Signs And Symptoms Of Cerebral Edema In Dka

Diabetic Ketoacidosis/cerebral Edema

How can diabetic ketoacidosisrelated cerebral edema be prevented? OVERVIEW: What every practitioner needs to know Are you sure your patient has diabetic ketoacidosisrelated cerebral edema? What are the typical findings for this disease? Cerebral edema is a potentially life-threatening complication of diabetic ketoacidosis (DKA) and is responsible for the majority of diabetes-related deaths in children. Cerebral edema typically occurs after several hours of treatment with insulin and intravenous fluids but can also occur at the time of presentation of DKA before treatment is started. The risk of cerebral edema is related to the severity of acidosis, hypocapnia, and dehydration at the time of presentation of DKA. Although severe, clinically apparent cerebral edema occurs in just 1% of DKA episodes in children, numerous studies have demonstrated that mild cerebral edema, associated with only minimal or no alterations in mental status, is present in the majority of children during DKA treatment. The relationship between intravenous fluid treatment and the risk of DKA-related cerebral edema is frequently debated; however, there are no clear associations between the use of particular fluid treatment protocols and increased risk of DKA-related cerebral edema. At present, whether and how cerebral edema can be prevented is unknown. Treatment for clinically apparent cerebral edema typically involves use of hyperosmolar agents (mannitol or hypertonic saline). DKA-related cerebral edema is a clinical diagnosis. Imaging studies may be helpful but are not always definitive. The most common symptoms of DKA-related cerebral edema include mental status changes (confusion, irritability, obtundation) associated with severe headache, recurrence of vomiting, seizures, hypertension, inappro Continue reading >>

Pediatric Diabetic Ketoacidosis

Author: William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH; Chief Editor: Timothy E Corden, MD more... Diabetic ketoacidosis, in pediatric and adult cases, is a metabolic derangement caused by the absolute or relative deficiency of the anabolic hormone insulin. Together with the major complication of cerebral edema, it is the most important cause of mortality and severe morbidity in children with diabetes. Symptoms of acidosis and dehydration include the following: Abdominal pain - May be severe enough to present as a surgical emergency Shortness of breath - May be mistaken for primary respiratory distress Confusion and coma in the absence of recognized head injury [ 1 ] Symptoms of hyperglycemia, a consequence of insulin deficiency, include the following: Polyuria - Increased volume and frequency of urination Nocturia and secondary enuresis in a previously continent child Weight loss - May be dramatic due to breakdown of protein and fat stores Patients with diabetic ketoacidosis may also have the following signs and symptoms: Signs of intercurrent infection (eg, urinary or respiratory tract infection) Weakness and nonspecific malaise that may precede other symptoms of hyperglycemia Kussmaul breathing or deep sighing respiration - A mark of acidosis Ketone odor - Patient may have a smell of ketones on his/her breath Impaired consciousness - Occurs in approximately 20% of patients Abdominal tenderness - Usually nonspecific or epigastric in location Most cases of cerebral edema occur 4-12 hours after initiation of treatment. Diagnostic criteria of cerebral edema include the following: Abnormal motor or verbal response to pain Cranial nerve palsy - Especially III, IV, and VI Abnormal neurogenic breathing pattern (eg, Cheyne-Stokes), apneusis Altered mentation, fluctuating Continue reading >>

Risk Factors For Cerebral Edema In Children With Diabetic Ketoacidosis

Cerebral edema is an uncommon but devastating complication of diabetic ketoacidosis in children. Risk factors for this complication have not been clearly defined. In this multicenter study, we identified 61 children who had been hospitalized for diabetic ketoacidosis within a 15-year period and in whom cerebral edema had developed. Two additional groups of children with diabetic ketoacidosis but without cerebral edema were also identified: 181 randomly selected children and 174 children matched to those in the cerebral-edema group with respect to age at presentation, onset of diabetes (established vs. newly diagnosed disease), initial serum glucose concentration, and initial venous pH. Using logistic regression, we compared the three groups with respect to demographic characteristics and biochemical variables at presentation and compared the matched groups with respect to therapeutic interventions and changes in biochemical values during treatment. A comparison of the children in the cerebral-edema group with those in the random control group showed that cerebral edema was significantly associated with lower initial partial pressures of arterial carbon dioxide (relative risk of cerebral edema for each decrease of 7.8 mm Hg [representing 1 SD], 3.4; 95 percent confidence interval, 1.9 to 6.3; P<0.001) and higher initial serum urea nitrogen concentrations (relative risk of cerebral edema for each increase of 9 mg per deciliter [3.2 mmol per liter] [representing 1 SD], 1.7; 95 percent confidence interval, 1.2 to 2.5; P=0.003). A comparison of the children with cerebral edema with those in the matched control group also showed that cerebral edema was associated with lower partial pressures of arterial carbon dioxide and higher serum urea nitrogen concentrations. Of the ther Continue reading >>

Treating Cerebral Edema In Diabetic Ketoacidosis: Caveats In Extrapolating From Traumatic Brain Injury

Treating Cerebral Edema in Diabetic Ketoacidosis: Caveats in Extrapolating from Traumatic Brain Injury Monica S. Vavilala, Departments of Anesthesiology & Pain Medicine and Pediatrics, University of Washington, Seattle, WA; Please direct all correspondence to: Monica S. Vavilala, MD, Professor of Anesthesiology & Pediatrics, Adjunct Professor of Neurological Surgery and Radiology, University of Washington and Harborview Injury Prevention and Research Center, Harborview Medical Center, 325 Ninth Avenue, Box 359724, Seattle, WA 98104, Phone: 206-744-3210, Fax: 206-744-8090, [email protected] The publisher's final edited version of this article is available at Pediatr Crit Care Med See other articles in PMC that cite the published article. When encountering children with diabetic ketoacidosis (DKA), the possibility of DKA related cerebral edema is usually at the forefront of anticipated worries facing treating clinicians. This is because neither the pathophysiology of cerebral edema is well understood, nor are proven treatments for cerebral edema available. Both these gaps force clinicians to rely on either theoretical conceptual frameworks of other neurological diseases or a given body of general knowledge of pharmacological agents to address this devastating complication in DKA. Evidence suggests that an ischemic ( 1 ) and/or vasogenic ( 2 ) process play a role in the genesis of DKA related cerebral edema, but details of the time course of these processes are not clear. Thus, clinicians are left with employing treatment strategies in DKA with some level of scientific evidence from other neurological conditions where cerebral edema occurs. In children, the reference disease state is typically traumatic brain injury (TBI). The issue of how best to prevent or treat Continue reading >>

Ketoacidosis

Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition), 2017 Introduction Although ketoacidosis is a form of metabolic acidosis because of the addition of acids, it is discussed separately in this chapter to emphasize the metabolic and biochemical issues required to understand the clinical aspects of this disorder (see margin note). We discuss the metabolic setting that is required to allow for the formation of ketoacids in the liver at a high rate and what sets the limit on the rate of production. Removal of ketoacids occurs mainly in the brain and kidneys. We examine what sets the limit on the rate of removal of ketoacids by these organs. We believe that understanding the biochemical and metabolic aspects of ketoacidsis provides the clinician with a better understanding of this disorder and allows for a better design of therapy in the individual patient with ketoacidosis. Relevant to the pathophysiology of this case, the soft drinks the patient consumed contained a large quantity of glucose, fructose, and caffeine. Ketoacids • A ketone is an organic compound that has a keto group (C=O) on an internal carbon atom. • Acetone is a ketone but not an acid. • Only acetoacetic acid is a ketoacid. β-Hydroxybutyric acid has a hydroxyl group (C–OH) on its internal carbon, so it is a hydroxy acid and not a ketoacid. Abbreviations β-HB, beta hydroxybutyrate anion AcAc, acetoacetate anion ADP, adenosine diphosphate ATP, adenosine triphosphate NAD+, nicotinamide adenine dinucleotide NADH,H+, reduced form of NAD+ FAD, flavin adenine dinucleotide FADH2, hydroxyquinone form of FAD EABV, effective arterial blood volume PAnion gap, plasma anion gap PGlucose, concentration of glucose in plasma POsmolal gap, plasm Continue reading >>

Children's Mercy Kansas City - Cerebral Edema Therapy

Those at increased risk include younger age (<5 y/o), newonset diabetes, and longer duration of symptoms. Additional risk factors at diagnosis or during treatmentinclude - more severe acidosis or very elevated BUN atpresentation, use of bicarbonate for treatment of acidosis, greatervolumes of fluid given in the first 4 hours of treatment,administration of short acting insulin in the first hour of fluidtreatment. Signs and symptoms - headache, slowing or irregular heart rate,change in neurologic status (restlessness, irritability, increaseddrowsiness, incontinence), cranial nerve palsies or other specificneurologic signs, increasing blood pressure, decreased oxygensaturation. One diagnostic criterion, 2 major criteria, or one major and 2minor criteria have a sensitivity of 92% and a false positive rateof only 4% for detecting cerebral edema. Diagnostic criteria - abnormal motor or verbal response topain, decorticate or decerebrate posture, cranial nerve palsy,abnormal neurogenic respiratory pattern (grunting, tachypnea) Major criteria - altered mental status, fluctuating level ofconsciousness, sustained heart rate deceleration (decrease morethan 20 beats per minute) not attributable to improved hydration orsleep, age-inappropriate incontinence Minor criteria - vomiting, headache, lethargy, diastolic BP>90 mm Hg, age <5 years. Begin immediate transfer to pediatric intensive care unit ifpatient is currently on a medical/surgical unit. Give mannitol 0.5-1 g/kg IV over 20 minutes Hypertonic saline (3%), 5-10 mL/kg over 30 minutes may be usedas an alternative to mannitol Obtain CT head after treatment has been started to rule outother possible intracerebral causes of neurologic deterioration(thrombosis or hemorrhage). These guidelines do not establish a standard of care to b Continue reading >>

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Cerebral Edema In Diabetic Ketoacidosis.

1. Pediatr Crit Care Med. 2008 May;9(3):320-9. doi: 10.1097/PCC.0b013e31816c7082. (1)Dartmouth Medical School, Lebanon, NH, USA. [email protected] Erratum in Pediatr Crit Care Med. 2009 May;10(3):429.Comment in Pediatr Crit Care Med. 2009 Mar;10(2):276; author reply 276. OBJECTIVE: To review the causes of cerebral edema in diabetic ketoacidosis(CEDKA), including pathophysiology, risk factors, and proposed mechanisms, toreview the diagnosis, treatment, and prognosis of CEDKA and the treatment ofdiabetic ketoacidosis as it pertains to prevention of cerebral edema.DATA SOURCE: A MEDLINE search using OVID was done through 2006 using the searchterms cerebral edema and diabetic ketoacidosis. RESULTS OF SEARCH: There were 191citations identified, of which 150 were used. An additional 42 references listed in publications thus identified were also reviewed, and two book chapters wereused.STUDY SELECTION: The citations were reviewed by the author. All citationsidentified were used except 25 in foreign languages and 16 that were duplicatesor had inappropriate titles and/or subject matter. Of the 194 references, therewere 21 preclinical and 40 clinical studies, 35 reviews, 15 editorials, 43 casereports, 29 letters, three abstracts, six commentaries, and two book chapters.DATA SYNTHESIS: The data are summarized in discussion.CONCLUSIONS: The causes and mechanisms of CEDKA are unknown. CEDKA may be due as much to individual biological variance as to severity of underlying metabolicderangement of the child's state and/or treatment risk factors. Treatmentrecommendations for CEDKA and diabetic ketoacidosis are made taking intoconsideration possible mechanisms and risk factors but are intended as generalguidelines only in view of the absence of conclusive evidence. Continue reading >>

Cerebral Edema In Dka

Please donate! Funds go solely to hosting and development costs that allow medical practitioners around the globe to freely access WikEM. Almost all affected patients are <20yr [2] Associated with initial bicarb level; not rate of glucose drop Overaggressive fluid resuscitation is NOT a risk factor Begins 6-12hr after onset of therapy or may begin before initiation of treatment or up to 48h afterward Many appear to be improving from their DKA before deteriorating from cerebral edema Mannitol 0.5-1gm/kg IV bolus over 20 minutes Give a repeat does if there is an inadequate response If 2 doses of mannitol are ineffective, consider 3% saline 10mL/kg over 30min Fluid restriction - decrease the IVF infusion rate by 30% Treat noncardiogenic pulmonary edema , if present Cooke & Plotnick. Management of diabetic ketoacidosis in children and adolescents. Pediatr Rev. 2008 Dec;29(12):431-5 Glaser NS, Wootton-Gorges SL, Buonocore MH, Marcin JP, Rewers A, Strain J, et al. Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis. Pediatr Diabetes. Apr 2006;7(2):75-80. Cooke & Plotnick. Management of diabetic ketoacidosis in children and adolescents. Pediatr Rev. 2008 Dec;29(12):431-5 Continue reading >>

Aetiology Of Cerebral Oedema In Diabetic Ketoacidosis | Emergency Medicine Journal

Aetiology of cerebral oedema in diabetic ketoacidosis Aetiology of cerebral oedema in diabetic ketoacidosis Department of Emergency Medicine, Royal Brisbane Hospital, Herston, Brisbane, Queensland 4029, Australia; af.brownuq.edu.au The excellent evidence based review of the emergency management of diabetic ketoacidosis (DKA) in adults by Hardern and Quinn perpetuates the premise that unnecessarily large volumes of intravenous fluids should be avoided because of the high case fatality rate of cerebral oedema. 1 This presupposes that the rate of fluid delivery is causally related to the development of cerebral oedema, which has not been proved. The large 15 year paediatric study in the USA that analysed 6977 hospitalisations for DKA found among the 61 cases of cerebral oedema (0.9%) that after multiple logistic-regression analysis with random and matched controls, the only variables statistically associated with cerebral oedema were higher initial serum urea nitrogen concentrations and lower partial pressures of carbon dioxide at presentation. 2 In addition, smaller increases in serum sodium concentration during treatment and the use of bicarbonate were also implicated. Importantly, the rate of fluid, sodium, and insulin administration were not associated with the development of cerebral oedema, nor was the initial serum glucose or its rate of change. Clearly these findings relate to patients aged 18 years or less but most occurrences of cerebral oedema in DKA are in children and adolescents, with only rare cases in adults. However, the underlying aetiology should be no different. One unifying hypothesis is that the cerebral oedema is related to cerebral vasoconstriction, brain ischaemia, and hypoxia, as hypocapnoea causing cerebral vasoconstriction and extreme dehydrati Continue reading >>

Symptomatic Cerebral Oedema During Treatment Of Diabetic Ketoacidosis: Effect Of Adjuvant Octreotide Infusion

Abstract A potentially lethal complication of diabetic ketoacidosis (DKA) in children is brain oedema, whether caused by DKA itself or by the therapeutic infusion of insulin and fluids. A 10-year old previously healthy boy with DKA became unconscious and apnoeic due to cerebral oedema (confirmed by abnormal EEG and CT-scan) during treatment with intravenous fluids (36 ml/h) and insulin (0.1 units/kg/h). He was intubated and artificially ventilated, without impact on EEG and CT-scan. Subsequently, adjuvant infusion of octreotide was applied (3.5 μg/kg/h), suppressing growth hormone (GH) and IGF-1 production and necessitating the insulin dose to be reduced to 0.05 - 0.025 units/kg/h. The brain oedema improved and the boy made a full recovery. Co-therapy with octreotide was associated with a favourable outcome in the present patient with DKA and cerebral oedema. Whether this could be ascribed to the effects of octreotide on the insulin requirement or on the GH/IGF-axis remains to be elucidated. Introduction Cerebral oedema is the most feared complication of DKA. The pathogenesis appears complex and is poorly understood [1]. According to a recent working hypothesis, dehydration and hypocapnia diminish cerebral perfusion, resulting in mild brain ischaemia and subsequent cytotoxic and vasogenic cerebral oedema [1]. In this context, hypoxia-induced VEGF activity may play a role [2]. Insulin treatment might also contribute, for example via its sodium-retaining effects, or by its effects on the growth hormone (GH)/insulin-like growth factor (IGF)-axis [3]. Insulin increases serum IGF-1 and decreases IGFBP-1, thereby increasing free IGF-1 activity. IGF-1 increases capillary permeability [4] and oedema formation [5, 6], probably via increasing the activity of VEGF [7, 8]. As insu Continue reading >>

Unusual Case Of New Onset Diabetes Mellitus Presenting With Diabetic Ketoacidosis And Cerebral Edema With Literature Review

Nitasa Sahu*, Emma Punni, Chandra Chandran and Medhat Ismail Department of Internal Medicine, St. Joseph’s Regional Medical Center, New York Medical College, Paterson, USA Citation: Sahu N, Punni E, Chandran C, Ismail M (2016) Unusual Case of New Onset Diabetes Mellitus Presenting with Diabetic Ketoacidosis and Cerebral Edema with Literature Review. J Nephrol Ther 6: 262. doi:10.4172/2161-0959.1000262 Copyright: © 2016 Sahu N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License; which permits unrestricted use; distribution; and reproduction in any medium; provided the original author and source are credited. Visit for more related articles at Journal of Nephrology & Therapeutics Abstract Diabetic ketoacidosis (DKA) is typically treated with volume replacement (most commonly normal saline), insulin and monitored via serial chemistry and glucose lab values. Cerebral edema, a complication occurring in approximately 1% of DKA presentations in children, with a mortality of 40-90%, has no clear identifiable risk factors. While many cases have been reported in children, there are only a few cases of clinically significant cerebral edema in adults. It is postulated the underlying mechanism is similar to that in children; excessive fluid resuscitation, rapid reduction in plasma osmolarity, and/or the administration of sodium bicarbonate. We are reporting a case of a 26 year old male with no prior medical history, who presented in diabetic ketoacidosis and was treated as per the American Diabetic Association guidelines, however, deteriorated rapidly after acute complaints of headache and irritability consistent with diffuse cerebral edema. Keywords Diabetic ketoacidosis; Cerebral edema; Adult; Mortality Introduction Dia Continue reading >>

Cerebral Edema In Diabetic Ketoacidosis: A Look Beyond Rehydration

Cerebral Edema in Diabetic Ketoacidosis: A Look Beyond Rehydration Department of Pediatrics University of Florida Gainesville, Florida 32610 Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 509513, Andrew Muir; Cerebral Edema in Diabetic Ketoacidosis: A Look Beyond Rehydration, The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 509513, INJUDICIOUS fluid resuscitation is frequently suggested as the cause of the cerebral edema that is the most common cause of mortality among pediatric patients with diabetic ketoacidosis (DKA) ( 1 ). The evidence, however, supports the hypothesis that neurological demise in DKA is a multifactorial process that cannot be reliably prevented by cautious rehydration protocols. Mortality and severe morbidity can, however, be reduced when healthcare providers watch vigilantly for and respond rapidly to the sentinel neurological signs and symptoms that precede, often by hours, the dramatic collapse that is typically described in these patients. Children being treated for DKA develop clinically important neurological compromise about 0.21.0% of the time ( 2 ). Subclinical neurological pathology, causing raised intracranial pressure, likely precedes the initiation of therapy in almost all cases of DKA ( 3 5 ). Intracranial hypertension has been considered to be aggravated by therapy of the DKA ( 4 , 6 , 7 ), but in keeping with the physicians perplexity about the problem, even this widely held tenet has recently been challenged ( 8 ). The pathogenic mechanism for this terrifying complication remains unknown. Hypothetical causes of cerebral edema in children with DKA must account for: 1) its occurrence (with rare excep Continue reading >>

Pediatric Diabetic Ketoacidosistreatment & Management

Pediatric Diabetic KetoacidosisTreatment & Management Author: William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH; Chief Editor: Timothy E Corden, MD more... In patients with diabetic ketoacidosis, the first principals of resuscitation apply (ie, the ABCs [airway, breathing, circulation]). [ 3 ] Outcomes are best when children are closely monitored and a changing status is promptly addressed. [ 39 , 2 ] Give oxygen, although this has no effect on the respiratory drive of acidosis. Diagnose by clinical history, physical signs, and elevated blood glucose. Fluid, insulin, and electrolyte (potassium and, in select cases, bicarbonate) replacement is essential in the treatment of diabetic ketoacidosis. Early in the treatment of diabetic ketoacidosis, when blood glucose levels are very elevated, the child can continue to experience massive fluid losses and deteriorate. Strict measurement of fluid balance is essential for optimal treatment. Continuous subcutaneous insulin infusion therapy using an insulin pump should be stopped during the treatment of diabetic ketoacidosis. Children with severe acidosis (ie, pH < 7.1) or with altered consciousness should be admitted to a pediatric intensive care unit. In cases in which the occurrence of diabetic ketoacidosis signals a new diagnosis of diabetes, the process of education and support by the diabetes team should begin when the patient recovers. In cases in which diabetic ketoacidosis occurs in a child with established diabetes, explore the cause of the episode and take steps to prevent a recurrence. Following recovery from diabetic ketoacidosis, patients require subcutaneous insulin therapy. Edge JA, Roy Y, Bergomi A, et al. Conscious level in children with diabetic ketoacidosis is related to severity of acidosis and not to blood g Continue reading >>

Cerebral Edema And Diabetic Ketoacidosis

Cerebral edema is the most feared emergent complication of pediatric diabetic ketoacidosis. Fortunately, it is relatively rare, but the rarity can lead to some confusion when it comes to its management. We recently discussed the use of mannitol and hypertonic saline for pediatric traumatic brain injury, but when should we consider these medications for the patient presenting with DKA? Cerebral Edema is a relatively rare. Incidence <1% of patients with DKA. Overall tends to occur in the newly diagnosed diabetic patient (4.3% vs 1.2%). While rare, it is a devastating complication. 1990 study showed case fatality rate was 64%. Those treated BEFORE respiratory failure had lower rate of mortality (30%). Lesson = treat early! The exact mechanism is not known… and may be varied between individual patients. Signs and Symptoms develop in: 66% within the first 7 hours of treatment (these tend to be younger). 33% within 10-24 hours of treatment. The diagnosis is clinical! ~40% of initial brain imaging of kids with cerebral edema are NORMAL! This is the area that often leads to finger pointing… most often those fingers being pointed toward the Emergency Physician who was initially caring for the kid. Much of the literature focused on interventions, but: Administration of Bicarb Sodium Bicarb was shown to be associated with Cerebral Edema in one study… Unfortunately, this study did not adjust for illness severity. Type of IV Fluids Generally, there is an absence of evidence that associates volume, tonicity, or rate change in serum glucose with Cerebral Edema development. There are cases presenting with cerebral edema prior to any therapies. Risk Factors that seem to stay consistent: Kids < 5 years of age More likely to have delayed diagnosis More severely ill at presentation S Continue reading >>