Pediatrics High Yield Topics from Past Questions
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Pediatrics High Yield Topics from past questions
Gastroenteritis
Acute gastroenteritis is characterized by the sudden onset of vomiting and/or diarrhea and/or fever.
Mortality and morbidity related with gastroenteritis are usually related to dehydration and electrolyte imbalance. The main focus of therapy is replacement of fluid and electrolytes.
Etiology Major cause of AGE in infants and young children Rotavirus 20-40% Campylobacter jejuni 8-10% Adenovirus 6-8% Salmonella species 4-8% Small round viruses 2-4% Other bacteria 2-5%
Differential diagnosis Common other causes to consider Surgical Acute appendicitis, intussusceptions, peritonitis, volvulus Infective UTI, septicemia, pneumonia, meningitis Metabolic DM (DKA), inborn errors Others Anaphylaxis, chronic GIT disorders, IBD
Assessment of dehydration Symptom/sign Mild (<5%) Moderate (5-10%) Severe (>10%) Thirst + ++ +++ (may be obtunded) Oliguria + ++ Anuric Dry mouth, eyes, - + ++ decreased skin turgor Tachypnea (from - + ++ acidosis) Tachycardia -/+ + ++ Shock - - +
Investigations Stool bacterial cultures should be one if: o Bloody stools + high temperature o Other family members with similar complaints o Child attends daycare o Child recently travelled overseas o Leucocytes on microscopy If child is sick enough to need admission – conduct stool viral and bacterial cultures Serum electrolytes in any child with moderate to severe AGE at outset and repeated at 6-8 hrs Septic work up if child is toxic and febrile Common electrolytes abnormalities Hypokalemia (<3.5 mmol/L) and hyponatremia (<135 mmol/L) Usually due to electrolyte loss in stool Sodium loss due to osmotic diarrhea Potassium loss due to aldosterone action on small/large intestines and kidneys Acidosis Usually caused due to bicarbonate loss in stool → low bicarbonate, high chloride with low anion gap May occur from lactic acidosis (shock), ketoacidosis (diabetes, starvation), unrecognized inborn error of metabolism Ingestion of drugs such as salicylates → high anion gap with low bicarbonate, low chloride and unmeasured anions Usually responds to treatment of dehydration Hypernatremia Results from osmotic water loss in excess of electrolytes. Can be caused by severe carbohydrate intolerance or use of hyperosmolar feeds e.g. undiluted carbonated drinks and concentrated infant formula Rapid rehydration may lead to complications of sudden sodium correction – cerebral edema Rehydration carried out over 36-48 hrs.
Treatment Resuscitation In severely dehydrated and shocked children with anuria, fluid expansion is urgently indicated Early IV or IO cannulation Replacement with 20mls/kg of crystalloids NS or hartmann’s boluses until patient has reasonable BP. Mode of replacement Mild dehydration → oral route Any child with >5% dehydration should be managed as in-patient, oral route may be tried but IV therapy most commonly used. Fluid replacement calculation Deficit volume (ml) = % dehydration X weight (kg) X 10 Calculate maintenance requirements o First 10 kg – 4ml/kg per hour
o Second 10 kg – add 2ml/kg/hour for every kg over 10 kg to above (40ml/kg/hr + x)
o Over 20 kg – add 1ml/kg/hour for every kg over 20 kg to above (60ml/kg/hr + y)
Add ongoing losses and subtract any expected oral intake. Oral rehydration therapy Commercially prepared ORS preferred. ORS contain glucose/sodium in proportions designed to stimulate glucose coupled sodium absorption Gastrolyte – Na 60mmol/L, K 20mmol/L, Cl 60mmol/L and HCO3 10 mmol/L Can be administered via NGT Non-dehydrated children can be treated with diluted sweet drinks e.g. carbonated drinks, fruit juices but need to be diluted 1:4 since they are hyperosmolar Maybe used in Inpatient or outpatient setting with detailed parental instructions IV therapy Choice of fluid dependent on electrolyte disturbance present. Normally N/2 with 2.5% D with 20mmol/L potassium will replace losses from diarrhea and vomiting Deficit to be replaced over 24 hrs Hypernatremic dehydration corrected with same fluid but over 48hrs. Do not need to administer bicarbonate unless life-threatening acidosis, and usually corrects itself. Medications No role for anti-emetics, anti-motility or anti-diarrheal agents in children with AGE Anitmicrobials only indicated for o Invasive infections shigella or salmonella GE in infants <6mths o Parasitic infections such as Giardia or Strongyloides Diet Breastfeeding to continue Normal dietary intake of formula to continue as usual Children will chose to eat when they are well enough Intussusception
Clinical features Peak incidence between 2 months and 2 years Pain is colicky with quiescent periods, often with marked pallor Vomiting clear initially, but bile stained after 12-24 hrs. Red currant stool – always conduct a PR examination to look for this Palpable sausage shaped mass or fullness with some tenderness Great mimicker and should be considered in all infants with symptoms of AGE Treatment Urgent fluid resuscitation if child is in hypovolemic shock Early IV access so there is no delay in specific treatment Specific treatment o Urgent enema reduction with air or barium, if not successful o Open manual surgical reduction or resection Epiglottitis/ Croup Croup The term croup refers to a symptom complex characterized by harsh barking cough, with or without inspiratory stridor and with or without respiratory difficulty. Causes: Viral laryngotracheitis o Most common type – parainfluenza virus and others o Particularly in first 5 years of life; peak incidence 1 – 2 years o Preceded by coryzal symptoms o Usually self-limiting but occasional severe, requiring treatment. Spasmodic croup o Associated with asthma/ atopy o No viral prodrome o Rapid onset and cessation of croup symptoms o Recurrent Pseudomembranous croup (staphylococcal tracheitis) o May represent secondary bacterial infection o Thick secretions form ‘pseudomembrane’. o Usually affects older children, often toxic and very unwell o Obstruction more severe with much softer stridor Diptheric croup o Consider in un-immunized child o Associated with toxicity with rapidly progressive airway obstruction o Laryngeal membrane – grey, foul-smelling, bleeds on suction and not easily removed (adherent). o Tonsillar/ pharyngeal membrane or exudates Management Initial assessment: aimed at determining severity of obstruction and the need for hospital admission o General appearance – w/f preoccupied or agitated child who could be significantly obstructed and hypoxemic o Degree of respiratory difficulty – respiratory and pulse rates, tracheal tug, chest wall retractions and palpable paradox Need for admission influenced by: o h/o sever obstruction or previous severe croup o degree of respiratory difficulty – stridor at rest is an indication for admission o child’s fluid intake o level of parental anxiety, proximity to home and transport availability pulse oximetry – may point toward poorer prognosis but normal does not rule out siginifcant obstruction oxygen if SaO2 <95% Oral corticosteroid therapy to all but trivial cases. o Oral dexamethasone 0.15 – 0.3 mg/kg/dose well tolerated or o 0.5 – 1 mg/kg of prednisolone Nebulised adrenaline 1:1000 (0.5 ml/kg, maximum 5ml) for moderate or severe obstruction – closely monitored by medical staff, need for multiple nebulizers an indication for ICU admission for monitoring. Nebulised budesonide 2mg may be used if steroids no tolerated or adrenaline contraindicated as in tetralogy of Fallot. IV corticosteroids may be used Assessment of need for intubation: o Impending respiratory collapse o Tired, agitated, worried or restless child o Increasing respiratory difficulty and chest retractions o Marked use of accessory muscles and increasing heart rate o Cyanosis o Decreased LOC o Decreasing respiratory effort with decreasing stridor and breath sounds
Acute epiglottitis Acute epiglottitis (supraglottitis) is characterized by inflammatory swelling of the epiglottis and aryepiglottic folds. It is a dangerous condition with a high mortality if undiagnosed early. Most commonly due to infection with Hib, become rare since advent of Hib immunization, though may still occur due to Hib, group A streptococci and some other viruses. Differentiating features from croup Toxic child with high fever Child often sits up, leans forward and drools (due to inability to swallow) Obstruction is more severe and stridor if present is soft Cough is absent or minimal, muffled but not croupy Management Call anesthetic registrar, who should remain with child Notify ENT, ICU and respiratory teams Arrange for urgent transfer to operating rooms for endoscopy and artificial airway, do not do anything unless respiratory collapse occurs o Have parents hold the child, sitting up o Do not examine the throat or insert cannulas or collect blood o Do not attempt lateral airway x-rays o Do not give nebulised adrenaline Cefotaxime is given following blood cultures and epiglottic swabs Rifampicin prophylaxis in epiglottitis cases with Hib isolated. Hib vaccine later given to children <2years due to poor immune response. Status Epilepticus This is an emergency situation and the seizures should be stopped ASAP. Seizures continuing for >30 – 60 minutes may cause permanent neurological damage.
All patients should have full cardiac monitoring, and facilities for rapid resuscitation and assisted ventilation must be available.
Acute control of seizures Drug Route Dosages Comments Midazolam Buccal, nasal or 0.3mg/kg maximum All routes doses can be intramuscular if no IV 10mg/dose for B, N repeated if no response in access 0.15mg/kg maximum 5 mins 5mg/dose for IM IV access + 0.15mg/kg maximum 5mg/dose Diazepam IO or IV 0.25mg/kg maximum Higher risk of resp 10mg/dose depression PR 0.5mg/kg maximum dose Slower action than 10mg/dose midazolam when given PR Phenytoin IV only 15-20mg/kg in NS over Check phenytoin levels 20-30mins followed by daily during early phases 3mg/kg IV or PO q6hrs for 48hrs Maintenance 5-10mg/kg/day Phenobarbitone IM or IV diluted 10mg/kg maximum High risk of resp. 500mg/dose over 20mins depression when given with benzo. Paraldehyde PR 0.15-0.3ml/kg up to Avoid IM due to risk of 10mls/dose abscess.
Usual drug of first choice in common forms of epilepsy Type of seizure Drug of choice Partial seizures and generalized tonic-clonic Carbamazepine, sodium valproate seizures Absence epilepsy Ethosuximide, sodium valproate Juvenile myoclonic epilepsy Sodium valproate, lamotrigine
Investigations Bedside BSL – beware of missing hypoglycemia as a cause for seizures as this is life threatening Blood gases – may suggest the level of hypoxia, tissue hypoperfusion and need for further fluid therapy. EEG – no role in acute management or diagnosis of status but may be helpful in anesthetized or intubated patients to rule out non convulsive status epilepticus Metabolic studies – fasting BSL, electrolytes, calcium, magnesium and urine metabolic screen CT or MRI scan – indicated when there are partial seizures, focal neurological signs or focal seizures or a recent change in seizure pattern or new onset seizures with questionable histories. Drug levels – for patients already on AEDs to rule out sub-therapeutic levels and toxicity. Limp
Acute or subacute onset of limp is common in children. In 80% it is caused by pain but it can be related to muscle weakness and/or neuropathy. History History is an important aspect in the evaluation of limp. Take into account a h/o recent trauma, but this may be present even in the case of inflammatory or infective causes of limp. Red flag symptoms include o Constant pain o Severe pain o Night pain o Short duration o Increasing pain o Functional impairment Careful physical examination including assessment of gait and check for range of movements Hip pain commonly causes referred pain to the knee and both joint should be examined in patient with c/o hip or knee pain. Investigations tailored across likely causes Etiology Age specific causes of limp Toddler (1 – 3 years) Transient synovitis (hip) Septic arthritis Juvenile idiopathic arthritis Discitis Developmental dysplasia of hip Leg length discrepancy Cerebral palsy Non-accidental injury Muscular dystrophy Child (3 – 10 years) Transient synovitis Septic arthritis Juvenile idiopathic arthritis Perthes disease Leg length discrepancy Kohler’s disease Adolescent (10 – 16 years) Overuse syndromes Tarsal coalition Slipped capital femoral epiphyses All ages Trauma Osteomyelitis Neoplasia
Frequency of non-traumatic limp presenting to ED Cause Frequency (%) Inflammatory Transient synovitis 39.5 Other 3.2 Osteomyelitis 1.6 Perthes disease 2.1 Neoplasia 0.8 Unknown diagnosis 31.1
Acute osteomyelitis The treatment of acute osteomyelitis is based on early commencement of effective antibiotic therapy on a presumptive diagnosis made from clinical features. Diagnosis Suggested by pain of recent onset usually in a limb near a joint. May or may not be associated with fever and toxemia Limitation of movement and localized bony tenderness with or without swelling and redness Differential diagnosis Cellulitis Septic arthritis Juvenile idiopathic arthritis Trauma Leukaemia and Bony tumors Investigations Blood cultures and swabs from any infective skin lesions Examination of blood film, WCC, ESR, CRP – useful baseline for comparison X-ray of affected part – usually normal in early stages and also as baseline for later comparison. May help in excluding other causes e.g. tumors Bone scan – more useful in early stages than x-rays Microbiology Staphylococcus aureus accounts for 80% of cases Community acquired MRSA and salmonella account for the remainder In neonates group B streptococcus and S.aureus are major causes Management Antibiotic therapy – flucloxacillin + cefotaxime for children <5 not immunized against Hib in high doses Vancomycin or clindamycin considered for MRSA. Risk factors for MRSA are o Aboriginal or Maori-polynesian ethnicity o Previous MRSA colonization o h/o boils modify antibiotics after culture results available antibiotics until patient is afebrile, local swelling and tenderness diminished, CRP decreasing – several days oral antibiotics in older children started as inpatient to gauge tolerance and then continued as out- patients for 3-4 weeks IV route for full course for infants/neonates General care – analgesia, sedation and splinting Surgery – indicated when there is collection of pus. Antibiotics will not work if pus present andmay lead to chronic osteomyelitis Septic arthritis
Acute septic arthritis may be of hematogenous origin or caused by spread from a neighboring bone lesion.
Diagnosis Acute onset symptoms may be those of acute osteomyelitis Malaise, pyrexia and pain Joint involvement may be indicated by effusion and swelling Muscle spasm and sever pain on slightest movement of joint are usual Investigations Blood culture and culture of any purulent skin lesions White cell counts, ESR, CRP – for baseline and follow up X-ray of the joint – soft tissue swelling and later on porosis of the bone ends. Ultrasound of joint – effusion Joint aspiration – diagnostic as well as therapeutic – performed in sterile conditions preferably in OR – fluid sent for gram stain and culture to confirm diagnosis Bone scan to rule out osteomyelitis Microbiology Commonly due to S.aureus, including CA-MRSA Others include S.pyogenes, Hib, N.meningitidis and S.pneumoniae N.gonorrhoae in sexually active children and is strong indicator of sexual abuse Hib more likely in children,5 years and un-imunised Management Antibiotic therapy – IV flucloxacillin ± cefotaxime (for Hib) Appropriate changes made depending on culture results If commenced early antibiotics need to continue for 3 weeks. General care – adequate analgesia and sedation Surgery – in weight-bearing joints e.g. hip, early surgical drainage and lavage by arthroscopy – will decrease risk of delayed degenerative arthritis. Legg-Calvé-Perthes disease
LCPD is a hip disorder that generally has onset between the ages of 4 and 9 years in 80% of cases, but can occur between ages 2 – 13 years. Most well know form of avascular necrosis of the femoral head. Pathophysiology Significant male preponderance 4:1, with 10% of cases being bilateral Most children are short with average or above average weight with delayed skeletal maturation Exact cause unknown but pathophysiology is vascular occlusion Begins with repeated episodes of ischemia of the femoral head, leading to infarction and necrosis. The avascular necrosis is then complicated by subchondral stress fracture Process of reossification and remodeling (resorption) may take place over 2 -4 years Resultant collapse and flattening of femoral head may occur with subsequent potential for subluxation Outcome is a painful hip joint with a restricted range of motion, muscle spasms and contractures of the soft tissues Clinical features Usually insidious onset with emergency presentation rare Mild hip pain and limp may have been present for weeks to months before diagnosis is made Initially pain is mild and radiates/ refers to the anterolateral thigh or knee Physical findings include hip abduction and internal rotation In advanced cases, proximal thigh atrophy and limb shortening may be noted Radiology Radiographically, LCPD progress and is divided into four stages: 1. Initial 2. Fragmentation 3. Reossification and 4. Healed Initial stage (1 -3 months) capital femoral epiphysis fails to grow due to lack of blood supply → widening of the cartilage space of the affected hip and a smaller size of ossific nucleus of the femoral head Second sign → appearance of subchondral stress fracture line in the femoral head (Caffey sign) Third sign → increased radiopacity of the femoral head caused by new bone deposition on avascular trabeculae Calcification of necrotic marrow and resultant crushing of the avascular trabeculae in the dome of the epiphysis. Further distortions of femoral head during healing process → subluxation and extrusion of femoral head from the acetabulum Differential diagnosis toxic synovitis, acute rheumatic fever, tuberculosis arthritis, tumors such as eosinophilic granuloma, osteoid osteoma, and osteoblastoma, and lymphoma Diagnosis High degree of suspicion is necessary to diagnose the condition before the appearance of irreversible changes on the x-ray. Bone scan and MRI are helpful early on to make the diagnosis. Technetium-99m bone scan – markedly reduced uptake of isotope within the affected femoral head MRI – provides superior resolution and sensitivity, with areas of low signal intensity reflecting necrotic regions within the femoral head. Treatment Patients diagnosed with LCP disease should be made non-weight bearing and referred to a pediatric orthopedist for management. Current treatment focuses on maintaining containment of the femoral head through the use of splints or occasionally surgery. Prognosis Factors related to a poorer prognosis include: Older age at clinical onset, Extensive capital femoral epiphyseal involvement, Premature epiphyseal closure, and Reduced range of hip motion. Non-accidental Injuries in children Child abuse and neglect
Child maltreatment may occur either within or outside the family. Types of child maltreatment include: Physical abuse Most often inflicted by a caregiver or family member and occasionally by strangers Most common manifestations of physical abuse include o Bruises o Fractures o Head trauma and o Abdominal injuries A small but significant amount of unexpected pediatric deaths are related to physical abuse Sexual abuse Sexual abuse is defined as the engaging of dependent, developmentally immature children in sexual activites that they do not fully comprehend and to which they cannot give conset, or activities that violate the laws and taboos of a society. It includes all forms of incest, sexual assault or rape and pedophilia. This includes: Fondling Oral-genital-anal contact All forms of intercourse or penetration Exhibitionism Voyeurism Exploitation or prostitution and Involvement of children in the production of pornography Emotional abuse and neglect Emotional or psychological abuse has been defined as the rejection, ignoring, criticizing, isolation or terrorizing of children, all of which have the effect of eroding their self-esteem. The most common form is verbal abuse and denigration. The most common feature of emotional neglect is the absence of normal parent-child attachment and a subsequent inability to recognize and respond to an infant’s or child’s needs. A common manifestation of emotional neglect in infancy is nutritional (nonorganic) failure to thrive Medical care neglect Medical care neglect is the failure to provide the needed treatment to infants or children with life-threatening illness or other serious chronic medical conditions. Münchausen syndrome by proxy MSP is a relatively unusual disorder in which the caregiver, usually the mother, either simulates or created the symptoms or signs of illness in a child. Also called as factitious disorder by proxy. Child can present with a long list of medical problems or often bizarre, recurrent complaints. Persistent doctor shopping and enforced invalidism. Recognition of Abuse and Neglect History Common Historical Features in Child Abuse Cases. Discrepant, evolving, or absent history Delay in seeking care Event or behavior by child that triggers a loss of control of caregiver History of abuse in the caregiver's childhood Inappropriate affect of the caregiver Pattern of increasing severity or number of injuries if no intervention Social or physical isolation of the child or the caregiver Stress or crisis in the family or the caregiver Unrealistic expectations of caregiver for the child Approach to the family should be supportive, non-accusatory and empathetic Individual bringing patient for care may not be offender 1/3rd cases occur in extrafamilial settings
Presentations of Sexual Abuse. General or direct statements about sexual abuse Sexualized knowledge, play, or behavior in developmentally immature children Sexual abuse of other children by the victim Behavioral changes Sleep disturbances (eg, nightmares and night terrors) Appetite disturbances (eg, anorexia, bulimia) Depression, social withdrawal, anxiety Aggression, temper tantrums, impulsiveness Neurotic or conduct disorders, phobias or avoidant behaviors Guilt, low self-esteem, mistrust, feelings of helplessness Hysterical or conversion reactions Suicidal, runaway threats or behavior Excessive masturbation Medical conditions Recurrent abdominal pain or frequent somatic complaints Genital, anal, or urethral trauma Recurrent complaints of genital or anal pain, discharge, bleeding Enuresis or encopresis Sexually transmitted infections Pregnancy Promiscuity or prostitution, sexual dysfunction, fear of intimacy School problems or truancy Substance abuse
Physical findings Physical abuse May include abrasions, alopecia, bites, burns, dental trauma, fractures, lacerations, ligature marks or scars Injuries may be in multiple stages of healing Patterned bruise may be found e.g. belt marks, grab or pinch marks Any bruise in an infant not developmentally mobile should be considered suspicious Lacerations of frenulum or tongue Bruising of lips associated with force feeding Pathognomic burn patterns include stocking and glove distribution Immersion burns to buttocks Branding burns as with cigarettes or hot objects Absence of splash marks or a pattern consistent with spillage Head and abdominal trauma may present with its signs and symptoms Shaken baby syndrome (inflicted head trauma) have no visible findings on examination. Findings of retinal hemorrhages in absence of medical condition e.g. leukemia must be considered very suspicious Sexual abuse Usually there may be no visible signs depending on type of abuse and time since incident Nonspecific changes of genital and rectal regions such as erythema, rashes and irritation in absence of corroborative history. Certain STIs should strongly suggest sexual abuse e.g. N.gonorrhoae, syphilis, HIV beyond perinatal period Chlamydia, HSV trichomoniasis and HPV are all STIs but may have a protracted history from perinatal period. Neglect and nonorganic failure to thrive Relative absence of subcutaneous fat in the cheeks, buttocks and extremities Deprivation dwarfism Head circumference is usually normal in nonorganic failure to thrive Münchausen syndrome by proxy Most common reported presentations are recurrent apnea, dehydration induced by vomiting or diarrhea, sepsis where contaminants are injected into a child, change in mental status, fever, GI bleeding and seizures. Radiological and laboratory findings Certain radiological findings are strong indicators of physical abuse, they include: Metaphyseal “corner” or “bucket-handle” fractures of long bones in infants Spiral fractures of the extremities in nonambulatory infants Rib fractures Spinous process fractures Fractures in multiple stages of healing Skeletal survey x-rays should be conducted in all children under suspicion CT findings of subdural hemorrhage in absence of clear accidental injury Investigations Blood tests – FBC, blood film, coagulation studies, platelet aggregation studies, EUC, LFTs, serum amylase to detect any explanation for bruising and evidence of abdominal trauma Urine examination for blood Skeletal survey – to look for findings as above Nuclear bone scan – may reveal stress fractures in different stages of healing CT brain Ophthalmic examination is indicated in all infants suspected to have shaken baby syndrome CT abdomen – in case of suspected abdominal trauma with suggestive other signs to suggest intra- abdominal bleed or solid organ injury – ultrasound may be used first if stable. Arrange for a case management meeting with CPU, DOCs and other community services if feasible Referrals for family to drug and alcohol counseling, community health and other services as required Management of suspected physical abuse children Document history and injuries precisely and provide emergency care as needed Document all relevant observations which justify concerns e.g. inappropriate behavior or language, observations of parent child interactions Discuss your concerns with the inpatient team and consultant Inform parent of concerns about child’s injuries and need for further investigations Refer to local child protection unit if present or DOCs helpline for further assessment Refer to the CPU social worker or social worker in hospital for further liaison activity Form an initial case plan consulting with the pediatrician and child protection e.g. admission, discharge into foster care etc. Involve security, police or necessary authorities as deemed necessary In case of suspected sexual abuse, the relevant state authority for pediatric sexual assault needs to be contacted after all emergent treatment has taken place. Other aspects of post-sexual assault care would need to incorporate STI testing, need for post-exposure prophylaxis, patient and family counseling etc. Head injury
Head injury is the leading cause of death in children >1 year. It is the third most common cause of death in infants < 1 year. Boys suffer head injury twice as often as girls and are 4 times as likely to suffer a fatal head injury. Immediate priorities Establish: A – Airway B – Breathing C – Circulation C – Cervical spine stability Assess each of these and treat as necessary. Poor outcome following head injury correlates closely with persisting hypotension and hypoxemia. Head injury is further classified on the basis of Glasgow coma scale (GCS): Mild head injury (GCS 13-15) It is the most common form of head injury and accounting for >85% of the pediatric head injuries. Assessment largely dependent on history and physical examination If child is neurologically normal and there is nothing to suggest the possibility of skull fracture, no imaging is required. Indications for skull x-ray Obvious injury to the scalp or skull h/o focal impact to head mechanism of injury unclear not conducted if CT scan is indicated Indications for CT scan neurological deterioration or failure to improve to a GCS of 15 focal neurological deficit skull fracture in association with an abnormal GCS possible penetrating skull injury CSF rhinorrhea, otorrhea or other suspicion of base of skull fracture Indications for admission for observation Strongly consider admission for observation if there is: Any h/o loss of consciousness Post-traumatic seizure Skull fracture or other abnormality on CT scan Neurological deficit Failure to improve to GCS of 15 Persistent headache, nausea or vomiting Suspected child abuse Absence of suitable caretaker to observe child at home or poor access at home Moderate head injury (GCS 9-12) The child will require admission under neurosurgeon to either a HDU or ICU. Assessment ABCC review and stabilization Venous access and send bloods for EUC, FBC, clotting studies, calcium, LFT and glucose. Assume cervical spine fracture and apply immobilization with hard collar until fracture radiologically and clinically cleared Close vitals monitoring including P, BP, RR, SaO2 and GCS every 15mins CT scan always indicated – intubation required if patient uncooperative. Do not sedate until airway secured Severe head injury (GCS 3-8) Child always requires intubation, ventilator support and admission under neurosurgeon in intensive care. Assessment Review and stabilize ABCC in preparation for urgent CT scan. Blood investigations as for moderate head injury and blood gase as indicated Ventilate for end-tidal CO2 35-40 mm Hg and SaO2 100%. Excessive hyperventilation i.e. ETCO2 <30mmhg and PaCO2 < 25 mm hg reduces cerebral flow and may be detrimental Continuously monitor P, BP, SaO2 and EtCO2 Mobilize operating rooms and neurosurgical teams for need of either evacuation of IC collections or for insertion of ICP monitoring Mannitol Indications for use in ED prior to CT scan are: o Evidence of herniation – papillary dilatation, bradycardia o Evidence of mass effect – hemiparesis o Serious deterioration prior to CT scan Contraindications to use o Hypotension/ hemodynamic instability o Renal failure Dose 0.5 – 1.0 g/kg IV over 20 minutes Post-traumatic seizures Occurs in about 6% of children with minor head injury and incidence increases with severity of head injury Seizures are associated with twice the risk of poor outcome Timing of seizures o 20% impact seizures o 98% occur in first 24 hrs o 1% between 1 – 7 days o 1% occur after 7 days Type of seizure o 70% are generalized tonic-clonic seizures o 23% focal motor seizures o 7% atypical seizures Post-traumatic seizures usually benign and self-limited rarely progressing to epilepsy or recurrent seizures. Indication for drug treatment include o Prolonged seizures o Recurrent seizures o Seizures within first week Skull fractures Common in children and increasingly common with severity of head injury Vast majority do not require any specific treatment, but more risk for poor outcome and operative intervention Always consider NAI with any skull fracture especially any other markers for physical abuse are present Child abuse At least 10% of children < 10 years presenting to hospital with alleged accidents are victims of abuse. Factors raising the suspicion of abuse include: Retinal hemorrhages Bilateral chronic subdural hygromas Multiple skull fractures of different ages Absence of external signs in case of shaken baby syndrome Vomiting in Infants (predominantly) The principle variables in assessment of vomiting are age and colour of the vomit. Newborn, with mucosy clear froth Esophageal atresia is the major condition to diagnose o Polyhyramnios antenatally o Diagnosis made with 10FG feeding tubes’ inability to pass beyond 10cm and gasles abdomen in case there is no fistula o Refer urgently to surgeon and cease feeding o Leave 10FG in place for frequent aspirations o Nursing and transport in supine position Newborn to 2 days with bilious vomiting Atresia or Hirschsprung’s disease – serious surgical conditions to consider, but also rule out medical conditions e.g. sepsis Plain abdominal x-ray will help pick level of atresia Abdominal distension usually present Early referral to neonatal unit Infant with bilious vomiting Malrotation is the major condition requiring exclusion Usually presents at 4 weeks but can present at any age Infant with green vomit has malrotation and potential volvulus until proven otherwise – major surgical emergency and increased risk of necrosis of small bowel Less urgent situations – malrotation can be excluded by a contrast meal and follow through by pediatric radiologist. Infant with milk vomiting Pyloric stenosis o 20% positive family history o Sudden or progressive onset of increasing volumes that become more forceful and projectile o Early presentation with no weight loss and normal electrolytes or at other end of spectrum o Careful examination of abdomen and test feed if needed o If child healthy, passing urine and no weight loss – can be followed up next day o Early surgical opinion if child unwell Gastro-esophageal reflux – if small amounts of milk vomited from birth, effortless regurgitation opposed to forceful vomiting Wheezing in children
Wheeze reflects lower airway obstruction and is usually caused by dynamic compression of the intrathoracic airway proximal to the equal pressure point. It is predominantly expiratory and has a whistling quality. Although the intensity of wheeze may reflect the severity of the obstruction, wheeze may be absent in severe obstruction because of significant reduction in airflow.
Causes of lower airway obstruction Acute asthma Acute viral bronchiolitis Chemical bronchitis/ bronchiolitis Suppurative lung disease Cystic fibrosis Immune deficiency Primary ciliary dyskinesia Bronchiectasis Chronic lung disease of prematurity Bronchial malformations Bronchomalacia Stenosis
Wheezing in children is a common problem and 25 – 30% of infants will have ateast one wheezing episode. The most common causes of wheezing in children include o Asthma o Allergies o Infections o GORD o Obstructive sleep apnea o Congenital abnormalities o Foreign body aspiration and o Cystic fibrosis History Family history – viral illnesses, h/o eczema, asthma or allergies Age of onset – helps distinguish congenital and noncongenital Pattern of wheezing – episodic vs. persistent in congenital/ anatomical causes Seasonality – asthma and also viral illnesses such as RSV, metapneumovirus Suddenness of onset – to rule out foreign body aspiration Association with feeding - GERD Cough – GERD, sleep apnea, asthma and allergies Respiratory illnesses and Positional changes – tracheomalacia and anamolies of great vessels Physical examination Chronically ill appearing child – tested for metabolic disorders, immunodeficiency and cystic fibrois Infants with audible wheezing without respiratory distress usually signifies congenital airway lesion Look for signs of respiratory distress – retractions, nasal flaring, grunting Severity of wheeze and absence of wheeze in c/o sever obstruction Skin, cardiac and ENT examination Differential diagnosis and further investigations Signs and symptoms Presumptive diagnosis Further evaluation Associated with feeding, cough and GORD 24-hour pH monitoring vomiting Barium swallow Associated with positional changes Tracheomalacia, great vessel Angiography anomalies Bronchoscopy Chest X-ray CT or MRI Echocardiography Auscultatory crackles, fever Pneumonia Chest X-ray Episodic pattern, cough, response Asthma PFT to bronchodilators Trial of bronchodilators Allergy testing Exacerbated by neck flexion, Vascular ring Angiography relieved by neck hyperextension Barium swallow Bronchoscopy Chest X-ray CT or MRI Heart murmurs or cardiomegaly, Cardiac disease Angiography cyanosis without respiratory Chest X-ray distress Echocardiography History of multiple respiratory Cystic fibrosis or Ciliary function testing illnesses, failure to thrive immunodeficiency Immunoglobulin level Sweat chloride testing Seasonal pattern, nasal flaring, Bronchiolitis, RSV, croup, Chest X-ray if indicated intercostals retractions allergies Sudden onset of wheezing and Foreign body aspiration Chest X-ray choking CT or bronchoscopy Sudden Infant Death Syndrome
The sudden death of an infant younger than 1 year of age that remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene and a review of the clinical history. The diagnosis of SIDS is one of exclusion and thus poses specific challenges for the emergency departments they present to. Although death from SIDS is much more common than death from child abuse, the possibility of homicide is an omnipresent etiologic overlay. Informing parents of the death of the child is cited as the most stressful experience physicians confront in emergency medicine. These events are compounded by feeling of guilt and inadequacy, which are experienced by many emergency physicians following an unsuccessful pediatric resuscitation. These reactions are markedly different to those which an emergency physician faces during other crises in the department.
Pathophysiology Although multiple hypotheses have been proposed as the pathophysiologic mechanisms responsible for SIDS, none have been proven. The triple-risk model of SIDS proposes that the cause of SIDS is multifactorial, and that the sudden death of an infant may occur when a predisposed infant is in an unstable period of homeostatic control and is exposed to triggering factors. The three hypothesis that have been put forward in the past with most evidence include: The QT interval hypothesis The Apnea hypotheses Other hypotheses – vertebral artery compression, behavioral theory, autonomic instability, receptor deficiencies and genetic polymorphism, immunopathogenesis theory, Infections etc. Apnea hypothesis has the most evidence noted to date. Triggering factors Vulnerable periods in maturation of the brain stem may be critical when associated with the prone sleeping position. An infant sleeping prone, surrounded by a soft mattress, blankets, or other bedding, and possibly co- bedding with adults and compressed by or between large bodies, is in an environment that predisposes to progressive increase in carbon dioxide-rich, oxygen-poor air. The normal response to rebreathing expired air is increased ventilation and arousal, but with these normal responses blunted, hypoxia and hypercarbia may proceed unchecked. There is an association between breathing warm air ans risk of SIDS and rebreathing of warm expired air during prone sleep seems to have an increased risk. Though the risk is increased with breathing warm air, SIDS seems to be more common in cold temperatures probably due to cold-induced autonomic dysfunction. Lying prone cause infants to lift their heads and rotate neck to one side to maintain airway and this could support the vertebral artery compression theory. Passive smoking impairs vasodilatation in children, this may explain the inability for vertebral artery to dilate in response to compression and thus increase risk of SIDS associated with passive smoking. SIDS is probably caused by maldevelopment, or delayed maturation, of the neural network in the brainstem that operates to affect arousal and physiological responses to life-threatening events during sleep. Most cases of SIDS probably result from a lethal sequence of events initiated by a temporary defect in neural control of either respiratory or cardiac function during vulnerable periods in the maturation of respiratory control, sleep-wake development, and thermoregulation. Epidemiology Sex – approximately 60 – 70% of SIDS deaths occur in males Age – 80% < 5months of age, peak incidence between 2 – 4 months, only 1% in neonates, rest in last six months of first year. History Classic presentation of SIDS begins with an infant who is put to bed, typically after a feed Baby is found dead, usually in the position in which he/she had been placed Most infants are apparently healthy, many parents may state that the baby was not themselves in the hours before death Diarrhea, vomiting and listlessness have been reported in the 2 weeks prior to death Abuse should be considered in the DD of infants presenting in SIDS Autopsy cannot distinguish death due to SIDS from death by suffocation and certain discrepancies in history may raise suspicion as to abuse, these include: Atypical history, prolonged interval between bedtime and death Atypical age Age > 6months Suspicious factors for child abuse in perinatal period include: Unwanted pregnancy, Late arrival for delivery Birth outside hospital No well baby care of few visits No immunizations D&A issues during and after pregnancy Deviant feeding practices Previous unexplained medical disorders Previous episodes of apnea reported by same person H/o previous SIDS in family H/o child abuse in other siblings of family
Physical examination should include documenting of any signs of physical abuse e.g. bruises, pinch marks, scalds, burns etc. Also look for signs of malnutrition, neglect, cutaneous injuries, traumatic lesions etc. All physical examination findings need to be made during the period of CPR and should cease once the infant is declared death. Any examination of the infant conducted after declaration of death is considered violation of criminal law.
Emergency department care If the infant is pronounced dead, inform the family in a quiet environment. Refer to the child by name, not as "the baby." Detailing resuscitative efforts before telling the parents of the death is not helpful and may engender parents' resentment. Specifically and directly tell parents that their child has died; use of words such as dead or died avoids confusion that may result from gentler terms such as "passed on." Expressions of sorrow and sympathy are appropriate and desirable, but avoid statements such as, "I know how you feel." Follow the protocol of the local medical examiner or coroner's office concerning retention or removal of an endotracheal tube or lines for vascular access. In NSW, leave all medical equipment in place. The family may see the infant after pronouncement of death. Some coroner or medical examiner offices do not want the infant's body left alone with the family, and they also do not want family members to hold the infant, until arrival of a medicolegal death investigator. Local policy should be followed and, where appropriate, diplomatically explained to the family. Issues such as baptism, grief counseling, religious support, reactions of surviving siblings, and risk of SIDS in subsequent siblings may have to be addressed. Return clothes or personal belongings to the parents, after receipt of permission from the coroner or medical examiner. In addition, a physical memento may be offered (eg, a lock of the child's hair, a handprint or footprint). Only after permission from coroner. Spend time with families to offer comfort, answer questions, and provide information. Health professionals must be compassionate, empathic, supportive, and nonaccusatory, while simultaneously conducting a thorough investigation. The parents may be told that their child's demise is a sudden unexpected death in infancy (SUDI), and that classification of the type of SUDI can be established only through review of records, thorough scene investigation, and complete postmortem examination. While sudden infant death syndrome (SIDS) is one category of SUDI, it should be emphasized that such a final diagnosis may only be made through exclusion of all other causes of death. Parents' reactions encompass the spectrum of negative human emotion, and may range from silence to hysteria. Parents often experience intense feelings of guilt, including most cases in which there is no reason for such recriminations. The death of a child in the ED is not a common event; thus, most emergency physicians do not have a depth of experience in telling parents their child is dead. Furthermore, only 14% of emergency physicians, in one study, recalled having received any training in notifying parents of the death of a child. Health professionals experience many of the same emotions as the parents (eg, guilt, anger, sadness, self-reproach, shock). Consideration should be given to critical incident stress debriefing following an infant death or other particularly stressful case.
Advice to parents seeking information on prevention of SIDS The Task Force on Sudden Infant Death Syndrome (2005) makes the following recommendations for healthy infants only:
Do not smoke during pregnancy. Back to sleep: Place infants in the supine position for sleep. Avoid soft surfaces and gas-trapping objects in an infant's sleeping environment. Of particular importance, do not place soft objects, such as pillows or quilts, under a sleeping infant. A certain amount of tummy time, while the infant is awake and observed, is recommended for developmental reasons and to help prevent flat spots on the occiput. Separate but proximate sleeping environment. While bed-sharing is hazardous, the risk of SIDS is reduced when the infant sleeps in the same room as the mother. Consider offering a pacifier at nap and bedtime. Pacifiers may have a number of effects: protecting infants from nasal compression, enlarging the infant’s pharyngeal airway, lowering arousal thresholds, and strengthening the pharyngeal muscles responsible for maintaining the airway. Avoid overheating. A previous recommendation from this Task Force raised the caution flag especially when the infant is ill, or when he or she is recovering from an illness. Avoid commercial devices advertised to reduce the risk of SIDS, such as devices purported to maintain sleep position or reduce the risk of rebreathing, as none of these devices have been tested sufficiently for efficacy or safety. Do not routinely use home monitors to reduce the risk of SIDS; rather their use is indicated only for selected infants who have extreme cardiorespiratory instability. A previous recommendation from the American Academy of Pediatrics Task Force on Infant Positioning and SIDS was to put infants to bed in the supine position when they can turn easily from the prone position but allow them to adopt whatever position they prefer. Neonatal resuscitation At birth, assess if baby is breathing and/or crying and assess muscle tone – if both are good routine care of baby should follow which includes Dry the baby Provide warmth Clear the airway only if needed Assess breathing, colour and heart rate A normal baby should be breathing normally with a heart rate of > 100/min and begin to look pink. Birth
Breathing or crying? Good Muscle tone?
No
Dry and stimulate Position head and neck to open the airway Provide warmth
Assess breathing and heart rate
If heart rate <100/min or inadequate breathing
Give PPV until heart rate >100 and infant breathing
Inadequate breathing and heart rate <60/min
Assess adequacy of ventilation and optimize If heart rate does not increase >60/min Give chest compressions with PPV at 3:1
If heart rate still does not >60/min, reassess ventilation technique Give adrenaline, continue CPR, consider fluid bolus
Consider endotracheal intubation at any of the above stages when thought appropriate.
Bacterial meningitis Diagnostic principles Should be considered in any child with unexplained fever Headache, photophobia, neck stiffness and drowsiness likely in older children, may be absent in younger children and infants Very young infants have non-specific signs – lethargy, reluctance to feed, weak cry, apnoea, hypothermia and shock Presence of another source of infection does not rule out possibility of meningitis Should be considered in children presenting with first febrile seizure Differential diagnosis: Viral, fungal and protozoal intracranial infections, including malaria Intracranial abscess and hemorrhage Tuberculous meningitis Raised intracranial pressure Can occur at any stage of disease with meningitis and should be suspected when there are: Focal neurological signs Rapidly deteriorating consciousness or deep coma (GCS<8) Signs of transtentorial herniation such as o One of both pupils dilated and poorly reacting o Decorticate or decerebrate posturing o Abnormal fluctuations in pulse, BP or RR o Episodic apnea Fundoscopic changes s/o papilledema Continuous uncontrolled seizures Under these circumstances LP may be fatal and should not be performed. If meningitis strongly suspected: Attempt bacteriological diagnosis by blood and urine cultures, meningococcal PCR on blood Commence appropriate antibiotics Lower ICP with mannitol, hyperventilation Exclude SOL by CT head, once child is stable Reconsider LP later when it can be done safely Lumbar puncture LP is indicated when meningitis is suspected. Contraindications Evidence of raised ICP Immediately overlying skin infection Bleeding disorder – prior to clotting factor replacement Distance to dura Approximate guide is: Children < 10kg: 1.5mm/kg Children 10 – 40kg: 1mm/kg Initial assessment Same as any unwell child, special attention to antibiotic allergy, developmental history and neurological signs including head circumference, circulation and hydration Bedside investigations: BSL and correct if needed, blood gases Blood investigations: EUC – w/f hyponatremia and investigate for SIADH Steroids – dexamthasone 0.4mg/kg/dose 12 hrly for 2 days – reduces complications of Hib and pneumococcal meningitis, ideally 10 mins before the antibiotics CT scan not generally required but requested urgently if there are any signs of raised ICP, though it does not diagnose raised ICP, it can rule ICSOL. Initial management Fluids – resuscitation and correction of hypovolemic shock and acidosis, to ensure adequate tissue perfusion – IV boluses 20ml/kg of NS or hartmann’s. fluid restriction only recommended if proven SIADH. Steroids – as above Give antibiotics early – do not wait for CT scan or LP results Treat seizures – benzodiazepines and phenytoin Consider artificial ventilation for sever disease Rifampicin prophylaxis for family and close contacts Antibiotic therapy IV antibiotic therapy ASAP When possible based on gram stain and subsequent culture result Pneumococci increasingly resistant to both penicillin and cefotaxime, so include vancomycin when strong possibility of it suspected. Review when LP results available 5 days IV therapy for meningococcal and 7 days for most other bacterial meningitis. Longer duration for severe or complicated, neonatal and gram negative meninigitis. Age Situation Antibiotics 0 – 6 months Presumed bacterial meningitis Ampicillin + cefotaxime >6 months Presumed bacterial meningitis Cefotaxime Any age Hib – culture proven or urinary Cefotaxime antigen positive Any age Pneumococcus considered, or LP Cefotaxime + vancomycin contraindicated Any age Suspected meningococcal Cefotaxime Any age Culture proven meningococcal Penicillin Management of cardiac arrest Immediate steps (ABC;E) – cardiopulmonary resuscitation (CPR) Recognition that the child is unconscious – judged by lack of response to either a loud call or tapping the child. Call for assistance while commencing basic life support. o Maintain AIRWAY – clear mouth and pharynx, lift chin up and forward and place an oropharyngeal airway if necessary o Determine if BREATHING is present – if not, provide 2 – 5 effective slow breaths with self- inflating bag and mask. Maintain breathing with bag and mask or if unavailable, use resucitube or mouth-to-mouth. o Assess CIRCULATION – if no pulse felt over 10 seconds or if heart rate ,60/min and/or signs of circulatory inadequacy, commence external cardiac compressions o Call for help – summon arrest team – immediate duties of emergency team are to simultaneously: . Secure airway with intubation . Achieve vascular access . Establish cardiac rhythm using ECG monitoring o Ventilation must be adequate but not excessive. Duration of inspiration 1 – 1.5 seconds at rate of 4 – 8/min. . Ventilate using 100% O2 with BVM and flow rate at 15 L/min. o Confirm tube position by one of many methods o ECC – . Area of compression – lower half of sternum with patient on firm surface . Depth – chest compressed approximately 1/3rd the AP diameter . Rate – 100/min for all ages . Duration – compression phase = release phase = 0.3seconds each . Compression ventilation ratio – 30:2 for single rescuer and 15:2 for two rescuers. No need to synchronise breaths and compressions once intubated Vascular access – try IV for ≤ 90 seconds, then go for IO if unsuccessful, ET route only as last resort, avoid intracardiac route Defibrillation – for VF/ pulseless VT DC shock initially 2j/kg followed by 2 minutes of CPR then 4j/kg, then adrenaline 10µg/kg IV/IO and repeat 4j/kg + 2 minutes CPR, then amiodarone 5mg/kg IV/IO then DC shock 4J/kg, then cycle with adrenaline 10µg/kg IV/IO and DC shocks 4J/kg. Reversible causes – consider 4Hs and 4Ts o Hypoxemia, hypovolemia, hypo/hyperkalemia, hypo/hyperthermia o Tamponade, tension pneumothorax, thromboembolism, toxins/ poisons/ drugs Consider alkanizing agents as last resort If asystolic, cycle between adrenaline 10µg/kg IV/IO every 3 min CPR. Intubation in infants/children
Normal pediatric airway anatomy The normal airway of a pediatric patient has important anatomic differences from that of the adult. These differences are most apparent in infants and become relatively insignificant by age 8 years. Differences include: The size of the occiput and the tongue in the infant, The high position of the larynx, The configuration of the larynx, and The position of the vocal cords. The size of the occiput and the tongue in the infant The infant has a large occiput. Positioning of the head to obtain the optimum orientation for laryngoscopy, or the “sniffing position”, is accomplished simply by rotating the head so that it rests on the occiput. Elevating the head with padding can lead to excessive flexion of the neck and may contribute to upper airway obstruction and difficulty during intubation. The infant’s tongue is also relatively large, and this can impair laryngoscopy and contribute to upper airway obstruction. The high position of the larynx An infant’s larynx is higher in the neck, located at the C3 level, than that of an adult, which is found at the C4-5 level. The configuration of the larynx The larynx also has a funnel shape in infants, with the narrowest portion at the subglottic area, rather than at the level of the vocal cords as in adults. Hence, in infants and small children, an ET tube that passes easily through the vocal cords may encounter resistance more distally. The position of the vocal cords Infant’s vocal cords are slanted anteriorly rather than being perpendicular to the trachea as in adults, and thus can result in difficult visualization and intubation in pediatric population. Congenital abnormal pediatric airways Pediatric Syndromes and Associated Airway Abnormalities Prominent Airway Abnormality Syndromes Mandibular hypoplasia Hallermann-Steiff-François Pierre-Robin Goldenhaber Nager Treacher Collins Maxillary hypoplasia Apert Pfeiffer Crouzon Macroglossia Trisomy 21 Beckwith-Wiedemann Hurler Tracheomalacia Apert Crouzon Acquired abnormal pediatric airways ACUTE Foreign body aspiration Infection Laryngotracheobronchitis Epiglottits Subglottic edema Previous intubation Allergy Internal or external airway trauma CHRONIC Subglottic stenosis Posttraumatic or post-surgical Tumor or abscess formation Pediatric airway equipment Bag-Valve-Mask devices Should provide an airtight seal between the mask and patient’s face Child-size or adult-size self-inflating bags may be used for the entire range of infants and children Maximum oxygen delivery occurs at an oxygen floe of 15L/min Laryngoscope blades A straight blade is superior to a curved blade in children younger than 2 years of age. Tip of Macintosh (curved) blade is inserted into the vallecula anterior to the epiglottis The tip of the Miller (straight) blade is placed beneath the epiglottis Laryngoscope Blade Selection for Pediatric Patients Age Miller Macintosh Premature 0 Neonate 0 or 1 1 month to 2 years 1 2–6 years * 2 6–12 years 2 2 or 3 12 or older 2 or 3 3
Endotracheal tubes For neonates >1.5 kg body weight 2.5mm Between 1.5 and 2.5 kg body weight 3.0mm Above 2.5kg 3.5mm For children > 1year of age Tube size (in mm) = 4 + age (in years)/4 Use of Broselow tape measures – slightly more accurate Diameter of the fifth digit – most crude method Method to confirm accurate size after insertion – no leakage up to pressures of 10 cm H2O but should leak at 30cm H2O Cuffed tubes generally avoided in patients <8 years Appropriate placement of ET tube is midway between glottis and the carina
Laryngeal Mask Airway Widely used in pediatric population Extremely useful rescue device in management of difficult airways and in failed intubation scenarios May be used as a conduit for fibroptically guided ET intubation.
Rapid sequence intubation of the pediatric patient THE SEVEN “PS” OF RSI 1. Preparation 2. Preoxygenation 3. Pretreatment 4. Paralysis with induction 5. Positioning 6. Placement of tube 7. Postintubation management
Preparation All necessary tools and materials should be prepared Well functioning IV line must be in place All drugs to be used for RSI should be predrawn in syringes and labelled. Laryngoscopes of appropriate calculated size and sizes above/ below checked for functionality Rescue maneuvers and airways thought about and procured handy Appropriate size ET tube prepared with stylet, with tube size larger and smaller handy Personnel allocated duties e.g. drugs, cricoid pressure etc. Continuous pulse oximetry and cardiac monitoring instilled with CO2 detection device/ machine ready for use Preoxygenation Due to relatively high O2 consumption, smaller children and infants undergo rapid desaturation, even with normal lungs Preoxygenation is effectively denitrogenation of functional residual capacity, and it increases the oxygen reservoir by roughly five-fold. Usually achieved by having the patient breathe 100% O2 from a tight fitting mask for 2min or for four vital capacity Premedication Atropine should be given pre-emptively when succinycholine administration is been considered (0.015 to 0.2 mg/kg IV) for all RSI to prevent bradycardia associated with posterior pharynx stimulation. In patients with increased intracranial pressure, consider lidocaine (1.5mg/kg IV), 1-5 min prior to intubation. Lidocaine is believed to decrease the adrenergic response to laryngoscopy, sedatives and neuromuscular blocking agents. Lidocaine is also shown to attenuate cough and increases in intracranial and intraocular pressures. Paralysis with induction Drugs for Pediatric Intubation Drug Dose Duration Comments Neuromuscular blockade Vecuronium 0.15–0.20 mg/kg to 60 min Atropine 0.02 mg/kg Rocuronium 0.9–1.2 mg/kg to 60 min Atropine 0.02 mg/kg Succinylcholine 1–2 mg/kg 3–5 min Atropine 0.02 mg/kg Anesthetic agents Etomidate 0.3 mg/kg 5–10 min Cardiostable; not an analgesic Midazolam 0.1–0.2 mg/kg 30–45 min Cardiostable; reversible Ketamine 2 mg/kg 20–60 min Cardiostable; use atropine Thiopental 4 mg/kg 5–10 min Hypotension, histamine release Propofol 2.5–3.5 mg/kg 4–8 min Hypotension
Drugs Thiopentone Most commonly used agent for induction of anaesthesia in emergency Relatively inexpensive with reliable induction within 1 minute. Causes significant venodilation and moderate direct myocardial suppression, with resultant decreases in blood pressure and cardiac output despite tachycardia. Lowers intracranial and intraocular pressures Only barbiturates have been shown to provide cerebroprotection in acute brain injury Side effects – o histamine release – flushing, exaggerated hypotension and wheezing o neuroexcitatory effects – twitching, cough and hiccups o extensive tissue necrosis if extravasated Propofol Onset of action similar to thiopentone with comparable decreases in blood pressure and cardiac output No reflex tachycardia Superior to thiopentone in suppressing pharyngeal and laryngeal reflexes Lowers intracranial and intraocular pressures although more expensive, comparable to thipentone in most instances of use. Side effects – o Pain in injection attenuated by preadministration of lidocaine o Prepared in emulsion and can have bacterial contamination, so has to be used within 6hours of opening the container o Does not histamine release, bronchospasm or necrosis on extravasation like thiopentone Ketamine Unlike other agents, ketamine tends to increase heart rate, blood pressure and cardiac output by central sympathetic stimulation Attractive for use in low volume states and trauma. Bronchodilator with no suppression of ventilator drive – excellent choice in patients with airway disease Significant analgesic and amnestic properties and can be given IM (4-6 mg/kg) with onset in 5 minutes Side effects – o Bronchorrhea o Increases cerebral blood flow, ICP and IOP o Significant incidence of emergence hallucinations (less common in children) Midazolam Most popular benzodiazepine for induction of anesthesia due to rapid onset time and lack of venous irritation Much larger doses required for induction of anesthesia than sedation At induction doses, recovery time is prolonged but unlike other agents an effective antagonist is available. Hypotension uncommon in cardiovascularly stable patients, but may be significant in hypovolemic patients Side effects – o Hypotension in hypovolemic patients o Apnea common and increased risk when administered with opioids o Amnesia most reliable as compared to others Succinylcholine Only depolarizing agent available and remains the drug of choice in RSI Extremely reliable with rapid time to onset of action, intubating conditions within 45 seconds Spontaneous respirations usually returns within 3-5 minutes Side effects – o Hyperkalemia o Malignant hyperthermia o Elevations in ICP, IOP and intragastric pressures o Prolonged blockade and fasciculations o Risk of hyperkalemic arrest in children subsequently found to have underlying undiagnosed myopathies. o Bradycardia may occur in children especially after the second dose and therefore atropine premedication is advised o Masseter spasm in a small number of patients may occur When succinylcholine is contraindicated, fast acting nondepolarizing NMB such as Rocuronium may be used. Management of the febrile child Early recognition and effective treatment of serious sepsis is of the highest priority. Definitions Fever – rectal temperature > 38 C or oral/axillary temperature > 38.5 C Serious bacterial infection – meningitis, septicemia, bone or joint infection, UTI, pneumonia, bacterial enteritis Occult bacteremia – bloodstream bacterial infection without clear focus of infection Toxic appearance – lethargy (reduced consciousness with poor or absent eye contact), poor perfusion, hypoventilation, hyperventilation, cyanosis History and examination: Respiratory symptoms e.g. cough, tachypnea may or may not signify pneumonia Abdominal pain may suggest UTI or enteritis h/o foreign travel must be sought h/o animal contact e.g. cat scratch Assess if child is ‘toxic’. Following signs suggest serious illness o A – poor arousal, reduced alertness and reduced activity o B – breathing difficulty, tachypnea and increased effort o C – circulatory impairment (mottling, tachycardia, decreased capillary return, hypotension and pale colour o D – decreased drinking (<1/2 usual), decreased urine output (<4nappies/day) Sinister signs – apnea, convulsions, cyanosis and petechial rash More features – more serious, lower age – less likely to have signs, no signs does not rule out serious illness Recent antibiotic use may obscure the clinical signs of sepsis Febrile child without a focus A non-toxic febrile child <3 years without obvious focus infection most likely has a viral infection. 10% of febrile children with no focus have occult bacteremia – positive cultures despite normal LP, Urine and CXR. S. pneumoniae (pneumococcus) is commonest but ↓since immunization, HIb rare now. N. meningitides and salmonella species less common. Most pneumococcus bacteremia spontaneously resolve without therapy but 1-2% may develop meningitis. But HIb bacteremia or meningococcal bacteremia carries much larger risk. Risk factors for serious infection o Neonate o High fever o Raised WBC o Toxic appearance Clinical acumen important Investigations: o FBC, blood culture o MSU, LP o CXR Management options for febrile child without focus Indications for admission, investigations and empiric antibiotics o All febrile neonates <28 days o All febrile infants <3 months o All toxic appearing febrile children <60 months Indications for no investigations and review in ED o Well looking febrile child aged 3 – 60 months who will reliably return for follow up Indications for investigations with decision on results o Moderately unwell children 3 – 60 months old. Neonatal jaundice Jaundice of the newborn is common and may be feature of a serious and treatable disorder. A very high level of unconjugated bilirubin can cause kernicterus and resultant neurological damage – choreoathetoid cerebral palsy from basal ganglia damage. Etiology and investigation: Jaundice at birth or <24 hrs is likely due to hemolysis or congenital infection Jaundice beyond 7-10 days requires exclusion of bile duct obstruction Jaundice is pathological if it; o Appears too early <24hrs o Appears too late >3-4 days o Is too high – requiring treatment o Lasts too long > 2 weeks o Is associated with an elevated direct or conjugated fraction Following investigations for pathological jaundice required: o Total and direct bilirubin o Total protein o Blood film to examine red cell morphology o Blood group, Direct coombs test Further investigations if persistent prolonged jaundice looking for hemolysis Hemolysis Jaundice within 24hrs suggests Hemolysis which can be immune or non-immune Following investigations are required o Maternal and infant blood groups o Direct coombs test o Total and direct serum bilirubin o FBC and blood film Non-immune causes: o Abnormal RBC shape – hereditary spherocytosis o Red cell enzyme defects – G6PD deficiency o Abnormal hemoglobins – thalassemia Prolonged unconjugated jaundice Prolonged jaundice for >2 weeks in wel infant is usually breast milk jaundice DD: congenital hypothyroidism or Crigler-Najjar syndrome If infant unwell consider UTI, galactosemia and congenital hypopituitarism Investigations o Newborn screening test o TFT o Urine for non glucose reducing substances o Urine culture o RBC galactose-1-phosphate uridyl transferase o Plasma cortisol or short synacthen test Neonatal cholestasis (obstructive, conjugated or direct jaundice) Present when direct (conjugated) bilirubin > 25-35 µmol/L and >20% of total bilirubin Cholestasis may be secondary to o Shock, parenteral nutrition or bacterial or congenital infection o Inborn errors of metabolism o Biliary obstruction or hepatocellular disease o Rarer causes: e.g. cystic fibrosis, congenital hypothyroidism Imaging: o Ultrasound to rule out extrahepatic biliary atresia, choledochal cyst or intrahepatic obstruction
Treatment o Phototherapy and exchange transfusion o Fluids Acute Asthma Assessment Take into account previous history including o interval symptoms, o sleep disruption, o exercise-induced symptoms, o triggers for asthma episodes o frequency of attacks o regular medications and medications during current episode o past admissions and ICU admissions Guidelines for assessing attack severity in children Presentation Mild Moderate Severe Life-threatening Altered No No Agitated Agitated, confused, consciousness drowsy Physical No No Yes Yes exhaustion Talks in Sentences Phrases Words Words Accessory muscle No Minimal Moderate Severe use Pulsus paradoxus Not palpable May be + Palpable Palpable Wheeze intensity Variable Moderate to loud Often quiet Often quiet Pulse rate <100 Tachycardia Marked tachycardia Marked tachy- or brady-cardia Central cyanosis Absent Absent Likely + Likely + SaO2 >94% 90 – 94% <90% <90% PEF or FEV1 >60% 40 – 60 % <40% <40% (% predicted)
Treatment Initial treatment determined by severity Presentation Mild Moderate Severe or life-threatening Admission Probably not Probably Consider ICU Oxygen Probably not Monitor with SaO2 Monitor with SaO2, ABG Β2 agonists Salbutamol via spacer Salbutamol via spacer as Salbutamol via nebulizer: <6yrs – 6puffs (600µg) before, repeat q20mins <6yrs – 2.5mg, ≥6yrs – >6yrs – 12puffs (1200µg) x2, if poor response use 5mg; initially q20min X 3 nebulizer or continuously Nebulised ipratropium Not necessary Optional 250µg added to <6yrs – 4puffs (80µg) salbutamol nebulizer >6yrs – 8puffs (160µg) q20min x 3, then 4hrly Steroids Yes consider Oral prednisolone IV methylprednisolone 1mg/kg/dose daily x 3- 1mg/kg 6hrly day 1, 5days 12hrly day 2, then oral as before IV salbutamol No No - only consider if Consider IV salbutamol multiple nebs needed bolus (15µg/kg over 10mins) if poor response to nebs. Continuous IV 1- 5µg/kg/min may be used IV aminophylline No No Only in ICU Loading: 5mg/kg over 30min Maintenance: <9y – 0.9mg/kg/hour >9y – 0.7mg/kg/hour Monitor blood levels at 6hrs Chest x-ray Not necessary unless No necessary unless focal Necessary if no response focal signs signs to therapy and to r/o pneumothorax ABG Not necessary Consider if initial May be required response poor Observations Regular Frequent Continuous
Salient points about above therapies: Maintain SaO2>95%. Oxygen does not cause CO2 retention in children IV steroid options are methylprednisolone 1mg/kg maximum 50mg every 6-8 hrs or hydrocortisone 4- 5mg/kg, maximum 200mg, every 4-6hrs. Magnesium sulphate can be considered for life threatening asthma o Bolus 50mg/kg over 20mins or continuously 30mg/kg/hour Other therapies IV fluids if patient not tolerating oral fluids or in c/o sever episode CPAP or assisted ventilation may occasionally be necessary despite aggressive medical terapy Antibiotics seldom necessary Physiotherapy only in convalescent phase, if there is lung collapse. Assessing response to therapy: Increased patient comfort; reduced feeling of tightness Reduced use of accessory muscles of breathing Reduction in RR Improved air entry Reduced length of expiratory phase and wheeze Improved oximetry and oxygen requirement Discharge criteria Ready for discharge when clinically stable on bronchodilator 3hrly. Oximetry not a criterion but should be at least >90% Discharge documentation At time of discharge all asthma patients should receive: o Discharge summary o Asthma action plan including post discharge plan o Discharge medications o Follow up arrangements o Carer fact sheets o Referral to pediatric outreach service if required Hyponatremia
Hyponatremia may be factitious or true. Causes of factitious hyponatremia include: Hyperglycemia Hyperlipidemia Hypertriglyceridemia Hyperproteinemia Classification and etiology
Clinical features Mild symptoms of nausea and malaise progress to headache, lethargy, and disorientation as the sodium concentration drops. The most serious symptoms are respiratory arrest, seizure, coma, permanent brain damage, brainstem herniation, and death. Laboratory assessment Serum electrolytes Serum creatinine Serum osmolality Urine sodium Etiology of most cases of hyponatremia will be apparent from the history, physical and basic laboratory tests. Additional tests of thyroid function and adrenal function will occasionally be required.
Calculation of sodium deficit Na deficit = (Na desired – Na observed) X bodyweight (kg) X 0.6 Treatment Half of the deficit is replenished in the first 8 hours of therapy, and the remainder is given over the following 16 hours. Maintenance and replacement fluids should also be provided. The deficit plus maintenance calculations generally approximate 5% dextrose with 0.45% saline. The rise in serum [Na+] should not exceed 2 mEq/L/h. The dangers of too rapid correction of hyponatremia include cerebral dehydration and injury due to fluid shifts from the ICF compartment. Hypovolemic patients require adequate fluid resuscitation from isotonic fluids (either normal saline or lactated Ringer solution) to suppress the hypovolemic stimulus for ADH release. Patients with cerebral salt wasting may require hypertonic saline to prevent circulatory collapse; some may respond to fludrocortisone. Hypervolemic patients may require loop diuretics or dialysis, or both, to correct increased total body water and sodium. Euvolemic patients may respond to free water restriction alone. Hypernatremia Hypernatremia is defined as a sodium concentration > 145 mEq/L. All patients with hypernatremia have hyperosmolality, unlike hyponatremic patients who can have a low, normal, or high serum osmolality. An intact thirst mechanism and access to water are the primary defense against hypernatremia. The hypothalamus can sense minimal changes in serum osmolality, triggering the thirst mechanism and increased water intake. Thus, whatever the underlying disorder (eg, dehydration, lactulose or mannitol therapy, central and nephrogenic DI), excess water loss can cause hypernatremia only when adequate water intake is not possible.
Clinical findings Symptoms and signs Dehydration, orthostatic hypotension Oliguria Lethargy, irritability and weakness are early signs Hyperthermia, delirium, seizures and coma may be seen with sever Hypernatremia (>158 mmol/L) Laboratory findings Urine osmolality > 400mosm/kg – renal water conserving ability is functioning Urine osmolality < 250mosm/kg – Hypernatremia with dilute urine characteristic of diabetes insipidus Central DI – inadequate ADH release Nephrogenic DI – renal insensitivity to ADH e.g. lithium, demeclocycline, relief of urinary obstruction, interstitial nephritis, hypercalcemia and Hypokalemia Treatment Hypernatremia with hypovolemia Isotonic saline to restore euvolemia and treat hyperosmolarity since NS is hypo-osmolar (308mosm/kg) After adequate fluid resuscitation change over fluid to ½ NS or 5% D Hypernatremia with euvolemia Water ingestion and 5%D → natriuresis If GFR decreased diuretics may be used but may need further fluid resuscitation Hypernatremia with hypervolemia 5% D + loop diuretics → natriuresis Severe cases with renal failure may need hemodialysis Calculation of water deficit Total body water (TBW) = 40 – 60% of current body weight (more in children) Volume to be replaced = current TBW X (Na – 140) / 140 Hyperkalemia Hyperkalemia usually occurs in patients with advanced kidney disease but can also develop with normal kidney function. Acidosis causes intracellular potassium to shift extracellularly. Serum potassium concentration rises about 0.7 mEq/L for every decrease of 0.1 pH unit during acidosis. Causes of hyperkalemia. Spurious Leakage from erythrocytes when separation of serum from clot is delayed (plasma K+ normal) Marked thrombocytosis or leukocytosis with release of intracellular K+ (plasma K+ normal) Repeated fist clenching during phlebotomy, with release of K+ from forearm muscles Specimen drawn from arm with intravenous K+ infusion Decreased excretion Kidney disease, acute and chronic Renal secretory defects (may or may not have frank kidney disease): kidney transplant, interstitial nephritis, systemic lupus erythematosus, sickle cell disease, amyloidosis, obstructive nephropathy Hyporeninemic hypoaldosteronism (often in diabetic patients with mild to moderate nephropathy) or selective hypoaldosteronism (some patients with AIDS) Drugs that inhibit potassium excretion: spironolactone, NSAIDs, ACE inhibitors, angiotensin II receptor blockers Shift of K+ from within the cell Massive release of intracellular K+ in burns, rhabdomyolysis, hemolysis, severe infection, internal bleeding, vigorous exercise Metabolic acidosis (in the case of organic acid accumulation—eg, lactic acidosis—a shift of K+ does not occur since organic acid can easily move across the cell membrane) Hypertonicity (solvent drag) Insulin deficiency (metabolic acidosis may not be apparent) Hyperkalemic periodic paralysis Drugs: succinylcholine, digitalis toxicity, β-adrenergic antagonists α-Adrenergic stimulation? Excessive intake of K+ Especially in patients taking medications that decrease potassium secretion (see above)
Clinical findings Hyperkalemia impairs neuromuscular transmission, causing muscle weakness, flaccid paralysis and ileus. ECG is not a sensitive method of detecting hyperkalemia ECG changes in hyperkalemia include: o Bradycardia o PR interval prolongation o Peaked T waves o QRS widening o Biphasic QRS-T complexes o Conduction disturbances such as bundle branch blocks and AV-blocks o Ventricular fibrillation and cardiac arrest terminally Treatment of hyperkalemia. EMERGENCY Modality Mechanism of Onset Duration Prescription K+ Action Removed from Body
Calcium Antagonizes 0–5 1 hour Calcium gluconate 10%, 5–30 0 cardiac minutes mL intravenously; or calcium conduction chloride 5%, 5–30 mL abnormalities intravenously + Bicarbonate Distributes K 15–30 1–2 NaHCO3, 44–88 mEq (1–2 0 into cells minutes hours ampules) intravenously
Note: Sodium bicarbonate may not be effective in end-stage renal disease patients; dialysis is more expedient and effective. Some patients may not tolerate the additional sodium load of bicarbonate therapy. Insulin Distributes K+ 15–60 4–6 Regular insulin, 5–10 units 0 into cells minutes hours intravenously, plus glucose 50%, 25 g (1 ampule) intravenously Albuterol Distributes K+ 15–30 2–4 Nebulized albuterol, 10–20 mg 0 into cells minutes hours in 4 mL normal saline, inhaled over 10 minutes
Note: Much higher doses are necessary for hyperkalemia therapy (10–20 mg) than for airway disease (2.5 mg). NONEMERGENCY Modality Mechanism of Duration of Prescription K+ Action Treatment Removed from Body + Loop diuretic ↑CO2 Renal K 0.5–2 hours Furosemide, 40–160 mg Variable excretion intravenously or orally with or
without NaHCO3, 0.5–3 mEq/kg daily
Note: Diuretics may not be effective in patients with acute and chronic kidney diseases. Sodium Ion-exchange 1–3 hours Oral: 15–30 g in 20% sorbitol 0.5–1 polystyrene resin binds K+ (50–100 mL) mEq/g sulfonate Rectal: 50 g in 20% sorbitol (Kayexalate) Note: Resins with sorbitol may cause bowel necrosis and intestinal perforation. Hemodialysis1 Extracorporeal 48 hours 200–300 + K removal Blood flow 200–300 mEq mL/min Dialysate [K+] ~ 0
Note: A fast and effective therapy for hyperkalemia, hemodialysis can be delayed by vascular access placement and equipment and staffing availability. Peritoneal Peritoneal K+ 48 hours Fast exchange, 3–4 L/h 200–300 dialysis removal mEq