1. Brain death is defined as the irreversible loss of function of the brain, including the brainstem. It is diagnosed through clinical examinations demonstrating coma, absence of brainstem reflexes, and apnea.
2. The diagnosis of brain death requires meeting certain prerequisites, performing a neurological exam to demonstrate no response to stimuli and no brainstem reflexes, and conducting an apnea test to show the inability to breathe independently.
3. Confirmatory tests such as an EEG, angiogram, or nuclear scan may be used but are not required for the diagnosis of brain death. Proper documentation of meeting criteria is important.
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.
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.
The document discusses the diagnosis of brain death through neurological criteria. It begins by describing the main parts of the brain and their functions. It then discusses the concepts, laws, and types of brain death in India. The key components of determining brain death are described, including establishing the cause of coma, achieving normal temperature and blood pressure, performing neurological examinations to check for absence of brainstem reflexes and response to stimuli, and conducting an apnea test. Potential mimics of brain death and pitfalls in the clinical evaluation are outlined. Confirmatory ancillary tests like cerebral angiography and EEG are also discussed.
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.
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
Brain death is a clinical diagnosis based on the absence of neurologic function and irreversible coma. A complete neurologic examination is required to determine brain death, which must show no brainstem reflexes, no response to stimuli, apnea on testing, and flaccid muscle tone. Ancillary tests like EEG or angiography can assist in diagnosis but are not required. Special considerations are needed for diagnosing brain death in newborns and preterm infants due to the potential for reversible conditions and lack of brain development. Death is declared after two examinations show no changes confirming an irreversible condition.
This presentation consist information about Brain death with special emphasis to differences between Indian and Western Guidelines. Also consist information about Organ transplantation and related act.
This document discusses brain death and how it is defined. It explains that brain death is a legal definition of death that means the complete and irreversible cessation of all brain function. The brain has died due to blocked blood flow even though the heart may still be beating with the help of life support. Signs of brain death include the absence of reflexes and the inability to breathe without a ventilator. Tests like EEG can confirm no brain activity remains. The document provides details on clinical evaluations and confirmatory tests used to determine brain death.
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.
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.
The document discusses the diagnosis of brain death through neurological criteria. It begins by describing the main parts of the brain and their functions. It then discusses the concepts, laws, and types of brain death in India. The key components of determining brain death are described, including establishing the cause of coma, achieving normal temperature and blood pressure, performing neurological examinations to check for absence of brainstem reflexes and response to stimuli, and conducting an apnea test. Potential mimics of brain death and pitfalls in the clinical evaluation are outlined. Confirmatory ancillary tests like cerebral angiography and EEG are also discussed.
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.
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
Brain death is a clinical diagnosis based on the absence of neurologic function and irreversible coma. A complete neurologic examination is required to determine brain death, which must show no brainstem reflexes, no response to stimuli, apnea on testing, and flaccid muscle tone. Ancillary tests like EEG or angiography can assist in diagnosis but are not required. Special considerations are needed for diagnosing brain death in newborns and preterm infants due to the potential for reversible conditions and lack of brain development. Death is declared after two examinations show no changes confirming an irreversible condition.
This presentation consist information about Brain death with special emphasis to differences between Indian and Western Guidelines. Also consist information about Organ transplantation and related act.
This document discusses brain death and how it is defined. It explains that brain death is a legal definition of death that means the complete and irreversible cessation of all brain function. The brain has died due to blocked blood flow even though the heart may still be beating with the help of life support. Signs of brain death include the absence of reflexes and the inability to breathe without a ventilator. Tests like EEG can confirm no brain activity remains. The document provides details on clinical evaluations and confirmatory tests used to determine brain death.
The document discusses increased intracranial pressure (ICP), including its causes, signs and symptoms, and treatment approaches. ICP is normally 7-15 mmHg but can increase due to mass effects from tumors or swelling, increased venous pressure, or obstruction of CSF flow. Goals of treatment are to maintain cerebral perfusion pressure and prevent ischemia. Management includes positioning, monitoring vitals, controlling seizures, administering diuretics like mannitol, and in severe cases, surgical intervention.
Brain death current concepts and legal issues in indiaNeurologyKota
This document discusses the history and criteria for determining brain death. It begins by outlining the historical definitions of death from the 1960s onwards, which evolved from cardiopulmonary criteria to brain-based criteria with the development of life-support technologies. The document then examines the anatomical basis of brainstem death and causes that can lead to it. It provides details on the clinical evaluation process for determining brain death in both adults and children based on guidelines from the US and UK. The document also discusses legal aspects of brain death certification in India according to the Transplantation of Human Organs Act.
This document provides an overview of radiological imaging in the management of stroke. It discusses:
1) Various imaging modalities used including unenhanced CT, CT angiography, MRI, and their benefits. Diffusion weighted MRI can detect acute ischemia within 30 minutes.
2) Examples of imaging findings for different stroke types like ischemic and hemorrhagic strokes. Ischemic strokes appear as bright lesions on DWI MRI.
3) Surgical interventions for acute stroke management include decompressive hemicraniectomy to reduce intracranial pressure for large hemispheric infarcts, and external ventricular drainage for intraventricular hemorrhage and hydrocephalus.
Management of patient with increased intracranial pressuresalman habeeb
This document discusses the management of increased intracranial pressure. It defines intracranial pressure and its normal compensatory mechanisms. Common causes of increased ICP including brain edema are explained. Signs and symptoms as well as diagnostic tests and methods for measuring ICP are covered. Goals and approaches for medical and surgical management to reduce ICP are outlined.
This document discusses cerebral blood flow and its regulation. It begins with an introduction to the components inside the skull and the Monro-Kellie doctrine. It then covers the anatomy of brain circulation discovered by Willis in 1664, including the anterior and posterior circulations and collateral pathways. Regulation of cerebral blood flow is achieved through hemodynamic autoregulation, metabolic and chemical mediators, neural control, and circulatory peptides. Clinical measurement techniques include laser Doppler flowmetry, transcranial Doppler, and imaging modalities like CT, MRI, PET, and SPECT. Factors like age, hypertension, and failure of autoregulation can impact cerebral blood flow and its regulation.
Intracerebral hemorhage Diagnosis and managementRamesh Babu
About ICH - Diagnosis and management, Discussed the clinical presentation, evaluation, radiological features and management including recent guidelines
This document discusses cerebral edema, which occurs when excess fluid accumulates in the brain tissue leading to increased intracranial pressure. It classifies edema into cytotoxic, vasogenic, and interstitial types based on etiology. Cytotoxic edema results from cellular damage while vasogenic edema stems from blood-brain barrier disruption. Managing cerebral edema focuses on optimizing ventilation, intravenous fluids, blood pressure control, and using osmotherapy agents like mannitol to reduce brain water content.
This is a presentation on brain death, its background, definition, related neurological conditions, criteria of brain death, brain stem reflexes, causes of coma, confounding factors, observation compatible with brain death, ancillary test, medical record documentation, prognosis, Management of brain death patient.
You tube link of this presentation
https://www.youtube.com/watch?v=3MzE5lHfglI&t=38s
This document summarizes key points from a review course on critical care medicine given by Dr. Anand Tiwari. It discusses traumatic brain injury epidemiology and mechanisms of injury. It also covers principles of prevention, emergency care, critical care, and brain-specific therapies. Specific topics include intracranial hypertension management, imaging and monitoring, and guidelines for neurosurgical intervention.
ICU management of traumatic brain injury FemiOpadotun
This document provides information on the management of traumatic brain injury (TBI) in the intensive care unit (ICU). It discusses the epidemiology, pathophysiology, clinical features, and management of TBI. Key points include that TBI is a leading cause of death and disability, with falls, motor vehicle accidents, and assaults being common causes. Primary brain injury results directly from trauma, while secondary brain injury involves downstream effects that can exacerbate damage. Clinical assessment involves the Glasgow Coma Scale and monitoring for signs of increased intracranial pressure. Aggressive ICU management is aimed at preventing secondary injury.
1. The document discusses the history and techniques of intracranial pressure (ICP) monitoring. It describes historical figures who contributed to the understanding of ICP and various monitoring methods that have been developed over time.
2. The current gold standard for ICP monitoring is an external ventricular drain, though fiberoptic and strain gauge monitors provide alternatives. Newer methods like optic nerve sheath ultrasound provide noninvasive options.
3. Careful analysis of ICP waveforms can provide insights into intracranial compliance and dynamics that help guide management of conditions with elevated ICP like traumatic brain injury.
This document provides an overview of traumatic brain injury (TBI), including its definition, pathophysiology, types (closed and open head injuries), specific injuries (contusions, hematomas, fractures), assessment (Glasgow Coma Scale), management (preventing secondary brain injury, ICP monitoring and treatment), and long-term outcomes (cognitive deficits, epilepsy, headaches). It describes the primary and secondary injury mechanisms of TBI, including diffuse axonal injury. Imaging and diagnostic criteria for different types of brain injuries are outlined. Guidelines for initial evaluation, monitoring, and medical and surgical management of increased ICP are also reviewed.
Management of Traumatic Brain Injury in ICUDr.Tarek Sabry
This document discusses the management of traumatic brain injury (TBI) patients in the intensive care unit (ICU). It outlines the key aspects of care including general monitoring, intracranial pressure (ICP) monitoring, analgesia and sedation, mechanical ventilation, hemodynamic support, maintaining normothermia and cerebral perfusion pressure, and preventing secondary insults. The goal of management is to stabilize the patient, prevent intracranial hypertension, and maintain adequate cerebral blood flow and oxygenation through various treatment strategies and intensive care measures.
This document discusses coma and disorders of consciousness. It defines coma as a state of unresponsiveness and unconsciousness, and notes that coma can be a medical emergency requiring intervention. The document outlines different levels of arousal from alert to coma and describes conditions like encephalopathy, locked-in syndrome, and persistent vegetative state. Causes of impaired consciousness discussed include alcohol, epilepsy, intoxication, trauma, infection, stroke, and hypoxia-ischemia. The Glasgow Coma Scale for assessing coma is also summarized.
This document discusses brain death and organ donation. It begins by outlining the history of defining brain death from 1959 to present. It then explains how brain death is determined, including establishing the cause of coma, performing a clinical examination to demonstrate signs of brain death like coma, brainstem areflexia and apnea, and confirming with ancillary tests if needed. The document provides details on specific tests like the apnea test and discusses special considerations for determining brain death in children. It also outlines conditions that must be excluded before declaring brain death. Finally, it discusses the importance of organ donation and the types of donations possible.
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.
The document discusses brain death, its diagnosis and pathophysiology. It defines brain death as the complete and irreversible loss of brain function. The diagnosis involves meeting strict clinical criteria demonstrating the absence of brainstem reflexes as well as confirmatory tests like EEG. Brain death results in no prospect of survival without life support or recovery of brain function. Proper diagnosis is important for organ donation where brain death constitutes legal death.
The document defines various types of strokes and transient ischemic attacks. It discusses the epidemiology, risk factors, clinical features, investigations, and management of strokes. The main types are ischemic and hemorrhagic strokes. Investigations include brain imaging like CT scan and MRI to identify the type of stroke and underlying causes. Treatment focuses on minimizing brain damage, preventing complications, rehabilitation, and reducing the risk of recurrence.
70% of RTA patients have head injury(HI).
One of the most important public health problems of today.
70% of deaths in RTA are due to HI.
At Risk population
Males 15-24
Infants
Young Children
Elderly
This document outlines the clinical criteria and procedures for determining brain death in adults. Brain death is defined as the irreversible loss of brain function, including the brainstem. The diagnostic criteria include coma or unresponsiveness, absence of brainstem reflexes, and apnea during an apnea test where respiratory movements are absent and blood gases meet specified levels. Confirmatory tests like EEG, angiography, or nuclear scans can be used if clinical criteria cannot be reliably tested. The medical record must document the criteria used to determine brain death.
1) Brain death is the irreversible loss of all brain and brainstem functions and is diagnosed clinically through examination of coma, absent brainstem reflexes, and apnea on testing.
2) The role of the intensivist is to determine if the patient meets criteria for brain death through clinical examination and ancillary testing, and to prepare potential organ donors.
3) Brain death results from severe brain injury or lack of oxygen that causes raised intracranial pressure, cessation of cerebral blood flow, and ultimately complete necrosis of brain tissue.
The document discusses increased intracranial pressure (ICP), including its causes, signs and symptoms, and treatment approaches. ICP is normally 7-15 mmHg but can increase due to mass effects from tumors or swelling, increased venous pressure, or obstruction of CSF flow. Goals of treatment are to maintain cerebral perfusion pressure and prevent ischemia. Management includes positioning, monitoring vitals, controlling seizures, administering diuretics like mannitol, and in severe cases, surgical intervention.
Brain death current concepts and legal issues in indiaNeurologyKota
This document discusses the history and criteria for determining brain death. It begins by outlining the historical definitions of death from the 1960s onwards, which evolved from cardiopulmonary criteria to brain-based criteria with the development of life-support technologies. The document then examines the anatomical basis of brainstem death and causes that can lead to it. It provides details on the clinical evaluation process for determining brain death in both adults and children based on guidelines from the US and UK. The document also discusses legal aspects of brain death certification in India according to the Transplantation of Human Organs Act.
This document provides an overview of radiological imaging in the management of stroke. It discusses:
1) Various imaging modalities used including unenhanced CT, CT angiography, MRI, and their benefits. Diffusion weighted MRI can detect acute ischemia within 30 minutes.
2) Examples of imaging findings for different stroke types like ischemic and hemorrhagic strokes. Ischemic strokes appear as bright lesions on DWI MRI.
3) Surgical interventions for acute stroke management include decompressive hemicraniectomy to reduce intracranial pressure for large hemispheric infarcts, and external ventricular drainage for intraventricular hemorrhage and hydrocephalus.
Management of patient with increased intracranial pressuresalman habeeb
This document discusses the management of increased intracranial pressure. It defines intracranial pressure and its normal compensatory mechanisms. Common causes of increased ICP including brain edema are explained. Signs and symptoms as well as diagnostic tests and methods for measuring ICP are covered. Goals and approaches for medical and surgical management to reduce ICP are outlined.
This document discusses cerebral blood flow and its regulation. It begins with an introduction to the components inside the skull and the Monro-Kellie doctrine. It then covers the anatomy of brain circulation discovered by Willis in 1664, including the anterior and posterior circulations and collateral pathways. Regulation of cerebral blood flow is achieved through hemodynamic autoregulation, metabolic and chemical mediators, neural control, and circulatory peptides. Clinical measurement techniques include laser Doppler flowmetry, transcranial Doppler, and imaging modalities like CT, MRI, PET, and SPECT. Factors like age, hypertension, and failure of autoregulation can impact cerebral blood flow and its regulation.
Intracerebral hemorhage Diagnosis and managementRamesh Babu
About ICH - Diagnosis and management, Discussed the clinical presentation, evaluation, radiological features and management including recent guidelines
This document discusses cerebral edema, which occurs when excess fluid accumulates in the brain tissue leading to increased intracranial pressure. It classifies edema into cytotoxic, vasogenic, and interstitial types based on etiology. Cytotoxic edema results from cellular damage while vasogenic edema stems from blood-brain barrier disruption. Managing cerebral edema focuses on optimizing ventilation, intravenous fluids, blood pressure control, and using osmotherapy agents like mannitol to reduce brain water content.
This is a presentation on brain death, its background, definition, related neurological conditions, criteria of brain death, brain stem reflexes, causes of coma, confounding factors, observation compatible with brain death, ancillary test, medical record documentation, prognosis, Management of brain death patient.
You tube link of this presentation
https://www.youtube.com/watch?v=3MzE5lHfglI&t=38s
This document summarizes key points from a review course on critical care medicine given by Dr. Anand Tiwari. It discusses traumatic brain injury epidemiology and mechanisms of injury. It also covers principles of prevention, emergency care, critical care, and brain-specific therapies. Specific topics include intracranial hypertension management, imaging and monitoring, and guidelines for neurosurgical intervention.
ICU management of traumatic brain injury FemiOpadotun
This document provides information on the management of traumatic brain injury (TBI) in the intensive care unit (ICU). It discusses the epidemiology, pathophysiology, clinical features, and management of TBI. Key points include that TBI is a leading cause of death and disability, with falls, motor vehicle accidents, and assaults being common causes. Primary brain injury results directly from trauma, while secondary brain injury involves downstream effects that can exacerbate damage. Clinical assessment involves the Glasgow Coma Scale and monitoring for signs of increased intracranial pressure. Aggressive ICU management is aimed at preventing secondary injury.
1. The document discusses the history and techniques of intracranial pressure (ICP) monitoring. It describes historical figures who contributed to the understanding of ICP and various monitoring methods that have been developed over time.
2. The current gold standard for ICP monitoring is an external ventricular drain, though fiberoptic and strain gauge monitors provide alternatives. Newer methods like optic nerve sheath ultrasound provide noninvasive options.
3. Careful analysis of ICP waveforms can provide insights into intracranial compliance and dynamics that help guide management of conditions with elevated ICP like traumatic brain injury.
This document provides an overview of traumatic brain injury (TBI), including its definition, pathophysiology, types (closed and open head injuries), specific injuries (contusions, hematomas, fractures), assessment (Glasgow Coma Scale), management (preventing secondary brain injury, ICP monitoring and treatment), and long-term outcomes (cognitive deficits, epilepsy, headaches). It describes the primary and secondary injury mechanisms of TBI, including diffuse axonal injury. Imaging and diagnostic criteria for different types of brain injuries are outlined. Guidelines for initial evaluation, monitoring, and medical and surgical management of increased ICP are also reviewed.
Management of Traumatic Brain Injury in ICUDr.Tarek Sabry
This document discusses the management of traumatic brain injury (TBI) patients in the intensive care unit (ICU). It outlines the key aspects of care including general monitoring, intracranial pressure (ICP) monitoring, analgesia and sedation, mechanical ventilation, hemodynamic support, maintaining normothermia and cerebral perfusion pressure, and preventing secondary insults. The goal of management is to stabilize the patient, prevent intracranial hypertension, and maintain adequate cerebral blood flow and oxygenation through various treatment strategies and intensive care measures.
This document discusses coma and disorders of consciousness. It defines coma as a state of unresponsiveness and unconsciousness, and notes that coma can be a medical emergency requiring intervention. The document outlines different levels of arousal from alert to coma and describes conditions like encephalopathy, locked-in syndrome, and persistent vegetative state. Causes of impaired consciousness discussed include alcohol, epilepsy, intoxication, trauma, infection, stroke, and hypoxia-ischemia. The Glasgow Coma Scale for assessing coma is also summarized.
This document discusses brain death and organ donation. It begins by outlining the history of defining brain death from 1959 to present. It then explains how brain death is determined, including establishing the cause of coma, performing a clinical examination to demonstrate signs of brain death like coma, brainstem areflexia and apnea, and confirming with ancillary tests if needed. The document provides details on specific tests like the apnea test and discusses special considerations for determining brain death in children. It also outlines conditions that must be excluded before declaring brain death. Finally, it discusses the importance of organ donation and the types of donations possible.
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.
The document discusses brain death, its diagnosis and pathophysiology. It defines brain death as the complete and irreversible loss of brain function. The diagnosis involves meeting strict clinical criteria demonstrating the absence of brainstem reflexes as well as confirmatory tests like EEG. Brain death results in no prospect of survival without life support or recovery of brain function. Proper diagnosis is important for organ donation where brain death constitutes legal death.
The document defines various types of strokes and transient ischemic attacks. It discusses the epidemiology, risk factors, clinical features, investigations, and management of strokes. The main types are ischemic and hemorrhagic strokes. Investigations include brain imaging like CT scan and MRI to identify the type of stroke and underlying causes. Treatment focuses on minimizing brain damage, preventing complications, rehabilitation, and reducing the risk of recurrence.
70% of RTA patients have head injury(HI).
One of the most important public health problems of today.
70% of deaths in RTA are due to HI.
At Risk population
Males 15-24
Infants
Young Children
Elderly
This document outlines the clinical criteria and procedures for determining brain death in adults. Brain death is defined as the irreversible loss of brain function, including the brainstem. The diagnostic criteria include coma or unresponsiveness, absence of brainstem reflexes, and apnea during an apnea test where respiratory movements are absent and blood gases meet specified levels. Confirmatory tests like EEG, angiography, or nuclear scans can be used if clinical criteria cannot be reliably tested. The medical record must document the criteria used to determine brain death.
1) Brain death is the irreversible loss of all brain and brainstem functions and is diagnosed clinically through examination of coma, absent brainstem reflexes, and apnea on testing.
2) The role of the intensivist is to determine if the patient meets criteria for brain death through clinical examination and ancillary testing, and to prepare potential organ donors.
3) Brain death results from severe brain injury or lack of oxygen that causes raised intracranial pressure, cessation of cerebral blood flow, and ultimately complete necrosis of brain tissue.
Protocols For Organ Donation powerpoint format.pptxRahulJankar4
This document provides guidelines for the management of potential organ donors. It begins with definitions of brain death and potential organ donor. It then discusses the history and criteria for determining brain death, including the Harvard criteria from 1968 and the Uniform Determination of Death Act from 1981. The document outlines the tests used to diagnose brain stem death in India, including neurological exams and the apnea test. It notes the physiological changes that occur after brain stem death and provides guidelines for multisystem management and care of the potential organ donor to optimize organ donation.
The document discusses guidelines for determining brain death. It begins with historical context for defining death and the need for brain death criteria. Key points include:
- Brain death is the irreversible loss of all brain function, including the brain stem. It allows for legal death even if other organs are functioning.
- Tests to determine brain death include examining for the absence of brain stem reflexes and apnea testing to check for respiratory drive.
- If full criteria are met, including examinations showing no brain activity, the time of death is determined to be when respiratory criteria were met on tests.
This document summarizes the key updates from the 2010 American Academy of Neurology evidence-based guidelines on determining brain death. It outlines the clinical evaluation process including the neurologic assessment and apnea test to determine the irreversible cessation of brain and brainstem functions. While ancillary tests are not required, they may be used when the neurologic exam is uncertain or the apnea test cannot be done. Proper documentation of the determination is also important.
This document discusses brain death and its determination. It begins by introducing the concept of brain death and how advances in medicine led to its development. It then covers the anatomical and physiological basis of brain death, focusing on the brainstem and its role in consciousness and vital functions. Several sections define the criteria for determining brain death, including clinical assessments and tests to confirm the diagnosis. Complicating factors and observation periods are also outlined. The document concludes by noting guidelines for determining brain death in children.
This document discusses brain death, including its definition, criteria, and controversies. It begins by explaining how advances in medicine led to the development of neurological criteria for determining death. It then covers the anatomical and physiological basis of brain death, focusing on damage to the brainstem and reticular formation. The document outlines the clinical criteria for diagnosing brain death, including the absence of brainstem reflexes and apnea testing. It notes complicating factors and observation periods. The history and acceptance of brain death criteria internationally is reviewed. Some bioethical controversies are also presented, such as debates around the definition of death and higher brain formulations.
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.
The document discusses the pathophysiology of brain death in pediatric patients. It begins with a brief history of the concept of brain death and outlines the key findings required for a diagnosis, including coma, absence of brainstem reflexes, and apnea. The document then describes the specific brainstem reflexes and other tests used in the clinical examination, including precautions that must be taken. It emphasizes that determination of brain death requires two examinations by different physicians, separated by an observation period, as well as an apnea test. The role of ancillary tests is also outlined.
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
Brain death & Potential Brain Dead Donor (PBDD)Krishn Undaviya
This document discusses brain death and the determination of brain death. It provides:
1) A definition of brain death as the irreversible loss of all functions of the brain, including the brainstem, as evidenced by coma, absence of brainstem reflexes, and apnoea.
2) Details the clinical criteria for determining brain death, including neurological examination to check for absence of brainstem reflexes and an apnoea test.
3) Outlines the general care and management of a potential organ donor who is brain dead, including maintaining body temperature and position, treating for infections, and eye and airway care.
Brain death and care for cadaveric organ donarKrishna R
The document discusses the history and criteria for determining brain death. It begins by outlining the evolution of the concept of brain death from the 1960s onwards. Key events included distinguishing brain death from cardiac death with the advent of life support technologies. The document then discusses the anatomy and functions of the brainstem and how brainstem death criteria focus on irreversible loss of brainstem function. It provides details on the tests and criteria used in India to determine brain death, including loss of consciousness, absence of brainstem reflexes, apnea testing, and rule out of confounding factors. Spinal cord reflexes that can occur after brain death are also addressed.
This document discusses brain death determination and organ donation. It begins by outlining the history of brain death criteria internationally and in India. It then describes the clinical examination process for determining brain death, including prerequisites, testing of brainstem reflexes, and requirements for the apnea test. Alternative confirmatory tests are also outlined. Considerations for special populations like children and potential mimics of brain death are discussed. The document concludes by discussing organ donation types and outcomes of donation.
Brain death refers to the irreversible loss of all brain function. It is diagnosed through examinations showing the absence of brainstem reflexes and apnea during an oxygen challenge. Organ donation from brain dead donors provides organs for transplantation but there is a shortage due to misperceptions about the process. The document discusses the criteria for determining brain death in adults and children, confirmatory tests, organ donation laws in India, and efforts to increase donation rates.
Brain death occurs when there is irreversible cessation of all functions of the entire brain, including the brain stem. It can be caused by conditions that lead to loss of oxygen to the brain like cerebral anoxia, hemorrhage or trauma. Diagnosing brain death involves assessing for the absence of brain stem reflexes and response to stimuli, as well as a positive apnea test where the patient fails to breathe independently with high carbon dioxide levels. Ancillary tests like EEG, angiography or PET scans may be used to confirm the diagnosis when clinical assessment is limited.
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.
This document discusses the history and guidelines for determining brain death. It provides:
1) A timeline of major events in defining brain death from 1959 to present.
2) Details on the Uniform Determination of Death Act definition of brain death as "irreversible cessation of all functions of the entire brain."
3) Guidelines for determining brain death in India based on the Transplantation of Human Organs Act including requiring certification by a board of medical experts.
The document summarizes key aspects of death and brain death from a medicolegal perspective. It defines death and outlines the vital systems that cease to function at death. It discusses the presumption of death and survivorship under Indian law. The document then examines the historical definitions of death and milestones in determining brain death. It provides details on the anatomy of the normal brain and causes, mechanisms, and conditions distinct from brain death. The neurological examination for determining brain death and confirmatory testing are described. The key provisions of the Transplantation of Human Organs Act of 1994 and its amendment in 2009 are summarized.
This document discusses brain death, including:
1) Historical definitions and guidelines for determining brain death from 1959 to present.
2) Normal brain anatomy and the functions of the cerebral cortex, brain stem, and reticular activating system.
3) Causes and mechanisms of cerebral death such as anoxia, hemorrhage, trauma, and meningitis.
4) Conditions distinct from brain death like persistent vegetative state, locked-in syndrome, and minimally responsive state.
5) Neurological examinations and tests used to determine brain death, including absence of brain stem reflexes and apnea testing.
6) Confirmatory tests like EEG, cerebral angiography, isotope brain scans, and
This document provides recommendations for different types of epilepsy and the antiepileptic drugs that are most effective for each. Generalized tonic-clonic seizures are best treated with valproate, while complex partial seizures respond well to carbamazepine, oxcarbazepine, or valproate. Valproate is also recommended for myoclonic epilepsy and infantile spasms. Lamotrigine or valproate are suggested for juvenile myoclonic epilepsy in females, and valproate in males.
The document discusses the evaluation and management of dizziness and vertigo. It outlines the main categories of dizziness including otologic, central, medical, and unlocalized causes. Evaluation involves taking a thorough history, performing a physical exam including tests of nystagmus, and ordering investigations like an audiogram or MRI. Common diseases discussed in more detail include benign paroxysmal positional vertigo (BPPV), vestibular neuritis, Meniere's disease, and migraine-associated vertigo. Treatment focuses on treating the underlying cause, patient education, rehabilitation, and medications in some cases.
This document discusses several epileptic encephalopathies:
- Early myoclonic encephalopathy presents in neonates and is characterized by fragmentary myoclonus, erratic seizures, and a suppression-burst EEG pattern. Prognosis is poor with over 50% mortality.
- Ohtahara syndrome presents from 10 days to 3 months of age with tonic spasms and a suppression-burst EEG pattern in both waking and sleep states. It can progress to West syndrome and Lennox-Gastaut syndrome.
- Lennox-Gastaut syndrome typically starts between ages 1-7 and is characterized by multiple seizure types, cognitive issues, and EEG showing slow spike-wave dis
This document summarizes 7 medical case presentations given by Dr. Srirama Anjaneyulu on thalamic hyperintensities. The cases included patients with abnormal behavior, seizures, tremulousness, urinary retention, dystonic posturing, and sudden weakness. Diagnostic tests discussed included MRI, CT, CSF analysis, and biochemical markers. The cases covered a range of ages from adolescents to geriatric patients and various acute neurological conditions.
This document discusses migraine headaches. It notes that lifetime prevalence is around 90% for women and 95% for men. Migraines affect 18.2% of females and 6.5% of males. Three quarters of migraine sufferers experience severe or extremely severe pain, and over half experience severe disability, with 31% missing at least one day of work or school in the past three months. It then discusses anatomical structures involved in migraine pain transmission both inside and outside the skull. The document outlines several theories for migraine triggers and mechanisms of pain transmission and modulation in the central nervous system. It lists warning signs that could indicate an underlying condition is causing headache symptoms. Finally, it references a meta-analysis on the use of oral t
This document discusses refractory epilepsy, including definitions, epidemiology, mechanisms, diagnosis, and treatment approaches. It defines refractory epilepsy as the absence of response to two anti-epileptic drugs at reasonable doses, with a minimum seizure frequency of one per month. It estimates that 20% of people with epilepsy have refractory seizures, totaling around 1 million people in India. Causes of refractory epilepsy include drug transporter issues, target resistance, and intrinsic disease severity. Surgical treatment and alternative therapies like the ketogenic diet, vagus nerve stimulation, polymers, and electrical brain stimulation are reviewed as potential treatment options.
This document summarizes treatment options for different types of seizures and epilepsy syndromes. It lists antiepileptic drugs and their levels of efficacy evidence for adults, children, and elderly patients with partial onset seizures, generalized tonic-clonic seizures, and absence seizures. It also mentions vagal nerve stimulation as a treatment option.
The document discusses the embryology of the brain, including:
- The formation of the neural tube and its subdivisions into primary brain vesicles.
- The development of the medulla, pons, midbrain, cerebellum, and cerebral hemispheres from the brain vesicles.
- The formation of structures within each brain region like the cranial nerve nuclei in the medulla and pons.
- The timeline of important developmental events from the formation of the neural plate to myelination.
This document discusses the management of epilepsy. It provides an overview of treatment options for epilepsy including antiepileptic drugs (AEDs), surgical management, vagus nerve stimulation, and ketogenic diets. It describes indications for treatment, classifications and side effects of AEDs, management of generalized and partial epilepsies, refractory epilepsy, status epilepticus, and treatments still under investigation.
This document discusses stroke in children. Key points include:
- Stroke in children differs from adults and can have developmental, genetic, or environmental causes rather than lifestyle factors.
- Presentation is often subtle with a wide differential diagnosis. Risk factors are multiple and poorly understood.
- Neonates are at highest risk. Incidence of ischemic stroke is around 1 in 4000-5600 term births. Cerebral venous thrombosis accounts for 0.67 cases per 100,000 children per year.
- Evaluation involves detailed history and physical exam looking for signs of bleeding disorders, infections, cardiac abnormalities, or genetic syndromes. Imaging and lab tests are needed to make an accurate diagnosis.
This document provides an overview of ventricle anatomy and common masses and pathologies seen within the ventricles. It describes the anatomy and features of the lateral, third and fourth ventricles. Common masses are discussed such as choroid plexus papilloma, colloid cyst, and subependymoma. Types of hydrocephalus like obstructive and normal pressure hydrocephalus are summarized. Considerations for shunt complications are also provided in brief.
EEG artifacts can arise from various physiological and extraphysiological sources other than brain activity. Physiological artifacts originate from the patient's own generator sources like eye movements, muscle activity, movement, and cardiac activity. Extraphysiological artifacts are externally generated, such as from medical devices, electrical equipment, or the environment. Common EEG artifacts include cardiac artifacts like ECG signals, ballistocardiographic artifacts from head or body movement, pacemaker signals, and pulse artifacts. Electrode artifacts can be transient pops or low frequency rhythms across electrodes from poor contact or movement. External artifacts include 50/60 Hz ambient noise, intravenous drips, and signals from devices like pumps and ventilators. Muscle and ocular artifacts
- Prion diseases are rapidly progressive dementias caused by infectious proteins called prions. They include Creutzfeldt-Jakob disease (CJD), Gerstmann-Sträussler-Scheinker syndrome (GSS), fatal familial insomnia (FFI), and kuru.
- Prion diseases occur sporadically in 85% of cases, are inherited in 15% of cases, and are infectious in less than 1% of cases. They result from the accumulation of abnormal prion protein (PrPsc) which differs from its normal cellular form (PrPc).
- Clinically, prion diseases present with dementia, myoclonus, and death usually within a year
The document summarizes the process of presurgical evaluation for epilepsy patients. It discusses how modern imaging techniques like video EEG monitoring, high-resolution MRI, fMRI, PET and SPECT are used to localize the epileptogenic zone noninvasively in most patients. When noninvasive methods are insufficient, invasive EEG monitoring using subdural or depth electrodes may be used. The goal is to precisely identify the brain area responsible for seizure generation to allow its surgical resection, while avoiding damage to critical functions. A classical example where surgery is often curative is mesial temporal lobe epilepsy.
Heat stroke is a life-threatening condition defined as a core body temperature above 41°C with neurological dysfunction. It can be exertional, caused by strenuous physical activity in heat, or nonexertional, often affecting the elderly, chronically ill, or very young. Risk factors include impaired thermoregulation, dehydration, and medications that interfere with sweating. Complications involve multiple organ systems and can include delirium, seizures, hypotension, liver and kidney damage, and disseminated intravascular coagulation. Immediate cooling and medical care are crucial to prevent high mortality rates from heat stroke.
1. Stroke is a common complication in cancer patients that can be caused by direct tumor effects, coagulation disorders, infections, or cancer therapies.
2. Studies have found strokes occur in 3.5-15% of cancer patients, with ischemic strokes being more common than hemorrhagic. Risk factors include certain cancers like lung cancer or blood cancers.
3. Diagnosis involves blood tests, imaging like MRI, and treatment focuses on anticoagulation though established treatments are still lacking. Differentiating between causes like coagulopathies or conventional vascular risk factors is important.
Carotid artery stenosis refers to atherosclerotic narrowing of the carotid arteries. While a correlation between stenosis level and stroke risk is expected, the relationship is unclear. Carotid artery stenosis is variably defined as 60-99% or 50-99% narrowing. Screening for carotid artery stenosis can be done with neck auscultation or ultrasound, but both have limitations in sensitivity and specificity compared to angiography. Noninvasive imaging techniques like ultrasound and MRI are better options for screening and diagnosis of carotid artery stenosis.
Heat stroke is a life-threatening condition defined as a core body temperature above 41°C with neurological dysfunction. It can be exertional, caused by strenuous physical activity in heat, or nonexertional, often affecting the elderly, ill, or young. Risk factors include impaired thermoregulation, dehydration, and medications. Symptoms include hyperthermia, altered mental status, sweating cessation, and potentially multi-organ failure. Immediate cooling and medical care are crucial to prevent high mortality.
Progressive myoclonus epilepsies are characterized by myoclonic seizures, tonic-clonic seizures, and progressive neurological dysfunction including ataxia and dementia. The document discusses several specific causes of progressive myoclonus epilepsy including Unverricht-Lundborg disease, Lafora's disease, myoclonus epilepsy with ragged-red fibers, sialidoses, neuronal ceroid lipofuscinoses, and others. It provides details on clinical features, pathogenesis, diagnosis, and genetic basis for several of these conditions.
2. Brain death is defined as the irreversible loss of function of the brain, including the brainstem. Primary neurologic diseases; severe head injury , aneurysmal subarachnoid hemorrhage. Medical and surgical intensive care units, hypoxic-ischemic brain insults and fulminant hepatic failure. In children, abuse is a more common cause than motor vehicle accidents or asphyxia in USA. In large referral hospitals, neurologists make the diagnosis of brain death 25 to 30 times a year. Overview
3. Physicians, health care workers, members of the clergy, and laypeople throughout the world have accepted fully that a person is dead when his or her brain is dead. In the United States, the principle that death can be diagnosed by neurologic criteria (designated as brain death) is the basis of the Uniform Determination of Death Act. There is a clear difference between severe brain damage and brain death. The physician must understand this difference, because brain death means that life support is useless, and brain death is the principal requisite for the donation of organs for transplantation. OVERVIEW
4. Prior to the advent of mechanical respiration, death was defined as the cessation of circulation and breathing. 1968 Irreversible Coma/Brain Death Harvard Medical School Ad Hoc Committee. 1981 Uniform Determination of Death Act - President’s Commission for the Study of Ethical Problems in Medicine. 1994 American Academy of Neurology Guidelines for the determination of Brain Death. 2005 NYS Guidelines for Determining Brain Death. Historical Perspective
12. Mechanism of Cerebral Death ICP>MAP is incompatible with life Increased Intracranial Pressure
13. Persistent Vegetative State Locked-in Syndrome Minimally Responsive State Conditions Distinct From Brain Death
14. Persistent Vegetative State Normal Sleep-Wake Cycles. No Response to Environmental Stimuli. Diffuse Brain Injury with Preservation of Brain Stem Function.
19. “An organ, brain or other, that no longer functions and has no possibility of functioning again is for all practical purposes dead.” A. determine presence of “a permanently nonfunctioning brain.” B. confirmatory data Report of the Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death. A definition of irreversible coma. JAMA 1968;205:337-340 Harvard Criteria
20. 1. Unreceptivity and Unresponsitivity: “total unawareness to externally applied stimuli…even the most intensely painful stimuli evoke no vocal or other response, not even a groan, withdrawal of a limb, or quickening of respiration.” 2. No Movements or Breathing: no spontaneous movements or spontaneous respiration (turn off respirator for 3 minutes; prior to trial breathing room air for ≥10 minutes and pCO2 normal) or response to pain, touch, sound or light for an hour. 3. No reflexes: pupils fixed, dilated and absence of: Pupillary response to bright light ocular movement to head turning and ice water irrigation of ears blinking postural activity (decerebrate ) Swallowing, yawning, vocalization Corneal reflexes Pharyngeal reflexes Deep tendon reflexes Respnse to plantar or noxious stimuli A. determine presence of “a permanentlynonfunctioning brain.”
21. 4. isoelectric EEG (specifies technique; “At least 10 full minutes of recording are desirable, but twice that would be better.” [!]) EEG: “when available it should be utilized” If EEG unavailable, “the absence of cerebral function has to be determined by purely clinical signs…or by absence of circulation as judged by standstill of blood in the retinal vessels, or by absence of cardiac activity.” A and B all need to be repeated 24 hours later in the absence of hypothermia (<90˚F [32.2˚C]) or CNS depressants, such as barbiturates, and determined only by a physician. B. confirmatory data
22. Diagnostic criteria for clinical diagnosis of brain death A. Prerequisites. Brain death is the absence of clinical brain function when the proximate cause is known and demonstrably irreversible. B. The three cardinal findings in brain death are coma or unresponsiveness absence of brainstem reflexes apnea. Practice parameters for determining brain death in adults: (summary statement) NEUROLOGY 1995;45:1012-1014:
23. Brain death is the absence of clinical brain function when the proximate cause is known and demonstrably irreversible. 1.Clinical or neuroimaging evidence of an acute CNS catastrophe that is compatible with the clinical diagnosis of brain death. 2. Exclusion of complicating medical conditions that may confound clinical assessment (no severe electrolyte, acid-base, or endocrine disturbance). 3. No drug intoxication or poisoning. 4. Core temperature ≥ 32° C (90°F). Prerequisites
24. Coma or unresponsiveness--no cerebral motor response to pain in all extremities (nail-bed pressure and supraorbital pressure). In step 1, the physician determines that there is no motor response and the eyes do not open when a painful stimulus is applied to the supraorbital nerve or nail bed.
25. 2. Absence of brainstem reflexes a) Pupils (a) No response to bright light (b) Size: midposition (4 mm) to dilated (9 mm) b) Ocular movement (a) No oculocephalic reflex (testing only when no fracture or instability of the cervical spine is apparent) (b) No deviation of the eyes to irrigation in each ear with 50 ml of cold water (allow 1 minute after injection and at least 5 minutes between testing on each side) c) Facial sensation and facial motor response (a) No corneal reflex to touch with a throat swab (b) No jaw reflex (c) No grimacing to deep pressure on nail bed, supraorbital ridge, or temporomandibular joint d) Pharyngeal and tracheal reflexes (a) No response after stimulation of the posterior pharynx with tongue blade (b) No cough response to bronchial suctioning
26. In step 2, a clinical assessment of brain-stem reflexes is undertaken. The tested cranial nerves are indicated by Roman numerals; the solid arrows represent afferent limbs, and the broken arrows efferent limbs. Depicted are the absence of grimacing or eye opening with deep pressure on both condyles at the level of the temporomandibular joint (afferent nerve V and efferent nerve VII), the absent corneal reflex elicited by touching the edge of the cornea (V and VII), the absent light reflex (II and III), the absent oculovestibular response toward the side of the cold stimulus provided by ice water (pen marks at the level of the pupils can be used as reference) (VIII and III and VI), and the absent cough reflex elicited through the introduction of a suction catheter deep in the trachea (IX and X).
27. 3. Apnea--test a) Prerequisites (a) Core temperature ≥ 36.5°C or 97°F (b) Systolic blood pressure ≥ 90 mm Hg (c) Euvolemia. Option: positive fluid balance in the previous 6 hours (d) Normal PCO2. Option: arterial PCO2 ≥ 40 mm Hg (e) Normal PO2 Option: preoxygenation to obtain arterial PO2 ≥ 200 mm Hg b) Connect a pulse oximeter and disconnect the ventilator. c) Deliver 100% O2, 6 l/min, into the trachea. Option: place a cannula at the level of the carina. d) Look closely for respiratory movements (abdominal or chest excursions that produce adequate tidal volumes). e) Measure arterial PO2, PCO2, and pH after approximately 8 minutes and reconnect the ventilator. f) If respiratory movements are absent and arterial PCO2 is ≥ 60 mm Hg (option: 20 mm Hg increase in PCO2 over a baseline normal PCO2), the apnea test result is positive (ie, it supports the diagnosis of brain death). g) If respiratory movements are observed, the apnea test result is negative (ie, it does not support the clinical diagnosis of brain death), and the test should be repeated. h) Connect the ventilator if, during testing, the systolic blood pressure becomes ≤ 90 mm Hg or the pulse oximeter indicates significant oxygen desaturation and cardiac arrhythmias are present; immediately draw an arterial blood sample and analyze arterial blood gas. If PCO2 is ≥ 60 mm Hg or PCO2 increase is ≥ 20 mm Hg over baseline normal PCO2, the apnea test result is positive (it supports the clinical diagnosis of brain death); If PCO2 is < 60 mm Hg or PCO2 increase is < 20 mm Hg over baseline normal PCO2, the result is indeterminate, and an additional confirmatory test can be considered.
28. In step 3, the apnea test is performed; the disconnection of the ventilator and the use of apneic diffusion oxygenation require precautionary measures. The core temperature should be 36.5°C or higher, the systolic blood pressure should be 90 mm Hg or higher, and the fluid balance should be positive for six hours. After preoxygenation (the fraction of inspired oxygen should be 1.0 for 10 minutes), the ventilation rate should be decreased. The ventilator should be disconnected if the partial pressure of arterial oxygen reaches 200 mm Hg or higher and if the partial pressure of arterial carbon dioxide reaches 40 mm Hg or higher. The oxygen catheter should be at the carina (delivering oxygen at a rate of 6 liters per minute). The physician should observe the chest and the abdominal wall for respiration for 8 to 10 minutes and should monitor the patient for changes in vital functions. If there is a partial pressure of arterial carbon dioxide of 60 mm Hg or higher or an increase of more than 20 mm Hg from the normal base-line value, apnea is confirmed. ABP denotes arterial blood pressure, HR heart rate, RESP respirations, and SpO 2oxygen saturation measured by pulse oximetry.
29. The diagnosis of brain death -EELCO FM WIJDICKS N Engl J Med, Vol. 344, No. 16 April 19, 2001
30. Pitfalls in the diagnosis of brain death Some conditions may interfere with the clinical diagnosis of brain death, so that the diagnosis cannot be made with certainty on clinical grounds alone. Confirmatory tests are recommended. A. Severe facial trauma B. Preexisting pupillary abnormalities C. Toxic levels of any sedative drugs, aminoglycosides, tricyclic antidepressants, anticholinergics,antiepileptic drugs, chemotherapeutic agents, or neuromuscular blocking agents D. Sleep apnea or severe pulmonary disease resulting in chronic retention of CO2
31. These manifestations are occasionally seen and should not be misinterpreted as evidence for brainstem function. A. Spontaneous movements of limbs other than pathologic flexion or extension response. B. Respiratory-like movements (shoulder elevation and adduction, back arching, intercostal expansion without significant tidal volumes). C. Sweating, blushing, tachycardia. D. Normal blood pressure without pharmacologic support or sudden increases in blood pressure. E. Absence of diabetes insipidus. F. Deep tendon reflexes; superficial abdominal reflexes; triple flexion response. G. Babinski reflex. Clinical observations compatible with the diagnosis of brain death
32. Brain death is a clinical diagnosis. A repeat clinical evaluation 6 hours later is recommended, but this interval is arbitrary. A confirmatory test is not mandatory but is desirable in patients in whom specific components of clinical testing cannot be reliably performed or evaluated. It should be emphasized that any of the suggested confirmatory tests may produce similar results in patients with catastrophic brain damage who do not (yet) fulfill the clinical criteria of brain death. Confirmatory laboratory tests (Options)
33. The diagnosis of brain death EELCO FM WIJDICKS N Engl J Med, Vol. 344, No. 16 April 19, 2001
39. A. Conventional angiography. No intracerebral filling at the level of the carotid bifurcation or circle of Willis. The external carotid circulation is patent, and filling of the superior longitudinal sinus may be delayed. B. Electroencephalography. No electrical activity during at least 30 minutes of recording that adheres to the minimal technical criteria for EEG recording in suspected brain death as adopted by the American Electroencephalographic Society, including 16-channel EEG instruments. C. Transcranial Doppler ultrasonography 1. Ten percent of patients may not have temporal insonation windows. Therefore, the initial absence of Doppler signals cannot be interpreted as consistent with brain death. 2. Small systolic peaks in early systole without diastolic flow or reverberating flow, indicating very high vascular resistance associated with greatly increased intracranial pressure. D. Technetium-99m hexamethylpropyleneamineoxime brain scan. No uptake of isotope in brain parenchyma ("hollow skull phenomenon"). E. Somatosensory evoked potentials. Bilateral absence of N20-P22 response with median nerve stimulation. The recordings should adhere to the minimal technical criteria for somatosensory evoked potential recording in suspected brain death as adopted by the American Electroencephalographic Society. The following confirmatory test findings are listed in the order of the most sensitive test first.
40. A. Etiology and irreversibility of condition B. Absence of brainstem reflexes C. Absence of motor response to pain D. Absence of respiration with PCO2 ≥ 60 mm Hg E. Justification for confirmatory test and result of confirmatory test F. Repeat neurologic examination. Option: the interval is arbitrary, but a 6-hour period is reasonable. Medical record documentation (Standard)
41. Guidelines of 80 countries reviewed Legal standards on organ transplantation present in 69% (55 of 80 countries) Practice guidelines for brain death for adults in 88% 50% guidelines require >1 physician to declare All guidelines specified exclusion of confounders, presence of irreversible coma, absent motor response, and absent brainstem reflexes Apnea testing required in 59% differences in time of observation and required expertise of examining physicians Confirmatory laboratory testing mandatory in 28 of 70 (40%) guidelines Conclusion: “uniform agreement on the neurologic exam with exception of the apnea test; but other major differences found in the procedures for diagnosing brain death in adults, and standardization should be considered.” Brain Death around the worldWijdicks EFM. Brain death worldwide: Accepted fact but no global consensus in diagnostic criteria NEUROLOGY 2002;58.
43. 1. Evaluate the irreversibility and potential causes of coma; 2. Initiate the hospital policy for notifying the next of kin; 3. Conduct and document the first clinical assessment of brain stem reflexes; 4. Observe the individual during a defined waiting period for any clinical inconsistencies with the diagnosis of brain death; 5. Conduct and document the second clinical assessment of brain stem reflexes; 6. Perform and document the apnea test; 7. Perform confirmatory testing, if indicated; 8. If the individual’s religious or moral objection to the brain death standard is known,implement hospital policies for reasonable accommodation; 9. Certify brain death; and 10. Withdraw cardio-respiratory support in accordance with hospital policies, including those for organ donation. NEW YORK STATE DEPARTMENT OF HEALTHGUIDELINES FOR DETERMINING BRAIN DEATHDECEMBER 2005