DOCSLIB.ORG

Intracerebral Hemorrhage After Carotid Endarterectomy

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Intracerebral Hemorrhage After Carotid Endarterectomy Henry Ford Hospital Medical Journal Volume 32 Number 3 Special Issue on Medical Computing Article 11 9-1984 Intracerebral Hemorrhage After Carotid Endarterectomy José Biller Andrew C. Hayes Fred N. Littooy William H. Baker Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Biller, José; Hayes, Andrew C.; Littooy, Fred N.; and Baker, William H. (1984) "Intracerebral Hemorrhage After Carotid Endarterectomy," Henry Ford Hospital Medical Journal : Vol. 32 : No. 3 , 197-203. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol32/iss3/11 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hosp Med j Vol 32, No 3, 1984 Case Reports Intracerebral Hemorrhage After Carotid Endarterectomy Jose Biller, MD,* Andrew C. Hayes, PA-C,** Fred N. Littooy, MD,** and William H. Baker, MD** Intracerebral hemorrhage (ICH) is a rare complication operatively. The third patient, who was hypertensive, of carotid endarterectomy (CE). In our multicenter se­ had a nonfatal ipsilateral thalamic hemorrhage on the ries of 1,180 CE (Baker-Littooy), three ICH occurred, of third postoperative day. Though these three patients which two were fatal. One patient was receiving anti­ represent only 0.25% of our series, they constitute 12% coagulants because ofa prosthetic aortic valve; another of our total strokes. ICH constitutes the largest per­ had rupture of a known ipsilateral intracranial an­ centage of nontechnically-related strokes and non- eurysm. Both occurred more than six weeks post­ cardiac deaths after CE. stroke after carotid endarterectomy is usually ascribed heparin, and a standard endarterectomy was performed to occlusion of the carotid artery, embolization, intimal through a lateral arteriotomy. Her immediate postoperative flap formation, or hemodynamic factors. Intracranial condition was satisfactory, and Doppler ultrasonic exam­ hemorrhagic complications after this procedure are ination was unremarkable. On the first postoperative day she considered rare. They embrace hemorrhagic infarction, had a three-hour episode of hypertension and incurred a subendocardial anterolateral wall myocardial infarction. No intracerebral hematomas with or without ventricular or neurological abnormalities were noted then, but 36 hours subarachnoid penetration, and instances of hem­ later, when her blood pressure was 190/80 mm/Hg, she de­ orrhagic cerebrospinal fluid associated with increased veloped left-sided weakness, left hemiparesis, left-sided as- intracranial pressure. Bruetman and associates (1) re­ tereognosis, and a left homonymous visual field defect. CT ported six hemorrhagic complications among 900 showed a right thalamic hemorrhage with no interval change (0.66%) patients surgically treated for carotid stenosis or of the previously noted right parietal infarct (Fig. 3). occlusion. More recently Sundt, et al (2,3) noted five cases in a series of 1,145 (0.43%) carotid endarterec- Case 2 tomies. We noted three cases in our series of 1,180 A 70-year-old woman was admitted in October 1978 with a three-week history of ischemic rest pain in the left foot. Past (0.25%) carotid endarterectomies and report our expe­ medical history was remarkable for valvular heart disease, a rience in conjunction with a review of 36 previously thrombosed prosthetic aortic valve, previous left hemispheric published cases. transient ischemic attacks, arterial hypertension, and diabetes mellitus. Medications included NPH insulin, digoxin, Cou­ Case Reports madin, and dipyridamole. Ten days after a left femoropop­ liteal bypass, transient paralysis of the right upper and lower Case 1 extremities and confusion were noted. CT was obtained and A 63-year-oId woman was admitted in March 1983 for elective was normal. The next day she developed aphasia and right right carotid endarterectomy. Four weeks previously, she had hemiparesis. Repeat CT was unchanged. Partial recovery oc­ had an episode of headache and persistent left arm and leg curred over the next 24 hours. Cerebral arteriogram revealed numbness. Cranial computerized tomography (CT) at that 99% stenosis atthe origin ofthe left internal carotid artery with time revealed a right superior parietal infarction (Fig. 1). Cer­ an occluded middle cerebral artery stem (Fig. 4). Heparin was ebral arteriography demonstrated greater than 80% stenosis continued, and on November 7, 1978, a left carotid end­ of the origin of the right internal carotid artery (Fig. 2) and a arterectomy was performed under general anesthesia. small nonulcerated plaque at the origin of the left internal carotid artery. There was cross filling to the right side, and the Although the patient developed postoperative hypertension posterior cerebral arteries filled from the carotid injection. of 220 mm/Hg systolic (which required sodium nitroprusside The posterior circulation was unremarkable. The patient im­ for control), her neurological status improved. However, proved steadily. on the second day after endarterectomy, neurological dete­ rioration was evident, and CT showed a small infarction in the One month later, a right carotid endarterectomy was per­ formed under general anesthesia. At operation, inspection of the right carotid revealed an atheroma at its bifurcation. After Submitted for publication; june 4, 1984 it was opened, a stenotic lesion was found with old and new Accepted for publication: july 19, 1984 clots situated on the intimal surface. Internal carotid artery Departments of Neurology^ and Surgery^^, Loyola University Medical Center back pressure was 86/60 mm/Hg with a mean of 70 mm/Hg; Address reprint requests to Dr, Biller, Division of Cerebrovascular Disease, systemic pressure was 180/80 mm/Hg. The patient was given Department of Neurology, University of lowa, lowa City, lowa 52242, 197 Biller, Hayes, Littooy, and Baker left basal ganglia (Fig. 5). She had significant recovery of neurological function and was discharged on the tenth postoperative day receiving Coumadin. Two months later she suffered sudden global aphasia, dense right hemiparesis, and lethargy. Prothrombin time was 19.8 seconds (N: 11.0-12.6 seconds), and CT revealed a large intracerebral hematoma located in the left temporal region extending into the external capsule (Fig. 6). She underwent successful removal of the hematoma and was discharged to a nursing home. Case 3 An 84-year-old woman experienced an episode of right mono­ cular blindness and transient left hemiparesis, but her neu­ rologic examination was normal. Blood pressure was 150/90 mm/Hg. Cerebral arteriography demonstrated severe stenosis of the internal carotid arteries bilaterally and an incidental 5 x 10 mm left internal carotid - posterior communicating junction aneurysm. Aphasia developed after angiography when left carotid endarterectomy was performed. Back pressure was 32/29 mm/Hg with a systemic pressure of 198/76 mm/Hg. The aphasia gradually resolved, but seven months later she was found comatose and died the same day. Autopsy revealed that the previously noted aneurysm had ruptured. A previously unrecognized 2 mm aneurysm was found in the right middle cerebral artery, and a small cystic infarction had occurred in the left parieto-occipital junction (4). Fig. 1. Case 1. CT scan obtained at time of original symptoms demonstrates low density area in right superior parietal region consistent with an ischemic infarction. Fig. 2. Case 1. Fig. 3. Case 1. Selective right carotid arteriogram demonstrates severe internal carotid CT scan obtained three days after right carotid endarterectomy, demon­ artery stenosis and ulceration. strates right thalamic hemorrhage. Area of prior infarction was un­ changed (not shown). 198 Intracerebral Hemorrhage After Carotid Endarterectomy Fig. 6. Case 2. CT scan demonstrates large left lateral ganglionic hemorrhage with mass effect. Fig. 4. Case 2. Selective left carotid arteriogram shows severe stenosis at origin of internal carotid and occlusion of middle cerebral artery system. Discussion Intracerebral hemorrhage following carotid end­ arterectomy is rare, and elevated blood pressure has usually been implicated as the primary risk factor. Hemorrhage most often occurs in the area of previous infarction, ipsilateral to the operation. In order to evaluate more completely the mechanism(s) of this complication, we have reviewed the reported cases of ICH after carotid endarterectomy. In addition to our three patients, we have reviewed 36 previously reported cases (1-3, 5-14), details of which are illustrated in the Table. During the past two dec­ ades, indications for carotid endarterectomy have changed, and some of these patients would not now be referred for surgery. Thirteen patients had operations to reopen occluded internal carotid arteries, most within days of a stroke. Three additional patients underwent surgery for severe internal carotid artery stenosis within five days of a major stroke. For six patients, information about the severity of neurologic deficit and the timing of endarterectomy was incomplete. Only 14 of these 36 patients had generally acceptable indications for operation. In three patients emergency Fig. 5. Case 2. surgery was undertaken for complications of an­ Immediate postoperative
Load more

Recommended publications
  • 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
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Of These, About 62% Are Women. STROKE: an OVERV
    STROKE: AN OVERVIEW It is estimated that more than 700,000 Americans suffer a cerebrovascular event, or stroke, each year. Approximately 500,000 of these are first strokes, and 200,000 are recurrent attacks. On average, someone suffers a stroke every 45 seconds, and a stroke death occurs every 3.1 minutes (1). According to American Heart Association data, approximately 4,700,000 stroke survivors are alive in the United States today (2). Stroke is the leading In West Virginia, between 1,200 and cause of adult disability in the United States and the 1,300 people die from stroke each year; third leading cause of death nationwide. In West of these, about 62% are women. Virginia, stroke ranks as the fourth leading cause of death, after heart disease, cancer, and chronic lower respiratory disease; between 1,200 and 1,300 people die from stroke each year in the state. Death rates from stroke declined markedly in the 1970s and 1980s in both the state and the country as a whole; however, this decline leveled off in the 1990s (3). Figure 1 illustrates the latter part of this trend, showing 20 years of stroke mortality rates in West Virginia among men and women. Rates among both men and women decreased in the state rather consistently until 1992, after which slight increases occurred. -1- Even though the mortality rate for stroke declined 12.3% from 1990 to 2000 in the United States, the actual number of stroke deaths rose nearly 10% (2) and stroke-related hospitalizations increased 19% (4). National projections for stroke mortality are bleak.
    [Show full text]
  • Canadian Stroke Best Practice Recommendations
    CANADIAN STROKE BEST PRACTICE RECOMMENDATIONS MANAGEMENT OF SPONTANEOUS INTRACEREBRAL HEMORRHAGE Seventh Edition - New Module 2020 Ashkan Shoamanesh (Co-chair), M. Patrice Lindsay, Lana A Castellucci, Anne Cayley, Mark Crowther, Kerstin de Wit, Shane W English, Sharon Hoosein, Thien Huynh, Michael Kelly, Cian J O’Kelly, Jeanne Teitelbaum, Samuel Yip, Dar Dowlatshahi, Eric E Smith, Norine Foley, Aleksandra Pikula, Anita Mountain, Gord Gubitz and Laura C. Gioia(Co-chair), on behalf of the Canadian Stroke Best Practices Advisory Committee in collaboration with the Canadian Stroke Consortium and the Canadian Hemorrhagic Stroke Trials Initiative Network (CoHESIVE). © 2020 Heart & Stroke October 2020 Heart and Stroke Foundation Management of Spontaneous Intracerebral Hemorrhage Canadian Stroke Best Practice Recommendations Table of Contents CANADIAN STROKE BEST PRACTICE RECOMMENDATIONS MANAGEMENT OF SPONTANEOUS INTRACERBRAL HEMORRHAGE SEVENTH EDITION, 2020 Table of Contents Topic Page Part One: Canadian Stroke Best Practice Recommendations Introduction and Overview I. Introduction 3 II. Spontaneous Intracerebral Hemorrhage Module Overview 3 III. Spontaneous Intracerebral Hemorrhage Definitions 4 IV. Guideline Development Methodology 4 V. Acknowledgements, Funding, Citation 6 VI. Figure One: Intracerebral Hemorrhage Patient Flow Map 8 Part Two: Canadian Stroke Best Practice Recommendations Spontaneous Intracerebral Hemorrhage 1. Emergency Management of Intracerebral Hemorrhage 9 1.1 Initial Clinical Assessment of Intracerebral Hemorrhage 9 1.2 Blood Pressure Management 10 1.3 Management of Anticoagulation 11 1.4 Consultation with Neurosurgery 12 1.5 Neuroimaging 12 1.5.1 Recommended additional urgent neuroimaging to confirm ICH diagnosis 12 1.5.2 Recommended additional etiological neuroimaging 13 1.6 Surgical management of Intracerebral Hemorrhage 13 Box One: Symptoms of Intracerebral Hemorrhage: 15 Box Two: Modified Boston Criteria (Linn 2010) 16 2.
    [Show full text]
  • Your Health Matters Intracerebral Hemorrhage (ICH)
    Your Health Matters Intracerebral Hemorrhage (ICH) Overview Intracerebral hemorrhage happens when a diseased blood vessel inside the brain bursts, letting the blood leak inside the brain. (The name means within the cerebrum or brain). This problem is also called a hemorrhagic stroke. The sudden increase in pressure inside the brain can cause damage to the brain cells exposed to the blood. If the amount of blood increases too fast, the sudden buildup in pressure can lead to unconsciousness or death. Intracerebral hemorrhage usually happens in selected parts of the brain, including the basal ganglia, cerebellum, brain stem, or cortex. *The most common cause of intracerebral hemorrhage is high blood pressure. Since high blood pressure by itself often causes no symptoms, many people with intracranial hemorrhage are not aware that they have high blood pressure, or that it needs to be treated. Less common causes of intracerebral hemorrhage include trauma, infections, tumors, blood clotting deficiencies, drug abuse and abnormalities in blood vessels (such as an aneurysm or arteriovenous malformations AKA “AVM”). Symptoms **Symptoms usually come on suddenly and can change depending on the location of the bleed. They may sometimes develop in a stepwise pattern, or they may get worse over time. Common symptoms include: • Sudden weakness or numbness of face, arm or leg; especially if the numbness is all on one side of the body • Sudden confusion, trouble speaking or understanding • Sudden trouble seeing in one or both eyes • Sudden trouble walking,PROOF
    [Show full text]
  • Migraine with Vasospasm and Delayed Intracerebral Hemorrhage
    Migraine With Vasospasm and Delayed Intracerebral Hemorrhage Andrew J. Cole, MD, Michel Aub\l=e'\,MD \s=b\Three women with well-documented brain-stem lesions have each been de¬ difficult to arouse, and was again brought to migraine associated with intracerebral scribed. In the majority, neurological the emergency department. She was hyper- hemorrhage are described. In each case, dysfunction is attributed to ischemie tesive, bradycardic, and stuporous, but, af¬ ter was able to follow migraine headaches began during adult- stroke, presumably secondary to vas¬ stimulation, simple commands. She had a dense left hemiplegia hood. Unusually severe and protracted cular spasm. Intracerebral hemor¬ associated with a left-sided homonymous headache heralded the onset of fixed neu- in has rhage migrainous patients only hemianopia and right gaze preference. rological deficits associated with lobar in- rarely been reported,7 and has some¬ Brain computed tomographic scanning tracerebral carotid hemorrhage. Striking times been associated with preexisting demonstrated a right frontoparietal intra¬ artery tenderness was characteristic. Ex- arteriovenous malformations.8·9 This cerebral hemorrhage (Fig 1, center). A ca¬ cept for a history of migraine, no cause for article describes a group of patients, rotid arteriogram showed narrowing of the intracerebral hemorrhage could be estab- all of whom are female, affected with Ml segment of the right middle cerebral lished. In each case arteriography showed migraine who presented with lobar in¬ artery (Fig 1, right). There was mass effect related to the but no evidence of extensive spasm of the appropriate ex- tracerebral hemorrhage either during hematoma, arteriovenous or tracranial or intracranial artery. Surgical or mi¬ malformation, aneurysm, immediately following typical tumor.
    [Show full text]
  • Endovascular Management of Acute Epidural Hematomas: Clinical Experience with 80 Cases
    CLINICAL ARTICLE J Neurosurg 128:1044–1050, 2018 Endovascular management of acute epidural hematomas: clinical experience with 80 cases Carlos Michel A. Peres, MD,1 Jose Guilherme M. P. Caldas, MD, PhD,2 Paulo Puglia Jr., MD,2 Almir F. de Andrade, MD, PhD,3 Igor A. F. da Silva, MD,3 Manoel J. Teixeira, MD, PhD,3 and Eberval G. Figueiredo, MD, PhD3 1Hospital Universitário Francisca Mendes, Manaus; and Divisions of 2Neuroradiology and 3Neurosurgery, University of São Paulo School of Medicine, São Paulo, Brazil OBJECTIVE Small acute epidural hematomas (EDHs) treated conservatively carry a nonmeasurable risk of late en- largement due to middle meningeal artery (MMA) lesions. Patients with EDHs need to stay hospitalized for several days, with neurological supervision and repeated CT scans. In this study, the authors analyzed the safety and efficacy of the embolization of the involved MMA and associated lesions. METHODS The study group consisted of 80 consecutive patients harboring small- to medium-sized EDHs treated by MMA embolization between January 2010 and December 2014. A literature review cohort was used as a control group. RESULTS The causes of head injury were falls, traffic-related accidents (including car, motorcycle, and pedestrian vs vehicle accidents), and assaults. The EDH topography was mainly temporal (lateral or pole). Active contrast leaking from the MMA was seen in 57.5%; arteriovenous fistulas between the MMA and diploic veins were seen in 10%; and MMA pseudoaneurysms were found in 13.6% of the cases. Embolizations were performed under local anesthesia in 80% of the cases, with N-butyl-2-cyanoacrylate, polyvinyl alcohol particles, or gelatin sponge (or a combination of these), obtaining MMA occlusion and complete resolution of the vascular lesions.
    [Show full text]
  • Intracranial Hemorrhage
    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
    [Show full text]
  • Primary Intracerebral and Subarachnoid Hemorrhage
    PRIMARY INTRACEREBRAL AND SUBARACHNOID HEMORRHAGE AN APPROACH TO DIAGNOSIS AND THERAPY MARC FISHER * SUMMARY — The diagnosis of primary intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH) has become easier with the advent of modern imaging techniques. The incidence of ICH has declined, while SAH has remained relatively constant. The prognosis for both disorders remains dismal and the mortality rate is substantially higher than that observed with ischemic stroke. Early imaging with CT or MRI is important for rapid and accurate diagnosis. General medical management in a skilled nursing facility should be available for patients who are not moribund. Therapy for ICH is predominantly supportive and effective medical and surgical intervention remains elusive. For SAH, calcium channel blockers may reduce cerebral ischemic complications related to vasospasm, but effective medical therapy to prevent rebleeding has not been established. Early surgery after SAH should be considered in clinically stable patients. Many challenges remain regarding the prevention and treatment of both these cerebral hemorrhage subtypes. Hemorragia intracerebral primária e subaracnóidea: uma avaliação do diagnóstico e da terapêutica. RESUMO — O diagnóstico da hemorragia intracerebral primária (HIP), bem como o da hemorragia subaracnóidea (HSA), ficou mais fácil com o advento das modernas técnicas de imagem. A incidência da HIC tem declinado, ao passo que a da HSA tem permanecido relativamente constante. O prognóstico de ambas ainda é desanimador e a taxa de morta­ lidade substancialmente maior que a observada nas afecções isquêmicas. A indicação pre­ coce da TC ou da RNM do crânio é importante para um diagnóstico rápido e preciso. Pacientes que não estejam moribundos devem receber cuidados médicos gerais em instalações com equipes de enfermagem especializada.
    [Show full text]
  • Acute Headache Due to Intracerebral Hemorrhage Secondary to Brain Metastases
    Open Access Case Report DOI: 10.7759/cureus.16889 Acute Headache Due to Intracerebral Hemorrhage Secondary to Brain Metastases Zachary J. Cohen-Neamie 1 , Latha Ganti 2, 3, 4, 5 , Thor S. Stead 6 , Joshua Walker 4, 2, 7 , Frank Fraunfelter 4, 2, 8 1. Emergency Medicine, Trinity Preparatory School, Maitland, USA 2. Emergency Medicine, Envision Physician Services, Plantation, USA 3. Emergency Medicine, University of Central Florida College of Medicine, Orlando, USA 4. Emergency Medicine, Ocala Regional Medical Center, Ocala, USA 5. Emergency Medicine, HCA Healthcare Graduate Medical Education Consortium Emergency Medicine Residency Program of Greater Orlando, Olrando, USA 6. Medicine, Warren Alpert Medical School, Providence, USA 7. Emergency Medicine, University of Central Florida, Orlando, USA 8. Emergency Medicine, University of Central Florida, Providence, USA Corresponding author: Latha Ganti, [email protected] Abstract Intracerebral hemorrhage (ICH) is a relatively common condition seen throughout the world, with the vast majority of cases referring to primary ICH. However, secondary ICH from other underlying conditions is also possible. In the present case, the patient presented with severe headaches. An initial computed tomography (CT) was taken which showed hyperdense regions in both the occipital lobe and right lateral ventricle. The patient was hypertensive upon arrival, so medication was given to lower his blood pressure. Due to the patient’s history of hypertension, it was believed to be a case of primary ICH caused by high blood pressure, but because of the odd positioning of the hemorrhaging, it was recommended for magnetic resonance imaging (MRI) and angiography (MRA) to be taken. Using the MRI and MRA, it was found out that growing nodes were responsible for the hypodense regions on the CT.
    [Show full text]
  • Traumatic Intraventricular Hemorrhage in Severe Blunt Head Trauma: a One Year Analysis
    Medical Journal of the Volume 20 Islamic Republic of Iran Number 1 Spring 1385 May 2006 TRAUMATIC INTRAVENTRICULAR HEMORRHAGE IN SEVERE BLUNT HEAD TRAUMA: A ONE YEAR ANALYSIS G.R. BAHADORKHAN, M.D.* From Dept. of Neurosurgery, Mashhad University of Medical Sciences, P.O. Box 91375-3983, Mashhad, I.R. Iran. ABSTRACT Background: High resolution CT scan has made early diagnosis of intra- ventricular hemorrhage (IVH) easier. Posttraumatic intraventricular hemor- rhage has been reported to a greater extent because of the CT scan. Methods: 904 patients were admitted in the NSICU from March 2001 to March 2002 with severe closed head injury, of those only 31 patients with in- traventricular hemorrhage (GCS less than 8) are reported herein and the mechanism involved is discussed. Results: Nine cases had intracerebral hemorrhage (contusional group), four cases in the frontal lobe, three cases in the temporal lobe and two cases in the parietal lobe. Nine cases (basal ganglia hemorrhage group) had hemorrhage in basal ganglia, six in the caudate nucleus and three in the thalamus, all spread- ing into the ventricles. In thirteen cases the original site of hemorrhage could not be determined. In this group six cases had accompanying peri-brain stem hemorrhage (peri-brain stem hemorrhage group) and different brain stem injury signs. Four cases had IVH less than 5 mL with or without minor intracranial le- sions (minor intracranial lesion group). Accompanying major intracranial hem- orrhage was found in sixteen cases, six cases had epidural hematoma, four cases had subdural hematoma, and seven had a combination of ASDH, EDH and contusional prarenchymal hemorrhages, all requiring primary surgical evacuation, and seven cases had different degrees of minor abnormalities (i.e.
    [Show full text]