1. Coma is defined as a state of unconsciousness from which the patient cannot be aroused. It results from diffuse or focal injuries to the brain.
2. The document discusses the pathophysiology, etiology, examination, investigations, management, and diagnosis of brain death in patients presenting with coma.
3. Key points include differentiating structural from metabolic comas, evaluating for reversible causes, monitoring vital signs and neurological exam including brain stem reflexes, treating increased intracranial pressure, and confirming brain death through apnea testing and clinical criteria.
This document discusses pediatric brain death. It defines brain death as the irreversible cessation of all brain functions, including the brain stem. Two examinations by two physicians are required to diagnose brain death in children, separated by 12-24 hours depending on age. The diagnostic criteria that must be fulfilled are a Glasgow Coma Scale of 3/15, apnea confirmed by an apnea test, and absent brain stem reflexes as shown by tests of cranial nerves and response to stimuli. Precautions must be taken to rule out factors that could mimic brain death.
This document discusses brain death, including its historical definition, current diagnostic criteria, pathophysiology, and management of organ donors. Key points include:
- Brain death is defined as irreversible cessation of all functions of the entire brain, including the brain stem.
- Diagnosis requires two examinations at least 6 hours apart showing coma, absence of brainstem reflexes, and apnea during a standardized test. Ancillary tests like EEG can be used if clinical criteria are inconclusive.
- After brain death, pathophysiological changes occur like hypotension, diabetes insipidus, and coagulopathies due to loss of autonomic and endocrine functions regulated by the brain.
General approach and differential diagnosis of comaAn Chang
This document provides guidance on evaluating and managing comatose patients. It outlines the following key steps:
1. Ensure airway, breathing and circulation are stabilized. Treat any rapidly reversible causes of coma like hypoglycemia.
2. Use the Glasgow Coma Scale to assess the level of consciousness. Common causes of coma include head injuries, strokes, infections, tumors, and metabolic derangements.
3. Perform a full neurological exam including pupil size and response, motor function, and posture. Request diagnostic tests like bloodwork and CT or MRI as indicated.
4. Manage increased intracranial pressure with osmotic diuretics if present. Treat any identifiable structural or metabolic causes. Monitor
This document discusses brain death and the criteria used to diagnose it. It begins by describing different states of consciousness including coma, persistent vegetative state, and locked-in syndrome. It then defines brain death as the total and irreversible loss of brain and brainstem function. The key criteria for determining brain death are the absence of cortical function, absence of brainstem reflexes, and apnea during a specific oxygen challenge. Confirmatory tests like angiography, EEG, transcranial Doppler, and nuclear medicine scans can also support the diagnosis. Precise clinical evaluations and testing are required to distinguish brain death from other severe neurological conditions.
This document discusses brain death and the criteria used to diagnose it. It begins by describing different states of consciousness including coma, persistent vegetative state, and locked-in syndrome. It then defines brain death as the total and irreversible loss of brain and brain stem functions. The key criteria for determining brain death are the absence of cortical function, absence of brainstem reflexes, and apnea during a specific oxygen challenge. Confirmatory tests like angiography, EEG, Doppler ultrasound, and scintigraphy can also be used when clinical criteria cannot be reliably assessed.
This document discusses brain death and the criteria used to diagnose it. It begins by describing different states of altered consciousness including coma and vegetative states. It then defines brain death as the total and irreversible loss of brain and brainstem function, and notes that spinal reflexes may remain. Several prerequisites and criteria for diagnosing brain death are provided, including the absence of brainstem reflexes and apnea testing. Confirmatory tests like angiography, EEG, Doppler ultrasound and nuclear scans are also summarized. Guidelines for diagnosing brain death in children of different ages are presented.
Brain cut up for the general pathologistEffiong Akang
Simplified procedure for brain cut up examination for general pathologists that emphasises the importance of good clinicopathological correlation in post-mortem CNS examination. Presented at TSL workshop in Lagos on 25 November 2014
1. The document discusses the approach to patients presenting in a comatose state, including definitions of different levels of consciousness, pathophysiology, common causes, management, and prognosis.
2. Management involves stabilization of airway, breathing, circulation, disability, and exposure, then detection of the underlying cause through history, exam, and investigations like imaging and labs.
3. Definitive therapy focuses on treating the specific cause, monitoring intracranial pressure, controlling seizures, and providing supportive care measures. Prognosis is generally poor when the GCS is very low or signs of herniation are present.
This document discusses pediatric brain death. It defines brain death as the irreversible cessation of all brain functions, including the brain stem. Two examinations by two physicians are required to diagnose brain death in children, separated by 12-24 hours depending on age. The diagnostic criteria that must be fulfilled are a Glasgow Coma Scale of 3/15, apnea confirmed by an apnea test, and absent brain stem reflexes as shown by tests of cranial nerves and response to stimuli. Precautions must be taken to rule out factors that could mimic brain death.
This document discusses brain death, including its historical definition, current diagnostic criteria, pathophysiology, and management of organ donors. Key points include:
- Brain death is defined as irreversible cessation of all functions of the entire brain, including the brain stem.
- Diagnosis requires two examinations at least 6 hours apart showing coma, absence of brainstem reflexes, and apnea during a standardized test. Ancillary tests like EEG can be used if clinical criteria are inconclusive.
- After brain death, pathophysiological changes occur like hypotension, diabetes insipidus, and coagulopathies due to loss of autonomic and endocrine functions regulated by the brain.
General approach and differential diagnosis of comaAn Chang
This document provides guidance on evaluating and managing comatose patients. It outlines the following key steps:
1. Ensure airway, breathing and circulation are stabilized. Treat any rapidly reversible causes of coma like hypoglycemia.
2. Use the Glasgow Coma Scale to assess the level of consciousness. Common causes of coma include head injuries, strokes, infections, tumors, and metabolic derangements.
3. Perform a full neurological exam including pupil size and response, motor function, and posture. Request diagnostic tests like bloodwork and CT or MRI as indicated.
4. Manage increased intracranial pressure with osmotic diuretics if present. Treat any identifiable structural or metabolic causes. Monitor
This document discusses brain death and the criteria used to diagnose it. It begins by describing different states of consciousness including coma, persistent vegetative state, and locked-in syndrome. It then defines brain death as the total and irreversible loss of brain and brainstem function. The key criteria for determining brain death are the absence of cortical function, absence of brainstem reflexes, and apnea during a specific oxygen challenge. Confirmatory tests like angiography, EEG, transcranial Doppler, and nuclear medicine scans can also support the diagnosis. Precise clinical evaluations and testing are required to distinguish brain death from other severe neurological conditions.
This document discusses brain death and the criteria used to diagnose it. It begins by describing different states of consciousness including coma, persistent vegetative state, and locked-in syndrome. It then defines brain death as the total and irreversible loss of brain and brain stem functions. The key criteria for determining brain death are the absence of cortical function, absence of brainstem reflexes, and apnea during a specific oxygen challenge. Confirmatory tests like angiography, EEG, Doppler ultrasound, and scintigraphy can also be used when clinical criteria cannot be reliably assessed.
This document discusses brain death and the criteria used to diagnose it. It begins by describing different states of altered consciousness including coma and vegetative states. It then defines brain death as the total and irreversible loss of brain and brainstem function, and notes that spinal reflexes may remain. Several prerequisites and criteria for diagnosing brain death are provided, including the absence of brainstem reflexes and apnea testing. Confirmatory tests like angiography, EEG, Doppler ultrasound and nuclear scans are also summarized. Guidelines for diagnosing brain death in children of different ages are presented.
Brain cut up for the general pathologistEffiong Akang
Simplified procedure for brain cut up examination for general pathologists that emphasises the importance of good clinicopathological correlation in post-mortem CNS examination. Presented at TSL workshop in Lagos on 25 November 2014
1. The document discusses the approach to patients presenting in a comatose state, including definitions of different levels of consciousness, pathophysiology, common causes, management, and prognosis.
2. Management involves stabilization of airway, breathing, circulation, disability, and exposure, then detection of the underlying cause through history, exam, and investigations like imaging and labs.
3. Definitive therapy focuses on treating the specific cause, monitoring intracranial pressure, controlling seizures, and providing supportive care measures. Prognosis is generally poor when the GCS is very low or signs of herniation are present.
approach to a child with altered sensorium.pptxdrgsvt
The document provides guidance on assessing and managing an altered sensorium in a child. It describes stabilizing the child's airway, breathing, and circulation. It also recommends treating potential causes like hypoglycemia, infections, seizures and raised intracranial pressure. The primary goals are saving the child's life and achieving intact neurological recovery through a multidisciplinary approach.
1) The document discusses a seminar on unconsciousness presented by a nurse. It defines consciousness and different levels of unconsciousness.
2) It reviews the anatomy of the brain and describes various causes of unconsciousness including structural lesions, metabolic disorders, drugs, and psychological factors.
3) Clinical manifestations involving different body systems are outlined. Assessment tools like the Glasgow Coma Scale and brainstem reflexes are also discussed.
Vital signs and neurological examination can provide clues to the cause of coma in children. Bradycardia, hypertension, and abnormal breathing patterns like Cheyne-Stokes suggest increased intracranial pressure. Signs of head trauma include "raccoon eyes", mastoid ecchymosis indicating basilar skull fracture, and retinal hemorrhages. Etiology may also be suggested by findings like jaundice/fetor (liver disease), petechiae (coagulopathy), or ketotic breath (metabolic disease). The Glasgow Coma Scale assessed severity of coma, while meningeal signs, posturing, and brainstem reflexes provide further neurological information about location and extent of injury.
NurseReview.Org - Nursing Management of the Adult Client with Neurologic Alte...Nurse ReviewDotOrg
This document provides an overview of nursing management for adult clients with neurologic alterations. It discusses anatomy and physiology of the nervous system, common health problems like altered level of consciousness and increased intracranial pressure. Diagnostic studies and neurological assessments are outlined. Intracranial pressure complications like cerebral herniation, diabetes insipidus, and SIADH are covered. Medical management goals and nursing interventions for conditions like altered level of consciousness and increased intracranial pressure are summarized.
Brain Death and Preparation for Organ DonationRanjith Thampi
This document discusses brain death, including definitions, causes, mechanisms, diagnostic criteria and confirmatory tests. It provides details on:
- Loss of brainstem and cortical function constituting brain death
- Common causes like stroke, trauma, hypoxia
- Mechanism of increased intracranial pressure leading to circulatory arrest
- Clinical criteria including apnea testing over multiple examinations
- Confirmatory tests like EEG, evoked potentials, angiography and imaging to demonstrate lack of cerebral blood flow
This document provides an overview of coma, including its anatomical and physiological bases, definition, causes, evaluation, and management. Coma requires dysfunction of the pontine reticular activating system and/or bilateral cerebral hemispheres. Common causes include drug overdose, metabolic derangements, head trauma, anoxia, and stroke. Evaluation involves assessing ABCs, looking for signs of increased intracranial pressure, and performing tests to identify potential causes. Management priorities are supporting ABCs, treating potentially reversible causes like hypoglycemia, and controlling intracranial pressure if elevated.
Birth asphyxia, or deprivation of oxygen during birth, can cause brain damage and other health issues in newborns. It occurs when a newborn does not begin breathing effectively at birth, leading to low oxygen levels and high carbon dioxide levels in the blood. This can damage organs like the brain, heart, and lungs. Brain damage from asphyxia is the most severe and least likely to fully recover from. Asphyxia affects over 1 million newborns annually and can cause disabilities like cerebral palsy and intellectual impairments. Symptoms range from mild issues that resolve within days to severe, long-term complications like coma. Prognosis depends on severity and duration of oxygen deprivation, as well as effectiveness
1. Brain death is defined as the irreversible loss of all brain function, including the brainstem. The three essential findings are coma, absence of brainstem reflexes, and apnea on testing.
2. Common causes of brain death include traumatic brain injury, intracerebral hemorrhage, hypoxic-ischemic injury from cardiopulmonary arrest. A thorough exam is required to determine the cause and rule out potential confounders.
3. Evaluation of brain death involves assessing for coma, absence of brainstem reflexes on exam, and a positive apnea test showing lack of respiratory drive and rising CO2 levels. Ancillary tests like angiography or EEG can also be
1. The document discusses the approach to evaluating and managing a comatose patient. It defines consciousness and the components of arousal and content of consciousness.
2. Evaluation of a comatose patient involves obtaining a detailed history, performing a physical exam including neurological assessment of pupil size and reactivity, eye and motor movements, and determining the level of coma.
3. Management begins with addressing airway, breathing, and circulation (ABCs), treating potentially life-threatening metabolic disorders, evaluating for increased intracranial pressure, and providing supportive care measures.
This document discusses coma, including its etiology, physical and laboratory evaluation, management and treatment, and prognosis. Coma is assessed using the Glasgow Coma Scale and signs such as eye opening, verbal response, motor response, and pupillary light reflex. Causes of coma are evaluated through history, examination, and tests of the blood, cerebrospinal fluid, imaging, and more. Treatment focuses on stabilizing the patient and removing the underlying cause, while nursing care includes positioning, nutrition, hygiene and physiotherapy. The prognosis depends on the cause, whether it can be corrected, and the duration of the coma, with higher rates of recovery for drug poisonings and head injuries treated promptly.
Hypoxic ischemic encephalopathy (HIE) is a brain injury caused by impaired oxygen delivery to the brain before, during or after birth. It affects 2-3% of live births globally and can result in death or disabilities like cerebral palsy. The primary injury is due to energy failure in neurons from lack of oxygen and glucose, leading to cell death. Secondary energy failure occurs later from oxidative stress and inflammation, worsening the injury. Clinical presentation ranges from mild abnormalities to severe complications involving multiple organ systems. Management involves supportive care, seizure control, ventilation and therapeutic hypothermia in severe cases to prevent further brain injury. Outcomes depend on severity of the initial insult and subsequent care.
This document provides an overview of the approach to a patient in a coma. It defines coma as a state of profound unconsciousness where the patient cannot be aroused or respond to stimuli. The etiology of coma can include metabolic disturbances, intoxications, infections, trauma, and other conditions. The assessment of a comatose patient involves evaluating vital signs, performing a neurological exam including brain stem reflexes, and considering differential diagnoses. Investigations may include blood and imaging tests. Management focuses on airway, breathing, circulation, treating the underlying cause, preventing complications, and providing supportive care.
This document discusses several topics related to neurology. It begins by describing upper and lower motor neuron lesions, including that pronator sign is an early sign of upper motor neuron lesion. It then discusses different types of headaches like tension-type headache and migraine, providing details on their symptoms. Raised intracranial pressure and space-occupying lesions as secondary causes of headache are also mentioned. Management strategies for various conditions like tension headaches, migraines, seizures and more are outlined. Neural tube defects, febrile seizures, and Duchenne muscular dystrophy are also summarized.
- Head injuries are a major health issue worldwide, with over 200 cases per 100,000 people and 25 cases of severe head injury.
- The brain is susceptible to both primary injury from the initial impact and secondary injury from processes that occur afterwards like swelling, bleeding and increased intracranial pressure.
- Assessment of head injury focuses on the Glasgow Coma Scale to monitor mental status changes, as this is the earliest indicator of worsening intracranial pressure. Prehospital management emphasizes spinal immobilization, oxygenation, ventilation and maintaining circulation and blood pressure.
This document discusses birth asphyxia, including its definition, causes, pathophysiology, clinical manifestations, assessment, effects, classification, management, investigations and prognosis. Some key points:
- Birth asphyxia is defined as reduction of oxygen delivery and accumulation of carbon dioxide around birth, leading to respiratory failure in newborns. It is assessed using Apgar scores and fetal monitoring.
- Causes include maternal, delivery and fetal factors that interfere with maternal-fetal circulation such as prematurity, cord problems and placental issues.
- Effects depend on severity and can involve multiple organs, particularly the brain, heart and lungs. Management focuses on stabilizing vital functions and preventing further injury through temperature control
All concepts compiled in an easy way including recent advances in the treatment of hie. For pediatricians, residents working in nicu i hope it will help you both in practical aspect as well as your academic needs.
Nurses as the primary care providers would be the immediate health care professional to assess the patient's response and to determine whether he is improving or deteriorating. Signs of brain death can be identified and reported early by a nurse with adequate knowledge.
This document discusses the management of Japanese encephalitis. It begins by outlining that JE is a leading cause of viral encephalitis in Asia. It has been effectively controlled through national vaccination programs. The document then discusses the virus, geographic distribution, pathogenesis, clinical presentation, investigations including lab diagnostics, differential diagnosis, treatment including supportive care, prevention including vaccination and vector control, and rehabilitation.
1) Brain death is defined as irreversible cessation of all functions of the entire brain, including the brainstem. Tests to determine brain death include examining brainstem reflexes and performing an apnea test.
2) Organ donation provides terminally ill patients a new lease on life but organ availability is low in India. Living donors can donate renewable tissues while deceased donors are a major source of organs.
3) For organ donation to occur, all reversible causes of coma must first be excluded through testing and the diagnosis of brain death must be certified by a board of medical experts according to the law.
approach to a child with altered sensorium.pptxdrgsvt
The document provides guidance on assessing and managing an altered sensorium in a child. It describes stabilizing the child's airway, breathing, and circulation. It also recommends treating potential causes like hypoglycemia, infections, seizures and raised intracranial pressure. The primary goals are saving the child's life and achieving intact neurological recovery through a multidisciplinary approach.
1) The document discusses a seminar on unconsciousness presented by a nurse. It defines consciousness and different levels of unconsciousness.
2) It reviews the anatomy of the brain and describes various causes of unconsciousness including structural lesions, metabolic disorders, drugs, and psychological factors.
3) Clinical manifestations involving different body systems are outlined. Assessment tools like the Glasgow Coma Scale and brainstem reflexes are also discussed.
Vital signs and neurological examination can provide clues to the cause of coma in children. Bradycardia, hypertension, and abnormal breathing patterns like Cheyne-Stokes suggest increased intracranial pressure. Signs of head trauma include "raccoon eyes", mastoid ecchymosis indicating basilar skull fracture, and retinal hemorrhages. Etiology may also be suggested by findings like jaundice/fetor (liver disease), petechiae (coagulopathy), or ketotic breath (metabolic disease). The Glasgow Coma Scale assessed severity of coma, while meningeal signs, posturing, and brainstem reflexes provide further neurological information about location and extent of injury.
NurseReview.Org - Nursing Management of the Adult Client with Neurologic Alte...Nurse ReviewDotOrg
This document provides an overview of nursing management for adult clients with neurologic alterations. It discusses anatomy and physiology of the nervous system, common health problems like altered level of consciousness and increased intracranial pressure. Diagnostic studies and neurological assessments are outlined. Intracranial pressure complications like cerebral herniation, diabetes insipidus, and SIADH are covered. Medical management goals and nursing interventions for conditions like altered level of consciousness and increased intracranial pressure are summarized.
Brain Death and Preparation for Organ DonationRanjith Thampi
This document discusses brain death, including definitions, causes, mechanisms, diagnostic criteria and confirmatory tests. It provides details on:
- Loss of brainstem and cortical function constituting brain death
- Common causes like stroke, trauma, hypoxia
- Mechanism of increased intracranial pressure leading to circulatory arrest
- Clinical criteria including apnea testing over multiple examinations
- Confirmatory tests like EEG, evoked potentials, angiography and imaging to demonstrate lack of cerebral blood flow
This document provides an overview of coma, including its anatomical and physiological bases, definition, causes, evaluation, and management. Coma requires dysfunction of the pontine reticular activating system and/or bilateral cerebral hemispheres. Common causes include drug overdose, metabolic derangements, head trauma, anoxia, and stroke. Evaluation involves assessing ABCs, looking for signs of increased intracranial pressure, and performing tests to identify potential causes. Management priorities are supporting ABCs, treating potentially reversible causes like hypoglycemia, and controlling intracranial pressure if elevated.
Birth asphyxia, or deprivation of oxygen during birth, can cause brain damage and other health issues in newborns. It occurs when a newborn does not begin breathing effectively at birth, leading to low oxygen levels and high carbon dioxide levels in the blood. This can damage organs like the brain, heart, and lungs. Brain damage from asphyxia is the most severe and least likely to fully recover from. Asphyxia affects over 1 million newborns annually and can cause disabilities like cerebral palsy and intellectual impairments. Symptoms range from mild issues that resolve within days to severe, long-term complications like coma. Prognosis depends on severity and duration of oxygen deprivation, as well as effectiveness
1. Brain death is defined as the irreversible loss of all brain function, including the brainstem. The three essential findings are coma, absence of brainstem reflexes, and apnea on testing.
2. Common causes of brain death include traumatic brain injury, intracerebral hemorrhage, hypoxic-ischemic injury from cardiopulmonary arrest. A thorough exam is required to determine the cause and rule out potential confounders.
3. Evaluation of brain death involves assessing for coma, absence of brainstem reflexes on exam, and a positive apnea test showing lack of respiratory drive and rising CO2 levels. Ancillary tests like angiography or EEG can also be
1. The document discusses the approach to evaluating and managing a comatose patient. It defines consciousness and the components of arousal and content of consciousness.
2. Evaluation of a comatose patient involves obtaining a detailed history, performing a physical exam including neurological assessment of pupil size and reactivity, eye and motor movements, and determining the level of coma.
3. Management begins with addressing airway, breathing, and circulation (ABCs), treating potentially life-threatening metabolic disorders, evaluating for increased intracranial pressure, and providing supportive care measures.
This document discusses coma, including its etiology, physical and laboratory evaluation, management and treatment, and prognosis. Coma is assessed using the Glasgow Coma Scale and signs such as eye opening, verbal response, motor response, and pupillary light reflex. Causes of coma are evaluated through history, examination, and tests of the blood, cerebrospinal fluid, imaging, and more. Treatment focuses on stabilizing the patient and removing the underlying cause, while nursing care includes positioning, nutrition, hygiene and physiotherapy. The prognosis depends on the cause, whether it can be corrected, and the duration of the coma, with higher rates of recovery for drug poisonings and head injuries treated promptly.
Hypoxic ischemic encephalopathy (HIE) is a brain injury caused by impaired oxygen delivery to the brain before, during or after birth. It affects 2-3% of live births globally and can result in death or disabilities like cerebral palsy. The primary injury is due to energy failure in neurons from lack of oxygen and glucose, leading to cell death. Secondary energy failure occurs later from oxidative stress and inflammation, worsening the injury. Clinical presentation ranges from mild abnormalities to severe complications involving multiple organ systems. Management involves supportive care, seizure control, ventilation and therapeutic hypothermia in severe cases to prevent further brain injury. Outcomes depend on severity of the initial insult and subsequent care.
This document provides an overview of the approach to a patient in a coma. It defines coma as a state of profound unconsciousness where the patient cannot be aroused or respond to stimuli. The etiology of coma can include metabolic disturbances, intoxications, infections, trauma, and other conditions. The assessment of a comatose patient involves evaluating vital signs, performing a neurological exam including brain stem reflexes, and considering differential diagnoses. Investigations may include blood and imaging tests. Management focuses on airway, breathing, circulation, treating the underlying cause, preventing complications, and providing supportive care.
This document discusses several topics related to neurology. It begins by describing upper and lower motor neuron lesions, including that pronator sign is an early sign of upper motor neuron lesion. It then discusses different types of headaches like tension-type headache and migraine, providing details on their symptoms. Raised intracranial pressure and space-occupying lesions as secondary causes of headache are also mentioned. Management strategies for various conditions like tension headaches, migraines, seizures and more are outlined. Neural tube defects, febrile seizures, and Duchenne muscular dystrophy are also summarized.
- Head injuries are a major health issue worldwide, with over 200 cases per 100,000 people and 25 cases of severe head injury.
- The brain is susceptible to both primary injury from the initial impact and secondary injury from processes that occur afterwards like swelling, bleeding and increased intracranial pressure.
- Assessment of head injury focuses on the Glasgow Coma Scale to monitor mental status changes, as this is the earliest indicator of worsening intracranial pressure. Prehospital management emphasizes spinal immobilization, oxygenation, ventilation and maintaining circulation and blood pressure.
This document discusses birth asphyxia, including its definition, causes, pathophysiology, clinical manifestations, assessment, effects, classification, management, investigations and prognosis. Some key points:
- Birth asphyxia is defined as reduction of oxygen delivery and accumulation of carbon dioxide around birth, leading to respiratory failure in newborns. It is assessed using Apgar scores and fetal monitoring.
- Causes include maternal, delivery and fetal factors that interfere with maternal-fetal circulation such as prematurity, cord problems and placental issues.
- Effects depend on severity and can involve multiple organs, particularly the brain, heart and lungs. Management focuses on stabilizing vital functions and preventing further injury through temperature control
All concepts compiled in an easy way including recent advances in the treatment of hie. For pediatricians, residents working in nicu i hope it will help you both in practical aspect as well as your academic needs.
Nurses as the primary care providers would be the immediate health care professional to assess the patient's response and to determine whether he is improving or deteriorating. Signs of brain death can be identified and reported early by a nurse with adequate knowledge.
This document discusses the management of Japanese encephalitis. It begins by outlining that JE is a leading cause of viral encephalitis in Asia. It has been effectively controlled through national vaccination programs. The document then discusses the virus, geographic distribution, pathogenesis, clinical presentation, investigations including lab diagnostics, differential diagnosis, treatment including supportive care, prevention including vaccination and vector control, and rehabilitation.
1) Brain death is defined as irreversible cessation of all functions of the entire brain, including the brainstem. Tests to determine brain death include examining brainstem reflexes and performing an apnea test.
2) Organ donation provides terminally ill patients a new lease on life but organ availability is low in India. Living donors can donate renewable tissues while deceased donors are a major source of organs.
3) For organ donation to occur, all reversible causes of coma must first be excluded through testing and the diagnosis of brain death must be certified by a board of medical experts according to the law.
This document appears to be a report from the geriatric team at RSUD Dr. Soetomo Surabaya hospital in October 2022. It discusses several topics in brief sections with titles but no identifying details are provided about the content of each section. The document closes with an expression of gratitude from the geriatric team at the hospital.
Pasien perempuan 25 tahun mengeluh nyeri kepala dan sering kesemutan sisi kanan. EEG menunjukkan gelombang tajam di area frontopolar kiri. Pasien laki-laki 17 tahun mengalami kejang tonik klonik. EEG menunjukkan kompleks gelombang tajam di area frontopolar kiri.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central19various
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kol...rightmanforbloodline
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Versio
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
1. Approach to a Child with Coma
Prof Rashmi Kumar
Department of Pediatrics,
KG Medical University,
Lucknow
2. Coma: Definition
• Derived from the Greek word ‘Koma’ or
deep sleep
• Various grades – ‘spectrum’
• State of altered consciousness with
reduced capacity for arousal and reduced
responsiveness to visual, auditory and
tactile stimulation
3. • The word coma should be differentiated
from
– Syncope (transient alteration of consciousness)
– Seizure
4. Coma : Pathophysiology
• Normal consciousness is maintained by integrity of
certain areas of the cerebral cortex, thalamus and
brain stem
• Altered consciousness due to
– Diffuse lesions of cerebral cortex (metabolic, toxic,
hypoxic)
– Focal lesions of ARAS - central core of brain stem
5. Coma: Pathophysiology
• Diffuse insult to both cerebral hemispheres
(metabolic/toxic/hypoxic/ischemic)
or
• focal lesion affecting ascending reticular activating
system (ARAS) located in upper pons, midbrain &
diencephalon. Affected by compression (herniation)
Lesion in one cerebral hemisphere will not produce coma
ICT generalised ischemia (CPP=MAP-ICT)
focal ARAS damage by herniation
12. Coma: Immediate Management
Is resuscitation required?
• A – airway prevent tongue falling
back, suction
• B – breathingrespiratory support,
oxygen
• C- circulationiv fluids, monitor BP,
vasopressors
• If any evidence of poisoning GL
13. Coma : Quick History & Examn
• Circumstances?
• Duration & onset? Acute in CNS infection, trauma,
seizure, poisoning, metabolic, vascular
• H/o poisoning?
• H/o trauma?
• H/o fever?
• H/o seizure?
• Past medical history
– H/o seizures in the past?
– H/o known endocrine disorder?
– H/o headache/vomiting/visual symptoms?
14. Coma: Quick History & Examn
• Vitals
• Fever
• BP
• S/o shock
• S/o ICP bradycardia, hypertension
• Respiration rapid in acidosis & CNS lesions also
• General Physical:
– Evidence of trauma, injury, tongue bite
– Jaundice
– Breath - for odor of ketones, fetor hepaticus etc
– Skin peticheae, exanthem
– Dry, flushed skin in belladonna poisoning
– Moist skin with salivation in organophosphorus poisoning
• Complete systemic exam
15. Coma : Neurological Examn
Painful stimuli- strong pinch, pressure on nail bed, pressure on globe
Glasgow Coma Scale:
Best Motor Best Verbal Eye opening
1. none none none
2. extension to incomprehensible to pain
pain sounds
3. flexion to inappropriate to call
pain words
4. withdraws confused speech spontaneous
5. localises well oriented
6. Moves on
command
16. Coma : Neurological Examn
Modified Coma Scale for children < 2 yrs
Best Motor Best Verbal Eye opening
1. none none none
2. extension to moaning to to pain
pain pain
3. flexion to crying to to call
pain pain
4. withdraws irritable cry spontaneous
5. localises coos, babbles
6. Moves on
command
17. Coma : Neurological Examn
• Meningeal signs
• Tone/posturing
– Decerebrate- lesion in upper pons
– Decorticate- b/l cortical lesion with preservation of brain stem
function
– Flaccidity – when all cortical & brain stem function till
pontomedullary junction are lost
• Fundus
• Pupils
– Pinpoint in pontine lesions/morphine poisoning
– B/l fixed dilated in terminal state, severe ischemic damage,
atropine/belladonna poisoning
– U/l unreactive pupil ? transtentorial herniation
– Pupils generally small, equal & reactive in toxic/metabolic causes
19. Structural vs functional coma
• Meningeal signs
• Focal deficits
• Brain stem reflexes
lost
• Pupils unequal or
fixed dilated
• Absent
• Absent
• Present
• Semidilated and
reactive
20. Coma: Investigations
• Counts
• Blood glucose, urea, electrolytes, acid base
• Ammonia, liver function, lactate
• Toxicology
• Lumbar puncture – CI if ICP. Abnormal in
CNS infections
• Cultures
• EEG – usually non specific
• Imaging – r/o mass lesion
21. Coma: Treatment
Treat the cause
Supportive care – antipyretics, anticonvulsants
Management of ICP
Mannitol – 0.25 – 1 gm/kg of 20% solution (1.25 – 5 ml/kg) bolus iv
Frusemide
Diamox, glycerine
Steroids – esp vasogenic edema
Hyperventilation lowers CBVCPP
Maintain PCO2 between 25 – 30 mm Hg
Nursing care:
Position
Nutrition
Care of eyes
Care of skin
Chest physiotherapy
Care of bowel & bladder
Physiotherapy
22. Persistent vegetative state:
• patients after recovery from coma return to a
wakeful state without cognition/ awareness of
environment
• Children who remain in this state for > 3
months do not regain functional skills
• Causes –
anoxia/ischemia/metabolic/encephalitic
coma/head trauma
• Survival indefinite with good nursing care
23. Coma: Diagnosis of Brain Death
Importance
(American Academy of Neurology, 1995)
Prerequisites:
– Cessation of all brain function
– Proximate cause of brain death is known
– Condition is irreversible
Cardinal features:
• Coma
• Absent brain stem reflexes
– Pupillary light reflex
– Corneal reflex
– Oculocephalic
– Oculovestibular
– Oropharyngeal
– Apnea
• Confirmatory tests (optional)
– Cerebral angiography
– Electroencephalography
– Radioisotope cerebral blood flow study
– Transcranial Doppler ultrasonography
• 2 examinations – interval depends
• One/two physicians
24. Apnea Test
• Prerequisites:- Core temperature > 36.5O C (97o F).
- Systolic blood pressure > 90 mm Hg (Adults only).
- Euvolemia (or positive fluid balance in the previous 6 hours).
- Normal PCO2 (or arterial PCO2 > 40 mm Hg).
- Normal PO2 (or preoxygenation to obtain arterial PO2 > 200 mm Hg).
• Connect a pulse oximeter. Disconnect the ventilator or place the patient on CPAP at an
appropriate level or place a cannula at the level of the carina and administer 100% O2
endotracheally at 8L per minute.
• Look closely for respiratory movements abdominal or chest excursions that produce
adequate tidal volumes).- Measure arterial PO2 , PCO2 , and pH after approximately 8
minutes (10 minutes for children). Resume mechanical ventilation.
• Absence of spontaneous respiratory effort with PCO2 20 mm Hg > baseline (PCO2 > 60
mm Hg) confirms apnea and supports the diagnosis of death. If respiratory efforts are
present, the test is inconsistent with brain death and should be repeated. For children, if
the rise in PCO2 fails to reach 60 mm Hg, perform the test again for a duration of 15
minutes.- If the blood pressure becomes unstable or significant oxygen desaturation and
cardiac arrhythmias are present during testing, resume ventilation. Immediately draw an
arterial blood sample. If PCO2 > 60 mm Hg or the increase is 20 mm Hg > baseline
normalized PCO2, the apnea test is consistent with brain death. If not, the result is
indeterminate. A confirmatory test may be useful.
25. A. History: determine the cause of coma to eliminate remediable or reversible conditions
B. Physical examination criteria:
1. Coma and apnea
2. Absence of brain stem function
(a) Mid-position or fully dilated pupils
(b) Absence of spontaneous oculocephalic (doll's eye) and caloric-induced eye movements
(c) Absence of movement of bulbar musculature, corneal, gag, cough, sucking and rooting
reflexes
(d) Absence of respiratory effort with standardized testing for apnea
3. Patient must not be hypothermic or hypotensive
4. Flaccid tone and absence of spontaneous or induced movements excluding activity
mediated at spinal cord level
5. Examination should remain consistent for brain death throughout the predetermined
period of observation
26. Observation period according to age:
• 7 days to 2 months: Two examination and EEGs 48 hours apart
• 2 months to 1 year: Two examination and EEGs 24 hours apart or one
examination and an initial EEG showing ECS combined with a
radionuclide angiogram showing no CBF.
• More than 1 year: Two examinations 12 to 24 hours apart; EEG and
isotope angiography are optional
• (No criteria for neonates < 7days of age)
27. MCQ
1. Cerebral Perfusion Pressure equals:
a) Mean arterial pressure + intracranial pressure
b) Mean arterial pressure - intracranial pressure
c) Intracranial pressure – Mean arterial pressure
d) None of the above
28. 2. The following is true about Glasgow Coma Scale:
a) The highest score is 10
b) Lowest score is 3
c) There are 5 possible scores for Best Motor Response
d) Lowest score is 0
29. Unilateral unresponsive pupil is found in:
a) Morphine poisoning
b) Impending trantentorial herniation
c) Belladona poisoning
d) Brain death
30. A 7 year old child is brought to the emergency in coma. On
deep painful stimulus there is no verbal response, no eye
opening and slight extension of limbs. What is his
Glasgow Coma Score?
a) 7
b) 9
c) 5
d) 4
31. Signs of raised intracranial tension include all
except:
a) Hypertension
b) Shallow breathing
c) Bradycardia
d) Papilledema
32. Prerequisites for diagnosis of brain death
include all except:
a) Cessation of all brain function
b) Flat EEG
c) Proximate cause of coma is known
d) Condition is irreversible