5 - Recognising and managing the seriously ill child

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Flashcards on 5 - Recognising and managing the seriously ill child , created by Elizabeth Then on 15/06/2018.
Elizabeth Then
Flashcards by Elizabeth Then, updated more than 1 year ago
Elizabeth Then
Created by Elizabeth Then over 6 years ago
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Asthma - pathophysiology common - cause unknown classic features of acute asthma- - cough, wheeze, breathlessness, breathing probelms - bronchioles surrounded by smooth muscle, contract to triggers: colds (virus), exercise, weather, smoke, dust, stress - inflammation, oedema, broncho-constriction result in narrowing of small airways, irritate lining of lungs - excessive mucus generated - constriction/blockage of airways - allergen perceived as foreign bodies inflammatory response and broncho-constriction
Spacer use in young children MDI requires cooperation and coordination spacers double the amount of medication getting into lungs above 5 years can use a spacer masks easier for young children nebs require 8-10 minutes - cannot cooperate this long
Convulsioins/seizures (epilepsy) - paroxysmal, time-limited change in motor activity/sensory/perception/behaviour that results from abnormal electrical activity in brain -common in child under 5 50% outgrow seizures as they mature
Causes of epilepsy NOT causes by fever or new brain injury Causes - idiopathic, CNS, electrolyte abnormalities, drug, toxic ingestion, CNS vascular abnormality
Pathophysiology of epilepsy uncontrolled, interrupted neuronal messengers to brain, triggers electrical activity in brain hyperexcitability of neurones group of neurones
Classifications of epilepsy partial - short, subtle lapse of awareness, simple (focal) - starts in one area of brain (staring, confusion) Complex (psychomotor) - lip smacking, part twitching generalised (grand mal) - crosses both hemispheres, myoclonic, tonic clonic muscle movement
Unclassified seizures Infantile spasms (drop attacks) - onset 6-8 months, fall forward, poor prognosis pseudo seizure - looks like seizure but is not * may be mix of classified and unclassified
Epilepsy diagnosis difficult in some children - need detailed history - detailed description of seizure EEG MRI CT scan
Effects and management of epilepsy effects: low self esteem, poor discipline, learning difficulties, behavioural probelms, developmental delay, dental probelms (side effects of medications) management: medication, only if frequent, type of medication varies, lethargy side effects
Cont management of a seizure ABCD * for seizures lasting more than 5 minutes - midazolam IV/IM 0.15mg/kg Buccal 0.5mg/kg Intranasal 0.2mg/kg *max 5 mg) if cont for further 5 min - repeat and look for resp depression if cont for another 5 min: phenobarbitone 20mg/kg (max 600mg) phenytoin 20mg/kg (max 1.5kg) *should be cardiac monitored
Status epilepticus any tonic/clonic seizure convulsion lasting more than 30 minutes
Management of epilepsy longer term encourafe normal life and routines medications as ordered supervison when swimming, and needed etc
Cystic Fibrosis (Mucoviscocoidosis) diagnosis: inherited autosomal recessive disorder of exocrine glands need 2 carriers to be affected diagnosis: via NNST in infancy, malaabsorption in ileus and failure to thrive, positive sweat test, genetic testing
Pathophysiology of CF gene mutation affects specific protein CFTR, which regulates sweat, dgestive juices, mucus this protein controls movement of chloride and sodium in and out of cells in CF, the CTFR does not function properly, and thick mucus blocks narrow passgaes of affected organs, e.g. lungs, pancreas, bowel
Manifestations of CF abnormal accumulation of viscous, dehydrated mucus result in: inflammation of lungs, chest infections, SOB, blockage of pancreatic duct, malnourished due to poor absorption, sterility in male no vans deferans forms, muscle cramps, lethargy, poor appetite
Management of CF Respiratory therapy to promote lung function, gastro tract therapy, nutrition, to promote essential nutrient balance for health and growth
Resp function and management in CF chest physio 2-3 times daily with bronchodilators to open airways usually admitted with signs and symptoms central venous line inserted
Promoting optimum nutrition pancreatic enzymes supplemented calories and vitamins (water soluble) and minerals enteral feeding
Diabetes major of children have type 1 onset is usually 8 years cause unknown
Pathophysiology of diabetes 1 autoimmune disease - beta cells destroyed by body's immune system in genetically susceptible individuals triggered by diabetogenic infection trigger dont make enough insulin for body requirements glucose remains in blood stream
Pathophysiology of type 2 diabetes more mature onset overweight and inactive individuals at risk cant be prevented cells don't respond to insulin insulin resistance results glucose remains in blood stream and body compensates by burning fats for energy - produces ketones and glycouria excess glucose stored in liver or converted to fat in body tissues
Symptoms of diabetes polydipsia, polyuria, weight loss (1), weight gain (2), fatigue, visual disturbances, itchy skin, nausea and vomiting, coma, dizy, sweating, LOC
Diagnosis of diabetes fasting BGL more than 7mmol 2 hours pc more than 11.1 mmol and glycated HB more than 6.5% glycated HB - form of HB to identify plasma glucose concentration also indicator of long term (2-3 months)
If untreated or undiagnosed builds up ketones in blood stream and dehydration -FATAL kidney function impaired - nephron damage increase in infections eye damage - retina, blindness poor circulation in feet and legs (gangrene) nerve damage in feet heart disease
BGL monitoring in children hypoglycaemia Hypoglycaemia in paediatric diabetic patients less than 2.3 - 2.8mmol (newborns -neonates) less than 4mmol (paediatric patients) *neonate heel prick rather than finger height, weight, BMI monitoring in children
Age appropriate Glycaemic aims in diabetic children infant: day 5-12, bed 7-12 toddler 1-3: day 5-12, bed, 7-12 school 5-7: day 4-10, bed, 7-12 school 7-11: day4-12, bed 7-12 adolescent: day 4-8, bed 7-12
Ideal BGL groups in children Toddlers - 5-12 mmol/L school age children - 7-12 mmol/L adolescents 4-8mmol/L night 7-12mmol/L
Tonsilitis/ adenoiditis tonsils and adenoids located in pharynx, composed of lymph tissue, part of body's defense system, mainly cause by virus, may be acute/chronic
Pathophysiology of tonsilitis toxins released from microorganism cause inflammation and infection on tonsils causes hypertrophy of tissue lymph nose involvement, infiltrate the epithelial germ layers
Clinical manisfestations of tonsilitis frequent throat infections - can recur breathing and swallowing diffculties dry mucus membranes, N& V, loss of energy, pain, excessive clearing of throat chronic - bacteria lodge in tonsillar bed
Diagnosis and treatment of tonsilitis visual inspection and symptoms tonsils lagre and inflamed on observation enlarged adenoids seen on x-ray conservation management - rest, fluids, analgesia, abx,
Nursing management of tonsilitis airway management left lateral until breathing established after surgery if bleeding sit up and support chin anad neck haemorrhage, pain, infection frequent swallowing (cardinal sign of bleeding) difficulty in swallowing pallor, restlessness, vomiting, decreasing BP, increasing temp and pulse regular panadol, vital signs
Discharge planning tonsilitis rest few days, eat food to make swallow and avoid scar tissue, protect against infection, other children, adults, panadol, follow up apt
Otitis media - and risk factors causes inflammation or infection of middle ear cold, usually precedes risk factors: boys, dummy use, smoke, child care causes: viral, strep, influenzae serous: non-suppurative, purulent, suppurative
Pathophysiology of otitis media eustachian tube of child - shorter/angled than adults infection moves from throast via tuse into middle ear tissue surrounding tube swell, and block tube negative pressure creates vacuum in middle ear fluid (serous) moves in increased pressure - pain intense
Clinical manisfestation of otitis media history, cold, fever, ear pain, anorexia, vomiting, lethargy, loss of hearing long term
Examination of otitis media tympanic membrane dull, opaque, bulging (pressure), cough, sneezing, runny nose, febrile, crying
Complications of otitis media perforation of TM, febrile convulsions, supparative - meningitis facial nerve palsy
Serous otitis media as a result of a cold, persists of 7 weeks/months, fluid does not move, conductive hearing loss, cognitive development may insert grommter
Nursing management of otitis media Abx analgesia topical lignocaine encourage drinking and eating ear drops PRN quiet actvitities, no swimming, report purulent discharge
Foreign bodies Inhaled - depend on where in body main bronchus - sudden catastrophic coughing, chocking, possible vomiting total obstruction - unconscious, cardiac arrest open airway - check for FB PP ventilation to force FB down L or R main bronchus
Choking in FB- assess severity effective cough - mild airway obstruction, encourage coughing, continue to monitor ineffective cough - conscious - call ambo, 5 back blows, 5 chest thrust, 5 back blows unconscious - begin CPR
Foreign Body in lower main bronchus 6 months to 4 years are at greatest risk symptoms include: wheese, cough, dyspoes, asymmetrical chest movement, lobal collapse, chest x- ray for dx total oesophageal obstruction- needs anaesthetic for removal partial obstruction - observe, may pass in stomach if drooling, chest pain , unable to eat, abdo pain, vomiting, melaena, then remove
Bronchiolitis acute viral resp tract infection effects children under 2 years RSV main cause transmitted through direct contact via resp secretions incubation period 2-8 days acute illness - lasts 3-7 days 1-2 weeks recovery period
Pathophysiology of bronchiolitis inflammation of bronchioles, virus infects epithelial cells, necrosis of epithelial cells and cilated lining oedema and increase in production of mucous plugs resp distress - acute
Signs and symptoms of bronchiolitits initial illness - pharyngitis, conjunctivitis, otitis media, low grade fever, lethergy, irritability, dyspoea, difficulty feeding, coughing, sneezing, audible wheeze, crackle on auscultation
Progression of illness - bronchiolitis tachypnoea, tachycardia, increased coughing, audible wheeze, crackles on auscultation, prolonged expiratory phase, nasal flaring, poor oral intake, increased lethargy
Severe illness in bronchiolitis tachypoea in increase in 70 breaths per min accessory muscle use air hunger, grunting, apnoea, cyanosis, marked lethargy, inability to suck
Admission criteria for bronchiolitis all infants with: accessory muscles withspo2 less than 94% underlying medical conditions apnoea, poor oral intake, signs of physical exhaustion
Treatment of bronchiolitis treat symptomatically oxygen to maintain saturation levels above 93%, monitor res status, vitals, hydration, additional precautions, minimal handling brochodilator therapy - salbutamol over 6 months with past history of wheeze vital signs and auscultation must be undertaken 30 minutes after each dose of salbutamol *steroids are not effective
Nasopharyngeal suction infant obligatory nose breather clear nasal pharyngeal airway size of catheter correct measurement to nose to ear
Nasal bleeding - think about and complications with suctioning trauma to mucous membranes complications with suctioning: bronchospasm, bradycardia, laryngospasm, MI
Croup (Laryngotracheobronchitis) most common in children 3 months - 3 years uncommon in children over 6 yeats usually viral - may be bacterial common cause is stridor
Pathophysiology of croup virus/bacteria enters throat infiltration of white cells leads to swelling of larynx, trachea, bronchi narrowed airways, noisy movement of air (stridor) over narrowed airways
Clinical presentation of croup barking cough, inspiratory stridor, hoarse voice, dyspnoea, sittin gup and forward to get breath, resp distress, anxious, agitated
Treatment of Croup humidified oxygen, adrenalin, dex 0.6mg/kg/IM not to exceed 10mg
Gastroenteritis - viral rotavirus major cause effect children under 4 years severe dehydration
gastroenteritis - bacterial rarely cause dehydration, stools often bloody
Pathophysiology of gastroenteritis inflammation stomach, bowels, caused by infection, decreases SA for absorption of nutrients and water alters parasympathetic innervations, increased bowel motility
Clinical manifestations of gastroenteritis poor feeding, vomiting, frequent, large watery stools - viral, small bloody stools with cramps - bacterial
Fractures in children bones softer than adults thicker periosteum highyl vascularised long bones not ossified ligaments stronger fractures heal faster, risk of compression fractures
Pathophysiology of fractures force bone greater than tensile or compression strength of bone disruption of periosteum, bv, cortex, bone marrow, soft tissue bleeding from damaged tissues, vasodilation, osteoblasts remodel bone,
Clinical presentation of fractures pain over fracture area, swelling, warmth, bruising, deformity, dysfunction
Influences on healing general health, nutrition status, anaemia, infections, compliance
Prevention of complications assess circulatoin, skin integrity, plaster care, pain, hygiene, modify clothing, prepare for d/c
Traction explanations +++ ensure analgesia hygiene, privace, neurovas obs, watch for swinging in traction, ensure weights are free
Febrile convulsions associated with fever more than 38 debress not associated with infection common in 6 months - 6 years rapid temperature rises cause the convulsion not the degree of fever
Signs and symptoms of febrile convulsions simple seizures, LOC, twitching, facial jerking, resp muscles, legs, arms, dyspoea, foaming at mouth, drowsiness keep them safe**
Head injury in a child leading cause of trauma and death in young children mostly preventable
Types of head injuries external force (mechanical) - shaking, strong head rotation - brain structure tear concussion - BV stretch on impact and damage to cranial nerves contusion - impact results in bleeding results damage/pressure penetration - object penetrate skull - breach of dura mater coup - contrecoup - impact on one side and damage on opposite side (contusion, bleed, clot)
Types of head injuries contued closed or penetrating mild, mod, sev acquired after birth - infection, bleeding
Trauma associated examples of head injuries skull fractures, cerebral lacerations, cerebral contusions, sheering injury
Examples of acquired injuries haemorrhage sub dural, extra- dural, intra-cerebral
Pathophysiology of head injuries brain structure tear or are compressed reduced blood flow - nerve tissues disturbed or damaged bleeding - increases ICP breach of dura mater loss of function - temp or permanent
Injury may be.. primary - mechanical. direct result of injury, haemotoma, contusion secondary - hours later, increase ICP, cerebral ischaemia
Assessment in head injuries symptoms - dizziness, ringing in ears, headache, nausea signs - slurred speech, convulsions, seizure, confusion, blurred vision primary survey secondary survey - neck , spine prec, head (swelling + lacerations), eyes - pupils, dental, facial fractures
Diagnosis of head injuries xray, CT, MRI, ICP, EEG
Management of head injuries aims aims: optimal pressure in brain, recognise secondary damage, prevent secondary damage
Severity of head injuries mild - no LOC, normal VS, GCS 14/15 mod - brief LOC, headache, normal VS, GCS 9-13 sev - LOC, seizure, CSF leak, GCS 3-8
Treatment and management of head injuries admission if: airway at risk, LOC, vital signs compromised Home if: no LOC, no transient symptoms, dizziness, headache, vomiting
Effects of head injuries difficulty concentrating and memory lethargy, sleep disorders, visual and hearing loss rehab - physio, speech, OT, care of parents
Paediatric setting patterns of injury and causes of taruma signiticant reduction of disease due to better housing, hygiene, immunisations common injuries: falls, fractures, MVAs, drownings, burns, FB inhalation
Accidental injuries MVA, drowning, burns
Culturally competent awareness, knowledge, skill, encounters, desire
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