Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
The Child with Hematologic or Immunologic Dysfunction Chapter 35 Assessment of Hematologic Function Complete blood count History and assessment findings Child’s energy and activity level Growth patterns Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 2 Anemia The most common hematologic disorder of childhood Decrease in number of RBCs and/or hemoglobin concentration below normal Decreased oxygen-carrying capacity of blood Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 3 Classification of Anemias Etiology and physiology RBC and/or Hgb depletion Morphology Characteristic changes in RBC size, shape, and/or color Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 4 Consequences of Anemia Decrease in oxygen-carrying capacity of blood and decreased amount of oxygen available to tissues When anemia develops slowly, child adapts Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 5 Effects of Anemia on Circulatory System Hemodilution Decreased peripheral resistance Increased cardiac circulation and turbulence May have murmur May lead to cardiac failure Cyanosis Growth retardation Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 6 Diagnostic Evaluation CBC Decreased RBCs Decreased Hbg and Hct Other tests for particular type of anemia Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 7 Therapeutic Management Treat underlying cause Transfusion after hemorrhage if needed Nutritional intervention for deficiency anemias Supportive care IV fluids to replace intravascular volume Oxygen Bed rest Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 8 Nursing Considerations Prepare child and family for laboratory tests Decrease oxygen demands Prevent complications Support family Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 9 Blood Transfusion Therapy Verify identity of recipient and donor’s blood group Monitor VS Use appropriate filter Use blood within 30 minutes of arrival Infuse over 4 hours maximum Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 10 Transfusion Reactions Hemolytic: the most severe, but rare Febrile reactions: fever, chills Allergic reactions: urticaria, pruritus, laryngeal edema Air emboli: may occur when blood is transfused under pressure Hypothermia Electrolyte disturbances: hyperkalemia from massive transfusions or with renal problems Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 11 Nursing Responsibilities Identify donor and recipient blood types and groups before transfusing Transfuse slowly for first 15 to 20 minutes Observe carefully for patient response Stop transfusion immediately if signs or symptoms of transfusion reaction; notify practitioner Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 12 Delayed Reactions to Blood Transfusion Transmission of infection Hepatitis, HIV, malaria, syphilis, other Blood banks test vigorously and discard units of infected blood Delayed hemolytic reaction Destruction of RBCs and fever 5 to 10 days after transfusion Observe for posttransfusion anemia Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 13 Family Concerns Difficult decision for HTSC transplant Child faces death without the transplant Preparing the child for transplant places the child at great risk No “rescue” procedure if complications follow HTSC transplants Nursing considerations Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 14 Apheresis Definition: the removal of blood from an individual; separation of the blood into its components Nursing considerations Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 15 Iron Deficiency Anemia Caused by inadequate supply of dietary iron Generally is preventable Iron-fortified cereals and formulas for infants Special needs of premature infants Adolescents at risk due to rapid growth and poor eating habits Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 16 Iron Deficiency Anemia (cont.) Pathophysiology Therapeutic management Prognosis Nursing considerations Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 17 Sickle Cell Anemia A hereditary hemoglobinopathy Ethnicity Occurs primarily in African-Americans • Occurrence 1 in 375 infants born in U.S. • 1 in 12 have sickle cell trait • Occasionally also in people of Mediterranean descent • Also seen in South American, Arabian, and East Indian descent Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 18 Etiology of Sickle Cell In areas of the world where malaria is common, individuals with sickle cell trait tend to have a survival advantage over those without the trait Autosomal recessive disorder 1 in 12 African-Americans are carriers (have sickle cell trait) If both parents have trait, each offspring will have 1 in 4 likelihood of having disease Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 19 Pathophysiology Partial or complete replacement of normal Hgb with abnormal hemoglobin S (HgbS) Hemoglobin in the RBCs takes on an elongated (“sickle”) shape Sickled cells are rigid and obstruct capillary blood flow Microscopic obstructions lead to engorgement and tissue ischemia Hypoxia occurs and causes sickling Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 20 Sickled Hemoglobin Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 21 Pathophysiology Large tissue infarctions occur Damaged tissues in organs lead to impaired function Splenic sequestration • May require splenectomy at early age • Results in decreased immunity Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 22 Prognosis No cure (except possibly bone marrow transplants) Supportive care/prevent sickling episodes Frequent bacterial infections may occur due to immunocompromise Bacterial infection is leading cause of death in young children with sickle cell disease Strokes in 5% to 10% of children with disease Result in neurodevelopmental delay, mental retardation Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 23 Sickle Cell Crisis Precipitating factors Anything that increases the body’s need for oxygen or alters transport of oxygen Trauma Infection, fever Physical and emotional stress Increased blood viscosity due to dehydration Hypoxia • From high altitude, poorly pressurized airplanes, hypoventilation, vasoconstriction due to hypothermia Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 24 Sickle Cell Crisis (cont.) Acute exacerbations that vary in severity and frequency Types Vaso-occlusive (VOC) thrombotic • Most common type of crisis—very painful • Stasis of blood with clumping of cells in microcirculation → ischemia → infarction • Signs: fever, pain, tissue engorgement Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 25 Sickle Cell Crisis (cont.) Types (cont.) Splenic sequestration • Life threatening—death can occur within hours • Blood pools in the spleen • Signs: Profound anemia, hypovolemia, shock Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 26 Sickle Cell Crisis (cont.) Types (cont.) Aplastic crises • Diminished production and increased destruction of RBCs • Triggered by viral infection or depletion of folic acid • Signs include profound anemia, pallor Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 27 Diagnosis of Sickle Cell Cord blood in newborns Newborn screening done in 43 states Genetic testing to identify carriers and children who have disease Sickle turbidity test Quick screening purposes in children older than 6 months Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 28 Medical Management Aggressive treatment of infection Possibly prophylactic antibiotics from 2 months to 5 years Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 29 Medical Management (cont.) Monitor reticulocyte count regularly to evaluate bone marrow function Blood transfusion, if given early in crisis, may reduce ischemia Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 30 Medical Management (cont.) Frequent transfusion leads to hemosiderosis (iron in tissues) Treat with iron-chelation such as feroxamine + vitamin C to promote iron excretion Rx—hydronurea (cytotoxic) leads to decreased production of abnormal blood cells and less pain Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 31 Nursing Management Monitor child’s growth—watch for failure to thrive Careful multisystem assessment Assess pain Observe for presence of inflammation or possible infection Carefully monitor for signs of shock Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 32 Sickle Cell Pain Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 33 Psychosocial Needs Coping mechanisms Support with genetic counseling Financial needs? Caregiver role strain Living with chronic illness in the family Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 34 Thalassemia Inherited blood disorders of hemoglobin synthesis Classified by Hgb chain affected and by amount of effect Autosomal recessive with varying expressivity Both parents must be carriers to have offspring with disease Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 35 Pathophysiology Anemia results from defective synthesis of Hgb, structurally impaired RBCs, and shortened life of RBCs Chronic hypoxia Headache, irritability, precordial and bone pain, exercise intolerance, anorexia, epistaxis Detected in infancy or toddlerhood Pallor, FTT, hepatosplenomegaly, severe anemia (Hgb <6) Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 36 Thalassemia -Thalassemia α chains affected Occurs in Chinese, Thai, African, and Mediterranean people -Thalassemia Occurs in Greeks, Italians, and Syrians is most common and has four forms Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 37 -Thalassemia Four types Thalassemia minor: asymptomatic silent carrier Thalassemia trait: mild microcytic anemia Thalassemia intermediate: moderate to severe anemia + splenomegaly Thalassemia major “Cooley anemia”: severe anemia requiring transfusions to survive Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 38 Patient with Thalassemia Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 39 Diagnosis By hemoglobin electrophoresis RBC changes often seen by 6 weeks of age Child presents with severe anemia, FTT Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 40 Medical Management Blood transfusion to maintain normal Hgb levels Side effect—hemosiderosis Treat with iron-chelating drugs such as deferoxamine (Desferal) • Binds excess iron for excretion by kidney Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 41 Nursing Management Observe for complications of transfusion Emotional support to family Encourage genetic counseling Parent and patient teaching for self-care Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 42 Prognosis Retarded growth Delayed or absent secondary sex characteristics Expect to live well into adulthood with proper clinical management Bone marrow transplant is potential cure Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 43 Aplastic Anemia All formed elements of the blood are simultaneously depressed: “pancytopenia” Hypoplastic anemia: profound depression of RBCs but normal WBCs and platelets Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 44 Aplastic Anemia (cont.) Etiology Primary (congenital) Secondary (acquired) Diagnostic evaluation Therapeutic management Nursing considerations Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 45 Hemophilia A group of hereditary bleeding disorders that result from deficiencies of specific clotting factors Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 46 Types of Hemophilia Hemophilia A Classic hemophilia Deficiency of factor VIII Accounts for 80% of cases of hemophilia Occurrence: 1 in 5000 males Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 47 Types of Hemophilia (cont.) Hemophilia B Also known as Christmas disease Caused by deficiency of factor IX Accounts for 15% of cases of hemophilia Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 48 Etiology of Hemophilia A X-linked recessive trait Males are affected Females may be carriers Degree of bleeding depends on amount of clotting factor and severity of a given injury Up to one third of cases have no known family history In these cases disease is caused by a new mutation Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 49 Manifestations Bleeding tendencies from mild to severe Symptoms may not occur until 6 months of age Hemarthrosis Mobility leads to injuries from falls and accidents Bleeding into joint spaces of knee, ankle, elbow, leading to impaired mobility Ecchymosis Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 50 Manifestations (cont.) Epistaxis Bleeding after procedures Minor trauma, tooth extraction, minor surgeries Large subcutaneous and intramuscular hemorrhages may occur Bleeding into neck, chest, mouth may compromise airway Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 51 Clinical Therapy Can be diagnosed through amniocentesis Genetic testing of family members to identify carriers Diagnosis on basis of history, labs, and exam Labs: low levels of factor VIII or IX, prolonged PTT Normal: platelet count, PT, and fibrinogen Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 52 Medical Management DDAVP IV Causes 2 to 4 times increase in factor VIII activity Used for mild hemophilia Replace missing clotting factors Transfusions At home with prompt intervention to decrease complications Following major or minor hemorrhages Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 53 Prognosis Historically, most died by age 5 years Now those with mild to moderate hemophilia live near-normal lives Gene therapy for the future Infuse carrier organisms into patient; these act on target cells to promote manufacture of deficient clotting factor Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 54 Interventions Close supervision and safe environment Dental procedures in controlled situation Shave only with electric razor Superficial bleeding—apply pressure for at least 15 minutes and ice to vasoconstrict If significant bleeding occurs, transfuse for factor replacement Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 55 Managing Hemarthrosis During bleeding episodes, elevate and immobilize the joint Ice Analgesics ROM after bleeding stops to prevent contractures PT Avoid obesity to minimize joint stress Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 56 von Willebrand Disease (vWD) A hereditary bleeding disorder involving deficiency of von Willebrand factor (a plasma protein and the carrier for factor VIII) von Willebrand factor needed for platelet adhesion Transmitted as autosomal dominant trait Occurs in both males and females The gene for the disease is located on chromosome 12 Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 57 Manifestations Easy bruising Epistaxis Gingival bleeding Excessive bleeding with lacerations or surgeries Menorrhagia Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 58 Diagnosis: Laboratory Findings Decreased von Willebrand factor levels von Willebrand antigen levels Decreased platelet agglutination Prolonged bleeding time PTT may be normal or prolonged Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 59 Treatment of vWD Infusion of von Willebrand protein concentrate DDAVP infusion before surgery or to treat bleeding episode Aminocaproic acid to treat bleeding in mucous membranes (in some cases) Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 60 Interventions Avoid aspirin or NSAIDs (increase bleeding time and inhibit platelet function) Manage bleeding episodes with prompt infusion therapy Children with vWD have normal life expectancy if well managed Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 61 Idiopathic Thrombocytopenic Purpura (ITP) An acquired hemorrhagic disorder characterized by: Thrombocytopenia: excessive destruction of platelets Purpura: discoloration caused by petechiae beneath the skin Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 62 ITP Forms Acute, self-limiting Often follows URI or other infection Chronic (more than 6 months’ duration) Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 63 ITP Diagnostic evaluation Therapeutic management Prognosis Nursing considerations Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 64 Disseminated Intravascular Coagulation (DIC) A disorder of coagulation that occurs as a complication of numerous pathologic processes Hypoxia Acidosis Shock Endothelial damage Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 65 Pathophysiology of DIC Coagulation process is abnormally stimulated Excessive amounts of thrombin are generated Fibrinolytic mechanisms are activated and cause extensive destruction of clotting factors Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 66 Mechanisms of DIC Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 67 DIC Diagnostic evaluation Therapeutic management Nursing considerations Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 68 Immunologic Deficiency Disorders HIV/AIDS Epidemiology Etiology and pathophysiology Clinical manifestations Diagnostics Therapeutic management Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 69 Components of Immune System Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 70 Common Clinical Manifestations of HIV Infection in Children Lymphadenopathy Hepatosplenomegaly Oral candidiasis Chronic or recurrent diarrhea Failure to thrive Developmental delay Parotitis Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 71 Common AIDS-Defining Conditions in Children Pneumocystis carinii pneumonia Lymphoid interstitial pneumonitis Recurrent bacterial infections Wasting syndrome Candidal esophagitis HIV encephalopathy CMV Cryptosporidiosis Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 72 Severe Combined Immunodeficiency Disease (SCID) Absence of both humoral and cell-mediated immunity Pathophysiology Graft-versus-host reaction Therapeutic management Nursing considerations Mosby items and derived items © 2007, 2003 by Mosby, Inc., an affiliate of Elsevier Inc. Slide 73 Nursing Care of the Child with a Neurologic Disorder Chapter 37 Assessment of Cerebral Function Infants and young children: observe spontaneous and elicited reflex responses Family history Health history Physical examination Increased Intracranial Pressure (ICP) Early signs and symptoms may be subtle As pressure increases, signs and symptoms become more pronounced and level of consciousness (LOC) deteriorates Clinical Manifestations of Increased ICP in Infants Irritability, poor feeding High-pitched cry, difficult to soothe Fontanels: tense, bulging Cranial sutures: separated Eyes: setting-sun sign Scalp veins: distended Clinical Manifestations of Increased ICP in Children Headache Vomiting: with or without nausea Seizures Diplopia, blurred vision Behavioral Signs of Increasing ICP Irritability, restlessness Drowsiness, indifference, decrease in physical activity and motor skills Complaint of fatigue, somnolence Inability to follow commands, memory loss Weight loss Late Signs of Increasing ICP Decreased LOC Decreased motor response to command Decreased sensory response to painful stimuli Alterations in pupil size and reactivity Papilledema Decerebrate or decorticate posturing Cheyne-Stokes respirations Levels of Consciousness (in Descending Order) Full consciousness Confusion: impaired decision making Disorientation: to time and place Lethargy: sluggish speech Levels of Consciousness (in Descending Order; cont.) Obtundation: arouses with stimulation Stupor: responds only to vigorous and repeated stimulation Coma: no motor or verbal response to noxious stimuli Persistent vegetative state: permanently lost function of cerebral cortex Pediatric Glasgow Coma Scale Three part assessment: Eyes Verbal response Motor response Score of 15: unaltered LOC Score of 3: extremely decreased LOC (worst possible score on the scale) Pediatric Glasgow Coma Scale Neurologic Exam Vital signs Skin Eyes Motor function Posturing Reflexes Variations in Pupil Size with Altered States of Consciousness Decorticate/Decerebrate Posturing Special Diagnostic Procedures Lab tests: glucose, CBC, electrolytes, blood culture if fever; evaluate for toxic substances, liver function Imaging: CT, MRI, echoencephalography, ultrasound, nuclear brain scan, PET Lumbar puncture EEG X-ray (rule out skull fractures, dislocations; evaluate degenerative changes, suture lines) Nursing Care of the Unconscious Child The outcome and recovery of the unconscious child may depend on the level of nursing care and observational skills Emergency management Airway Reduction of ICP Treatment of shock Assessment Parameters LOC Pupillary reaction Vital signs Frequency of assessment depends on condition: range from every 15 minutes to 2 hours Pain Management for the Comatose Child Signs of pain Increased agitation and rigidity Pain increases ICP Alterations in vital signs Usually increase in HR, RR, BP and decrease in oxygen saturation Drug Therapies for Pain Opioids Fentanyl + midazolam + vecuronium Acetaminophen and codeine Respiratory Management Airway management is primary concern Cerebral hypoxia lasting more than 4 hours may cause irreversible brain damage CO2 causes vasodilation, increased cerebral blood flow, and increased ICP May have minimal gag and cough reflexes Risk of aspiration of secretions ICP Monitoring Indications for ICP monitoring Glasgow coma scale <7 Glasgow coma scale <8 with respiratory distress Deteriorating neurologic condition Subjective judgment Nursing Care for Child with Increased ICP Patient positioning Avoid activities that may increase ICP Eliminate or minimize environmental noise Suctioning issues Nutrition and Hydration IV administration of fluids and parenteral nutrition Caution with overhydration Later begin gastric feedings via NG or GT Patient may continue to have risk of aspiration Altered Pituitary Secretion Syndrome of inappropriate antidiuretic hormone (SIADH) may accompany CNS diseases Decreased urine output with hyponatremia and hyposmolality Treatment of SIADH Fluid restriction, observe for electrolyte balance, vasopressin administered Medications (as Indicated) Osmotic diuretics for cerebral edema Antiseizure medications with or without sedatives Controversy with barbiturates Paralyzing agents Antipyretics Nursing Care Needs Elimination Hygienic care Position to prevent skin breakdown Exercise- range of motion Stimulation Family support Nursing Diagnoses Disturbed Sensory Perception related to CNS impairment Self-Care Deficits related to physical immobility, perceptual and cognitive impairments Risk for Aspiration related to depressed sensorium, impaired motor function Risk for Injury related to depressed sensorium Head Injury: Etiology Falls Motor vehicle injuries Bicycle injuries Falls – Leading Cause of Head Injury under 5 years Pathophysiology of Head Injury Force of intracranial contents cannot be absorbed by the skull and musculoligamentous support of the head Especially vulnerable to accelerationdeceleration injuries Primary Head Injuries Those injuries that occur at a time of trauma Include: Skull fracture Contusions Intracranial hematoma Diffuse injury Subsequent Complications of Head Injuries Hypoxic brain injury Increased ICP Infection Cerebral edema Concussion Transient and reversible Results from trauma to the head Instantaneous loss of awareness and responsiveness lasting for minutes to hours Generally followed by amnesia and confusion Contusion and Laceration Terms used to describe visible bruising and tearing of cerebral tissue Coup: bruising at the point of impact Contrecoup: bruising at a site far removed from the point of impact Skull Fractures in Children Great deal of force is required to produce a skull fracture in an infant Fracture on the underside of skull can tear the meningeal artery, causing severe hemorrhage with hypovolemic hypotension Types of Skull Fractures Linear Depressed Compound Basilar Diastatic Complications of Head Trauma Epidural hemorrhage Subdural hemorrhage Cerebral edema Hematomas Diagnostic Evaluation Assessment of ABCs Vital signs Neurologic exam Special tests: CT, MRI, behavioral assessment Posttraumatic Syndromes Postconcussion syndrome Posttraumatic seizures Structural complications such as hydrocephalu True mental retardation occurs only after severe injuries Therapeutic Management Care in hospital if severe injuries, loss of consciousness for several minutes, prolonged or continued seizures NPO initially Possible surgical interventions Prognosis Nursing Considerations Frequent assessment: vital sign and neurologic checks Provide analgesia and sedation Careful observation and recording Family support Rehabilitation Prevention Near Drowning Drowning is the second leading cause of accidental death in children Death occurs from asphyxia while submerged Can occur with even small quantity of water (even as little as a pail of water) Near-drowning: survived at least 24 hours after submersion Drowning – 2nd Leading Cause of Death Pathophysiology of Drowning Hypoxia Aspiration Hypothermia Therapeutic Management Emergency resuscitative efforts at the scene Management is based on degree of cerebral insult Aspiration is frequent complication Prognosis Nursing Considerations Care depends on condition of the child Helping parents cope with feelings of guilt Parental anxiety related to prognosis PREVENTION OF DROWNING CNS INFECTIONS CNS has limited response to injury Difficult to distinguish etiology by looking at clinical manifestations Lab studies required to identify causative agent Inflammation can affect the meninges, brain, or spinal cord Bacterial Meningitis Acute inflammation of the CNS Decreased incidence following use of Hib vaccine Can be caused by various bacterial agents Streptococcus pneumoniae Group β streptococci Escherichia coli Transmission of Bacterial Meningitis Droplet infection from nasopharyngeal secretions Appears as extension of other bacterial infection through vascular dissemination Organisms then spread through CSF Bacterial Meningitis Diagnostics: LP is the definitive diagnostic test Therapeutic management Nursing considerations Nonbacterial Meningitis (Aseptic Meningitis) Causative agents are principally viruses Frequently associated with other diseases Measles, mumps, herpes, leukemia Onset abrupt or gradual Manifestations: headache, fever, malaise Diagnosis and treatment Prognosis Tuberculosis (TB) Meningitis More likely to occur in very young children or in immunosuppressed children Ischemic infarction may occur Fever, altered LOC, seizures Common complication of this type of meningitis: hydrocephalus Brain Abscess Pyogenic organisms gain access to neural tissue by way of bloodstream from foci of infection or from direct inoculation Predisposing factors Most common sites Seizure disorders may be long-term complication Encephalitis Inflammatory process of CNS with altered function of brain and spinal cord Variety of causative organisms—viral most frequent Vector reservoir in U.S.: mosquitoes and ticks Clinical Manifestations of Encephalitis: Onset Sudden or Gradual Malaise Fever Headache/dizziness Stiff neck Nausea/vomiting Ataxia Speech difficulties Clinical Manifestation of Severe Encephalitis High fever Disorientation/stupor/coma Seizures/spasticity Ocular palsies Paralysis Encephalitis Diagnostic evaluation Therapeutic management Nursing considerations Rabies An acute infection of the CNS Caused by virus transmitted by saliva of infected animal Virus multiplies in muscles and fatal if untreated Highest incidence in humans is in children younger than 15 years Rabies (cont.) 12% of cases come from domestic animals, especially cats Infected wild animals are most commonly raccoons, skunks, foxes, and bats Unprovoked attack is more likely to indicate a rabid animal than a provoked attack Therapeutic Management of Rabies Inactivated rabies vaccines Globulins HRIG: human rabies immune globulin ASAP after exposure HDCV: human diploid cell rabies vaccine Guidelines for use from World Health Organization Nursing Considerations Support and reassurance for child and family Analgesia with EMLA cream to injection sites Reye Syndrome (RS) A disorder defined as toxic encephalopathy associated with other characteristic organ involvement Characterized by fever, profoundly impaired consciousness, and disordered hepatic function Reye Syndrome (cont.) Etiology is obscure Most cases follow a common viral illness Potential association between aspirin therapy for fever and development of RS Reye Syndrome (cont.) Pathophysiology Diagnostic evaluation Therapeutic management Prognosis Nursing considerations Seizures Caused by malfunctions of brain’s electrical system Determined by site of origin Most common neurologic dysfunction in kids Occur with wide variety of CNS conditions Seizures: Signs and Symptoms Change in LOC Involuntary movements Posturing Changes in perception, behaviors, or sensations Types of Seizures Epileptic Nonepileptic Most seizures are idiopathic May result from acute medical illness Etiology of Seizures Idiopathic (no known cause) Genetic factors –may alter sz threshold Acquired After brain injury Hypoxia Infections Toxins Incidence and Occurrence 2.3 million Americans affected Especially children and elderly More seizures in children younger than 2 years than any other age group Epilepsy Definition: ≥2 “unprovoked” seizures Idiopathic epilepsy: cause unknown Seizures are an indispensable characteristic of epilepsy Seizures A single seizure not generally classified as epileptic Single seizure not generally treated with LT Rx Major Causes of Seizures in Children Birth injuries (anoxia) or congenital defects of CNS Acute infections in late infancy and early childhood In children older than 3 years, usually is idiopathic Absence Seizures Formerly called petit mal or “lapses” Brief loss of consciousness Minimal or no change in muscle tone Almost always appear in childhood (4 to 12 years) Absence Seizures (cont.) Sudden onset of 20+ events per day No warning/no aura Duration 5 to 10 seconds Motor: lip smacking, twitching of eyes, face, slight hand movements May drop object; child rarely falls No incontinence Absence Seizures (cont.) Often misdiagnosed Inattention/daydreaming ADD/ADHDSchool issues Behavioral management School issues Atonic Seizures Sudden momentary loss of muscle tone Onset usually ages 2 to 5 years May or may not have loss of consciousness Sudden fall to ground, often on face Less severe—head droops forward several times Myoclonic Seizures Sudden brief contractions of muscle group May be single or repetitive No loss of consciousness Often occur when falling asleep May be nonspecific symptom in many CNS disorders May be mistaken as exaggerated startle reflex Status Epilepticus Definition: seizure lasting more than 30 minutes or series of seizures without regaining premorbid LOC Treatment: Maintain airway Establish IV access Medications Status Epilepticus (cont.) Medications: Diastat (prefilled rectal syringe) Versed (intranasal) IV Ativan or valproic acid IV loading with phenytoin for ongoing management Emergency Management High-dose sedatives Maintain patent airway Prepare for respiratory support Pediatric Diagnosis of Seizure Disorders Ascertain type of seizure History, observation Determine the cause of the event Diagnostics • EEG, MRI • Labs: glucose, electrolytes, BUN, Ca++ • LP Common Pediatric Seizure Triggers Changes in dark-light patterns (camera flashes, headlights, rotating fan blades, reflections off snow or water) Sudden loud noises Extreme temperature changes Dehydration Fatigue Febrile Seizures Transient disorder of childhood Affect approximately 3% of children Usually occur between ages 6 months and 3 years Rare after age 5 Twice as frequent in males Febrile Seizures (cont.) Cause ?????? Usually in temperatures higher than 101.8° Seizure occurs when temperature is rising, not after Seizure usually over before arriving in emergency department Febrile Seizure Treatment Fever reduction Evaluate history (episodic and family) Seizure control if ongoing Diazepam (rectal) Febrile Seizures 95% to 98% of children with febrile seizures do not have epilepsy or neurologic damage Management: Avoid tepid baths—usually ineffective Vigorous use of antipyretics Protect child from injury during seizure Call 911 if seizure lasts more than 5 minutes Febrile Seizure Treatment Prophylaxis with medications If focal or prolonged seizures If neurologic anomalies If first-degree relative has seizure history In child less than 1 year old If multiple seizures in 2-hour period RX Phenobarbital Febrile seizures, neonatal seizures Also for other seizures: front-line IV choice if patient does not respond to diazepam High dosage may require respiratory support Phenytoin (Dilantin) PO or slow IV push (<50 mg/min) Precipitates when mixed with glucose Side effects: Gingival hyperplasia, ataxia, rashes, acne, hirsutism, osteoporosis Onset 5 to 30 minutes; duration 12 to 24 hours Fosphenytoin May be given with saline or glucose Rate up to 150 mg/min IV or IM Valproic Acid Trade names: Depakote, Depakene IV or PO IV for status epilepticus S.E.: Hepatotoxicity! Diazepam Trade names: Valium IV, Diastat (rectal gel) Medication of choice for status epilepticus Rectal gel for home or prehospital management Onset 3 to 10 minutes; short duration (minutes) Concurrent loading with phenytoin for sustained control of seizures Ativan Alternative to diazepam May be preferable to diazepam Longer duration of action Less respiratory distress in children older than 2 years Midazolam (Versed) Intranasal route For acute epileptic seizures Onset 3 to 5 minutes; duration Pharmacologic Management Monotherapy is treatment of choice for pediatrics Gradual increase of dose until seizure control or signs of toxicity Polypharmacy if uncontrolled with one drug Pharmacologic Management (cont.) Monitor therapeutic levels Increase dosage as child grows Monitor for known side effects Avoid abrupt discontinuation—gradual dose reduction When to Discontinue When seizure free for 2 years Normal EEG Avoid DC during puberty or when subject to frequent infections Recurrence possible within first year Nursing Interventions Observe and document episode Protect from injury Stay calm Remain with child Privacy if possible Home Management of Seizures CPR training for family members Rectal diazepam available for intractable seizures Activity restriction on individual basis Safety devices—helmets, no swimming alone, awareness of school, other caregivers Migraine Headache Autosomal dominant disorder Cause unknown Precipitating factors Symptoms Symptomatic pain relief Pharmacologic options