DOCSLIB.ORG

Intracranial Hemorrhage

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Intracranial Hemorrhage MARK MOSS, M.D. INTERVENTIONAL NEURORADIOLOGY WASHINGTON REGIONAL MEDICAL CENTER Definitions Stroke Clinical syndrome of rapid onset deficits of brain function lasting more than 24 hours or leading to death Transient Ischemic attack (TIA) Clinical syndrome of rapid onset deficits of brain function which resolves within 24 hours Epidemiology Stroke is the leading cause of adult disabilities 2nd leading cause of death worldwide 3rd leading cause of death in the U.S. 800,000 strokes per year resulting in 150,000 deaths Deaths are projected to increase exponentially in the next 30 years owing to the aging population The annual cost of stroke in the U.S. is estimated at $69 billion Stroke can be divided into hemorrhagic and ischemic origins 13% hemorrhagic 87% ischemic Intracranial Hemorrhage Collective term encompassing many different conditions characterized by the extravascular accumulation of blood within different intracranial spaces. OBJECTIVES: Define types of ICH Discuss best imaging modalities Subarachnoid hemorrhage / Aneurysms Roles of endovascular surgery Intracranial hemorrhage Outside the brain (Extra-axial) hemorrhage Subdural hematoma (SDH) Epidural hematoma (EDH) Subarachnoid hematoma (SAH) Intraventricular (IVH) Inside the brain (Intra-axial) hemorrhage Intraparenchymal hematoma (basal ganglia, lobar, pontine etc.) Your heads compartments Scalp Subgaleal Space Bone (calvarium) Dura Mater thick tough membrane Arachnoid flimsy transparent membrane Pia Mater tightly hugs the brain surface Brain Ventricles • The extradural (epidural) space is a potential space between the calvarium and the dura mater. • Subdural space- potential space between the dura and arachnoid membrane • Subarachnoid space- relatively large space which is filled with CSF Intracranial hemorrhage Extra-axial hemorrhage Subdural hematoma (SDH) Epidural hematoma (EDH) Subarachnoid hematoma (SAH) Intraventricular (IVH) Intra-axial hemorrhage Intraparenchymal hemorrhage (basal ganglia, lobar, pontine ect) Subdural Hematoma Source of bleed: stretching and tearing of bridging cortical veins. Rarely caused by an arterial hemorrhage As blood accumulates, pressure on the brain increases. This mass effect causes a subdural hematoma's symptoms. Much slower to develop into a mass large enough to produce symptoms Cause: acceleration-deceleration injury (trauma) Risk factors: Elderly, dementia, alcoholics, pts on anticoagulation Subdural Hematoma • Clinical features: HA, fluctuating LOC, confusion, dilated fixed pupil, gaze deviation, can have high mortality Not a Aneurysm Treatment options Medical managent Neurosurgical Burr hole irrigation Craniotomy Intracranial hemorrhage Extra-axial hemorrhage Subdural hematoma (SDH) Epidural hematoma (EDH) Subarachnoid hematoma (SAH) Intraventricular (IVH) Intra-axial hemorrhage Intraparenchymal hemorrhage (basal ganglia, lobar, pontine ect) Epidural Hematoma Traumatic Intracranial bleed A neurologic emergency Bleed usually arterial but rarely can be venous Clinical Features: LOC>>>Lucid Interval>>unconsciousness s/s of raised ICP / cerebral herniation Focal neurological deficit Epidural hematoma Typically epidural hematomas are seen in young trauma patients Usually have a skull fracture (80%) Classically a torn meningeal artery (middle meningeal artery) Convex appearance Epidural Hematoma Treatment options Surgical emergency craniotomy Intracranial hemorrhage Extra-axial hemorrhage Subdural hematoma (SDH) Epidural hematoma (EDH) Subarachnoid hematoma (SAH) Intraventricular (IVH) Intra-axial hemorrhage Intraparenchymal hemorrhage (basal ganglia, lobar, pontine ect) Intraventricular Hemorrhage Blood within the ventricular system Usually from extension of aneurysmal subarachnoid hemorrhage or hypertension-related intracerebral hemorrhage Less likely etiologies Vascular malformations, anticoagulation, intraventricular tumor trauma Most immediate threat to life is the development of obstructive hydrocephalus. Mainstay of treatment is a External ventricular drain (EVD) Intracranial hemorrhage Extra-axial hemorrhage Subdural hematoma (SDH) Epidural hematoma (EDH) Subarachnoid hematoma (SAH) Intraventricular (IVH) Intra-axial hemorrhage Intraparenchymal hemorrhage (basal ganglia, lobar, pontine ect) Intraparenchymal Hematoma Clot is located within the substance of the brain Can extent to surface(SAH,SDH) or (IVH) Spontaneous intracerebral hematoma often the result of uncontrolled hypertension or amyloid angiopathy Underlying pathology (vascular malformation, tumor) Trauma Intra-parenchymal Hematoma Treatment options Clot evacuation Intracranial hemorrhage Extra-axial hemorrhage Subdural hematoma (SDH) Epidural hematoma (EDH) Subarachnoid hematoma (SAH) Intraventricular (IVH) Intra-axial hemorrhage Intraparenchymal hemorrhage (basal ganglia, lobar, pontine ect) Subarachnoid Space Contains larger cerebral blood vessels that penetrate into and out of brain parenchyma Contains cerebrospinal fluid (CSF) When these blood vessels tear or rupture they release blood into the subarachnoid space where it mixes with CSF. • Occasionally this blood can extend into the: brain parenchyma 20-40% • Extend into the ventricles 13-28% • Or into the subdural space 2-5% Subarachnoid Hemorrhage Etiology Trauma (most common) Spontaneous SAH Aneurysms 75-80% (aSAH) Arteriovenous malformations (AVM) 4-5% Vasculopathy / Vasculitis / RCVS Arterial dissection Coagulopathy Spinal AVM Drugs (cocaine , amphetamines) Sickle cell disease Pituitary apoplexy Benign perimesencephalic hemorrhage Unknown 15% Possible Risk Factors for SAH NON-MODIFIABLE MODIFIABLE • Age • HTN • Sex • Cholesterol • Race • Anti-coagulation • Asians>Afr. Amer.>White • Anti-platelets • Genetic • Smoking • Cerebral amyloid angiopathy, • High ETOH intake coagulation disorders • DM • Drugs (cocaine, amphetamines) Aneurysmal Subarachnoid Hemorrhage Trauma (most common) Spontaneous SAH Aneurysms 75-80% Arteriovenous malformations (AVM) 4-5% Vasculopathy / Vasculitis / RVCS Arterial dissection Coagulopathy Spinal AVM Drugs (cocaine , amphetamines) Sickle cell disease Pituitary apoplexy Benign perimesencephalic hemorrhage Unknown 15% What is a brain aneurysm ? Area of weakness in a brain blood vessel that over time can grow larger and thinner. Aneurysms are dangerous because they eventually rupture allowing blood to leak out of the vessel and cause a SAH. Aneurysm Definition A abnormal dilation of a blood vessel. Saccular 90%, fusiform, dissecting and mycotic Giant aneurysm (>25mm) Wide neck aneurysm is defined as a Fundus: neck ratio <1 or a neck greater than 4 mm. Aneurysm Incidence and Demographics Approximately 2-3% of the population have a intracranial aneurysm 10-12 million people in the U.S. Vast majority of aneurysms are asymptomatic 30,000 ruptured aneurysms a year in US 20% incidence of multiple aneurysms in those with aneurysms Estimated rate of aneurysmal SAH is 6-8/100,000 Peak age of aneurysm rupture is 55-60 Female>Male Aneurysm Biology What causes Brain Aneurysms? In most cases, the reason why aneurysms form is unclear. Intracranial arteries are relatively fragile with less muscle, elastic protein and thinner walls than that of peripheral arteries of a similar size. Intracranial arteries have less supporting tissues surrounding them. Aneurysms most often form at bifurcations where there is turbulent flow and stress. Congenital defects in the media layer of the arterial wall ? Infection and inflammation can cause weakening of the arterial wall. Trauma Aneurysm Formation Summary “Complex disease”, where some things are known to contribute to aneurysm formation: smoking, chronic high blood pressure, chronic alcohol abuse, illicit drug use, and genetic factors. They are acquired lesions, which is supported by the fact that aneurysm prevalence increases with increasing age Smoking and hypertension are major drivers in the formation and progression of aneurysms and thereby a target for therapeutic intervention Exact etiology of aneurysm formation remains uncertain Risk factors for Aneurysms Polycystic Kidney Disease (15% have aneurysms) Fibromuscular Dysplasia Atherosclerosis AVM Moya-moya Marfan’s syndrome Connective tissue disorder (Ehlers-Danlos) Bacterial endocarditis Smoking Familial aneurysms risk (at least 1 first-degree family member with an intracranial aneurysm, and especially if 2 first- degree relatives are affected) and family history of a SAH 80% aneurysms arise from the COW Why are Aneurysms Dangerous? Size and location are the most important factors that determine the likelihood that an aneurysm will rupture Small aneuryms <5mm are unlikely to rupture and are often not treated unless they begin to grow. The larger an aneurysm is the more likely it will rupture. Aneurysms located in the back half of the brain (vertebral arteries, basilar artery, and the posterior communicating artery) are higher risk than aneurysms found in the anterior half (carotid artery, middle cerebral artery, and the anterior cerebral artery) Other risk factors for rupture: Growth, multiple aneurysms, prior rupture, symptomatic aneurysms, irregular shape, and family history of ruptured aneurysms. Natural History of Aneurysmal SAH 10-15% die before reaching a hospital 10% die within first several days of reaching care Overall mortality is 32-67% for all comers 30% of survivors have significant disability
Recommended publications
  • Why Do Bridging Veins Rupture Into the Virtual Subdural Space?

    Why Do Bridging Veins Rupture Into the Virtual Subdural Space?

    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.47.2.121 on 1 February 1984. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry 1984;47:121-127 Why do bridging veins rupture into the virtual subdural space? T YAMASHIMA, RL FRIEDE From the Department ofNeuropathology, University of Gottingen, Gottingen, Federal Republic of Germany SUMMARY Electron microscopic data on human bridging veins show thin walls of variable thick- ness, circumferential arrangement of collagen fibres and a lack of outer reinforcement by arach- noid trabecules, all contributory to the subdural portion of the vein being more fragile than its subarachnoid portion. These features explain the laceration of veins and the subdural location of resultant haematomas. Most subdural haematomas due to venous bleeding walls are delicate, lacking muscle fibres, with only a have been attributed to lacerations in bridging veins. thin fibrous wall and a thin elastic lamina adjacent to These veins form short trunks passing directly from the endothelial layer. The conclusions of these two the brain to the dura mater, almost at right angles to authors, have gained wide acceptance, although guest. Protected by copyright. both. Between these two points, bridging veins take there was little evidence concerning the fragility of a straight course with no tortuosity to allow for the the vein walls. possible displacement of brain.' Trotter2 speculated The purpose of the present communication is to that subdural haematomas are invariably due to provide electron microscopic data on tissue fixed in trauma tearing large veins, an interpretation situ, which might throw some light on to the lacera- elaborated by Krauland.3 According to Leary,4 the tion mechanism of bridging veins and its relationship common sources of subdural haematomas are rup- to the development of subdural haematoma.
  • Management of the Head Injury Patient

    Management of the Head Injury Patient

    Management of the Head Injury Patient William Schecter, MD Epidemilogy • 1.6 million head injury patients in the U.S. annually • 250,000 head injury hospital admissions annually • 60,000 deaths • 70-90,000 permanent disability • Estimated cost: $100 billion per year Causes of Brain Injury • Motor Vehicle Accidents • Falls • Anoxic Encephalopathy • Penetrating Trauma • Air Embolus after blast injury • Ischemia • Intracerebral hemorrhage from Htn/aneurysm • Infection • tumor Brain Injury • Primary Brain Injury • Secondary Brain Injury Primary Brain Injury • Focal Brain Injury – Skull Fracture – Epidural Hematoma – Subdural Hematoma – Subarachnoid Hemorrhage – Intracerebral Hematorma – Cerebral Contusion • Diffuse Axonal Injury Fracture at the Base of the Skull Battle’s Sign • Periorbital Hematoma • Battle’s Sign • CSF Rhinorhea • CSF Otorrhea • Hemotympanum • Possible cranial nerve palsy http://health.allrefer.com/pictures-images/ Fracture of maxillary sinus causing CSF Rhinorrhea battles-sign-behind-the-ear.html Skull Fractures Non-depressed vs Depressed Open vs Closed Linear vs Egg Shell Linear and Depressed Normal Depressed http://www.emedicine.com/med/topic2894.htm Temporal Bone Fracture http://www.vh.org/adult/provider/anatomy/ http://www.bartleby.com/107/illus510.html AnatomicVariants/Cardiovascular/Images0300/0386.html Epidural Hematoma http://www.chestjournal.org/cgi/content/full/122/2/699 http://www.bartleby.com/107/illus769.html Epidural Hematoma • Uncommon (<1% of all head injuries, 10% of post traumatic coma patients) • Located
  • Hypertensive Intracerebral Hemorrhage Due to Autonomic Dysreflexia in a Young Man with Cervical Cord Injury

    Hypertensive Intracerebral Hemorrhage Due to Autonomic Dysreflexia in a Young Man with Cervical Cord Injury

    J UOEH（産業医科大学雑誌）35（ 2 ）: 159－164（2013） 159 ［Case Report］ Hypertensive Intracerebral Hemorrhage Due to Autonomic Dysreflexia in a Young Man with Cervical Cord Injury Tadashi Sumiya Department of Spinal Care Center, Division of Rehabilitation Medicine 219 Myoji, Katsuragi-cho, Ito-gun, 649-7113, Japan Abstract : The author reports the case of a 36 year old man with cervical cord injury in whom autonomic dysreflexia developed into intracerebral hemorrhage during inpatient rehabilitation. This patient showed complete quadriplegia (motor below C6 and sensory below C7) due to fracture of the 6th cervical vertebra. An indwelling urethral catheter had been inserted into the bladder for 3 months, diminishing bladder expansiveness. Bladder capacity decreased to 200 ml and the patient frequently experienced headaches whenever his bladder was full. To obtain smoother urine flow, a supra-pubic cystostomy was performed. The headaches were temporarily cured, but soon relapsed with extreme increases in blood pressure, representing typical symptoms of autonomic dysreflexia. However, no poten- tial triggers were identified or removed, and lack of blood pressure management led to left putaminal hemorrhage. Despite operative treatment, the right upper extremity showed progressive increases in muscle tonus and finally formed a frozen shoulder with elbow flexion contracture. Two factors contributed to this serious complication: first, autonomic dysreflexia triggered by minor malfunction and/or irritation from the cystostomy catheter; and second, the medical staff lacked sufficient experience in and knowledge about the management of autonomic dysreflexia. It is of the utmost importance for medical staff engaging in rehabilitation of spinal patients to share information regard- ing triggers of autonomic dysreflexia and to be thorough in ensuring proper medical management.
  • Intracerebral Hemorrhage ICH Fact Sheet

    Intracerebral Hemorrhage ICH Fact Sheet

    FACT SHEET FOR PATIENTS AND FAMILIES Intracerebral Hemorrhage (ICH) What is it? An intracerebral [in-truh-suh-REE-bruh l] hemorrhage [HEM-rij], Dura mater or ICH, is bleeding inside or around the brain, which Brain Skull can put pressure on the brain. An ICH robs the brain Intracerebral of oxygen, so it must be identified and managed right hemorrhage away. Other names for ICH are cerebral hemorrhage or intracranial [in-truh-KREY-nee-uh l] hemorrhage. ICH can happen because of trauma or as a result of no known cause (spontaneous ICH), which is a type of stroke called a hemorrhagic [hem-oh-RAJ-ik] stroke. In the U.S. each year, about 1 in 10 people who have strokes do so because of an ICH. Stroke is the leading cause of disability and the 5th-leading cause of death in the U.S. What are the symptoms of spontaneous ICH? Spontaneous ICH symptoms usually develop suddenly, without warning. Key symptoms can include a SUDDEN (see BE FAST on page 2): What causes it? • Loss of balance or coordination An ICH is often caused by a blood vessel leaking or • Change in vision breaking. This can be the result of: • Weakness of the face, arm, or leg • High blood pressure that has damaged a blood vessel • Difficulty speaking • Smoking, overuse of alcohol, or use of illegal drugs Other ICH symptoms can include: such as cocaine or methamphetamine • Severe headache with no known cause (patients • Diabetes often describe it as “the worst headache of my life”) • Abnormal blood vessel proteins in the elderly • Seizures An ICH can also be caused by: • Vomiting or severe nausea, when combined with • Anticoagulant therapy (treatment with blood thinners) other symptoms from this list • Problems with vein structure • Partial or total loss of conciousness • A brain tumor that bleeds • Head injuries caused by a fall or accident 1 How is it diagnosed? What can I expect afterward? Your doctor will explain what tests will be used to Your long-term outlook depends on the location and diagnose ICH, depending on your condition.
  • The Diagnosis of Subarachnoid Haemorrhage

    The Diagnosis of Subarachnoid Haemorrhage

    Journal ofNeurology, Neurosurgery, and Psychiatry 1990;53:365-372 365 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.53.5.365 on 1 May 1990. Downloaded from OCCASIONAL REVIEW The diagnosis of subarachnoid haemorrhage M Vermeulen, J van Gijn Lumbar puncture (LP) has for a long time been of 55 patients with SAH who had LP, before the mainstay of diagnosis in patients who CT scanning and within 12 hours of the bleed. presented with symptoms or signs of subarach- Intracranial haematomas with brain shift was noid haemorrhage (SAH). At present, com- proven by operation or subsequent CT scan- puted tomography (CT) has replaced LP for ning in six of the seven patients, and it was this indication. In this review we shall outline suspected in the remaining patient who stop- the reasons for this change in diagnostic ped breathing at the end of the procedure.5 approach. In the first place, there are draw- Rebleeding may have occurred in some ofthese backs in starting with an LP. One of these is patients. that patients with SAH may harbour an We therefore agree with Hillman that it is intracerebral haematoma, even if they are fully advisable to perform a CT scan first in all conscious, and that withdrawal of cerebro- patients who present within 72 hours of a spinal fluid (CSF) may occasionally precipitate suspected SAH, even if this requires referral to brain shift and herniation. Another disadvan- another centre.4 tage of LP is the difficulty in distinguishing It could be argued that by first performing between a traumatic tap and true subarachnoid CT the diagnosis may be delayed and that this haemorrhage.
  • Intracranial Hemorrhage As Initial Presentation of Cerebral Venous Sinus Thrombosis

    Intracranial Hemorrhage As Initial Presentation of Cerebral Venous Sinus Thrombosis

    Case Report Journal of Heart and Stroke Published: 31 Dec, 2019 Intracranial Hemorrhage as Initial Presentation of Cerebral Venous Sinus Thrombosis Joseph Y Chu1* and Marc Ossip2 1Department of Medicine, University of Toronto, Canada 2Department of Diagnostic Imaging, William Osler Health System, Canada Abstract Intracranial Hemorrhage (ICH) as initial presentation is an uncommon complication of Cerebral Venous-Sinus Thrombosis (CVT). Clinical and neuro-imaging studies of 4 cases of ICH due cerebral venous-sinus thrombosis seen at the William Osler Health System in Toronto will be presented. Discussion of the immediate and long-term management of these interesting cases will be reviewed with emphasis on the appropriate neuro-imaging studies. Literature review of Direct Oral Anticoagulants (DOAC) in the long-term management of these challenging cases will be discussed. Introduction The following are four cases of Cerebral Venous-Sinus Thrombosis (CVT) who present initially as Intracranial Hemorrhage (ICH). Clinical details, including immediate and long term management and neuro-imaging studies are presented. Results Case 1 A 43 years old R-handed house wife, South-Asian decent, who was admitted to hospital on 06- 10-2014 with sudden headache and right hemiparesis. Her past health shows no prior hypertension or stroke. She is not on any hormone replacement therapy, non-smoker and non-drinker. Married with 1 daughter. Examination shows BP=122/80, P=70 regular, GCS=15, with right homonymous hemianopsia, right hemiparesis: arm=leg 1/5, extensor R. Plantar response. She was started on IV Heparin after her unenhanced CT showed acute left parietal intracerebral hemorrhage and her MRV showed extensive sagittal sinus thrombosis extending into the left transverse OPEN ACCESS sinus (Figures 1,2).
  • Early Management of Retained Hemothorax in Blunt Head and Chest Trauma

    Early Management of Retained Hemothorax in Blunt Head and Chest Trauma

    World J Surg https://doi.org/10.1007/s00268-017-4420-x ORIGINAL SCIENTIFIC REPORT Early Management of Retained Hemothorax in Blunt Head and Chest Trauma 1,2 1,8 1,7 1 Fong-Dee Huang • Wen-Bin Yeh • Sheng-Shih Chen • Yuan-Yuarn Liu • 1 1,3,6 4,5 I-Yin Lu • Yi-Pin Chou • Tzu-Chin Wu Ó The Author(s) 2018. This article is an open access publication Abstract Background Major blunt chest injury usually leads to the development of retained hemothorax and pneumothorax, and needs further intervention. However, since blunt chest injury may be combined with blunt head injury that typically requires patient observation for 3–4 days, other critical surgical interventions may be delayed. The purpose of this study is to analyze the outcomes of head injury patients who received early, versus delayed thoracic surgeries. Materials and methods From May 2005 to February 2012, 61 patients with major blunt injuries to the chest and head were prospectively enrolled. These patients had an intracranial hemorrhage without indications of craniotomy. All the patients received video-assisted thoracoscopic surgery (VATS) due to retained hemothorax or pneumothorax. Patients were divided into two groups according to the time from trauma to operation, this being within 4 days for Group 1 and more than 4 days for Group 2. The clinical outcomes included hospital length of stay (LOS), intensive care unit (ICU) LOS, infection rates, and the time period of ventilator use and chest tube intubation. Result All demographics, including age, gender, and trauma severity between the two groups showed no statistical differences.
  • Iatrogenic Spinal Subarachnoid Hematoma After Diagnostic Lumbar Puncture

    Iatrogenic Spinal Subarachnoid Hematoma After Diagnostic Lumbar Puncture

    https://doi.org/10.14245/kjs.2017.14.4.158 KJS Print ISSN 1738-2262 On-line ISSN 2093-6729 CASE REPORT Korean J Spine 14(4):158-161, 2017 www.e-kjs.org Iatrogenic Spinal Subarachnoid Hematoma after Diagnostic Lumbar Puncture Jung Hyun Park, Spinal subarachnoid hematoma (SSH) following diagnostic lumbar puncture is very rare. Generally, Jong Yeol Kim SSH is more likely to occur when the patient has coagulopathy or is undergoing anticoagulant therapy. Unlike the usual complications, such as headache, dizziness, and back pain at the Department of Neurosurgery, Kosin needle puncture site, SSH may result in permanent neurologic deficits if not properly treated University Gospel Hospital, Kosin within a short period of time. An otherwise healthy 43-year-old female with no predisposing University College of Medicine, factors presented with fever and headache. Diagnostic lumbar puncture was performed under Busan, Korea suspicion of acute meningitis. Lumbar magnetic resonance imaging was performed due to hypo- Corresponding Author: esthesia below the level of T10 that rapidly progressed after the lumbar puncture. SSH was Jong Yeol Kim diagnosed, and high-dose steroid therapy was started. Her neurological symptoms rapidly deterio- Department of Neurosurgery, rated after 12 hours despite the steroids, necessitating emergent decompressive laminectomy Kosin University Gospel Hospital, and hematoma removal. The patient’s condition improved after the surgery from a preoperative Kosin University College of Medicine, 262 Gamcheon-ro, Seo-gu, Busan motor score of 1/5 in the right leg and 4/5 in the left leg to brace-free ambulation (motor grade 49267, Korea 5/5) 3-month postoperative.
  • Feigned Consensus: Usurping the Law in Shaken Baby Syndrome/ Abusive Head Trauma Prosecutions

    Feigned Consensus: Usurping the Law in Shaken Baby Syndrome/ Abusive Head Trauma Prosecutions

    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by University of Michigan School of Law University of Michigan Law School University of Michigan Law School Scholarship Repository Articles Faculty Scholarship 2020 Feigned Consensus: Usurping the Law in Shaken Baby Syndrome/ Abusive Head Trauma Prosecutions Keith A. Findley University of Wisconsin Law School D. Michael Risinger Seton Hall University School of Law Patrick D. Barnes Stanford University Medical Center Julie A. Mack Pennsylvania State University Medical Center David A. Moran University of Michigan Law School, [email protected] See next page for additional authors Available at: https://repository.law.umich.edu/articles/2102 Follow this and additional works at: https://repository.law.umich.edu/articles Part of the Criminal Procedure Commons, Evidence Commons, Juvenile Law Commons, and the Medical Jurisprudence Commons Recommended Citation Findley, Keith A. "Feigned Consensus: Usurping the Law in Shaken Baby Syndrome/Abusive Head Trauma Prosecutions." Michael Risinger, Patrick Barnes, Julie Mack, David A. Moran, Barry Scheck, and Thomas Bohan, co-authors. Wis. L. Rev. 2019, no. 4 (2019): 1211-268. This Article is brought to you for free and open access by the Faculty Scholarship at University of Michigan Law School Scholarship Repository. It has been accepted for inclusion in Articles by an authorized administrator of University of Michigan Law School Scholarship Repository. For more information, please contact [email protected]. Authors Keith A. Findley, D. Michael Risinger, Patrick D. Barnes, Julie A. Mack, David A. Moran, Barry C. Scheck, and Thomas L. Bohan This article is available at University of Michigan Law School Scholarship Repository: https://repository.law.umich.edu/articles/2102 FEIGNED CONSENSUS: USURPING THE LAW IN SHAKEN BABY SYNDROME/ ABUSIVE HEAD TRAUMA PROSECUTIONS KEITH A.
  • Symptomatic Intracranial Hemorrhage (Sich) and Activase® (Alteplase) Treatment: Data from Pivotal Clinical Trials and Real-World Analyses

    Symptomatic Intracranial Hemorrhage (Sich) and Activase® (Alteplase) Treatment: Data from Pivotal Clinical Trials and Real-World Analyses

    Symptomatic intracranial hemorrhage (sICH) and Activase® (alteplase) treatment: Data from pivotal clinical trials and real-world analyses Indication Activase (alteplase) is indicated for the treatment of acute ischemic stroke. Exclude intracranial hemorrhage as the primary cause of stroke signs and symptoms prior to initiation of treatment. Initiate treatment as soon as possible but within 3 hours after symptom onset. Important Safety Information Contraindications Do not administer Activase to treat acute ischemic stroke in the following situations in which the risk of bleeding is greater than the potential benefit: current intracranial hemorrhage (ICH); subarachnoid hemorrhage; active internal bleeding; recent (within 3 months) intracranial or intraspinal surgery or serious head trauma; presence of intracranial conditions that may increase the risk of bleeding (e.g., some neoplasms, arteriovenous malformations, or aneurysms); bleeding diathesis; and current severe uncontrolled hypertension. Please see select Important Safety Information throughout and the attached full Prescribing Information. Data from parts 1 and 2 of the pivotal NINDS trial NINDS was a 2-part randomized trial of Activase® (alteplase) vs placebo for the treatment of acute ischemic stroke. Part 1 (n=291) assessed changes in neurological deficits 24 hours after the onset of stroke. Part 2 (n=333) assessed if treatment with Activase resulted in clinical benefit at 3 months, defined as minimal or no disability using 4 stroke assessments.1 In part 1, median baseline NIHSS score was 14 (min: 1; max: 37) for Activase- and 14 (min: 1; max: 32) for placebo-treated patients. In part 2, median baseline NIHSS score was 14 (min: 2; max: 37) for Activase- and 15 (min: 2; max: 33) for placebo-treated patients.
  • What to Expect After Having a Subarachnoid Hemorrhage (SAH) Information for Patients and Families Table of Contents

    What to Expect After Having a Subarachnoid Hemorrhage (SAH) Information for Patients and Families Table of Contents

    What to expect after having a subarachnoid hemorrhage (SAH) Information for patients and families Table of contents What is a subarachnoid hemorrhage (SAH)? .......................................... 3 What are the signs that I may have had an SAH? .................................. 4 How did I get this aneurysm? ..................................................................... 4 Why do aneurysms need to be treated?.................................................... 4 What is an angiogram? .................................................................................. 5 How are aneurysms repaired? ..................................................................... 6 What are common complications after having an SAH? ..................... 8 What is vasospasm? ...................................................................................... 8 What is hydrocephalus? ............................................................................... 10 What is hyponatremia? ................................................................................ 12 What happens as I begin to get better? .................................................... 13 What can I expect after I leave the hospital? .......................................... 13 How will the SAH change my health? ........................................................ 14 Will the SAH cause any long-term effects? ............................................. 14 How will my emotions be affected? .......................................................... 15 When should
  • Overcoming Defense Expert Testimony in Abusive Head Trauma Cases

    Overcoming Defense Expert Testimony in Abusive Head Trauma Cases

    NATIONAL CENTER FOR PROSECUTION OF CHILD ABUSE Special Topics in Child Abuse Overcoming Defense Expert Testimony in Abusive Head Trauma Cases By Dermot Garrett Edited by Eleanor Odom, Amanda Appelbaum and David Pendle NATIONAL CENTER FOR PROSECUTION OF CHILD ABUSE Scott Burns Director , National District Attorneys Association The National District Attorneys Association is the oldest and largest professional organization representing criminal prosecutors in the world. Its members come from the offices of district attorneys, state’s attorneys, attorneys general, and county and city prosecutors with responsibility for prosecuting criminal violations in every state and territory of the United States. To accomplish this mission, NDAA serves as a nationwide, interdisciplinary resource center for training, research, technical assistance, and publications reflecting the highest standards and cutting-edge practices of the prosecutorial profession. In 1985, the National District Attorneys Association recognized the unique challenges of crimes involving child victims and established the National Center for Prosecution of Child Abuse (NCPCA). NCPCA’s mission is to reduce the number of children victimized and exploited by assisting prosecutors and allied professionals laboring on behalf of victims too small, scared or weak to protect themselves. Suzanna Tiapula Director, National Center for Prosecution of Child Abuse A program of the National District Attorneys Association www.ndaa.org 703.549.9222 This project was supported by Grants #2010-CI-FX-K008 and [new VOCA grant #] awarded by the Office of Juvenile Justice and Delinquency Prevention. The Office of Juvenile Justice and Delinquency Prevention is a component of the Office of Justice Programs. Points of view in this document are those of the author and do not necessarily represent the official position or policies of the U.S.