35. Treatment of aneurysm
• With the publication of the ISAT, the treatment of an unsecured aneurysm has
shifted from surgical clipping to mostly endovascular coiling.
• ISAT showed that patients in the endovascular coiling group had significantly
higher odds of survival free of disability 1 year after SAH and a lower risk of
epilepsy when compared to the surgical clipping group.
• Even 10 years after SAH, patients who underwent endovascular coiling had better
outcome.
38. Endovascular & Surgical Treatment
• Should be performed as early as possible in low to intermediate grade
SAH (HHS or WFNS grade 1-3)
• Severe grade pts may be candidate for delayed coiling or clipping
• Endovascular coiling is preferred due to less complication
• Follow-up vascular imaging is indicated
• Retreatment should be considered by repeat coiling or clipping if
there is clinically significant remnant
39. Coiling vs Clipping
Endovascular treatment is favored over open surgery in the
following situations:
• Aneurysms in the posterior circulation because of the high surgical
morbidity
• Patients with higher-grade SAH (i.e. Hunt and Hess/WFNS grades 4-5)
• Patients who are medically unstable
• Patients with symptomatic cavernous aneurysms
• Patients with vasospasm
• Patients in whom the aneurysm lacks a defined surgical neck
• Patients with multiple aneurysms in different arterial territories if the
surgical risk is high
40. Coiling vs Clipping contd..
Clipping is favored in cases of:
• Mass effect or large hematoma (>50 ml) associated with aneurysm
• Large and giant aneurysm
• MCA aneurysm
• Wide-necked aneurysms - A large neck-to-dome ratio makes acute
endovascular coiling of wide-necked aneurysms more difficult
• Recurrent aneurysm after coil embolization
41. Complications of Coiling
• Aneurysm rupture
• Thromboembolism with acute or delayed neurologic deficit
(stroke)
• Coil displacement or compaction
• Nonspecific access complications such as groin hematoma or
arterial dissection
43. Rebleeding
• Most dangerous complication
• Risk is 60% in first 24 hour, 20 % at 14 days
• Risk factors:
• Large aneurysm
• Poorly controlled BP
• Higher Hunt & Hess grade
• Delay in coiling or clipping
• Use of antiplatelet
45. Rebleeding contd..
Prevention:
• Bed rest in a quiet room
• Analgesia, preferably with short acting agent e.g. fentanyl
• Sedation, preferably with short acting agent e.g. midazolam
• Stool softener
• Management of BP
• Early coiling or clipping
• Antifibrinolytics reduce risk of rebleeding but increase risk of
infarction: may be given for short term (<72 hours)
46. Vasospasm & Cerebral Ischemia
• Occur 7-10 days after SAH & resolves spontaneously after 21 days
• Amount of blood on initial CT is a good predictor
• Hypovolemia & hypotension may precipitate vasospasm
• Presents with new focal neurological deficit or global symptom
• Prevention:
• Avoid hypotension
• Maintain euvolemia
• oral nimodipine for 21 days- (60 mg every 4 hours for 21 days)
• Monitoring: daily bedside transcranial Doppler USG
48. Vasospasm & Cerebral Ischemia contd..
Treatment of symptomatic vasospasm:
• Triple H therapy:
• Hypertension
• Hypervolemia
• Hemodilution. If bleeding site is not secured before, rebleeding may occur
• Transluminal balloon angioplasty
• Intra-arterial vasodilator therapy e.g. CCB, papaverine, Mg
49. Acute Hydrocephalus
• Usually within first 24 hours
• Occurs in 20% cases
• Obstructive type
• Blood in ventricles in initial CT is a good predictor
• Presents with sudden neurologic deterioration
• CT may differentiate from rebleeding
• In obtunded pt, emergency ventriculostomy is needed
50. Chronic Hydrocephalus
• After 10 days
• 10-15% cases
• Communicating type
• Presents with, incontinence, ataxia, cognitive impairment
• May be difficult to distinguish from vasospasm
• Permanent CSF diversion (Shunt) may be needed
51.
52. Seizure
• Occur in 26% cases
• Risk factors include hematoma, infarct, MCA aneurysm
• Short term prophylaxis may be considered in high risk pts
• Long term prophylaxis not recommended
• Phenytoin, Levetiracetam is the agent of choice
• Phenytoin i.v. can achieve rapid therapeutic concentration and it does
not cause alteration in consciousness
• Phenobarbital produces a sedative effect, which may mask the
neurologic evaluation
54. Hyponatremia
• Occur in 10-30% cases
• Cerebral salt wasting occur due to excess BNP
• SIADH may also occur
• CSW is hypovolemic, SIADH is euvolemic
• Isotonic saline prevents hypovolemia, but not hyponatremia for
which hypertonic saline may be needed
55. Cardiopulmonary dysfunction
• Ranges from minor ECG changes to severe stress cardiomyopathy and
neurogenic pulmonary edema.
• The severity of SAH is an independent predictor of cardiopulmonary injury,
• The cardiopulmonary injury is neurally mediated.
• Cardiopulmonary complications after SAH are usually transient and resolve
within several days to 2 weeks.
56. • Fever
- most common medical complication( up to 70% of patients)
- searching for infection & antipyretic
• Glycemic Dysfunction:
-current recommendations are to maintain a
blood glucose level between 80 mg/dL and
200 mg/dL.
57. Deep vein thrombosis
prophylaxis
• All pt should have pneumatic compression stocking
• UH can be used within 1-2 days following aneurysms treatment
• IVC filter if DVT or PE occurs after clipping
• Systemic anticoagulation if DVT or PE occurs after coiling..
58. Reference
• CONTINUUM (MINNEAP MINN) 2018;24(6, NEUROCRITICAL CARE):
1623–1657.
• Harrison's Principles of Internal Medicine, Twentieth Edition.
• Adams and Victor's Principles of Neurology 11th Edition