The classic concept of central chemosensitive sites as being located in restricted areas of the ventral medullary surface has finally been shown to be bunkum. Chemosensitive neurons are diffusely located in the CNS, and multiple regions contribute to the hypercapnic ventilatory response. Makes sense, because you want the system to be resistant to damage. Explains why central alveolar hypoventilation (eg with tumors, stroke) is not well explained by the brain lesions. The hypoxic hypercapnic response involves all manner of different excitatory and inhibitory responses from different centres. Neural plasticity (ie prior experience) is also a major influence, potentially maladapatively.
The Oxygen-Haemoglobin dissociation curve should probably be drawn the other way round with Sats on the bottom. This presents 2 evolutionary advantages:
So someone with sats of 85% is delivering only 10% less O2 to the tissues, which in itself is probably not cause for concern - on the other hand, there cardioresp function is probably 50% what it should be, indicating significant disease.
On the other hand, excessive O2 will lead to:
Work of breathing increases with falling FEV, so resp rate increases, sats fall. Sensitivity to CO2 falls, esp in REM sleep - headaches, daytime somnolence. Infants more at risk as more REM, more likely to tire.
Parents have varying ideas of what "wheezy" means. Usually to do with noisy breathing, but also difficulty in breathing. In kids attending A&E, less than 50% agreement between parental reports of wheeze and doctors finding wheeze. Cane, Arch Dis Child. 2000 Apr;82(4):327-32. PMID 10735844 Medically speaking, an expiratory whistling sound is meant, but this is rarely what parents think. Important to let parents use their own terms, but then clarify what exactly they mean! Atopic children with doctor confirmed wheeze have significantly poorer lung function compared to those with parentally reported but unconfirmed wheeze. Arch Dis Child. 2004 Jun;89(6):540-3. PMID 15155399
= congenital central hypoventilation. Genetic, onset at birth, cyanosis worse in sleep, better when crying. No response to hypercapnia. Involves other autonomic abnormalities. (Curr Op Ped)
2005 BTS/SIGN - main differences from previous guideline are: inhaled steroids introduced earlier in milder cases; Individualized management plan; Primary care should have specific training; Inpatients should be reviewed by clinicians with particular expertise in asthma, pref within 30 days. Otherwise see the previous SIGN/BTS guideline for details on management. Main points:
Differential: congenital abnormality eg CCAM, TB, CF, immunodeficiency, ciliary dyskinesia, postviral, Churg-Strauss.
Asthma appears to be a latecomer in the Allergic March - children often have a history of eczema or food allergy before they develop their first symptoms. Hay fever tends to come later. About 50% of asthmatics will have first degree family history.
Previous RSV bronciolitis seems to predispose, or at least there is remodellin of the airways that impacts on later asthma symptoms.
Other influences:
The mechanism of asthma, similar to other allergic manifestations, is an initial IgE response from Mast cells involving bronchoconstriction by histamine and leukotrienes (although there appear to be multiple pathways, hence some people do not get any benefit from leukotriene antagonists). Histamine is also vasoactive, leading to tissue (mucosal) oedema. Then there is a secondary, delayed pathway involving eosinophils - when these degranulate, apart from releasing more leukotrienes there are also all the cytotoxic substances eg Major Basic Protein (MBP) and Peroxidases that cause tissue damage. Prostaglandins appear to inhibit this later reaction. It is the mucosal damage and oedema that causes symptoms resistant to bronchodilator therapy (hence the need for steroids).
PEAK trial (Prevention of Early Asthma in Kids) tried giving fluticasone to well children at high risk of asthma at the age of 2-3 years - over 2 years less additional asthma therapy required but this benefit did not continue when all treatment stopped (and made them shorter). NEJM 2006
See Prescribing under Practical for inhalers.
Metanalysis of Magnesium in asthma - 5 studies, all ER based, vs steroids/nebs only. Only 1 did not find benefit, NNT=4 to prevent admission in moderate asthma. 40mg/kg over 20 mins, at 2mmol/ml. Data limited in under 6yrs (eg PEFR not feasible so not reported). Give on admission if severe else after 2 nebs if moderate and no improvement.Archives of Disease in Childhood 2005;90:74-77
Non-compliance is the most common cause for poor reponse to oral steroids. Monthly subcut injections? Anti-IgE monoclonal (Omalizumab) shows significantly fewer exacerbations and reductions in oral steroid doses (2-4wkly subcut injections) cf methotrexate. BAL to look for eosinophils (ciclosporin) vs neutrophils (azithromycin)? BMJ 2007; 335:253-6
Increasing inhaled steroid dose in asthma exacerbations by 5 times was effective in 1 study (adult?) but considering that many patients probably don’t take their steroid regularly, better to remind them to take what they’re prescribed. On the other hand, if on a low maintenance dose, probably not a bad idea to increase.
Marginally cheaper to prescribe combined steroid and long acting beta. Better compliance; less flexibility to adjust dose.
Parental beliefs influence adherence to management plan viz concern about drugs vs perceived necessity.
Asthma unresponsive to basic management - wash spacer regularly? Frequency of prescriptions? Abnormal voice?
2-6 yrs mostly. Snoring (but seen in 12% of normal kids) - not the same as obstruction , 10 snorers to 1 obstructor. May not make any noise when obstructed. Pauses, choking, apnoea, body position, loudness, school performance, wetting (suggests seizures but common in obstruction). Poor attention span, bad behaviour may be more noticeable than somnolence. There is evidence for impaired learning/memory: intermittent hypoxia worse than sustained in rats. Role in failure to thrive?
Clinical history not v reliable: 50-60% sens/spec. Only 5% of snorers have obstruction. Sats monitoring is specific not sens. Polysomnography shows REM or not, ?cause. 8 centres in UK. Adenotonsill'y 95% cure rate. Else BIPAP, wt loss, oxygen (but CO2?). Nasal steroids, tracheostomy, mandib surgery. NOT UPPP in kids - speech/feeding issues.
CF is the major cause of severe chronic lung disease in children and is responsible for most exocrine pancreatic insufficiency during early life. It is one of the most common inherited diseases. It is a systemic condition, affecting many different systems. Common CF presentations are recurrent chest symptoms/infections, meconium ileus (failure to pass meconium at birth), and failure to thrive.
CF is inherited as an autosomal recessive trait. All of the gene mutations that contribute to the CF syndrome occur at a single locus on the long arm of chromosome 7. The CF gene codes for the CF transmembrane regulator (CFTR) protein. The most prevalent mutation of CFTR is the deletion of a single phenylalanine residue at amino acid 508 (deltaF508). This mutation is responsible for the high incidence of CF in northern European populations (approximately 1 in 20 whites are carriers), explains 50% of individuals with CF and Northern European ancestry. The pathophysiology is an inability to secrete salt and secondarily to secrete water, leading to thick secretions.
Suggested recently that defective bicarb (HCO3-) transport is as important as chloride, due to effect on mucin expansion. PMID: 18675692
The high frequency of the CF gene has been hypothetically ascribed to cholera: intestinal epithelial cells may be less responsive to cholera toxin.
Nasal obstruction and rhinnorhoea are common, sometimes with polyposis.
15-20% present with meconium ileus - AXR shows distended loops with ground glass in the lower central abdomen. There may be meconium peritonitis. Distal intestinal obstruction syndrome or meconium ileus equivalent is a similar picture in older children. Give oral gastrograffin in orange juice (bad taste) - consider NG tube if not managing to take it. Consider Movicol.
Most have malabsorption from exocrine pancreatic insufficiency. Some mutations are less affected. Other GI problems are intussusception, reflux, rectal prolapse. Malnourished children may present with vitamin deficiencies eg peripheral neuropathy and dementia (vitamin E), coagulopathy (K). Symptomatic cirrhosis (jaundice, ascites, varices) occurs in only 2-3%. Cholelithiasis may occur in older children, neonatal hepatitis with massive fatty liver may occur in neonates. Liver disease is independent of genotype.
Sweat test involves electrical current enhancing skin penetration of pilocarpine. At least 50-100mg must be collected. Chloride above 60 mmol/l is diagnostic when other criteria are present (normal is under 40, sodium about the same if not higher but this is reversed in positive; total goes over 140). If intermediate, proceed to gene analysis. Can be performed after 2 weeks of age in infants greater than 3 kg who are normally hydrated and without significant systemic illness (grade C) - in term infants, sweat sodium and chloride can be high in the first seven days, especially the first 48 hours. Testing should be delayed in subjects who are oedematous or on systemic steroids.
False positives are:
Neonatal IRT will pick up 90% of cases. Newborn screening is associated with improved growth, reduced morbidity, and reduced therapy - but equivalent pulmonary outcome compared with late clinical diagnosis Jonathon's study, Pediatrics. 2007;119:19-28.
Does sweat chloride predict severity? CF patients with alleles associated with pancreatic sufficiency have less severe disease and lower sweat chloride. But sweat chloride concentration by itself did not correlate with the severity index.
(Pediatr Pulmonol. 2004 Sep;38(3):204-9.)
Neonatal screening: if IRT is >60 on 2 occasions, genotype recommended. In Scotland 31 genes screened, in proposed E&W scheme only 3 genes - to avoid detecting milder forms.
CF in S Asians 1:20 000. 25% are Delta F508, 25% unidentified. Standard panel not v sensitive! No delay in diagnosis but poorer outcome. Islam supports efforts to preserve life so transplantation permitted. Abortion illegal. "Dire need" overrides haraam (forbidden) drugs etc. Denial may reflect fear of family stigmatization esp marriage prospects. (Jonathon McCormick)
Growth hormone (crossover trial, n=18) resulted in significant improvement in height, weight, bone mineral content, lean tissue mass, and number of hospitalizations. Absolute forced vital capacity and forced expiratory volume in 1 minute significantly increased in GH treatment, but there was no significant change in percent predicted pulmonary function. Caloric intake was similar in both groups during both years. J Pediatr. 2005 Mar;146(3):324-8.
Carbon dioxide retention during exercise is associated with more rapid decline in lung function. Archives of Disease in Childhood 2005;90:792-795
Evidence that macrolides help FEV1, reduce exacerbations and help weight gain, even in the absence of Pseudomonas. But variable response. Equi A, Balfour-Lynn I, Bush A,et al. Long term azithromycin in children with cystic fibrosis: a randomized, placebo-controlled crossover trial. Lancet 2002;360:978�84
Some children with abnormal GTTs get better; others with normal GTTs and Hb1Ac are found to have transient hyperglycaemia and low dose insulin produces significant clinical improvement. Arch Dis Child 2002;87:430�1
NIPPV for neuromuscular disorder reduces hospital bed days by 85% and ICU days by 68%.
Home ventilation suitable if FiO2 <0.4. Aim for normal pCO2, off vent for periods - "sprint" weaning wih suppl O2 for increasing periods. Tracheostomy for young, lots of secretions, labile requirements. Longterm mask use leads to midfacial hypoplasia.
NIPPV is an important adjunct in palliative care. Apart from the fact that it may allow for successful treatment of an acute episode, it can also contribute to relief of dyspnoea and reduction in opiate doses. If used, its role and its limitations should be discussed, and endpoints clarified.
Starts off as pneumonia. Effusion is exudative reaction in pleural space, may become empyema ie fibropurulent after 3 days, begins to organized after 14 days. Unclear why some effusions become empyemas but not others: older child, some bugs eg staph and GAS more likely, less preceding antibiotics associated (68% vs 50%, but ceftriaxone associated!). Traditionally associated with staph, pneumococcus, TB, Hib. Now cultures are often negative, but PCR 70-80% positive esp Pneumococcus, esp serotype 1 (25-50% of empyemas, although only 5% of pneumonias). GAS also seen commonly.
Increasing incidence in recent years. Serotype 1 pneumococcus pneumonia is known to be associated with influenza and outbreaks. Surprisingly, this is not a common serotype in other forms of invasive pneumococcal disease, ?why. Not covered by 7 valent pneumococcal vaccine either. PIDJ Volume 25(6), June 2006, pp 559-560
Less empyema in US since Prevnar in most places but not all – where unchanged, replacement seen. MRSA has been seen.
5 grades of severity on American thoracic society guidelines. BTS guidelines have only 4 grade Bs, otherwise mostly Ds ie opinion.
Ultrasound diagnosis. Small effusions may resolve spontaneously. If large or causing significant symptoms, drain. At insertion, drain 500ml max then clamp for 1hr else pulmonary oedema may develop.
For pleural penetration, penicillin, cefotaxime, cipro, amikacin and meropenem all good.
Resolution of fever and inflammatory markers are indicators of recovery. CXR returns to normal within weeks.
Fibrinolysis - BTS recommended, in part because VATS less readily available. Intrapleural urokinase promotes drainage and may obviate surgery. In RCT reduced duration of stay from 9 to 7 days. Patients with percutaneous small pigtail drains did best, but possibly centre effect. Much more comfortable in any case... But recent NEJM study in adults found no overall benefit.
Video assisted thoracoscopy (VATS) - 2 trials:
Availability of VATS depends on having appropriate equipment and suitably trained surgeons.
Metanalysis of primary operative management vs not - lower in-hospital mortality rate (0% vs 3.3%), reintervention rate (2.5% vs 23.5%), length of stay (10.8 vs 20.0 days), duration of tube thoracostomy (4.4 vs 10.6 days), and duration of antibiotic therapy (12.8 vs 21.3 days). Pediatrics. 2005 Jun;115(6):1652-9.
But compared to fibrinolysis? Latest RCT from GOS shows no difference between fibrinolysis and VATS but latter more expensive.
Whooping cough, caused by Bordetella pertussis. B parapertussis can cause similar illness but usually less severe. Classically, Catarrhal phase (mild fever, productive cough, no pharyngitis) then Paroxysmal (coughing fits, often associated with vomiting, followed by characteristic inspiratory "whoop") then Convalescent - persistent cough, traditionally 4-12 weeks (100 days)! Fever is rarely marked, and in fact patients can often look relatively well between paroxysms, with clear chest and no respiratory signs. Young infants may present with apnoea rather than whooping.
But probably underdiagnosed, esp where symptoms are chronic but mild, or in the third of cases where symptoms last less than 3 weeks. Among children with a cough lasting 14 days or more attending their GP, 37.2% had serological evidence of recent Bordetella infection, even though most had been fully immunised. Oxford BMJ 2006 Jul 22;333(7560):174-7. Hence reported incidence depends on quality of surveillance rather than actual prevalence! Probably the same everywhere, with peaks every 2-5 yrs.
Rarely, associated with encephalopathy, including seizures. Probably a direct toxin effect, plus hypoxia during paroxysms. Hernias and rectal prolapse may occur. Secondary pneumonia is not uncommon, so if chest signs are present consider antibiotic treatment to cover other organisms.
The reason for the chronic, persistent cough is still not clear (many infections cause similar ciliary disruption, and don't cause such chronic symptoms).
Adult disease presents in its mild form as disturbed sleep, sweating, sinusitis or otitis, protracted cough so not usually diagnosed. Cough associated with choking is characteristic, whereas sweating is not very sensitive or specific. Cough is non-productive (although there may be a sensation of retained secretions - question carefully!).
Although part of universal immunization schedule, immunity (from immunization or exposure) is pretty shortlived viz 2-5yrs, so in vaccinated areas severe disease seen either pre-immunization ie young babies, or adolescent/adults after immunity has worn off. Most cases in unvaccinated infants are contracted from a family member, usually the mother. In low coverage areas burden of disease is in 5 yr olds, because of regular exposure through life. See Vaccines.
Notifiable!
7/7 isolation, 14/7 erythromycin. Makes little difference to clinical course, but does help reduce transmission. Treat within 3-4 weeks of start of illness. Still need full immunization course as natural disease does not confer long lasting immunity. Azithromycin (10 mg/kg on day 1, and 5 mg/kg on days 2 through 5) is as effective as erythromycin, gastrointestinal adverse events are much less, and compliance in general was markedly better (Pediatrics. 2004 Jul;114(1):e96-101 - pmid:15231980 )
Where vulnerable individuals eg unimmunized infants, asthmatics are exposed to a likely case, there is an argument for giving prophylactic erythromycin to all close contacts. See Health Protection Agency advice. Journal of Public Health Medicine 2002;24(3):200-206.
Increasing diagnosis with increased use of high resolution computed tomography (HRCT). Much higher incidence of bronchiectasis in certain groups eg Maoris, Aborigines and Inuits. The median interval between onset of respiratory symptoms and diagnosis is three years.
Main symptom is chronic cough, unresponsive to anti-asthma medications. Cough in the absence of wheeze is unlikely to be due to asthma. Presence of ear/nose discharge may suggest cilial problem or antibody deficiency.
Diagnosis: specimens (sputum, cough swab or NPA) for bacterial culture, radiological investigations, sweat test, and immune function tests. The most common pathogens isolated are H influenzae and S pneumococcus (although may also be upper airway commensals). Bronchoscopy will help differentiate, plus pathology may indicated endobronchial infection (see below) - esp focal anomalies. Brush biopsy for cilia studies.
Plain CXR is of very limited use, as not sensitive even in children with significant bronchiectatic changes on HRCT (the gold standard).
Bronchial dilatation is associated with loss of cilia, cubiodal and squamous metaplasia, hypertrophy of bronchial glands and lymphoid hyperplasia, along with marked vascular changes. These changes are related to chronic bacterial infection: the vicious cycle theory, chronic infection leads to inflammation and airway damage causing bronchial dilatation, mucociliary statis. But actually, bronchial dilation as seen in pneumonia or inhaled foreign body may resolve. It has become apparent that HRCT changes may not always progress as would be predicted from the vicious cycle theory - in many patients radiological changes remain static over several years and in some there may be improvement or even complete resolution. Hence HRCT bronchiectasis on a single scan should probably be distinguished from changes that persist or progress on repeat scans performed over a period of time eg two years.
Traditionally about 30% was considered idiopathic, but better diagnostic techniques may reduce this.
Management (no good clinical trial data, of course) -
Surgical options are limited because many patients have generalised disease. Lobectomy may be curative for a small number of patients in whom disease is limited to a single lobe and difficult to control by medical means alone.
The use of other therapies such as oral and inhaled corticosteroids, Rh DNase, and nebulised hypertonic saline remains speculative, and the best evidence available is based around case reports.
Archives of Disease in Childhood 2005;90:712-714 D A Spencer
Does disease recur in the same region? Implies localized area of intraluminal obstruction (foreign body), extraluminal compression (enlarged lymph nodes, enlarged or aberrant vessels, or parenchymal tumors) or structural abnormalities of the airway (localized bronchial stenosis or bronchomalacia, tracheobronchus or isolated areas of bronchiectasis) or lung parenchyma (pulmonary sequestration, cystic adenomatoid malformation and bronchogenic cysts).
Right middle lobe syndrome is a unique entity of recurrent right middle lobe pneumonia and atelectasis. That lobe is prone to infection and collapse because the bronchus arises at an acute angle and is relatively long before it subdivides into segments. Adjacent lymph nodes can compress it when they enlarge. The most common noninfectious cause is asthma; tuberculosis remains the most common infectious etiology.
Recurrent pneumonia in a single region demands airway endoscopy. For distal lesions or those outside of the airway lumen, chest CT, MRI and angiography are useful. When lymphadenopathy is present, tuberculin skin testing should be performed. If there is a suggestive history, acute and convalescent titers for histoplasmosis, blastomycosis or coccidioidomycosis should be obtained.
Children who develop recurrent pneumonia in varying lobes may have impairment in cough or mucociliary clearance mechanisms, diffuse airway narrowing that hampers airway clearance or local or systemic immune dysfunction. Aspiration is associated with impaired cough and diffuse airway narrowing. It results from swallowing dysfunction (due to central nervous system abnormality, neuromuscular disease or anatomic lesion of the oropharynx). A history of coughing during feeds should provoke evaluation of the swallowing mechanism by direct observation, videofluoroscopy or endoscopy. Patients who aspirate chronically may lose their cough reflex. Radionuclide salivagram with 99mTc-sulfur colloid is a sensitive and noninvasive method to detect chronic aspiration of oral contents.
Material from the oesophagus can be aspirated in cases of oesophageal stricture, foreign body, dysmotility, achalasia or gastroesophageal reflux. The association of gastroesophageal reflux with aspiration is difficult to prove. The utility of a lipid-laden macrophage index of cells obtained by bronchoalveolar lavage remains controversial, in that macrophages filled with exogenous lipid secondary to aspiration cannot be distinguished from those containing endogenous lipid associated with inflammation and cell death. Children who develop recurrent pneumonia from aspiration in association with gastroesophageal reflux tend to be younger than 2 years of age.
Children with recurrent pneumonia from asthma are older. CXR densities represent areas of infection, atelectasis or both. Recent polymerase chain reaction and culture evidence proves that the majority of asthma exacerbations are associated with viral infections. Children who have a history of nocturnal cough, cough or wheeze with exercise or protracted coughing after upper respiratory illnesses should undergo spirometry and assessment of bronchodilator responsiveness, or they should receive an empiric trial of inhaled corticosteroids and bronchodilators.
Cystic fibrosis (CF) and primary ciliary dyskinesia (PCD) are disorders of mucociliary transport. CF should be considered in any child with recurrent pneumonia, especially when symptoms of intestinal malabsorption are present. Recovery of Pseudomonas aeruginosa from the respiratory tract, especially the mucoid form, is highly suggestive of CF. Patients with PCD typically have chronic purulent rhinitis as well as recurrent middle ear disease. Approximately one-half have situs inversus. The triad of sinusitis, situs inversus and bronchiectasis, called Kartagener syndrome, is a subset of patients with PCD.
Systemic immunodeficiencies cause recurrent sinopulmonary infections as well as infections outside the respiratory system. Abnormalities in phagocytosis, the most common of which is chronic granulomatous disease (CGD), result in defective killing of bacteria and fungi. In a national registry of CGD patients, 80% had at least 1 episode of pneumonia, most commonly with Aspergillus spp. (41%), Staphylococcus spp. (12%) and Burkholderia cepacia (8%). Pulsed field gel electrophoresis patterns of isolates from serial episodes of illness revealed that these are new, rather than persistent infections.
Absence of immunoglobulins (Ig) which help opsonize and clear encapsulated bacteria results in recurrent infections. Complete absence of IgG (Bruton, or X-linked agammaglobulinemia) is an isolated B cell defect, while patients with common variable immunodeficiency (CVID) manufacture some Ig and have abnormalities of T cell function. In 19 patients with CVID, 68% had a reduced number of B cells and 79% had a decreased ratio of CD4+ to CD8+ cells. Recurrent pneumonia occurred in 74% most commonly with Streptococcus pneumoniae (37%) and Haemophilus influenzae (26%). Replacement therapy with intravenous gamma-globulin (IVIG) significantly reduces mortality and morbidity. In 23 patients with agammaglobulinemia treated with IVIG, the incidence of pneumonia fell from 0.82 to 0.12 episode per patient per year.
Some children with recurrent pneumonia have normal levels of IgG but low levels of IgG subclasses. IgG2 subclass deficiency is associated with poor antibody responses to polysaccharides. IgA deficiency is one of the most common antibody deficiencies, but most patients are asymptomatic unless there is a coexistent IgG subclass deficiency.
T cell abnormalities are associated with both pulmonary and extrapulmonary infections. Pneumocystis carinii (Pneumocystis jiroveci), fungi and viruses are important pathogens.
PIDJ Volume 24(3) March 2005 pp 265-266, Panitch, Howard
CCAM assoc with malignancy in 40s, pneumothorax.
Common after head trauma, status epilepticus, Subarachnoid haemorrhage. Tachypnoea, bibasal creps, haemoptysis. Mechanism? - sympathetic overload (myocardial infarction can occur in adults) drives raised LA pressure, pulmonary hypertension, increased capillary permeability. Diagnose by normal JVP, no gallop cf cardiogenic!
Think Pulmonary embolism. eg:
else bronchiectasis, haemangioma, tumour.
Meduri study in adults suggested benefit from methylprednisolone in late ARDS (no evidence of benefit early on) - n=24 only, study stopped early! Recent Steinberg (ARDS Clinical Trials Network, Harborview Medical Center, Seattle) RCT similar methods but no benefit in 60/180 day mortality (although reduced number of ventilated/shocked days, improved lung compliance, oxygenation and blood pressure. Worse mortality in late (14+days) enrolled (8 vs 35%!). No increase in infectious complications (less if anything!) but worse neuromuscular weakness. N Engl J Med 2006;354:1671–84
20% idiopathic. Known causes are pulmonary alveolar proteinosis (=surfactant deficiency, usually type B), alpha 1 Anti-Trypsin, chronic reflux aspiration. Associated with:
Differential: CF, pulmonary venous congestion (from cardiac disease). Hi res CT is gold standard (lung biopsy if often non-specific) - ground glass, then honeycombing (fibrosis around dilated obstructed bronchioles). Some respond to steroids, most do not improve unless v young. Usually long term suppl oxygen requirement.. ?prophylactic antibiotics.
Nose problems - clinically,look for misting, listen to voice.
Orbital cellulitis- commonly sinus related so refer.
Sinusitis - diagnose by inspection above inf turbinate for pus (use auroscope, 5mins otrivine on swab if poor view). CT only for planning surgery, as sinuses opaque in 2/3 of normal, and xray wholly unreliable. Sinus surgery for CF, ciliary dyskinesia.
Potts puffy tumour - sinusitis then neuro involvement with intracranial empyema +/- metastatic abscesses eg bone/lung cf Lemierre syndrome (below). Associated with IDDM, EBV.
Adenoidectomy v effective for glue ear/recurrent OM (besides grommets).
Tonsillectomy - For children with moderately frequent throat infections (3 in the previous year) a wait and see approach results in acceptable control of symptoms and avoids operative complications (1% need surgery for haemorrhage). Paradise trial suggested tonsillectomy of benefit if 7 infections in previous year, 5 per year for previous 2 years or 3 per year for previous 3 years but baseline unequal. BMJ 329:654. See Common.
TB lymphadenitis - Gene probe amplified mycobacterium tuberculosis direct test has sens 93% and spec 100% (J Clin Microbiol. 2004 Dec;42(12):5921-2.)
In Scotland, Automated Auditory Brainstem Response (AABR) for all babies x2 then diagnostic ABR/tympanometry/otoacoustic emissions (OAE) to establish thresholds. Behavioural testing (as was done by Health visitors) still useful from 6/12! Early support team- audiologist, advisory teacher for hearing impaired, SLT, educational audiologist, WOS National Deaf Children Society.
Inherited hearing loss can present late, or be progressive so any concern refer regardless of screening history.
Ludwig's angina - sublingual spread from dental abscess, airway compromise, septic shock. Rx benpen, metronidazole.
Similarly Lemierre's syncrome - metastatic lung abscesses from jugular thrombophlebitis, secondary to upper airway sepsis esp tonsils. Usually Fusobacterium, painful neck with palpable tender jugular veins. Surprisingly good prognosis!
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