Traumatic brain injury (TBI) can be classified in several ways including using the Glasgow Coma Scale or neuroimaging scales. The presentation outlines strategies to decrease secondary brain injury following TBI. It recommends treatments such as decompressive craniectomy, ventilation therapies, hyperosmolar therapy, cerebrospinal fluid drainage, infection prophylaxis, and intracranial pressure monitoring to reduce mortality and improve outcomes. Monitoring of cerebral physiology including intracranial pressure, cerebral perfusion pressure, and jugular venous oxygen saturation is advised to guide management of severe TBI.
Management Of High I C P And Traumatic Brain InjuryAndrew Ferguson
This document summarizes guidelines for the management of traumatic head injury. Key points include:
- Maintain cerebral perfusion pressure (CPP) above 70 mmHg using interventions like elevating blood pressure, ventricular drainage, and osmotherapy.
- Hyperventilation and barbiturates may be used temporarily for refractory increased intracranial pressure (ICP) over 25 mmHg, but prolonged hyperventilation should be avoided.
- Mannitol and hypertonic saline are effective for acute ICP control, while hypothermia, barbiturates, and decompressive craniectomy are options for salvage therapy when other measures fail.
- Avoidance of hypotension, hypo
TRAUMATIC BRAIN INJURY - DR DEVAWRAT BUCHERenuka Buche
1. The document discusses guidelines and management of traumatic brain injury (TBI). It outlines different levels of evidence and recommendations for treatment.
2. It describes the etiology, demographics, patterns of injury, and pathophysiology of primary and secondary brain injury following TBI. Secondary injuries like hypotension and hypoxia can worsen outcomes.
3. The document provides guidance on the initial management of TBI, including the primary and secondary surveys, with a focus on airway, breathing, circulation, and neurological assessment. It also discusses brain-specific resuscitation approaches.
The document discusses strategies and rationale for decreasing secondary brain injury following traumatic brain injury (TBI). It describes that TBI consists of primary and secondary brain injury, with primary injury occurring immediately from mechanical forces and secondary injury developing over time from cellular and biochemical cascades. The document outlines various mechanisms of secondary injury including excitotoxicity, inflammation, edema, and ischemia. It then provides recommendations for treating and monitoring TBI to decrease secondary injury, such as decompressive craniectomy, ICP/CPP monitoring, ventilation strategies, hypothermia, hyperosmolar therapy, and seizure prophylaxis.
This document discusses definitions of hypotension after traumatic brain injury (TBI) and management strategies. It summarizes several studies that identify optimal systolic blood pressure thresholds for defining hypotension in TBI patients of different ages, and find that aggressive fluid resuscitation is recommended to treat hypotension and improve outcomes for severe TBI patients. Maintaining a systolic blood pressure above 110 mmHg is important to prevent secondary brain injuries and reduced mortality.
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.
Traumatic brain injury compatible versionBharath T
This document discusses traumatic brain injury (TBI). It provides an overview of TBI including the problem statement, pathophysiology, pre-hospital management, monitoring in TBI patients, critical care management, current guidelines and evidence, and prognostication. Key points include that TBI is a leading cause of death and disability, secondary injury can worsen outcomes, and pre-hospital management focuses on oxygenation, ventilation, fluid resuscitation, and transport to a trauma center for further monitoring and treatment.
This document provides an overview of stroke rehabilitation and managing physical impairments. It defines stroke and discusses the importance of the ischemic penumbra in early rehabilitation. The document outlines the phases of rehabilitation and various interventions to address common impairments like weakness, spasticity, and balance issues. Evaluation tools and a sample rehabilitation plan addressing specific impairments are also presented.
Traumatic brain injury (TBI) can be classified in several ways including using the Glasgow Coma Scale or neuroimaging scales. The presentation outlines strategies to decrease secondary brain injury following TBI. It recommends treatments such as decompressive craniectomy, ventilation therapies, hyperosmolar therapy, cerebrospinal fluid drainage, infection prophylaxis, and intracranial pressure monitoring to reduce mortality and improve outcomes. Monitoring of cerebral physiology including intracranial pressure, cerebral perfusion pressure, and jugular venous oxygen saturation is advised to guide management of severe TBI.
Management Of High I C P And Traumatic Brain InjuryAndrew Ferguson
This document summarizes guidelines for the management of traumatic head injury. Key points include:
- Maintain cerebral perfusion pressure (CPP) above 70 mmHg using interventions like elevating blood pressure, ventricular drainage, and osmotherapy.
- Hyperventilation and barbiturates may be used temporarily for refractory increased intracranial pressure (ICP) over 25 mmHg, but prolonged hyperventilation should be avoided.
- Mannitol and hypertonic saline are effective for acute ICP control, while hypothermia, barbiturates, and decompressive craniectomy are options for salvage therapy when other measures fail.
- Avoidance of hypotension, hypo
TRAUMATIC BRAIN INJURY - DR DEVAWRAT BUCHERenuka Buche
1. The document discusses guidelines and management of traumatic brain injury (TBI). It outlines different levels of evidence and recommendations for treatment.
2. It describes the etiology, demographics, patterns of injury, and pathophysiology of primary and secondary brain injury following TBI. Secondary injuries like hypotension and hypoxia can worsen outcomes.
3. The document provides guidance on the initial management of TBI, including the primary and secondary surveys, with a focus on airway, breathing, circulation, and neurological assessment. It also discusses brain-specific resuscitation approaches.
The document discusses strategies and rationale for decreasing secondary brain injury following traumatic brain injury (TBI). It describes that TBI consists of primary and secondary brain injury, with primary injury occurring immediately from mechanical forces and secondary injury developing over time from cellular and biochemical cascades. The document outlines various mechanisms of secondary injury including excitotoxicity, inflammation, edema, and ischemia. It then provides recommendations for treating and monitoring TBI to decrease secondary injury, such as decompressive craniectomy, ICP/CPP monitoring, ventilation strategies, hypothermia, hyperosmolar therapy, and seizure prophylaxis.
This document discusses definitions of hypotension after traumatic brain injury (TBI) and management strategies. It summarizes several studies that identify optimal systolic blood pressure thresholds for defining hypotension in TBI patients of different ages, and find that aggressive fluid resuscitation is recommended to treat hypotension and improve outcomes for severe TBI patients. Maintaining a systolic blood pressure above 110 mmHg is important to prevent secondary brain injuries and reduced mortality.
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.
Traumatic brain injury compatible versionBharath T
This document discusses traumatic brain injury (TBI). It provides an overview of TBI including the problem statement, pathophysiology, pre-hospital management, monitoring in TBI patients, critical care management, current guidelines and evidence, and prognostication. Key points include that TBI is a leading cause of death and disability, secondary injury can worsen outcomes, and pre-hospital management focuses on oxygenation, ventilation, fluid resuscitation, and transport to a trauma center for further monitoring and treatment.
This document provides an overview of stroke rehabilitation and managing physical impairments. It defines stroke and discusses the importance of the ischemic penumbra in early rehabilitation. The document outlines the phases of rehabilitation and various interventions to address common impairments like weakness, spasticity, and balance issues. Evaluation tools and a sample rehabilitation plan addressing specific impairments are also presented.
Research guru and PI for the ARISE study, college examiner and semi-professional forrest-based carpenter, Anthony always gives a fascinating talk. This time he gives an intelligent and considered breakdown on the nebulous topic of cerebral protection.
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 provides information on the management of traumatic brain injury (TBI). It defines TBI as an alteration in brain function caused by a blow or jolt to the head. The primary survey for a TBI patient involves assessing the airway, breathing, circulation, disability or neurological status, and exposure. Disability is evaluated using the Glasgow Coma Scale. Mild TBI is defined as a brief alteration in mental status or consciousness with a Glasgow Coma Scale score between 13-15. The document also discusses complications, guidelines for CT scans, and classifications of mild versus severe TBI.
This document discusses recent trends in the management of traumatic brain injury. It provides an overview of the causes and statistics of TBIs in India. It then summarizes guidelines for managing factors like blood pressure, oxygenation, ICP thresholds, and various treatment strategies. These include hyperventilation, hyperosmolar therapy, blood transfusions, glycemic control, and neuromonitoring techniques. The document examines evidence for and against invasive ICP monitoring. While no RCTs definitively prove its benefits, ICP monitoring still forms the standard of care for managing severe TBIs.
This study investigated the effects of piracetam on post-concussion syndrome using SPECT imaging. Patients with minor head injuries and post-concussion symptoms were randomly assigned to receive either piracetam or a control treatment. SPECT scans found cerebral perfusion abnormalities in most patients. Those receiving piracetam showed significantly improved cerebral perfusion ratios compared to controls. The study concludes that piracetam may help reverse perfusion deficits and accelerate symptom recovery in post-concussion syndrome. A larger randomized controlled trial is still needed to confirm these preliminary results.
Anesthesiologists should concern about the risk of POCD by making prevention and attentive to the potential risk factors.
It should be remembered that research in animal models which represent the specific characteristics of POCD in human remains unclear.
With many factors still unknown, there is still a chance for sinchronized preclinical and clinical research on POCD.
Osmotic demyelination syndrome (ODS) occurs when hyponatremia is corrected too rapidly. It involves demyelination in the pons and other brain areas. The presentation depends on the location but may include dysarthria, dysphagia, quadriparesis, and mutism. Risk factors include serum sodium below 120 mEq/L, hyponatremia duration over 2-3 days, and sodium correction exceeding 6-8 mEq/L/day. Prevention involves differentiating acute vs chronic hyponatremia and limiting correction rates. Treatment focuses on supportive care while investigational therapies target reducing neuroinflammation.
This document discusses electrolyte disorders that can occur following a traumatic brain injury. A 13-year-old boy suffered a fall from a tree resulting in multiple injuries including a traumatic brain injury. Serial lab tests showed fluctuations in the patient's sodium, potassium, and creatinine levels. The document then discusses various electrolyte imbalances that can occur after head injuries like hypernatremia, hyponatremia, hypokalemia, and diabetes insipidus. It covers the causes, effects, diagnosis, and management of these conditions. Maintaining normal electrolyte levels is important to prevent secondary brain injuries in patients with head trauma.
Dr Awaneesh Katiyar-Brain Trauma Foundation 4 - copyAwaneesh Katiyar
This document summarizes the key guidelines from the 4th edition of the Brain Trauma Foundation guidelines for severe traumatic brain injury. Some of the major topics and recommendations included:
- Early prophylactic hypothermia within 2.5 hours of injury is not recommended to improve outcomes for diffuse brain injury.
- While hyperosmolar therapy may lower intracranial pressure, there is insufficient evidence on effects on clinical outcomes to recommend a specific agent.
- For elevated intracranial pressure refractory to other treatments, continuous drainage of cerebrospinal fluid with an external ventricular drain or high-dose barbiturates may be considered.
This document provides an overview of the approach to brain trauma management in the intensive care unit. It discusses:
1. Using a multidisciplinary team approach and following protocols to consistently provide great care for traumatic brain injury patients.
2. Identifying and treating both primary brain injuries from the initial trauma and secondary injuries that can develop over time through techniques like intracranial pressure monitoring and control, seizure prophylaxis, and infection prevention.
3. Preventing secondary injuries like herniation, edema, and reduced blood flow through careful monitoring, normalization of physiology, and medical or surgical interventions when needed. The goal is to prevent further brain damage after the initial trauma.
1. Status epilepticus is defined as a seizure lasting more than 5 minutes or recurrent seizures without recovery in between.
2. It can be generalized convulsive seizures or non-convulsive without motor symptoms but ongoing EEG seizure activity.
3. Treatment involves stabilizing the patient, identifying and treating the underlying cause, giving benzodiazepines as first line, then fosphenytoin, phenytoin, phenobarbital or levetiracetam if still seizing, with escalation to anesthetic drugs, coma or general anesthesia if refractory.
Seizures & status epilepticus in the intensive careKaveh Kazemian
This document discusses seizures and status epilepticus in the intensive care unit. It notes that persistent seizures or failure to regain consciousness after a witnessed seizure requires emergency neurological consultation. Early maximal anticonvulsant therapy is critical to reducing morbidity. The causes of seizures in the ICU include antiepileptic drug withdrawal, alcohol withdrawal, and various medical conditions. Non-convulsive status epilepticus is difficult to diagnose without EEG monitoring and can present as confusion, subtle movements, or behavioral changes. Early treatment of seizures within 30 minutes is associated with better outcomes.
One of the hardest specialties is neuro anesthesia. When I initially started, I were so dumb founded. The things in brain did not only change, they become instantly harder. The drugs which were supposed to work now did not because the brain had developed edema or there was no blood supply. I worked real hard on this presentation. Took help from the textbooks and my teachers and has helped me. I hope you will found it somewhat helpful. Some of the answers are beyond the scope of this presentation due to the diversity of the field.
The document summarizes responsive neurostimulation (RNS) as a treatment option for drug-resistant epilepsy. It describes the components of the RNS system, including implantable leads and a pulse generator. The system is able to record epileptic activity, detect seizures, and deliver targeted stimulation to reduce seizures. Clinical trials found RNS significantly reduced seizure frequency and improved quality of life. Complications were generally minor. The RNS provides an alternative to surgery for some patients and offers opportunities to study epileptic activity and evaluate new treatments.
This document discusses various neuroendocrine emergencies including pituitary apoplexy, myxedema coma, thyroid storm, adrenal crisis, hypercalcemia, hypocalcemia, and hyperglycemic emergencies. Pituitary apoplexy is caused by hemorrhage or infarction of the pituitary gland and presents with sudden severe headache, visual changes, and pituitary hormone deficiencies. Myxedema coma and thyroid storm are life-threatening complications of hypothyroidism and hyperthyroidism respectively that require prompt diagnosis and treatment with thyroid hormones, glucocorticoids, and supportive care. Adrenal crisis occurs in patients with primary or secondary adrenal insufficiency due to inadequate cortisol response to stress
Pediatric Severe Traumatic Brain Injury-1.pptxzahramoukhader
- The document describes the case of a 6-month-old girl who presented with agitation, somnolence, spastic movements, and a history of head trauma after a fall.
- Initial workup revealed a Glasgow Coma Scale of 8, dilated pupils, and abnormal movements indicative of severe traumatic brain injury and possible intracranial bleed.
- She was admitted to the PICU for monitoring and treatment including anti-seizure medications, steroids, hydration, and head elevation. Her condition gradually improved over the following days.
This document summarizes a seminar on head injuries presented by Dr. Soumen Kanjilal. It discusses the anatomy of the skull and meninges, types of head injuries including concussions, contusions, extradural and subdural hemorrhages. It covers the management of traumatic brain injuries including indications for CT scans, initial management, treatment of elevated intracranial pressure, and intensive care management. Diffuse axonal injury is also summarized.
Research guru and PI for the ARISE study, college examiner and semi-professional forrest-based carpenter, Anthony always gives a fascinating talk. This time he gives an intelligent and considered breakdown on the nebulous topic of cerebral protection.
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 provides information on the management of traumatic brain injury (TBI). It defines TBI as an alteration in brain function caused by a blow or jolt to the head. The primary survey for a TBI patient involves assessing the airway, breathing, circulation, disability or neurological status, and exposure. Disability is evaluated using the Glasgow Coma Scale. Mild TBI is defined as a brief alteration in mental status or consciousness with a Glasgow Coma Scale score between 13-15. The document also discusses complications, guidelines for CT scans, and classifications of mild versus severe TBI.
This document discusses recent trends in the management of traumatic brain injury. It provides an overview of the causes and statistics of TBIs in India. It then summarizes guidelines for managing factors like blood pressure, oxygenation, ICP thresholds, and various treatment strategies. These include hyperventilation, hyperosmolar therapy, blood transfusions, glycemic control, and neuromonitoring techniques. The document examines evidence for and against invasive ICP monitoring. While no RCTs definitively prove its benefits, ICP monitoring still forms the standard of care for managing severe TBIs.
This study investigated the effects of piracetam on post-concussion syndrome using SPECT imaging. Patients with minor head injuries and post-concussion symptoms were randomly assigned to receive either piracetam or a control treatment. SPECT scans found cerebral perfusion abnormalities in most patients. Those receiving piracetam showed significantly improved cerebral perfusion ratios compared to controls. The study concludes that piracetam may help reverse perfusion deficits and accelerate symptom recovery in post-concussion syndrome. A larger randomized controlled trial is still needed to confirm these preliminary results.
Anesthesiologists should concern about the risk of POCD by making prevention and attentive to the potential risk factors.
It should be remembered that research in animal models which represent the specific characteristics of POCD in human remains unclear.
With many factors still unknown, there is still a chance for sinchronized preclinical and clinical research on POCD.
Osmotic demyelination syndrome (ODS) occurs when hyponatremia is corrected too rapidly. It involves demyelination in the pons and other brain areas. The presentation depends on the location but may include dysarthria, dysphagia, quadriparesis, and mutism. Risk factors include serum sodium below 120 mEq/L, hyponatremia duration over 2-3 days, and sodium correction exceeding 6-8 mEq/L/day. Prevention involves differentiating acute vs chronic hyponatremia and limiting correction rates. Treatment focuses on supportive care while investigational therapies target reducing neuroinflammation.
This document discusses electrolyte disorders that can occur following a traumatic brain injury. A 13-year-old boy suffered a fall from a tree resulting in multiple injuries including a traumatic brain injury. Serial lab tests showed fluctuations in the patient's sodium, potassium, and creatinine levels. The document then discusses various electrolyte imbalances that can occur after head injuries like hypernatremia, hyponatremia, hypokalemia, and diabetes insipidus. It covers the causes, effects, diagnosis, and management of these conditions. Maintaining normal electrolyte levels is important to prevent secondary brain injuries in patients with head trauma.
Dr Awaneesh Katiyar-Brain Trauma Foundation 4 - copyAwaneesh Katiyar
This document summarizes the key guidelines from the 4th edition of the Brain Trauma Foundation guidelines for severe traumatic brain injury. Some of the major topics and recommendations included:
- Early prophylactic hypothermia within 2.5 hours of injury is not recommended to improve outcomes for diffuse brain injury.
- While hyperosmolar therapy may lower intracranial pressure, there is insufficient evidence on effects on clinical outcomes to recommend a specific agent.
- For elevated intracranial pressure refractory to other treatments, continuous drainage of cerebrospinal fluid with an external ventricular drain or high-dose barbiturates may be considered.
This document provides an overview of the approach to brain trauma management in the intensive care unit. It discusses:
1. Using a multidisciplinary team approach and following protocols to consistently provide great care for traumatic brain injury patients.
2. Identifying and treating both primary brain injuries from the initial trauma and secondary injuries that can develop over time through techniques like intracranial pressure monitoring and control, seizure prophylaxis, and infection prevention.
3. Preventing secondary injuries like herniation, edema, and reduced blood flow through careful monitoring, normalization of physiology, and medical or surgical interventions when needed. The goal is to prevent further brain damage after the initial trauma.
1. Status epilepticus is defined as a seizure lasting more than 5 minutes or recurrent seizures without recovery in between.
2. It can be generalized convulsive seizures or non-convulsive without motor symptoms but ongoing EEG seizure activity.
3. Treatment involves stabilizing the patient, identifying and treating the underlying cause, giving benzodiazepines as first line, then fosphenytoin, phenytoin, phenobarbital or levetiracetam if still seizing, with escalation to anesthetic drugs, coma or general anesthesia if refractory.
Seizures & status epilepticus in the intensive careKaveh Kazemian
This document discusses seizures and status epilepticus in the intensive care unit. It notes that persistent seizures or failure to regain consciousness after a witnessed seizure requires emergency neurological consultation. Early maximal anticonvulsant therapy is critical to reducing morbidity. The causes of seizures in the ICU include antiepileptic drug withdrawal, alcohol withdrawal, and various medical conditions. Non-convulsive status epilepticus is difficult to diagnose without EEG monitoring and can present as confusion, subtle movements, or behavioral changes. Early treatment of seizures within 30 minutes is associated with better outcomes.
One of the hardest specialties is neuro anesthesia. When I initially started, I were so dumb founded. The things in brain did not only change, they become instantly harder. The drugs which were supposed to work now did not because the brain had developed edema or there was no blood supply. I worked real hard on this presentation. Took help from the textbooks and my teachers and has helped me. I hope you will found it somewhat helpful. Some of the answers are beyond the scope of this presentation due to the diversity of the field.
The document summarizes responsive neurostimulation (RNS) as a treatment option for drug-resistant epilepsy. It describes the components of the RNS system, including implantable leads and a pulse generator. The system is able to record epileptic activity, detect seizures, and deliver targeted stimulation to reduce seizures. Clinical trials found RNS significantly reduced seizure frequency and improved quality of life. Complications were generally minor. The RNS provides an alternative to surgery for some patients and offers opportunities to study epileptic activity and evaluate new treatments.
This document discusses various neuroendocrine emergencies including pituitary apoplexy, myxedema coma, thyroid storm, adrenal crisis, hypercalcemia, hypocalcemia, and hyperglycemic emergencies. Pituitary apoplexy is caused by hemorrhage or infarction of the pituitary gland and presents with sudden severe headache, visual changes, and pituitary hormone deficiencies. Myxedema coma and thyroid storm are life-threatening complications of hypothyroidism and hyperthyroidism respectively that require prompt diagnosis and treatment with thyroid hormones, glucocorticoids, and supportive care. Adrenal crisis occurs in patients with primary or secondary adrenal insufficiency due to inadequate cortisol response to stress
Pediatric Severe Traumatic Brain Injury-1.pptxzahramoukhader
- The document describes the case of a 6-month-old girl who presented with agitation, somnolence, spastic movements, and a history of head trauma after a fall.
- Initial workup revealed a Glasgow Coma Scale of 8, dilated pupils, and abnormal movements indicative of severe traumatic brain injury and possible intracranial bleed.
- She was admitted to the PICU for monitoring and treatment including anti-seizure medications, steroids, hydration, and head elevation. Her condition gradually improved over the following days.
This document summarizes a seminar on head injuries presented by Dr. Soumen Kanjilal. It discusses the anatomy of the skull and meninges, types of head injuries including concussions, contusions, extradural and subdural hemorrhages. It covers the management of traumatic brain injuries including indications for CT scans, initial management, treatment of elevated intracranial pressure, and intensive care management. Diffuse axonal injury is also summarized.
Traumatic brain injury can cause primary and secondary brain damage. Secondary injuries like hypoxia, hypotension and increased intracranial pressure can worsen outcomes. A thorough history, examination and imaging investigations help classify injury severity and guide management. The goals of treatment are to prevent secondary injuries through airway control, ventilation, oxygenation and controlling blood pressure and ICP. Surgery is indicated for space occupying lesions causing mass effect or neurological deterioration while observation and conservative care may be sufficient for mild or stable injuries.
Traumatic brain injury (TBI) occurs when an external force causes brain damage. Primary injury is caused by the impact, while secondary injury involves swelling and reduced blood flow. TBI can be mild, moderate, or severe based on symptoms. Treatment focuses on preventing secondary injury by controlling swelling, blood pressure, and seizures. Patients require rehabilitation to regain abilities lost from brain damage. Long term issues may include headaches, depression, and cognitive impairments.
This document provides an overview of concussion including:
- Definitions of concussion and its symptoms and signs in the acute phase.
- Risk factors, assessment tools like SCAT3, and typical findings.
- Management including return to play guidelines in a 5-step progression and treatment of post-concussion syndrome.
- Rare and serious conditions like second impact syndrome and chronic traumatic encephalopathy are also discussed.
This document provides an overview of traumatic brain injury (TBI), including:
1) It defines TBI and outlines primary and secondary brain injury mechanisms. Common causes include motor vehicle accidents, falls, and assaults.
2) It discusses evaluation and treatment, including importance of preventing hypotension and hypoxia. Neuroimaging with CT is important for diagnosis and prognosis.
3) Management of elevated intracranial pressure is also covered, including osmotherapy, sedation, cerebral perfusion pressure maintenance, temperature control, and avoiding hypocapnia or steroids.
This document provides an overview of head injury management, including definitions of key terms like the Glasgow Coma Scale and intracranial pressure. It describes mechanisms of traumatic brain injury and the evaluation of head injuries through history, exam, and radiographic imaging. It outlines guidelines for both nonoperative management, which typically involves monitoring and treating intracranial pressure, and operative management when significant mass lesions are present like epidural or subdural hematomas. The guidelines provide recommendations for indications for intracranial pressure monitoring and therapies to reduce elevated intracranial pressure through medical, surgical, and in more severe cases, barbiturate-induced coma interventions.
Neuropsychiatric consequences of traumatic brain injuryDikshya upreti
This document discusses the neuropsychiatric consequences of traumatic brain injury (TBI). It covers the epidemiology, pathology, clinical features, cognitive disorders, personality changes, and depressive disorders that can result from TBI. It describes how TBI causes both primary and secondary brain damage through mechanical forces. Common neuropsychiatric outcomes include delirium, neurocognitive disorders, depression, bipolar disorder, anxiety, and psychosis. Cognitive deficits often involve memory, attention, and executive function. Personality changes like irritability and disinhibition are also frequent.
This document discusses traumatic brain injury (TBI), including its definition, severity classification, common causes, and pathophysiology involving primary and secondary injury. It describes various types of focal hemorrhages that can occur after TBI and outlines the spectrum of TBI from mild to severe forms involving coma and vegetative/minimally conscious states. Neuroimaging techniques like CT and MRI are discussed. Behavioral measures for assessing TBI patients and common cognitive, behavioral, and psychological complications are also summarized.
This document discusses traumatic brain injury (TBI), including definitions, classifications, symptoms, diagnostic criteria, rating scales, pathology, causes, risk factors, guidelines for management, prognostic factors, complications, rehabilitation programs, and prevention. It defines TBI as an injury to the brain caused by external forces and classifies TBIs as mild, moderate, severe or persistent vegetative state based on factors like loss of consciousness and Glasgow Coma Scale scores. Rating scales discussed include Glasgow Coma Scale, Glasgow Outcome Scale, and Rancho Los Amigos levels. Causes include falls, road traffic accidents, violence and other injuries. Risk factors include age, gender, socioeconomic status and child abuse. Guidelines are provided for management and rehabilitation
This document provides an overview of acute head injury, including definitions, pathophysiology, classifications, investigations, management, and references. Some key points:
- Head injury is defined as blunt and/or penetrating trauma to the head/brain causing temporary or permanent brain dysfunction. Primary injuries occur at impact while secondary injuries are subsequent damage from factors like hypoxia or raised intracranial pressure (ICP).
- Raised ICP can lead to herniation syndromes like cerebellar tonsillar herniation, which can compress brainstem centers and cause Cushing's triad of hypertension, bradycardia, and irregular breathing.
- Management goals include airway protection, maintaining cerebral perfusion pressure
Lessons from the TTM trial and planning for the nexstscanFOAM
1) Detailed neurological examinations and blinded prognostication were conducted in the TTM trials to minimize bias in outcomes.
2) Follow-up assessments at 6 months in TTM1 found cognitive impairment, depression, and reduced quality of life in about one third of patients despite similar mortality between groups.
3) Extended cognitive testing in TTM1 at 6 months revealed memory, executive function, and processing speed impairments in about half of patients, more than in risk-factor matched controls, showing long-term cognitive consequences after cardiac arrest.
1. The document discusses classification and management of traumatic head injuries, including grading severity based on Glasgow Coma Scale and anatomical findings on CT scans.
2. Management involves stabilizing patients through the pre-hospital and hospital phases, monitoring intracranial pressure, and treating to prevent secondary brain injuries using medical and surgical methods like intubation, sedation, osmotherapy, and surgical evacuation of hematomas if needed.
3. The goal of management is to control factors that raise intracranial pressure like hypoxia, hypotension, and cerebral edema in order to maintain adequate cerebral perfusion pressure and optimize outcomes.
Head injuries are a major cause of death and disability worldwide. Road traffic accidents are the most common cause of head injuries in India. The brain is encased within the rigid skull, so any increase in intracranial volume from bleeding or swelling can rapidly increase intracranial pressure. The document discusses the epidemiology, anatomy, physiology and classification of head injuries as well as guidelines for management including medical therapies to reduce intracranial pressure and criteria for surgical intervention for specific injuries like epidural hematomas.
The document provides an overview of traumatic brain injury (TBI) for medical professionals. It discusses the demographics of TBI, including that over 2.5 million TBIs occur in the US each year from causes like falls, assaults, and motor vehicle accidents. It outlines the approach to evaluating a TBI patient, including performing a full neurological exam and Glasgow Coma Scale. Common injuries from TBI like contusions, hematomas, and shearing are also reviewed. The document then discusses various medical and surgical treatment options as well as factors that influence prognosis. The goal is to educate medical professionals on understanding and managing TBI.
HEAD TRAUMA & CEREBRAL RESUSCITATION copy.pptxHarryArwin1
This document provides an overview of traumatic brain injury (TBI) management. It begins with definitions of TBI and mechanisms of injury such as blunt and penetrating trauma. It then discusses features such as site of injury, pathology, and severity. Evaluation involves assessments like Glasgow Coma Scale and investigations like CT brain. Management principles focus on stabilization, prevention of secondary brain injury, and intracranial pressure control for severe TBI through protocols like cerebral protection. It concludes with references for further information.
Similar to Approach to patients with minor head injury-Dr Sameep Koshti (Consultant Neurosurgeon) (20)
WHO classification of brain tumours - Dr Sameep Koshti (Consultant NeuroSurgeon)Sameep Koshti
This document discusses the classification of brain tumours according to the WHO. It begins by describing the main cell types in the central nervous system - astrocytes, oligodendrocytes, microglia and radial glia. It then lists the WHO classification of tumours from 2016 and provides details on the nomenclature and histopathological reporting of brain tumours. Key genetic markers and their roles in tumour classification are discussed.
Venous drainage system of brain - Dr Sameep Koshti (Consultant Neurosurgeon)Sameep Koshti
The venous drainage of the brain occurs through a complex system of deep and superficial veins. The superficial system drains the superficial fifth of the cerebrum while the deep system drains the remaining four-fifths. These veins pierce the arachnoid mater and dura mater to open into dural venous sinuses. The major veins include the superior and inferior cerebral veins, internal cerebral veins, basal vein of Rosenthal, vein of Galen, and petrosal and galenic vein groups which drain into dural sinuses like the superior sagittal sinus and transverse sinus. The brain's venous system lacks valves and has thin walls to facilitate drainage.
Third ventricle anatomy - Dr Sameep Koshti (Consultant Neurosurgeon)Sameep Koshti
The lateral wall of the third ventricle is formed by the medial surface of the thalamus superiorly and the hypothalamus inferiorly, separated by the hypothalamic sulcus. The lateral wall is limited superiorly by the stria medullaris thalami. The lateral walls are joined by the interthalamic connection. The blood supply of the tela choroidea and choroid plexuses of the third and lateral ventricles is derived from the choroidal branches of the internal carotid and basilar arteries. The document also contains an image showing structures of the right lateral ventricle such as the choroid plexus, thalamostriate vein, foramen of Monro, mammillary
Surface anatomy of brain - Dr Sameep Koshti (consultant Neurosurgeon)Sameep Koshti
1) The pterion is located 35 mm behind and 12 mm above the frontozygomatic suture, estimated to be 2 fingerbreadths above the zygomatic arch.
2) The central sulcus can be approximated by connecting a point 2 cm posterior to the midline nasion-inion line to a point 5 cm straight up from the external acoustic meatus.
3) The lateral ventricles can be circumscribed by a quadrilateral with an upper limit 5 cm above the zygomatic arch, a lower limit 1 cm above the arch, and vertical limits through the zygomatic arch and 5 cm behind the mastoid process.
Slit ventricles syndrome - Dr Sameep Koshti (Consultant Neurosurgeon)Sameep Koshti
Slit ventricles refer to complete collapse of the ventricles. Slit ventricle syndrome involves intermittent headaches in shunted patients with small ventricles and slow reservoir refilling. It is usually caused by chronic, nonphysiologic CSF drainage from the shunt. Management involves adjusting shunt valve pressure or adding an antisiphon device to drain less CSF while maintaining stable ventricle size. Evaluation assesses CSF pressure and attempts to identify patients who may no longer require the shunt.
This document describes several neurological syndromes that result from lesions in the posterior circulation of the brain. It outlines the anatomical structures and clinical deficits involved in Weber syndrome, Claude syndrome, Benedikt syndrome, Nothnagel syndrome, and Parinaud syndrome, which result from lesions in the midbrain. It also describes medial and lateral pontine syndromes, including Foville syndrome, Mills' syndrome, and anterior inferior cerebellar artery syndrome, which are caused by lesions in different regions of the pons.
Normal pressure hydrocephalus (NPH) - Dr Sameep Koshti (Consultant Neurosurgeon)Sameep Koshti
This document discusses normal pressure hydrocephalus (NPH), also known as Hakim-Adams syndrome. It defines NPH as a clinical syndrome characterized by a triad of altered mentation, gait difficulties, and sphincter disturbances, along with ventriculomegaly and normal cerebrospinal fluid pressure. The causes of NPH are often idiopathic but can include infection, hemorrhage, trauma, or other obstructions. Diagnosis involves evaluating history, clinical symptoms, physiological tests like lumbar puncture pressure, and brain imaging showing ventricle enlargement. Potential treatments include lumbar drainage tests and placement of a ventriculoperitoneal shunt, usually with a medium-pressure
Intervertebral disc anatomy - Dr Sameep Koshti (Consultant Neurosurgeon)Sameep Koshti
The document discusses the anatomy and structure of the intervertebral disc (IVD). It has three main components - the nucleus pulposus surrounded by the annulus fibrosus, which are flanked by cartilage end plates. The nucleus pulposus acts as a gel cushion, while the annulus fibrosus provides structural integrity through concentric layers of collagen. Nutrients diffuse through the end plates from surrounding vasculature. The IVD loses its vascular supply in early life, relying on diffusion, and undergoes degeneration with aging as water content and proteoglycans decrease.
Hydrocephalus - Dr Sameep Koshti (Consultant Neurosurgeon)Sameep Koshti
This document discusses the pathophysiology, causes, diagnosis, and management of hydrocephalus. It covers:
1. The causes of hydrocephalus including congenital, acquired, infections, hemorrhage, and tumors.
2. The diagnostic process including clinical exam, imaging like CT/MRI, and lumbar puncture to classify hydrocephalus.
3. The management approaches for different types of hydrocephalus including various endoscopic procedures and ventriculoperitoneal shunting.
4. It also provides details on normal pressure hydrocephalus (NPH), including criteria for diagnosis and predictive tests like CSF withdrawal responses.
Development of brain and spinal cord- Dr Sameep Koshti (Consultant Neurosurgeon)Sameep Koshti
This document summarizes the development of the brain and spinal cord from 7-12 days of gestation through formation of the meninges. It describes the progression from a bilaminar disc to formation of the trilaminar disc and notochord. It then covers primary and secondary neurulation, development of the individual brain regions including the telencephalon, diencephalon and myelencephalon. Secondary topics discussed include neural crest derivatives, secondary neurulation, ascent of the conus medullaris, and meninges development.
This document discusses the anatomy, embryology, biomechanics, imaging and classification of abnormalities at the craniovertebral junction. It defines the craniovertebral junction and describes the important bones, ligaments, blood supply and development from somites. The biomechanics of the atlanto-axial and atlanto-occipital joints are explained. Common radiological measurements used to evaluate the craniovertebral junction are provided. Overall, the document provides a comprehensive overview of the normal anatomy and evaluation of abnormalities at the cranio-vertebral junction.
Csf flow dynamics and ICP management - Dr Sameep Koshti (consultant Neurosurg...Sameep Koshti
This document discusses cerebrospinal fluid (CSF) flow dynamics and intracranial pressure (ICP) management. It covers normal ICP ranges, components of the ICP waveform, physical principles of pressure, the Monro-Kellie doctrine of volume equilibrium, CSF circulation and absorption, and a general model for CSF dynamics. The key points are that ICP is determined by the volume and elastance of intracranial contents; CSF is produced continuously and absorbed through arachnoid villi into venous sinuses; and steady-state ICP depends on CSF production rate, total resistance to outflow, and dural sinus pressure.
C2 fracture - Dr Sameep Koshti (Consultant Neurosurgeon)Sameep Koshti
This document discusses different types of C2 fractures including odontoid fractures, hangman's fractures, and other C2 fractures. It describes classification systems for these fractures and outlines treatment approaches including non-operative immobilization or operative stabilization depending on the fracture type, stability, displacement, and patient factors. Surgical options involve anterior odontoid screw fixation or posterior wiring/fusion techniques. Outcomes and considerations for each approach are provided.
Brain tumour genetic and markers - Dr Sameep Koshti (consultant Neurosurgeon)Sameep Koshti
This document discusses genetic markers and mutations involved in brain tumour development. It describes how somatic mutations can be distinguished from hereditary ones by comparing tumor and normal tissue DNA. Key genes discussed include oncogenes, tumor suppressor genes, and mutator genes. The document focuses on glioblastoma and describes the differences between primary and secondary GBM, including differing mutation spectra. Specific mutations discussed in relation to glioma subtypes and grades include p53, IDH1/2, ATRX, and chromosomal changes like 1p/19q codeletion in oligodendrogliomas.
Localization of brachial plexus injury- Dr Sameep Koshti (consultant Neurosur...Sameep Koshti
The brachial plexus is formed by the ventral rami of cervical and upper thoracic spinal nerves. It has three cords - lateral, medial, posterior. Injuries can occur at different levels, causing varying patterns of weakness and sensory loss. Total plexus paralysis from severe trauma causes paralysis and atrophy of the entire arm. Upper plexus injury involves C5-C6 roots, weakening shoulder muscles. Middle and lower injuries affect forearm and hand muscles respectively. Preganglionic injuries are closer to the spinal cord and may involve sympathetic fibers.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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2. MILD TRAUMATIC BRAIN INJURY
(M-TBI)
• Definition
• Scales
• Signs and symptoms
• Prehospital management of traumatic brain injury
• Management in ED/Triage
• Requirement of Imaging :?:
• Admission or safe discharge?
• Treatment
• Sequelae
• Post injury Neuropsychology and rehabilitation
3. WHO DEFINITION
• Mild TBI is an acute brain injury resulting from
mechanical energy to the head from external physical
forces.
• Operational criteria for clinical identification include:
– (i) 1 or more of the following:
• confusion or disorientation,
• loss of consciousness for 30 minutes or less,
• post-traumatic amnesia for less than 24 hours, and/or
• Other transient neurological abnormalities such as focal signs,
seizure, and intracranial lesion not requiring surgery;
– (ii) Glasgow Coma Scale score of 13-15 after 30 minutes
post-injury or later upon presentation for health care.
4. Contd..
• These manifestations of MTBI must not be due
to :
– drugs, alcohol, medications,
– caused by other injuries or treatment for other
injuries (e.g. systemic injuries, facial injuries or
intubation),
– caused by other problems (e.g. psychological
trauma, language barrier or coexisting medical
conditions) or
– caused by penetrating craniocerebral injury.
5. Concussion definition
• A complex pathophysiological process affecting the brain, induced by biomechanical forces.
• Several common features that incorporate clinical, pathologic and biomechanical injury
constructs that may be utilized in defining the nature of a concussive head injury include:
• 1. Concussion may be caused either by a direct blow to the head, face, neck or elsewhere on
the body with an “impulsive” force transmitted to the head.
• 2. Concussion typically results in the rapid onset of short-lived impairment of neurological
function that resolves spontaneously. However, in some cases, symptoms and signs may
evolve over a number of minutes to hours.
• 3. Concussion may result in neuropathological changes, but the acute clinical symptoms
largely reflect a functional disturbance rather than a structural injury and, as such, no
abnormality is seen on standard structural neuroimaging studies.
• 4. Concussion results in a graded set of clinical symptoms that may or may not involve loss
of consciousness. Resolution of the clinical and cognitive symptoms typically follows a
sequential course.
• However, it is important to note that in some cases symptoms may be prolonged.
15. Primary Survey
• Airway
– Clear and maintain airway
• Breathing
– Supply oxygen (target PaCO2 30-35 mmHg)
– Look for and treat injuries
• Circulation
– P/BP/Neck veins/external haemorrhage
– Temperature /capillary refill
• Disability
– Assess GCS
• The GCS score that has the most prognostic importance is referred to as the
postresuscitation GCS, obtained after the patient's airway and hemodynamic status have
been stabilized.
– Pupillary size and response
– Other brainstem reflexes: Corneal /Cough /gag reflex
– Signs of Spinal cord injury and Other lateralizing signs of injury
• Exposure
– After adequate collar immobilization of neck and log roll for back examination
– For Adequate complete examination
– Prevention of hypothermia
16. Secondary Survey
• History:
– Allergy
– Medication
– Past medical history (Including pregnancy)
– Last meal
– Events relating to injury
• Examination:
– Head
– Eyes
– Face
– Neck
– Chest
– Abdomen
– Pelvis
– Extremities
• Detailed Neurological reassessment:
– GCS/Pupils /Motor /Sensory
• Adjuvant Test
– CT Scan (“MAN SCAN”—tomogram from head to knee)
17. Requirement of Imaging
• ATLS guidelines :
– a goal of 30 minutes between initial assessment and CT
scan.
• The Canadian CT Head Rule is useful for indication of
CT scan: includes the following high-risk factors and
two additional medium-risk factors
• Other Imaging:
– MRI BRAIN
– CT ANGIOGRAPHY OF CEREBRAL VESSELS
18.
19.
20. CLASSIFY THE SEVERITY
• ONCE
– INITIAL ASSESSMENT AND
– RESUSCITATION
– IMAGING
THEN
Classify as per GCS scoring and management of
1. GCS score of 3 to 12 -- (moderate and severe TBI) and an abnormal CT
scan will require :
– Neurotrauma intensive care unit specialized care.
2. GCS scores of 13 to 15 (mild TBI) depends on the :
– degree of injury and
– the cause of the depressed GCS score (e.g., alcohol, illicit drugs, hypoxia).
21. MILD TBI
• commonly associated with transient
confusion, temporary loss of consciousness,
and amnesia without significantly poor GCS
scores.
• GCS: 13-15
• Watch for “Talk and Die” patient (ask for lucid
interval)
• WHO definition : Concussion and Mild TBI
• CDC guidelines
22. CDC Guidelines for Mild TBI
1. Any period of observed or self-reported transient
confusion, disorientation, or impaired
consciousness
2. Any period of observed or self-reported
dysfunction of memory (amnesia) around the time
of injury
3. Observed signs of neurological or
neuropsychological dysfunction
23. Neuropsychology testing
• ImPACT (Immedicate Post concussion
Assessment and cognitive testing) program
– measures verbal and
– visual memory,
– information processing time, and
– reaction time
• Other Computerized test
– (CogSport, and Headminders)
24. Post Imaging
• Patients with mild TBI and negative head CT scans :
– Can be safely discharged
– except those on anticoagulant or antiplatelet therapy or
– who have undergone prior neurosurgical procedures.
• Patients with head CT scans showing small contusions
and hemorrhages, but with GCS scores of14 or 15,
– inpatient observation for 24 to 48 hours with frequent
neurological examinations in a monitored setting (e.g.,
every 2 to 4 hours) and
– repeat imaging
25. Adjunct testing
• fMRI
• PET
• MR Spectroscopy-- (NAA : Cr) Ratio
• DTI
• HD Fibre tracking
• Serum markers:
– S100B Calcium binding protein
– GFAP
– By immuno assay:
• NSE
• MBP
• Tau Protein
• Neuropsychhologic assessment
• Post concussion SCAT 3
26. Concussion Management
• COGNITIVE
• PHYSICAL REST FOR first 48 hours
• Stepwise approach:
– period of no activity,
– followed by light aerobic exercise,
– sport-specific exercise,
– noncontact training drills,
– full-contact practice, and
– finally return to play/ Full activity
• with a period of 24 hours at each level
• In the event that postconcussion symptoms occur at any step:
– another 24-hour period of rest is completed, and the
– Patient /athelete drops back to the previous step in the program.
• Because of evidence that RTP(return to play) on the day of injury may be
associated with prolonged neuropsychological deficits with delayed onset,
same-day RTP should never be permitted.
27. Pharmacological treatment
– Not used for TBI deficit
– but useful for patients with postconcussion syndrome
or prolonged postconcussion syndrome
– during the recovery phase
• It is best to avoid medications
– that lower the seizure threshold or
– that cause confusion or contribute to cognitive
slowing, fatigue, or daytime drowsiness
28. In patient management
• strict monitoring
– GCS
– Vital
– Pupils
– Newer neurological defcit
• Cerebral protection
• Other systemic injuries to be ruled out and
managed accordingly
30. Post Head injury disease (Post
concussion)
• Post concussion syndrome (6weeks – 3 months)
– ICD 10 Diagnosis of PCS:
• requires the presence of three or more of the following symptoms:
– headache,
– dizziness,
– fatigue,
– irritability,
– insomnia,
– concentration difficulty, and
– Memory difficulty.
• Prolonged post concussion syndrome (>3 months)
• Mild cognitive deficit
• Chronic traumatic encephalopathy