CHAPTER 19 Infectious diseases 720 Meningitis 75% of cases of meningitis are believed to occur in those <15yrs of age. Three o rganisms (Streptococcus pneumoniae, Neisseria meningitides (mainly group B in the UK) and H aemophilus in \202 uenzae type b) account for 80% of the cases. H. in \202 uenzae and men ingococcal group C have declined very signi \201 cantly since the introduction of routine immunization in infancy. Three important practice points to remember are: Infants do not get classical symptoms of m eningism with meningitis and there should be an extremely low threshold for doing a lumbar puncture as part of the septic screen in infants with unexplained fever or seizures (see b pp.128, 180). Co-existing septicaemia in 20 \200\22330% is often the treatment priority to prevent death. Do not forget possibility of tuberculous meningitis. Pathogenesis The sequence of pathology involves: \200 \200 \200 \200 Colonization and invasion of the nasopharyngeal epithelium. Invasion of the blood stream. A ttachment to and invasion of the meninges. Induction of in \202 ammation with leak of prot eins leading to cerebral oedema. Alteration in cerebral blood \202 ow and metabolism. Cer ebral vasculitis. \200 Symptoms and signs In younger children symptoms may be non-speci \201 c including fever, p oor feeding, lethargy. Rash and seizures may or may not be present. In older children, feve r with headache and neck stiffness. Other features include: \200 \200 \200 General: Central: Seizures: subdural collection. Do not assume \200\230febrile convulsion \200\231 in child under 1yr of age or over 1yr of age with additional symptoms. Neck Neurol ogy: tuberculous or cryptococcal meningitis. Eyes: papilloedema is a late sign and not a re liable indicator of raised intracranial pressure. Retinal hemorrhages may be present and ma y indicate sagittal venous thrombosis or coagulopathy. However, these are rare and in the i nfant the possibility of non-accidental or in \202 icted head injury should be considered. fever, vomiting, and anorexia. irritability, disorientation, altered mental state. occur in 30%. Focal seizures suggest localized infarction or \200 stiffness: more common in older children. focal cranial nerve signs are more common in children with Lumbar puncture Lumbar puncture is a useful procedure to make the diagnosis of meningitis a nd identify the organism and it is generally safe. However, patients with bacterial meningi tis may have raised ICP so if there is a clinical suspicion of this problem (low heart rate with raised blood pressure, often \201 rst sign of which are transient changes seen on c ardiac monitors) then the procedure 19_McClure_19.indd 720 11/14/2012 3:51:56 PM MENINGITIS 721 should be deferred. (The cellular and chemical changes of meningitis will remain in the CSF for several days). The contraindications are: \200 \200 \200 \200 \200 \200 shock or cardiovascular instability; signs of raised intracranial pressure focal neurologic al signs or focal seizures infection of the skin at the lumbar puncture site (rare); eviden ce of coagulopathy; acute meningococcal disease Treatment See b Chapter 5 (b p.79). Suspected cases of meningococcal meningitis in the comm unity should receive IV benzylpenicillin (IM if no IV access) as an initial single dose. \200 \200 \200 (cid:2)10yrs, 1g. Children 1 \200\2239yr olds, 600mg. <1yr, 300mg. Suspected cases in hospital should receive 80mg/kg/od ceftriaxone (or cefotaxime 50mg/kg/td s). A management algorithm for health profession- als based on the NICE clinical guideline 102 is available at M www.nice. org.uk/CG102 Steroids In bacterial meningitis \200 \200 Do note use corticosteroids in children younger than 3mths There is bene \201 t from the u se of dexamethasone and the dosing schedule is 0.15mg/kg qds for 4 days to reduce the sever ity of neurological sequelae, particularly deafness, after bacterial meningitis (M www.nice .org.uk/CG102). If dexamethasone was not given before the \201 rst dose of antibiotics, b ut was indicated, try to give the \201 rst dose within 4hr of starting antibiotics, but d o not start dexamethasone more than 12 hours after starting antibiotics. In meningococcal septicemia \200 \200 Do not use the meningitic dosing of dexamethasone. In children with shock that is not respo nding to \202 uids and inotropes, physiological replacement of hydrocortisone (25mg/m2 qd s) should be considered after discussion with the intensive care team. 19_McClure_19.indd 721 11/14/2012 3:51:56 PM CHAPTER 19 Infectious diseases 722 Mycobacteria Pulmonary tuberculosis Pulmonary tuberculosis due to Mycobacterium tuberculosi s (an acid-fast ba- cillus) is discussed in b Chapter 9 (see b p.294). Atypical mycobacterial infection could be the cause of the following: Persistent a surgical ly resected node. Disseminated infection in the immunocompromised patient. Mycobacterium av ium intracellulare: is an infection often seen in patients with advanced disease due to HIV . lymphadenopathy: this infection is diagnosed after histology of Tuberculous meningitis (TBM) TBM is the most feared complication of M. tuberculosis infecti on. \200 usually occurs within 12mths of \201 rst infection. \200 group: most frequen tly occurs in those <5yrs of age. \200 Timing: Age Pathology: to the cerebral cortex from a p site (e.g. gut, lung). This increase s in size until it reaches the meninges and subarachnoid space. A thick gelatinous exudate is created especially around the brainstem so that cranial nerves III, IV, and VI are commo nly compromised. Hydrocephalus is common. Clinical course: the onset is insidious and is ch aracterized by apathy or disinterest, then intermittent headaches and anorexia. Fever is al most always present. Vomiting occurs in 50%. Focal neurological signs, seizures, or severel y depressed conscious level may occur. Diagnosis: or gamma interferon release assay often p ositive. 40 \200\22390% have CXR changes of pulmonary disease. Prognosis: most survive if t reated in the early insidious stage. There is a very high complication rate, especially if the focal neurological signs are present at the start of therapy. therapy with four antitub erculous agents and Treatment: corticosteroids is for at least 12mths and should be supervi sed by a specialist team. the initial pathology is occult haematogenous dissemination 50% will grow Mycobacteria from their CSF and the Mantoux 19_McClure_19.indd 722 11/14/2012 3:51:56 PM TROPICAL INFECTIONS 723 Tropical infections Tropical infections may be present in any child returning from the trop ics (see b p.1026). A general review in the febrile child should follow the process discuss ed in the section on \200\230Acute fever \200\231 (see b pp.696 \200\223701). Malaria \200 Agent: \200 Features: fever (often cyclical, though falciparum is not), di arrhea, vomiting, \202 u-like symptoms, jaundice, anemia, thrombocytopenia. Time occur af ter a few months in children. Diagnosis: thick and thin blood \201 lm should be examined in all children with fever from infected area without prophylaxis. Repeat daily for 3 sampl es if there is a high index of suspicion. Treatment: malaria, although not universally avai lable in the UK. For other forms of malaria consult specialist advice. Plasmodium falciparum (also P. vivax, P. ovale, P. malariae). course: onset usually occurs 7 \200\22310 days after inoculation, but may artesunate is now the \201 rst line therapy for P. falciparum Typhoid \200 Agent: \200 Features: GI symptoms a week later. Splenomegaly, bradycardia, and rose- colored spots on the trunk. Complications include GI perforation, myocarditis, h epatitis, and nephritis. Treatment: therapy following antimicrobial sensitivity testing. Salmonella typhi or paratyphi. fever, headache, cough abdominal pain, myalgia followed by third generation cephalosporin or cipro \202 oxacin, adjust Dengue fever \200 \200 Agent: Features: arthralgia, and high fever. s desquamation follows. Shock: another infecti on with a different strain. viral infection spread by mosquitoes. p infection produces a \201 ne erythematous rash, myalgia, Dengue shock occurs when a previously infected child has Viral haemorrhagic fevers \200 \200 \200 Agents: Features: Management: advice needed. Lassa, Marburg, Ebola, and other viruses. highly contagious and often lethal. if suspected, strict isolation is required and specialist 19_McClure_19.indd 723 11/14/2012 3:51:56 PM CHAPTER 19 Infectious diseases 724 Immunode \201 ciency disorders Immunode \201 ciency may be due to causes that are: \200 \200 Primary Secondary splenectomy, nephrotic syndrome, SCD, etc. : intrinsic abnormalities. : cancer, immunosuppressive agents, HIV infection, Primary immunode \201 ciency Caused by defects in the following. B lymphocytes and antibody production \200 X-linked severe bacterial infections Hyper agammaglobulinaemia: presents in early childhood with IgG \200 IgM syndrome: presents with bacterial infection and PCP subclass de \201 ciency: minor imm unode \201 ciency that may cause recurrent respiratory infection Tests Immunoglobulin levels and functional vaccine responses as indicated by clinical prese ntation T lymphocytes and cellular immunity Severe combined immunode \201 ciency (SCID) Presents i n \201 rst few months. Failure to thrive. Persistent infection due to viruses and fungi Tests FBC, blood \201 lm, lymphocyte subsets and function Neutrophil defects Leucocyte adhesion de \201 ciency Presents in infancy with delayed heal ing of the umbilical cord, chronic skin ulcers, bacterial and fungal infection involving ly mph nodes, liver, and lung Tests Assessment of chemotaxis, neutrophil surface adhesion molecules, and killing (e.g. ne utrophil oxidative burst test for chronic granuloma- tous disease) Opsonization and other innate immunode \201 ciencies Complement de \201 ciency or mannose binding lectin de \201 ciency Rare, but may present with severe meningococcal disease Tests Complement levels, TOLL receptor pathway assays (second line tests directed by clinic al presentation) Multisystem syndromes \200 \200 Ataxia Wiskott \200\223Aldrich immunode \201 ciency DiGeorge and immunode \201 ciency Dun can EBV infection telangiectasia: skin, neurological, and immune defects syndrome: eczema, thrombocytopenia, and syndrome: hypocalcaemia, branchial arch and heart defects, syndrome: X-linked lymphoproliferative disease due to prior Tests Chromosomal fragility, genetic polymorphisms 19_McClure_19.indd 724 11/14/2012 3:51:56 PM IMMUNODEFICIENCY DISORDERS 725 The investigation for these conditions in children with a history of recur- rent or severe infection requires a broad screen of tests, which can be directed by the type of infection (e.g. viral, bacterial, fungal). Treatment A variety of therapies is required for children with primary immunode- \201 cie ncy and they should be cared for in designated centers. Therapy in- cludes: \200 \200 \200 \200 \200 prophylactic antibiotics; supportive care and antibiotics for acute infections; replacement immunoglobulins and additional immunization; bone marrow transplantation; gene therapy (fu ture). 19_McClure_19.indd 725 11/14/2012 3:51:56 PM CHAPTER 19 Infectious diseases 726 Human immunode \201 ciency virus HIV infection in children is a global issue caused mainly by the retrovirus HIV (human immunode \201 ciency virus) type 1. Vertical transmission of HIV See b p.185. Children at risk of acquiring the virus are infan ts of HIV- positive mothers, although it is now rare because of the success of ante- natal preventative measures. \200 \200 Infants may become infected during labor and the postnatal period. Rate of vertical transmi ssion is 20 \200\22340% without suitable management but <1% with effective prophylaxis Prevention of vertical transmission \200 \200 \200 Use of antenatal, perinatal, and postnatal antiretroviral drugs. Avoid labor and birth cana l contact by elective Cesarean section. Avoidance of breastfeeding. Clinical features Dormant infection lasts a short period and has few or no clinical feature s. The later features of pediatric HIV infection are the following. \200 \200 \200 \200 \200 Gastrointestinal: CNS: Recurrent Lymphadenopathy Opportunistic Varicella, and atypical myco bacteria. Respiratory CXR. chronic diarrhea, failure to thrive. delayed development and cerebral palsy bacterial and viral infection. and hepatosplenomegaly. infections: Pneumocystis carinii, Candida, herpes virus, distress: cough, hypoxaemia, bilateral nodular in \201 ltrates on Acquired immune de \201 ciency syndrome (AIDS) Lymphocytic interstitial pneumonitis, Pneum ocystis carinii (PCP) infection, and Candida oesophagitis are \200\230AIDS de \201 ning \200\231 in an HIV-positive child; they signify progression to the AIDS phase. Diagnosis The diagnosis of HIV infection depends on demonstrating the following: \200 ant ibody response (anti-HIV antibodies): infants infected Speci \201 c perinatally have an im mune response by 4 \200\2236mths of age. However, an uninfected infant of a HIV-positive mo ther can test positive for anti- HIV antibodies for up to 12 \200\22318mths. Virus or its components in the blood (PCR): high speci \201 city tests. Treatment \200 \200 \200 \200 Prophylaxis against PCP. Avoidance of live oral polio vaccine and BCG. Antiretroviral thera py to suppress viral replication. Social, psychological, and family support. 19_McClure_19.indd 726 11/14/2012 3:51:56 PM HUMAN IMMUNODEFICIENCY VIRUS 727 19_McClure_19.indd 727 11/14/2012 3:51:56 PM CHAPTER 19 Infectious diseases 728 Immunizations \200 \200 \200 Immunizations are an important part of child health in the community. Immunization should b e delayed in the acutely ill child. In those where there is a family history of febrile con vulsion, advice should be given about control of fever with antipyretics, and when to seek medical assistance. Schedule The schedule for vaccinations to be given to an infant growing up in the UK is as follows: \200 BCG: TB, or those whose parents/grandparents were born in a TB high- prevalence country). H epatitis B: \200 \200 Diphtheria \200 \200 \200 Inactivated \200 \200 Haemoph ilus Neiserria infants. Pneumococcal Measles \200 \200 Human papilloma virus (HPV, agai nst cervical cancer): 6mths in girls 12 \200\22313-yr-old. birth in at-risk groups (e.g. those living in areas of high rate of birth, 1mth, 2mths in at risk groups; 12, 15, and 18mths in at risk groups. , pertussis, tetanus (DPT): 2, 3, and 4mths in all infants; booster at 3yrs 4mths to 5yrs old; booster for only diphthe ria and tetanus at 13 \200\22318-yr-olds. polio virus: 2, 3, and 4mths in all infants. boosters at 3yrs 4mths to 5yrs, and 13 \200 \22318yrs \200 in \202 uenzae type b: 2, 3, 4, and 12 \200\22313mths in all infants. meningitidis (mening ococcus) C: 3, 4 and 12 \200\22313mths in all \200 conjugate vaccine: 2, 4, and 12 \200\22313mths in all infants. , mumps, rubella (MMR): 12 \200\22313mths in all infants; booster at 3yrs 4mths to 5yrs. 3 doses within Live vaccines are contraindicated in children with immunode \201 ciency. Pertussis immuniz ation is contraindicated in infants who have had a severe local or general reaction to a pr evious injection. MMR is contraindicated in children allergic to excipients such as gelatin and neomycin. 19_McClure_19.indd 728 11/14/2012 3:51:56 PM IMMUNIZATIONS 729 Table 19.1 Routine childhood immunization program* When to immunize Diseases protected against Vaccine given DTaP/IPV/Hib & pneumococcal conjugate vaccine (PCV) 2mths old Diphtheria, tetanus, pertussis, polio, & Haemophilus in \202 uenzae type b (Hib) 3mths old Diphtheria, tetanus, pertussis, polio, & Haemophilus in \202 uenzae type b (Hib) DTaP/IPV/Hib, MenC Meningitis C (meningococcal group C) 4mths old Diphtheria, tetanus, pertussis, polio & Haemophilus in \202 uenzae type b (Hib) DTaP/IPV/Hib, MenC, & PVC Meningitis C Pneumococcal infection Around 12 \200\22313mths Haemophilus in \202 uenzae type b (Hib) & meningitis C Measles, mumps, & rubella (German m easles) Hib/MenC MMR & PCV Pneumococcal infection 3yrs 4mths to 5yrs old Diphtheria, tetanus, pertussis, & polio DTaP/IPV or dTaP/IPV & MMR Measles, mumps, & rubella 12 \200\22313yr old girls Cervical cancer 3 doses HPV 13 \200\22318yrs old Tetanus, diphtheria, & polio Td/IPV Each vaccination is given as a single injection into the muscle of the thigh or upper arm. Revised July 2011 M http://www.nhs.uk/Planners/vaccinations/Pages/Vaccinationchecklist.aspx 19_McClure_19.indd 729 11/14/2012 3:51:56 PM 19_McClure_19.indd 730 11/14/2012 3:51:56 PM 731 Chapter 20 Bones and joints Clinical assessment 732 The limping child 734 The limping child: differential diagnosis 736 Infections: septic arthritis 738 Infections: osteomyelitis 740 Spinal disorders 742 Spine: kyphosis 744 Spine: scoliosis 746 Hip disorders: developmental dysplasia of the hip 748 Hi p disorders: Perthes \200\231 disease 750 Hip disorders: slipped upper femoral epiphysis 75 2 Knee disorders 754 Orthopedic trauma 758 Osteochondroses 760 Osteogenesis imperfecta 762 Osteopetrosis 764 Cleidocranial dysplasia 765 Skeletal dysplasias 766 Juvenile idiopathic a rthritis 768 Juvenile idiopathic arthritis: clinical principles and management 770 Systemic arthritis 772 Oligoarticular juvenile idiopathic arthritis 773 Rheu matoid factor-positive polyarthritis 774 Rheumatoid factor-negative polyarthritis 776 Psori atic arthritis 777 Enthesitis-related arthritis 778 Systemic lupus erythematosus 780 Juveni le dermatomyositis 782 Mixed connective tissue disease \200\224overlap syndromes 784 Sclero derma 786 Henoch \200\223Sch nlein purpura 788 Polyarteritis nodosa 789 Wegener \200\231s granulomatosis 790 Takayasu \200\231s arteritis (pulseless disease) 791 20_McClure_20.indd 731 11/14/2012 3:24:02 PM CHAPTER 20 Bones and joints 732 Clinical assessment History This should focus on the following: \200 Presenting complaint: \200 \200\224site, severity, onset, nature, duration/chronicity, e xacerbating/ pain relieving factors, rest pain, radiation; if child presents with knee pain, always ask about and examine the hips; swelling limp morning stiffness/start-up pain; deformity \200 \200\224refusing to weight bear 9 history of trauma or injury; \200 \200 Associ ated systemic symptoms: \200 \200 Antenatal Neurodevelopmental milestones (see Past Spo rts and activities. Drug Family Neurological \200\224site, size, onset, duration, exacerbating/relieving factors; \200\224static/worsening or improving condition. infection (rigors, night sweats, \202 u-like symptoms); loss of appetite/weight. \200 \200 \200 \200 \200 \200 and birth history \200\224important with congenital conditions. b p.557). medical history \200\224previous trauma, surgery, medical illnesses. history \200\224glucocorticoid usage, allergies. history \200\224hereditary conditions. screening: \200\224important in syndromic children. Examination Inspection Observe the child walking and at play (don \200\231t forget to watch as they walk into the consulting room). \200 General: \200 \200 height, weight, proportion (long limbs, short trunk); soft tissue (swelling, muscle skin (s cars, lesions, color, discharge) \200\224 wasting, contractures), skeletal (alignment, rota tion, limb length); limb phocomelia (hand/foot attached directly to trunk), syndactyly (fus ed digits), polydactyly (additional digits); gait abnormalities of lower limb/spine (b pp.3 4, 496). \200\224amelia (absence), hemimelia (absence of distal half), \200\224antalgic, Trendelenburg, high stepping, short leg, crouch, Skeletal Spine \200 a lordosis at the cervical and lumbar spine (not noticeable in neonat es). look also for plagiocephaly, torticollis, scoliosis; lower varus/valgus deformity; alw ays examine the hips; feet during childhood. Look at the shoes! elbows especially in female s. alignment: \200\224normally there is a \202 exible kyphosis of the thoracic spine, limb \200\224check rotational pro \201 le, symmetric range of movement, \200\224babies have \200\230 \202 at \200\231 feet. The medial longitudinal arch develop s \200\224there is a mild valgus deformity when in extension 20_McClure_20.indd 732 11/14/2012 3:24:03 PM CLINICAL ASSESSMENT 733 Mobility and gait: matures (by the age of 7yrs), the gait becomes more \200\230adult-like \200\231 with the heel strike, stance phase (whole of foot to the ground), push off phase, and arm swing. The cadence decreases and the step length increases. antalgic \200 put wei ght on affected limb); high the ground to avoid tripping over); Trendelenberg gait \200 \224look at pelvis. When weight is loaded on the ipsilateral side, the contralateral hemipe lvis tilts downwards (due to weak abductors or neurological, muscular, or hip joint causes in the weight-bearing ipsilateral limb). The upper body is then used to counter-balance; to e boys consider DMD and check creatine kinase (CK). toddlers have a wide stepping jerky gait. As the child (painful) gait \200\224short stance phase (child does not want to stepping gait \200\224usually due to foot drop (child lifts foot higher off walking \200\224consider neurological causes (see b pp.34, 496). In Trendelenburg test: facing upwards. Ask the child to rest their hands (palms down) on your hands. Then ask the child to lift one leg. If the pelvis tilts downwards on the non-weight- bearing side (you will feel the downward pressure on your hand of this side) the test is po sitive. Gower \200\231s sign: sitting position without using their upper limbs. With weak l ower limb muscles, the child may \200\230crawl \200\231 hands up thighs in order to stand up, e.g. in muscular dystrophy. Neurodevelopmental assessment: Can the child hop on either foot? Can the child climb on to the examination couch? stand facing the child with your hands out, palms child should be able to independently stand from a \200 \200 see b p.557. Feel Tenderness, warmth, swelling ( \201 rmness, \202 uctuant), leg length discrepancy ( true leg length: measure from the anterior superior iliac spine to the medial malleolus), p ulses. Move \200 General: hyperlaxity/stiffness, contractures (are they \201 xed or can they be overcome?) . Spine: Hip: Knee: muscle tone, symmetric full joint range of movement, \200 \200 \201 xed/correctable deformity? Ortolani and Barlow tests (b p.748). patella instability, anterior drawer/Lachman test (ACL integrity). 20_McClure_20.indd 733 11/14/2012 3:24:03 PM CHAPTER 20 Bones and joints 734 The limping child Exclude trauma and infection before considering other disorders. Examination Lower limbs, back, and abdomen need to be examined. Observe the fol- lowing: \200 Limb position of least pain (e.g. in hip septic arthritis, the hip is held in \202 exion and external rotation). Gait ( Movement and mobility: \200 \200 \200 \200 b p.34). ability to weight bear passively and actively; ability to move the joints and limbs freely; palpate for tenderness, heat, and swelling around the joint; palpate the entire length of the extremity, the abdomen, and spine; leg length difference: anterior superior iliac spine (ASIS) to medial malleoli. to determine if discrepancy is in femur, or tibia perform galea zzi test ( \202 ex knees and hips and examine from the side); range of movement side; neur ological and vascular status: (ROM): in individual joint and compare with other abdominal examination. Beware of referred pain from joint above or from the abdomen (con- sider appendicitis, ingu inal hernia, UTI with hip pain). Always assess the joint above and below. Hip pathology may present as knee pain. Investigations \200 Temperature . \200 Bloods: rheumatoid factor (RF), antinuclear anti body (ANA), anti-streptolysin (ASO) titre, Lyme titre, HLA-B27. dipstick + MSU. Urine: X-ra ys: antero-posterior (AP), lateral plain X-ray of entire bone involved including joint abov e and below (e.g. if hip: AP pelvis and frog leg lateral views). US MRI: pathology. Three n ot speci \201 c. Radiation exposure. FBC, ESR (may be normal), CRP, blood cultures, blood \201 lm, \200 \200 scan: of muscle and bone. very sensitive and speci \201 c \200\224good for soft tissues and bone phase bone scan: when pain not easily localizable; sensitive, but 20_McClure_20.indd 734 11/14/2012 3:24:03 PM THE LIMPING CHILD 735 20_McClure_20.indd 735 11/14/2012 3:24:03 PM CHAPTER 20 Bones and joints 736 The limping child: differential diagnosis Table 20.1 Differential diagnosis according to area of lower limb affected Back Hip Femur Knee Foot & ankle Age 0 \200\2235yrs Discitis Developmental dysplasia of hip, transient synovitis, septic arthritis Osteomyelitis* Septic arthritis Age 5 \200\22310yrs Kohler \200\231s disease, Freiberg \200\231s disease, tarsal coalition, verruca Osteomyelitis* Discoid Discitis Transient synovitis, Perthes \200\231 disease, septic arthritis meniscus, septic arthritis Age 10 \200\22315yrs Discitis Slipped upper femoral epiphysis, septic arthritis Osteomyelitis* Osgood \200\223 Sever \200\231s disease, tarsal coalition, verruca, in growing toenails Schlatter \200\231s disease, osteochondritis dessicans, patellofemoral pain syndrome, chond romalacia patella Consider with septic joint. Causes of limp Tumor \200 \200 \200 b p.666). Neuroblastoma (age 0 \200\2235yrs) ( Ewing \200\231s sarcoma (age 5 \200\22315yrs) ( Osteos arcoma (age 5 \200\22315yrs) ( b p.670). b p.670). Benign tumor Osteoid osteoma (age 5 \200\22315yrs). Hematological causes (all ages) \200 Acute lymphocytic leukemia ( \200 HSP ( \200 SCD ( \200 Thalassaemia ( b p.656). b p.788). b p.620). b p.622). 20_McClure_20.indd 736 11/14/2012 3:24:03 PM THE LIMPING CHILD: DIFFERENTIAL DIAGNOSIS 737 Infection (all ages) \200 b p.722). \200 \200 \200 TB ( Malaria ( Lyme disease ( Viral. b p.723). b p.712). Neurological causes (all ages) \200 b p.550). \200 \200 \200 \200 Rheumatological causes (all ages) Juvenile idiopathic arthritis (JIA; b p.768). CP ( DMD ( Poliomyelitis. Hereditary motor sensory neuropathy ( Spina bi \201 da ( b p.546). b p.541). b p.170). Trauma (all ages) \200 \200 \200 \200 Non-accidental injury (NAI). Trauma (open/closed fractures). Sprains/contusions. Ill- \201 tting shoes. Congenital causes (all ages) Congenital limb de \201 ciency/shortening. 20_McClure_20.indd 737 11/14/2012 3:24:04 PM CHAPTER 20 Bones and joints 738 Infections: septic arthritis An infectious arthritis of a synovial joint. The frequency is highest in young children with half of all cases presenting in the \201 rst 2yrs. Males > female (2:1). Pathogenesis Septic arthritis can develop from osteomyelitis especially in neonates where i nfection spreads from the metaphysis via transepiphyseal vessels. It may also arise due to haematogenous spread of infection or by direct inoculation. Etiology \200 Age <12mths old: \200\223ve bacilli, Candida albicans. Age 1 \200\2235yrs: children), Grou p A streptococcus (pyogenes), Streptococcus pneumonia, Kingella kingae, Neisseria gonorrhea e (child abuse). Staph. aureus, Group A streptococcus. Age 5 \200\22312yrs: Staph. aureus, Neisseria gonorrhoeae (sexually active). Age 12 \200\22318yrs: Community acquired MRSA (CA- MRSA) is increasing worldwide. Staphylococcus aureus, Group B streptococcus, Gram Staph. aureus, Haemophilus in \202 uenza (rarely in immunized \200 \200 Common joints affected Most (75%) are in lower limb. Knee > hip > ankle. Other 25% are in u pper limbs. Differential diagnosis This depends on age and joint involved: \200 Hip: transient synovitis, Perthes, slipped capital femoral epiphysis, psoas abscess, proxim al femoral or vertebral osteomyelitis, discitis. Knee: distal femoral or proximal tibial os teomyelitis. Pain often referred from the hip. cellulitis, pyomyositis, other infectious ar thritis (viral, General: mycoplasmal, mycobacterial, fungal, Lyme disease), sickle cell, he mophilia, trauma, collagen vascular disease, Henoch \200\223Sch nlein purpura, reactive ar thritis from GI infections or GU infections, streptococcal pharyngitis, viral hepatitis, sa lmonella, or post-viral (HIV, CMV). joint involved: pauciarticular arthritis, rheumatic fev er, serum >1 sickness, HSP, collagen vascular disease, sickle cell disease, chronic recurre nt multifocal osteomyelitis (CRMO). Hemophilia: (predisposes to infection: pneumococci). increased risk of septic arthritis due to haemarthrosis Symptoms and signs Infants characteristically do not appear ill. 50% do not have fever. In the older child \200\224acute onset; decreased range of movements or pseudopa- ralysis; pai n on passive motion; hot, warm, swollen joint; inability to weight bear; systemic symptoms of infection. In <10% of cases more than one joint affected (except gonococcal infections). The clinical picture may be less acute if the child has received antibiotics. 20_McClure_20.indd 738 11/14/2012 3:24:04 PM INFECTIONS: SEPTIC ARTHRITIS 739 Investigations \200 \200 Blood: X-ray of joint: usually normal initially (widened joint space suggests an effusion). Subluxation/dislocation, joint space narrowing and erosive changes are later signs. Joint aspiration: microscopy and culture. PCR may be useful if already on antibiotics. US: MRI: t reatment while waiting for MRI). CT: Bone scan: Lumbar puncture: (increased incidence of me ningitis). FBC, ESR, CRP, blood cultures; Lyme titres if exposure. most useful diagnostic investigation. Send aspirate for \200 to detect effusion and guide aspiration. if diagnosis in doubt to exclude osteomyelitis, (d o not delay \200 \200 to imaging sternocalvicular and sacroiliac joints. Psoas abscess. if multiple sites and child too unwell to localize pain. if a septic joint with Haemophilus in \202 uenzae Treatment \200 Medical: in \202 ammatory markers normalize), followed by oral antibiotic s for a total of 4 \200\2236wks. Outcome of treatment is time dependent. early referral to orthopedic team as there is a low threshold Surgical: for irrigation and debridement of the affected joint (+ drainage of any associated osteomyelitis). Splintage: and allows in \202 ammation to settle. Splint in position of function. Physiotherapy: IV antibiotics, after aspirate taken, for up to 3wks (until In the acute setting a brief period of splintage improves pain to avoid joint stiffness. Prognosis Usually good unless the diagnosis is delayed. Recurrence of disease and developme nt of chronic infection occur in <10%. Long-term follow-up is needed as growth-related sequ elae may not become apparent for months or years. Hip joint infection has the worst prognos is for anatomical and functional impairment. Complications Chondrolysis, ongoing infection and bone destruction, joint incongruity/ stif fness, and growth disturbance. Avascular necrosis of the femoral head can occur. 20_McClure_20.indd 739 11/14/2012 3:24:04 PM CHAPTER 20 Bones and joints 740 Infections: osteomyelitis Infection of bone. The frequency of osteomyelitis is greatest in infants, with 33% of all cases in the \201 rst 2yrs, and 50% occurring by 5yrs. Male > fe male (2:1). Pathogenesis Infection usually seen in the metaphyseal region of bones. Most infections are spread via the haematogenous route from a p site of entry (e.g. res- piratory, GI, ENT, or skin sites). Infection may also occur by direct in- oculation (open fractures, penetrating wounds) or local extension from adjacent sites. In the infant, transphyseal vessels are pa tent and infection may spread to the adjacent joint causing a septic arthritis. In adolesce nts infection tends to spread through the medullary canal. Types of osteomyelitis \200 \200 \200 Acute. Subacute (2 \200\2233wks duration). Chronic: bone). Bone abscesses may become surrou nded by thick, \201 brous tissue and sclerotic bone (Brodie \200\231s abscess). may develop \200\230sequestrum \200\231 (dead bone) and \200\230involucrum \200\231 (new Etiology The yield for bacterial growth from synovial \202 uid and bone aspirate is small ; therefore organisms are not always isolated. Staphylococcus aure- us is most common in ch ildren in all age groups. Other organisms seen include the following: \200 < \200 2yrs: Haemophilus in \202 uenzae (rare). > \200 2yrs: Gram +ve cocci, Pseudomonas aeruginosa. \200 Neisseria gonorrhoeae. Neonates: group B streptococcus and Gram \200\223ve enteric bacilli. Adolescents: Consider salmonella in SCD. Tuberculosis is rare. Symptoms and signs \200 \200 Neonates characteristically do not appear ill and may not have fever. Older children have p ain, limping, refusal to walk/weight bear, fever, malaise, \202 u-like symptoms. Overlyin g bone may be tender (+ warm), with/without swelling. Long bones principally affected: Tibi a > femur > humerus. Differential diagnosis This includes: \200 b p.768). \200 \200 \200 \200 \200 \200 JIA ( Lyme/post-streptococcal arthritis ( Acute leukemia ( Neuroblastoma ( Neoplasm (e.g. o steoid osteoma, osteosarcoma, Ewing \200\231s sarcoma). CRMO. LCH. b pp.244, 712). b p.658). b p.666). 20_McClure_20.indd 740 11/14/2012 3:24:04 PM INFECTIONS: OSTEOMYELITIS 741 Investigations \200 \200 Blood: X-ray of bone: visible. Late stages reveal metaphyseal rarefaction. Destructive chan ges in bone appear after 10 days. US-guided aspiration: MRI: formation, joint effusion, sub periosteal extension. Bone scans: joint involvement (seen as hot spots) and differentiate j oint from bone involvement; good for infections of pelvis, proximal femur, and spine. Open biopsy may be necessary. Consider immunological evaluation if atypical organism. FBC, ESR, CRP, blood cultures (positive in 50%). early stages may be normal; soft tissue oedema may be \200 for microscopy and culture. soft tissue assessment \200\224bone marrow involvement; abscess good for acute osteomyelitis; can identify up to 90% of \200 Treatment \200 Medical: antibiotics for 4wks. Early liaison with microbiologist required. Surgical: a sequestered abscess or collection (not accessible to antibiotics). IV antibiotics for a minimum of 2wks, followed by oral drainage and debridement if there is frank pus on aspiration or Prognosis Usually excellent if treated early. Disease recurrence/pro- gression to chronic i nfection is seen in <10%. Complications \200 \200 Systemic: Local: may include septicaemia. pathological fracture, sequestration, growth disturbance. 20_McClure_20.indd 741 11/14/2012 3:24:04 PM CHAPTER 20 Bones and joints 742 Spinal disorders General management History Pain, onset of deformity, loss of weight, night sweats, family history, disa- bility, other disorders. Examination \200 Inspection: asymmetry, scapular prominence, skin lesions (especially mid line pits and haemangiomas), caf au lait spots (associated with neuro \201 bromatosis), foot deformity, leg atrophy. Feel: Move: General: Investigations: \200 \200 \200 spinal tenderness. forward \202 exion, hamstring tightness. neurological examination. radiographs, CT, MRI, bone scan. General spinal disorders Back pain Take it seriously! More likely to be caused by signi \201 cant pathology than in adult (e.g. osteoid osteoma, eosinophilic granuloma). Beware of the following, especially in young children \200\224several weeks of symptoms; night pain; increasing symptoms; abnormal neurology; recent onset of scoliosis; night sweats. Pain may be referred from intra-abdominal or intrathoracic process. Investigate thoroughly, but rem ember 50% of children experience back pain by 15yrs of age. Discitis In \202 ammation (probably infection) of the disc space: \200 \200 Age Symptoms: pain. Symptoms may be vague. Investigations: Treatment: in \202 ammatory mar kers return to normal. Outcome: group: any age (infants and children rather than adolescents). fever; irritability; unwilling to walk; back pain, abdominal \200 bloods (i CRP and ESR); MRI; bone scan. antibiotics (according to local policy), at least until usually do well. Congenital anomalies Diastematomyelia: spinal cord is split by a central cartilaginous/bony prom- inence. \200 Signs: foot); cutaneous lesions seen in most children; positive neuro logy seen in 50%. Management: progressive. Spina bi \201 da. other abnormalities are common (e.g. scoliosis, clubfoot, cavus consider resection of spur if neurology appears/is Regional spinal disorders Cervical spine: torticollis See b pp.127, 883. Thoracic spine See Scheuermann \200\231s disease (b p.744). 20_McClure_20.indd 742 11/14/2012 3:24:04 PM SPINAL DISORDERS 743 Lumbar spine: spondylolysis and spondylolisthesis \200 defect of pars interarticularis (spondylolysis). If bilateral and De \201 nition: at the s ame level may result in anterior displacement of one vertebra upon another (spondylolisthes is). Usually due to a stress fracture through a congenitally dysplastic pars. Incidence: os teopetrosis), connective tissue (e.g. Marfan \200\231s), hyperextension sports (e.g. gymnas tics). Symptoms/signs: Decreased forward \202 exion and straight leg raise. Investigation s: dog \200\231s collar \200\231. Bone scan/SPECT for occult fractures and evidence of heal ing. Management: consider short-term bracing, analgesia, hamstring stretches, and core stre ngthening. Operative intervention seldom required for stabilization. uncommon, associated with spina bi \201 da, metabolic (e.g. sudden/insidious onset of pain exacerbated by activity. X-rays \200\224lateral and oblique spinal views. Look for \200\230Scotty non-operative usually. Rest and change of activities; Sacral spine: sacral agenesis \200 De \201 nition: diabetic mothers. Signs: neurology. Management: hypoplastic/absent sacrum; most common in infants of abnormal pelvic ring affecting lower limbs with associated tailor towards severity of agenesis and neurology. 20_McClure_20.indd 743 11/14/2012 3:24:04 PM CHAPTER 20 Bones and joints 744 Spine: kyphosis \200 De \201 nition: from Greek Kyphos, a hump. Increased curvature of the spine in the sagitta l plane, visible from the side. Normally there is a 20 \200\22340 curvature of the thorac ic spine. History: neurological symptoms, family history. site, age of onset, rate of progression, associated scoliosis/pain/ Examination Assess: \200 \200 Flexibility: Ability to lie \202 at: greater severity of kyphosis). Hips for tight hamstr ings: Full respiratory (pulmonary function) and neurological examination. stand, bend forwards, bend backwards (hyperextension). associated lumbar lordosis (more pro minent with \200 limited straight leg raising. Investigation PA and lateral standing X-rays of entire spine. Diagnosis Three major causes are identi \201 ed by answers to: \200 \200 \200 Is it \202 exible? Is it painful? When did it start? Postural kyphosis (most common) Flexible, usually painless, onset <10yrs old. \200 Other poor at games. Investigations: complete correction. Treatment: for dorsal spine, educ ation, occasionally brace. Outcome: \201 ndings: tall; girls > boys; poor physical development; \202 at-footed;