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"Data.app 0CECG - a quick guide Normal Axis 1wk - 1 mth +140 - 180 1mth - 3 mth + 20 - 130 3mth - 3yrs +10 - 110 > 3 yrs +30 - 120 PR interval 0.1 sec in infancy 0.16 sec in adolescence QRS complex < 0.06 sec = normal 0.06 - 0.12 sec= incomplete BBB > 0.12 sec = complete BBB Look further for RVH (full criteria in Clarke Clinic) if R in V1 > 20 mm any age S in V6 > 10mm if under one mth or S in V6 > 5mm if over one mth Look further for LVH if S in V1 > 20mm any age R in V6 > 16mm under 6 mths orR in V6 > 19mm if over 6 mths Consider right atrial hypertrophy with Peaked P wave : > 3 mm if < 6 months > 2.5 mm > 6 months Consider left atrial hypertrophy with P wave lead 11 > 0.09 sec Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Roman Arial UGHEART FAILURE This is a state in which the heart cannot produce the cardiac output required to sustain the metabolic needs of the body. It can be difficult to diagnose in infancy where it may be confused with respiratory illnesses. Symptoms dyspnoea, feeding difficulties, sweating, growth failure older children may report poor exercise tolerance, anorexia, abdominal pain and cough Signs tachypnoea tachycardia hepatomegaly elevated JVP in a child cyanosis and grunting with pulmonary oedema displaced apex beat indicating enlarged heart hypotension with severe heart failure gallop rhythm on auscultation a heart murmur may indicate a structural anomaly intracranial bruit may indicate A-V malformation hypertension may cause congestive heart failure Note. Peripheral oedema is a late sign of heart failure in children Auscultation of the lungs is usually normal in young children with heart failure. Possible causes Congenital heart defects Myocarditis Cardiomyopathy Supraventricular tachycardia Systemic hypertension Anaemia Hyperthyroidism A-V malformations Suspect myocarditis with congestive heart failure distant heart sounds fever arrythymias reduced QRS voltages, ST and T wave changes Suspect dilated cardiomyopathy with congestive heart failure arrythmias LVH on ECG prominent p waves and ST changes Investigations Chest X-ray and ECG Arterial blood gases FBC, U+E,Creatinine,Calcium, Glucose,ESR Consider septic screen Consider viral titres, LDH and CK if myocarditis suspected Management ( may need to contact cardiologist) A. General measures monitor SaO2 and cardiac rhythm if severe. administer oxygen if necessary correct acidosis. correct anaemia if severe. B. Drug measures (Paediatric Prescriber) BFive out of six criteria must be fulfilled for diagnosis. 1. Fever persisting for at least one week 2. Conjunctivitis bilateral and non - purulent 3. Lips and oral mucosa dry, fissured lips, reddened oral and pharyngeal mucosa, prominent papillae, strawberry tongue 4.Peripheries acute - oedema and erythema convalescent - desquamation 5.Rash polymorphous exanthem, no vesicle or crust formation 6.Cervical lymphadenopathy at least one node of 1.5 cm diameter Investigations Full blood count - platelets usually increased ESR - elevated Chest x-ray Management Seek urgent cardiological advice so that echocardiography can be arranged. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Table1 ColA12 ColB12 ColA13 ColB13 ColA14 ColB14 ColA15 ColB15 ColA16 ColB16 ColA17 ColB17 ColA18 ColB18 Index1 ColA12 Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial bNHeart murmurs are most often heard in children as an incidental finding on routine examination. Some of these children will have congenita heart diseas but, in the majority, th murmur is innocent Very rarely, the child may have infective endocarditis. What should be done if a murmur is heard? 1. History shortness of breath or feeding difficulties episodes of duskiness or pallor or sweating family history of heart disease 2. Examination cyanosis (check SaO2 if necessary) failure to thrive or finger clubbing peripheral pulses and femoral pulses praecordial heaves and thrills character of heart sounds radiation of murmur and any change with position evidence of heart failure temperature,splinter haemorrages, Roth spots, Osler nodes, Janeway lesions, splenomegaly, ( all suggestive of infective endocarditis ) Innocent murmur Significant murmur Normal pulses Normal / abnormal No thrill Thrill may be present Soft Soft / loud Often variable Consistent Normal heart sounds May be abnormal Normal ECG,chestX-ray May be abnormal No added sounds ( clicks etc. ) 3. Investigations Ideally,all children in whom a murmur is heard should have an ECG, chest X-ray and four limb blood pressure measurements. Management If the murmur is heard incidentally and seems innocent the child should return for a repeat examination when well. If the murmur is persisting, perform the investigations at this stage. If the investigations are abnormal, then refer to the cardiologists. If the investigations are normal, the child may be discharged. If the murmurseems pathological, then investigations must be performed and the child referred to the cardiologists, even if the investigations are normal. Characteristics of some childhood murmurs Still s murmur ( innocent) A short ejection systolic murmur, loudest at the lower left sternal edge, usually midway between fourth intercostal space and apex, vibratory, attenuated in the sitting position, with very little radiation. Venous hum ( innocent) A soft humming sound heard in systole and diastole, loudest in the neck or upper chest The intensity varies with position of neck and it is softened by lightly compressing the jugular vein and in the supine position. Ventricular septal defect A pansystolic murmur, loudest at the lower left sternal border.The chest x-ray may show cardiomegaly, pulmonary plethora and enlarged pulmonary artery and the ECG may show biventricular hypertrophy. Atrial septal defect An ejection systolic murmur in th pulmonary areawith fixed splitting of the second heart sound.The chest x-ray is similar to that of a VSD and the ECG may show right axis deviation and incomplete RBBB. Pulmonary stenosis An ejection systolic murmur in the pulmonary area with a soft and widely split second sound + / - ejection click.The chest x-ray may show post stenotic dilation of the pulmonary artery and the ECG may show RVH. Patent ductus arteriosus A continuous murmur heard best in the pulmonary area radiating to the back. Peripheral pulses are collapsing. The chest x-ray may show cardiomegaly with pulmonary plethora and the ECG may show LVH. Aortic stenosis An ejection systolic murmur , loudest at the right sternal border and radiating to the neck + / - ejection click. Peripheral pulses have small volume. The chest x-ray may show post stenotic dilation of the ascending aorta and the ECG is usually normal unless the stenosis is severe. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial KA heart rate above the normal range when age is taken into account. Age Heart Rate - upper end of normal range 0-6 mths 160 / min. 6-12 mths 150 / min 1-2 130 / min 2-6 120 / min 6-10 110 / min 10-14 100 / min Possible causes Sinus tachycardia Supraventricular tachycardia Nodal ( Junctional ) tachycardia Ventricular tachycardia AS A GENERAL RULE, THE MANAGEMENT OF AN INFANT OR CHILD WITH A DYSRHYTHMIA SHOULD BE DISCUSSED WITH THE PAEDIATRIC CARDIOLOGIST ON CALL BEFORE STARTING THE TREATMENT EXCEPT IN A GRAVE EMERGENCY. Sinus tachycardia fever, anxiety, hypoxia, heart failure, dehydration + other causes of hypovolaemia myocarditis, pericarditis Heart rate : up to 200 / min. in an infant. QRS complex : each is preceded by a P wave. QRS waves are identical. P waves : all are identical Onset : often a history of recent illness. Management of sinus tachycardia depends on the underlying cause.The heart rate falls with treatment of the underlying illness. Supraventricular tachycardia Heart rate : over 220 / min. Up to 300 / min. in an infant. QRS complexes : all are identical in appearance. In 95% of cases the complex is narrow. If the complex is broad then ventricular tachycardia must be considered. P waves : may not be visible due to the tachycardia, may be visible but look abnormal , or may look normal. ( in this case the heart rate helps differentiate SVT and sinus tachycardia.) Other features : The child may be well or have signs of heart failure. The onset and cessation is sudden. In 70-80% of cases the heart is structurally normal.When sinus rhythm is resumed, then a slow upstroke on the QRS may be seen ( delta wave ) with a short PR interval ( Wolff - Parkinson-White). 30 - 40% of children with SVT present in the first weeks of life. Management of SVT A. General Monitor pulse rate, BP, SaO2 and cardiac rhythm. Establish intravenous or interosseous line. Before any treatment is administered. If the patient is normotensive and not in severe congestive heart failure document the tachycardia with a 12 lead ECG and rhythm strip before any treatment. B. Drugs See Paediatric Prescriber Ventricular tachycardia Heart rate : varies between 120 and 250/ min P wave P wave : none QRS complexes : wide in appearance .Very occasionally, a wide QRS complex may be due to a supraventricular tachycardia. If the patient is stable, try adenosine to distinguish between the two. Unstable patients should be treated as if they had ventricular tachycardia. Management of ventricular tachycardia A. General - see under SVT B. Drugs - see Paediatric Prescriber Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial DInflammation of the pericardium. Fluid gathers in the pericardial space and may cause cardiac tamponade. Symptoms chest pain, worse lying, better sitting sharp stabbing pain in the left shoulder cough dyspnoea Signs( depend on amount of fluid) fever tachycardia low volume pulse distant heart sounds friction rub pulsus paradoxus> 20 mmHg Constrictive pericarditis is rare. Hepatomegaly and ascites are out of proportion to the other signs and symptoms. Possible causes Infections Kawasakai Disease Neoplastic Connective tissue disease Metabolic / endocrine Trauma or surgery Post radiotherapy Investigations 1. Chest X-ray. A relatively large effusion must be present before the cardiac shadow enlarges. The lung fields are usually clear. With constrictive pericarditis the heart shadow is relatively small. Calcification may be present. 2. ECG. Low voltage QRS complexes, generalised T wave inversion, ST segment changes. 3. Echocardiography 4. Full blood count. Blood cultures. Viral titres( paired). 5. Consider fungal cultures. 6. Consider TB screening. Management Discuss with the cardiologists. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial ETHE CRYING INFANT All infants cry but persistent, inconsolable crying may be a symptom of disease. Possible causes for excessive crying without fever Infantile colic - see below Gastrooesophageal reflux Obstructing inguinal hernia, volvulus, intussusception Constipation Fractured limb or dislocated joint, especially hips Urinary tract or other infection Post vaccination Teething Child abuse Psychological Points in the history vomiting / diarrhoea / constipation feeding difficulties episodes of pallor recent trauma recent vaccination social and family history Points on examination Thorough general examination, remembering, abdomen for masses or faecal loading inguinal / perianal region parent - child interaction Investigations Urine for urgent direct microscopy Further investigations depend on symptoms and signs Management Admission may be necessary for observation and reassurance. Infantile colic describes episodes of inconsolable crying in the first three months of life, usually in the evening and often associated with excessive flatus,. No cause has yet been identified. In a thriving, otherwise healthy child, parents can be told it is likely to be self limiting. There are no cures. Gripe water or Infacol may be helpful and are well tolerated. Generally, the parents are not advised to change the type of milk. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial HThis is defined as wetting, in the absence of organic pathology, beyond the age when the majority of children have achieved dryness. Under the age of five, one in seven chidren still wet the bed. It is not usual to treat a child under seven years of age. Points in history and on examination presence of day time wetting other urinary symptoms e.g. frequency, urgency, dysuria seasonal variation, stresses at home or in school sleeping and toileting arrangements previous management strategies abdominal masses blood pressure lumbo - sacral spine and lower limb reflexes Baseline investigations ( simple nocturnal enuresis) urine for microscopy and culture urinalysis for protein, blood and glucose Note, renal investigations are generally required in those with day - time wetting , unusual urinary symptoms or proven infection.Refer for a nephrology opinion. Management (simple nocturnal enuresis ) Spontaneous cure rate is 10% per year. Motivation, patience and encouragement are vital. Involve both child and parent in the treatment plan. Strict fluid restriction is ineffective but be sensible. Lifting the child late at night is generally not effective. If used, ensure that the child is fully awake. Between the ages of 6 and 7 try a Star chart . This works in up to 50% of children. After the age of 7, an enuresis alarm will work in 90% of children if used correctly. It can take 4 - 6 weeks before improvement is seen. The child may need to keep the alarm for several months. Use with the star chart to monitor progress. Review regularly to maintain motivation. Drugs Desmopressin ( tablets or nasal spray ) may be indicated in those over 7 years for 1. short term use to cover special occasions 2. when a period of respite is required 3. as a primer with the alarm 4. older children not responding to other treatments Dose: spray 20 - 40 mg nocte; tablets 0.2 mg nocte The response rate is 60 - 70 % but relapse rate is > 80 % Treatment should be stopped within three months to assess the situation. Note, there is no role for the routine use of Oxybutinin. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial IFever is a symptom and not a diagnosis. Axillary and oral temperatures ( mouth closed ) correspond with a normal range of 36.8 - 37.8 (C. Rectal temperature best approximates to core body temperature with a normal range of 37.2 - 38.3 (C. Fever may be caused by infectious disease ( most common cause ) vaccines tissue injury drugs inflammatory disease endocrine disorders e.g thyrotoxicosis metabolic disorders e.g uraemia CNS pathology small infants may develop fever if overdressed on a hot day Fever does not always = infection. Aims of management lower the body temperature identify the cause for fever and treat be alert to children at increased risk Special risk factors congenital heart disease indwelling catheters, lines, shunts immunocompromised patients infants < 6 months Lowering the body temperature A combination of tepid sponging and regular paracetamol is most effective . In resistant cases, a NSAID such as Junifen may be given in addition to paracetamol. REMEMBER DUAL PATHOLOGY - tonsillitis and meningitis can occur together . A careful history and examination are required. Examination undress the child completely including nappy look for rashes palpate for generalised lymphadenopathy check fontanelle examine all systems including ENT and joints tap sinuses in older children examine teeth and mucosal membranes look for entry sites for osteomyelitis Investigations If there is an obvious focus on clinical examination e.g. tonsillitis, then treat without investigations. If there is no obvious focus and the child looks well then give advice about anti - pyretic measures , check urine microscopy + culture, allow home and arrange to reassess if the situation changes. If there is no obvious focus and the child looks unwell then organise a Septic Screen. Septic Screen FBC+ dWCC Blood cultures U+E, creatinine Glucose Urine for urgent direct microscopy and culture Chest X-ray if < 6 months or with respiratory symptoms in older children Lumbar puncture if < 6 months. Assess the need carefully in older children. Throat swab with upper respiratory tract symptoms. Drug therapy Ideally, a focus of infection should be identified before antibiotic treatment is initiated. Exceptions to this are ( 1 ) the situation where the child is very unwell. Intravenous cefotaxime is indicated while results are pending. (see Paediatric Prescriber ) ( 2 ) children at risk Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial -GThis is the commonest cause of seizure in childhood, affecting 4% of all children. By definition, it is a generalised convulsion lasting less than 20 minutes ,associated with an acute febrile illness which is not of CNS origin. It occurs between the ages of 6 mths - 5 years as a single episode in an otherwise healthy child.There is often a family history of febrile convulsions. Points in history and on examination child s general health and developmental status family or personal history of seizures duration of convulsion focal features evidence of recent infection If the seizure has any atypical features , inform a senior colleague. Management of any febrile seizure Aim to stop seizure lasting more than 5 mins (see Paediatric Prescriber). Check capillary glucose. If low, check blood glucose . Anti - pyretic measures. With first febrile seizure Admit for a period of observation. Try to identify the cause for the fever. Susequent investigations depend on the course of the fever and the child s well - being but a septic screen must be considered, especially in those under 18months. Advise the parents on prognosis and management ( literature is available on hand - out) Antibiotics should not be administered routinely but may be required to treat specific infections. With subsequent febrile seizure Admission may not be needed, depending on the clinical condition of the child. Investigations may not be needed, depending on the clinical condition of the child. Repeat advice about temperature control. Oral anti -convulsants are generally not indicated. Consider rectal diazepam to use at home. The dose is 1 mg / year + 1. Rectal tubes are available in 5 mg and 10 mg strengths. Parents should be instructed in the use of CPR. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial `FVomiting is a symptom and not a diagnosis. The aims of the initial management are to 1. identify the underlying cause 2. decide who needs admitted to hospital Possible causes in any age group Gastroenteritis GIT abnormality ( includes gastrooesophageal reflux ) Infection ( any focus ) Drugs or toxins Food intolerance Biochemical disturbances Raised intracranial pressure Middle ear disease Migraine Cylical vomiting Points in the history nature of vomiting - projectile, bilious, coffee grounds, early morning details of feeds / diet and relationship to vomiting weight loss or gain ( use centile charts ) associated symptoms - headache, diarrhoea, constipation,urinary symptoms, abdominal pain, dizziness other affected family members or contacts access to drugs ortoxins N.B. Bile stained vomiting is pathological until proven otherwise Points on examination assess hydration plot growth parameters thorough general examination including blood pressure consider palpation for pyloric tumour consider fundoscopy for papilloedema observe feeding / vomiting Initial investigations to consider urinalysis for glucose, protein, blood, ketones urine for microscopy and culture capillary blood glucose U+E, creatinine Other investigations depend on the clinical picture septic screen ( see guidelines) serum calcium barium swallow USS abdomen for pyloric tumour examination of stools blood gas analysis if pyloric stenosis, diabetic ketoacidosis or renal tubular acidosis suspected Save and freeze urine for organic and amino acids. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial FA child is said to be failing to thrive when his or her rate of growth fails to meet the potential expected. Growth rate depends on many factors e.g. ethinic origin, parental height, birth weight. Failure to thrive is not a diagnosis but a term which describes the end result of a great number of different conditions.Regular monitoring and a multidisciplinary approach are key factors in the management of a child who is failing to thrive. Some possible causes Inadequate diet psychosocial circumstances impact of organic disease Gastrointestinal problems gastrooesophageal reflux malabsorption e.g. coeliac disease, cystic fibrosis infalammatory bowel disease chronic GI infection e.g. giardiasIs Renal problems urinary tract infection renal tubular disorder Lung problems bronchopulmonary dysplasia cystic fibrosis continued... Endocrine problems Cardiac problems Chronic infection tuberculosis Immunodeficiency Malignancy Points in the history diet ( 3 day food diary may help) family history general systemic review ask G.P. and health visitor for information look at parent held child health record card Points on examination growth chart ( corrected for prematurity) poor hygiene, apathy, poor eye contact dysmorphic features Consider as baseline investigations FBC and dWCC Calcium, urea, creatinine, electrolytes Liver function tests Urine for microscopy and culture Consider in some cases Chromosomes Coeliac screen Thyroid function Sweat test Barium swallow Chest X-ray ECG, echocadiography Urine pH Bone age Stools for ova and cysts Stools for pH and reducing substances Heaf test Jejunal biopsy Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial vJThere are many forms of child abuse e.g.physical injury, sexual abuse, neglect, failure to protect, emotional or psychological abuse and Munchausen syndrome by proxy. If any form of child abuse is suspected when a child attends A/E, then the SHO should ask someone more senior to see the child from the outset. If there are allegations of sexual abuse the registrar on call should take the history and contact the consultant on call. If there are concerns about physical abuse the registrar on call may begin the initial assessment and examination but must inform a consultant as soon as possible.( A/E consultant by day and consultant on call if after hours) Child abuse is a consultant diagnosis. Assessment Careful history from each person accompanyiny the child. Include the alleged, precise mechanism of injury. Look for consistency if there are several histories. Note any concerns about delay in seeking help. Details of all household members and their relationships. Systematic questions including details of any wetting or soiling. Ask about recent changes in behaviour and mood. Examination No child should be examined against his / her will. Observe behaviour of parents and child. Record any comments made. Thorough general examination with special attention to - demeanour of the child - general hygiene - growth parameters -bruising ( note the colour, size and distribution)) - burns and scalds - frenulum - tympanic membranes - fundi if possible - ano genital inspection ( not invasive examination) Be especially alert for NAI with - fractures of ribs, scapula or sternum - multiple fractures of different ages - spiral fractures of long bones Document any positive findings with drawings and precise measurements. Investigations ( check with consultant first ) Skeletal survey if < 2 years FBC + coagulation screen if bruising or bleeding present Initial mananagement of suspected N.A.I. Contact appropriate medical consultant who is likely to suggest contacting the social worker on call (by ringing the Contactors Bureau in Belfast) Depending on individual circumstances and nature of the injury to the child a decision can be taken as to whether or not admission is appropriate. In any case, details of any proven or suspected cases of any form of child abuse should be left for the social workers in the RBHSC. Initial management of suspected sexual abuse Contact appropriate medical consultant who is likely to suggest contacting the social worke on call. Depending on circumstances, clinical examination by a forensic medical officer may be required. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial KConsultant paediatric pathologists Dr.Claire Thornton and Dr. Denis O Hara should be contacted as soon as it is practical as they will give advice about how to proceed with arranging the autopsy. They are available by phone throughout the week and over the weekend at the following numbers. Dr. C. Thornton Dr. M.D.O RVH: Ext. 2625 RVH: Ext. 2518 Home: 01247 467049 Home: 01232 662096 If the pathologists are unavailable at the above numbers, call their mobile phone 0374 408716 General information There are two forms of autopsy - the Coroner s autopsy and the hospital autopsy. The Coroner s autopsy is requested by the Coroner when the death falls into one of the following catagories 1. sudden, unexpected death ( at home or in hospital) 2. unnatural cause of death 3. anaesthetic death 4. when there is a possibility of litigation Parental consent is not required in these cases and the family cannot prevent the autopsy. If the death falls in to one of the above catagories, telephone the Coroner s office ( 01232 743040) and give the Coroner or his officer a short summary of the clinical history. Remember that both paediatric and forensic pathologists do autopsies for the Coroner so ask which pathologists are to perform the autopsy. If the paediatric pathologists are to carry out a Coroner s post mortem, this will be done in the RVH mortuary. If the forensic pathologists carry out the autopsy the body may be transferred to the Belfast City mortuary at Forster Green. When the Coroner requests an autopsy, the police are required to take a history from the family and you should let the parents know that this will happen. A clinical summary and the case notes are also required. The pathologist gives preliminary details of the cause of death to the Coroner who then issues a burial order to enable the funeral to take place. The completed autopsy report is sent to the Coroner who may then wish to hold an inquest. He ultimately provides the death certificate although this may happen weeks or months later. A hospital autopsy is requested by the clinicians and requires written consent forn the next of kin of the deceased. The autopsy will be performed by the paediatric pathologist or by their junior staff in the RVH mortuary. For a hospital autopsy, the pathologist requires the writen consent form and the clinical summary on a completed request form. When the autopsy is complete, the pathologist will telephone the ward with the result and a death certificate can be issued if this has not already been done. A provisional summary is issued the following day by the pathologist and the final report is sent to the consultant clinician severral weeks later. When the patient has been under the care of the paediatric neurologists or neurosurgeons, the autopsy, whether Coroner s or hospital in type, is generally caried out by the neuropathologists. When an autopsy is being arranged, please inform the RVH mortuary staff at RVH extension 3860 / 3855. GEczema associated with a personal or family history of atopy (asthma, allergic rhinitis, allergic conjunctivitis) Symptoms and signs pruritis erythema, scaling papulovesicles in acute or subacute cases lichenification and hacking in chronic cases Complications bacterial superinfection (look for frank pustules or secondary impetiginization) eczema herpeticum (look for a sudden deterioration in the eczema with groups of papulovesicles and punched out erosions) Management A.General measures Avoid iritants such as soap. Advise about clothing - use cotton, avoid wool. B. Emollients Apply liberally, frequently and long term. Ask parents in detail about quantities applied.(These are frequently inadequate and this is a common cause of an apparent poor response to treatment.) Use bath emollients, 3 - 4 caps per bath e.g. Diprobath, Oilatum, Emulsiderm, Balneum Use emollient creams or ointments e.g. Diprobase cream or ointment, Aqueous cream, Oily cream BP, Soft white paraffin and liquid paraffin ( 50:50 mix) C. Topical steroids Apply to active eczematous areas. The activity of the eczema will determine the potency. Only mild steroids should be applied to the face and body fold sites. Mild: 1 % hydrocortisone Moderate: Eumovate, Modrasone Potent: Elocon, Cutivate, Diprosone, Locoid D. Antihistamines Sedative agents are useful as a short term adjunctive measure in active cases e.g. Phenergan, Vallergan Non - sedative agents are of little benefit. E. Antibiotics Topical antibiotics with or without topical steroids are indicated for localised secondary infection e.g. Polyfax ointment, Bactroban ointment, Daktacort ointment, Gregoderm ointment. Systemic antibiotics are indicated with widespread secondary infection e.g. Erythromicin, Flucloxacillin. F. Fixed dressings and bandaging These are useful when excoriation is prominent. Contact the dermatologist on call for advice if you think that they are indicated. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial FAEczema Herpeticum Contact dermatologist on call in every suspected case. confirm diagnosis by examining vesicle fluid (air dried on slide) under electronmicroscopy stop topical steroids systemic acyclovoir is indicated (use the intravenous route if sytemically unwell or if there is poor response to oral treatment) Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial DNAPKIN DERMATITIS A primary irritant eczema due to prolonged contact with a soiled napkin. erythema over buttocks, genitalia, lower abdomen, upper thighs sparing of deep folds( in contrast to seborrhoeic eczema) superficial erosions rarely deep crater-like ulcers (Jacquet s dermatitis) Complications superimposed candidiasis secondary spread of eczema to sites outside napkin area Management 1. Parent education is essential. 2. Use disposable napkins. 3. Change napkins frequently and , if possible, the infant should have peroids completely napkin free. 4. Cleanse the skin thoroughly with cream ( not alcohol) based wipes. 5. Apply a water repellent emollient liberally e.g. soft white paraffin, Sudocream, Zinc and castor oil BP 6. Use 1 % hydrocortisone ointmnent with or without a topical antifungal component e.g. Daktacort but for short periods only and only in conjunction with hygiene measures. 7. For recurrent candidiasis, give Nystatin oral suspension100,000 units / ml, 1 ml q.i.d. for 7 days. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial BThere are two clinical forms- bullous and non-bullous. Non-bullous discrete erythematous base with yellow-brown crust often around nose, mouth and hands Bullous flaccid blister on an erythematous base ruptures rapidly may be mistaken for a cigarette burn Investigations Send swab to bacteriology. Management A. Topical antibiotics These are adequate for localised lesions e.g. Bactroban ointment, Polyfax ointment B.Systemic antibiotics These are indicated with widespread lesions or with systemic upset e.g. Flucloxacillin, Erythromycin. C.Frequent recurrence Swab the carrier sites of the child and of family members. Treat the carrier sites with nasal Bactroban ointment, using a separate tube for each individual. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial BEpidermal necrosis and blistering of skin and mucous membranes. Possible causes drugs( most common cause) viral infections lymphoma, leukaemia post-immunisation idiopathic Clinical features tender, erythematous skin evolving to flaccid blistering and development of raw denuded areas extent is variable inflammation of conjunctivae, mouth and genital mucosae may precede or develop with skin changes pyrexia, anorexia and malaise are common Management Contact the dermatologist on call in every suspected case. 1. Admission. 2. Analgesia. 3. Adopt general supportive measures with special attention to fluid balance and the possibility of secondary sepsis. 4. Skin dressings. 5. Request early opthalmological assessment. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial BThis describes a generalised erythema with superficial blistering and peeling due to infection with epidermolytic toxin-producing staphylococcus. Clinical features usually occurs in infancy and early childhood extent of involvement varies trunk, perioral and perigenital areas are especially affected sudden onset of tender erythema with flaccid blistering and peeling N.B. The precipitating staphylococcal infection is often occult especially if in the upper respiratory tract. Management Contact the dermatologist on call in every suspected case. 1. Admit. 2. Give adequate analgesia 3. Adopt general supportive measures. 4. Specific systemic anti-staphylococcal treatment is required. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial D pruritic, excoriorated eruption nocturnal itch often prominent itch may be present in close contacts distributed over finger webs, flexor aspects of wrists, axillae, periumbilical and genital areas involvement of soles is common in infancy a linear burrow is a pathognomonic lesion Complications secondary bacterial infection ( pustules, impetigo) secondary eczematous changes Management 1. Treat all close contacts simultaneously. 2. Explain that the itch will persist for 3 -4 weeks and that this is not an indication for re-treatment. 3. Symptomatic control may be achieved by using sedative antihistamines e.g. Phenergan, Vallergan and Eurax HC cream. 4. Scabicide. (a) Lyclear dermal cream. Apply to all areas except immediate perioral and periorbital areas. In infants a light application to the scalp should be included. Wash off after 24 hours. If any area is washed within 8 hours of the initial treatment the cream should be reapplied. Repeat the treatment one week later. (b) Malathion ( Derbac M)This is an alternative treatment, equally efficacious and equally well tolerated.Application is as described above. Both preparations are safe in pregnancy. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial APrimary herpes simplex virus infection of the finger. Clinical features tender, vesiculopustules on the finger tip sometimes a haemorrhagic element progression to erosions with crusting Management 1. Simple analgesia 2. Prevention of secondary bacterial infection by taking extra care with hygiene and using Betadine if necessary. N.B. As it is self resolving, acyclovoir is not generally indicated. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial B1. Apply topical wart paint daily for up to three months e.g. Occlusal, Cuplex, Salactac gel. 2. Cryotherapy is indicated when there is failure of resolution after three months of adequate topical treatment. The procedure is painful and is applied every 1-2 weeks so it is important that likely compliance is considered prior to referral. PLANTAR WARTS 1. Regular paring, twice a week. This should be demonstrated and a disposable scalpel provided. 2. Daily application of a wart preparation. Occlusal, Cuplex, Salactac gel, Verucasep, Veracur. N.B.Treatment is often required for months so persistence is required. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial BPossible causes viral infections, especially herpes simplex drugs bacterial infections e.g.mycoplasma malignancy (rare) collagen vascular disease (rare) Clinical features annular or targetoid lesions, sometimes with central bullae or haemorrhage often a urticarial background oral, genital and conjunctival involvement in severe cases( Stevens Johnson syndrome) Management 1. Treat or remove the triggering factor if identified. 2. Achieve symptom control in mild isolated cases using antihistamines with or without topical steroids. 3. Indications for dermatology referral include (a) severe involvement (b) mucosal involvement (c) recurrent cases Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial B pink, pruritic wheals sudden onset, resolution within 24 hours may be an isolated cutanoeus finding may be associated with a widespread hypersensitivity reaction giant urticaria common in childhood N.B. An accurate history is most important to identify an antigenic trigger. In childhood transient, self-resolving viral infections are the most common trigger. Management of isolated cutaneous urticaria 1. Avoidance or elimination of any identified trigger factors. 2. Symptomatic treatment with non-sedative antihistamines. 3. Referral to a dermatologist is indicated if the problem persistS for more than three months. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial FDA vasculitis presenting with urticarial type morphology. Clinical features urticarial wheals, distinguished from simple urticaria by (1) duration> 24 hours (2) residual bruising on resolution multisystem vasculitis complaints may be variably present - arthralgia, abdominal pain, malaise, anorexia, lower limb oedema, hypertension Points in the history and examination try to identify the trigger e.g. drugs(most common), viral infection thorough examination of all systems is essential including documentation of blood pressure urinalysis is essential Management Contact the dermatologist on call in every suspected case. In the absence of abnormal urinalysis or any multisystem complaints, commence non-sedative antihistamines and repeat urinalysis regularly while the process remains active. In the presence of abnormal urinalysis or multisystem complaints, admit for further assessment and treatment. It may be helpful to consult the guidelines on Henoch Schonlein Purpura. (This is a subtype of urticarial vasculitis.) Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial BThe morphology of eruptions varies widely. Common patterns include widespread, morbilliform pattern urticaria erythema multiforme-like elements toxic erythema or erythroderma An allergic hypersenstivity vasculitis may be manifest as palpable purpura urticarial elements erythema nodosum-type lesions necrotic ulcers N.B. Viral infections are often associated with exanthems. Be cautious in blaming a co-administered antibiotic as a cause of the eruption. Management 1. Withdrawal of the suspected drug if possible. 2. Antihistamines are helpful especially when the urticarial element is promInent. 3. Oily calamine lotion can be soothing. 4. Topical steroids may provide short term symptomatic relief. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial FClinical presentation Usually, an acute onset of bruising, purpura and petechiae. Serious mucosal bleeding is unusual. 80% will describe some infection in the preceding three weeks. Investigations Admit to hospital to confirm the diagnosis. The baseline investigations are FBC and film and coagulation screen. In addition, bone marrow aspiration should be considered for those with lassitude, pain, a limp, lymphadenopathy , hepato - splenomegaly or a FBC which is not in keeping. Management There is still contraversy about the place of steroids. Low dose steroids are unlikely to be harmful over a short period. They may protect against intracranial haemorrhage which is serious though rare. At present it is suggested that (1) for those with bruising only, without mucosal or more severe haemorrahge, with platelet counts above 30 x 10 6 / l , it may be reasonable to give no treatment at all. (2) Usually oral steroids are required for platelet counts less than 30 x10 6 / l. The suggested dose is 0.25 mg / kg / day of oral prednisolone for one weekwith a gradual reduction over the following three weeks. Give a steroid advice card home. Intravenous immunoglobulin may be helpful for short term emergency treatment e.g.serious bleeding or for operations. Follow up should be until the platelet count returns to normal and remains normal for 2- 3 months. After this, parents should be alerted to reattend if the bruising recurs. If the thrombocytopenia persists for > 6 months, it is by definition chronic. Many children with chronic thrombocytopenia still remit spontaneously. (Splenectomy is rarely required in children.) Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial ELymph node enlargement is a common finding in children. Significant pathology is uncommon.The difficulty arises in deciding whom to investigate. When is a lymph node enlarged? Nodes > 1 cm diameter are generally considered abnormally enlarged. Some possible causes of generalised lymphadenopathy many common viral infections inc. EBV and HIV infection toxoplasmosis leukaemia / lymphoma/ other malignancy Some possible causes of regional lymphadenopathy infection (the commonest cause) tuberculosis Kawasaki disease cat scratch disease (axillary and cervical nodes) malignancy Points in the history duration travel exposure to pets weight loss fever, night sweats pruritis, rashes drug history Points on examination full examination of all nodal sites document size of nodes hepato/spleno megaly skin rashes / infected skin lesions anaemia, petechiae or bruising ENT , teeth, scalp especially with cervical nodes Management of lymphadenopathy Investigate immediately if 1. unexplained generalised lymphadenopathy with nodes > 1 cm diameter 2. or significant constituitional symptoms 3. or hepato/ plenomegaly, anaemia, bleeding Otherwise reassess in 3 - 4 weeks and investigate if 1. progressive enlargement 2. or no reduction in size. Investigations FBC, dWCC, slides, ESR Chest X-ray Tuberculin skin test in some cases Paediatric oncology opinion or lymph node biopsy Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial NMeningitis is inflammation of the meninges. It may be caused by bacteria, viruses, fungi and chemicals. Meningoccocal septicaemia may occur with or without meningitis.Both are life threatening. Symptoms and signs vary depending on whether meningitis or septicaemia predominates. Infants Older children pyrexia pyrexia fretfulness joint pains and myalgia vomiting vomiting poor feeding photophobia drowsiness drowsiness high pitched cry headache pallor confusion RASH RASH Note, typically the rash is purpuric (fine or blotchy) but occasionally is macular in the early stages. Management of suspected meningococcal septicaemia ( In the RBHSC meningococcal packs of blood forms are available. Also, guideline sheets are available for individual patients which serve as check lists for all the management points) A. Recuscitation Seek senior help. Check Airway, Breathing, Circulation Apply oxygen saturation monitor B. Establish intravenous access Take blood for capillary blood glucose blood glucose blood cultures FBC + dWCC coagulation screen group and hold PCR ( 2 ml EDTA - microbiology form ) first serology sample (1 ml clotted - virology form ) C. Antibiotics give benzyl penicillin 300 mg / kg / day in 4-6 divided doses and / or cefotaxime 200 mg / kg / day in 3 - 4 divided doses. if allergic to penicillin or cephalosporins, give chloramphenicol 20 mg / kg q.i.d. D. Treat shock vigorously There is often severe capillary leak in sepsis. give 4.5 % albumin 20 ml / kg rapidly. This may have to be repeated. E. Other samples take throat swab take petechial rash scrapings. (No skin preparation. Scrape lesion with sterile needle until it bleeds. Smear 2-3 drops onto a slide for gram stain and let it dry.) Also send dry cotton wool swab for O+S to bacteriology for immediate processing. consider arterial blood gas sampling consider lumbar puncture F. Notification all cases, whether suspected or proven, should be notified to Public Health immediately .Telephone = 321313 Outside normal working hours telephone ambulance control at 402222 and they will contact Public Health. G. Prophylaxis arrange prophy;actic antibiotics for household contacts (prolonged contact at home over last 7 days ) and throat swabbing of contacts accompanying the index child on the ward. public health will arrange chemoprophylaxis and throat swabbing of other close contacts and, if indicated, vaccination for types A,C,W 135 or Y . the index case requires prophylaxis to remove nasal carriage if not on ceftrioxone). This should be given at changeover to oral antibiotics prior to discharge. Rifampicin dosages: Adult 600 mg b.d. for 48 hours child > 10 months 10 mg / kg b.d. for 48 hours child < 10 months 5 mg / kg b.d. for 48 hours Warn of orange secretions, staining of soft contact lenses and interference wtih oral contraceptives Management of suspected or proven meningococcal meningitis The guidelines for meningococcal septicaemia should be followed. Lumbar puncture is desirable as it may yield a specific organism but check for contraindications. Send CSF for O+S, protein, cells, glucose and consider sending a fourth sample for virology. If aged six weeks or under Cefotaxime 50 mg / kg stat and ampicillin 50 mg / kg stat. If aged over six weeks give antibiotics as for meningoccocal septicaemia. Note, acyclovir should be commenced if there are signs and symptoms suggestive of encephalopathy. A simple viral menengitis does not require extra treatment and so a lymphocytosis in the CSF is not an absolute indication for treatment with acyclovir. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial NDA primary, herpetic infection with herpes simples virus, usually type 1. Spread is from person to person via oral secretions from a lesion or, more often, from an asymptomatic carrier. Symptoms and signs painful mouth and difficulty drinking high fever vesicles and ulcers in orophayynx, gums and tongue Indications for admission (isolate if admitted) inadequate fluid intake immunosuppression Management Ensure an adequate intake of fluids.Give small amounts frequently.Try straws, ice-pops and ice-cream. Young babies who refuse a bottle may take fluids from a syringe. Give adequate analgesia.Again try using a syringe.A parent can be shown how to give rectal paracetamol. Use a mouthwash such as Corsodyl, after analgesia has taken effect, 3-4 times a day. Either let the older child rinse his mouth or dab the Corsodyl using cotton wool. Acyclovir is probably not necessary in most cases especially if the infection is well established and otherwise uncomplicated as it will not alter the course of the illness. Look carefully for oral candidiasis and treat if necessary. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial 2IClassically, this is caused by Bordetella pertussis and parapertussis but a sometimes indistinguishable disease is associated with adenovirus infection. It is highly infectious and spread is by direct contact or by respiratory droplets. Full immunisation is necessary to reduce the incidence and mortality from pertussis but, even then, does not always give full protection. A neonate is not protected by maternal antibodies. The incubation period is 7-10 days. 1. Catarrhal stage (1-2 weeks) Upper respiratory tract symptoms predominate. 2. Paroxymal stage (2-6 weeks) Episodes of forceful coughing spasms during a single expiration are followed by a sudden whoop. Post tussive emesis is characteristic. Some patients do not whoop. Young infants may present with apnoeic episodes. 3. Convalescent stage (1-2 weeks) The cough gradually decreases in severity but can persist for several months. Investigations FBC + d WCC. A raised white cell count with an absolute lymphocytosis is characteristc at the end of stage 1 and during stage 2 in pertussis (not in parapertussis) chest x-ray initially and again at the end of the illness to exclude persistent areas of collapse continued...... send a pernasal swab with a specific request for pertussis. The % of positive swabs falls rapidly after the catarrhal phase as the lymphocytosis increases. serology is expensive and takes several weeks. It is only indicated in a few hospital cases. Management Admit if < 6 months and remember to isolate. Commence erythromycin 50 mg / kg / day for 2 weeks at any stage of the illness. It will not alter the course of the illness but eliminates infectivity within five days. For close contacts, under 7 years of age, who are fully immunised, give a booster dose of DPT unless it has been given in the last 6 months commence erythromycin 50 mg / kg day for 2 weeks. For close contacts, over the age of 7 years, who are fully immunised, give erythromycin as above. For close contacts of any age who are not fully immunised, give erythromycin as above and immunise. Note, treatment of the cough is difficult. Chlorpromazine is possibly the only useful medication. For infants, skilled nursing care should ensure an adequate fluid intake. Mechanical ventilation is occasionally necessary. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial uLAn increase in frequency, fluidity and volume of stool. Possible causes infection in GIT - bacterial, viral, parasitic systemic infection e.g. otitis media, UTI oral antibiotics prolonged oral rehydration therapy malabsorption e.g.cystic fibrosis, coeliac disease, lactose intolerance, cows milk protein intolerance inflammatory bowel disease anatomical defects and surgical conditions neoplasms and immunosupressive disease endocrine disease Points in the history and on examination onset and duration vomiting, temperature or abdominal pain description of stool recent foods and drugs other family members affected recent travel assess hydration - mild, moderate or severe signs of shock including capillary refill time signs of acute infection signs of systemic disease signs of acute surgical conditions Management of acute infective diarrhoeal illness Normal hydration A child may be managed at home if tolerating oral fluids. Continue normal feeding. Mild dehydration If breast feeding, continue breast feeding throughout. Stop otherl feeds for 12-24 hours. Prescribe oral rehydration therapy.Give frequently in small volumes.Supply a 10 ml syringe for parents to give one ml at a time if vomiting. It is probably not helpful to send stools for examination unless they are blood stained. Moderate to severe dehydration Admit. Remember to isolate. Send stools for O+S , virology, ova + cysts and cryptosporadia Send blood for U+E, creatinine, FBP. Send blood cultures if febrile. Note, when restarting feeds, restart directly onto full strength normal feeds t treat with an antibiotic t treat with an antiemetic or antidiarrhoeal drug t suggest flat coke Do review the next day Shock Correct shock if present using 20 ml / kg of colloid Repeat if necessary.(Do not include in future fluid calculations) Subsequent management of moderate to severe dehydration Maintenance fluids may be calculated as Body weight Fluid requirement per day First 10 kg 100 ml / kg Second 10 kg 50 ml / kg Subsequent kg 20 ml / kg 5% dehydration = maintenance + 50 ml /kg 10% dehydration = maintenance +100ml /kg 15% dehydration = maintenance +150 ml /kg. In addition, remember to replace any ongoing losses. Try oral rehydration therapy although nasogastric or intravenous fluids may be necessary. With normal serum sodium, use 0.18% saline + 4 % dextrose as the intravenous fluid. Fluid may be replaced over 24 hours. With low serum sodium, treat shock if present. Then,use the above regime but with 0.45 % saline + 2.5 % dextrose as the intravenous fluid over 24 hours. With hypernatraemic dehydration, treat shock if present. Then, use 0.45% saline + 2.5% dextrose. Calculate maintenance and replacement fluid requirements. Rehydration must take place slowly. Give maintenance fluids over 24 hours but replace lost fluid over 48 hours or longer.The serum sodium should be reduced slowly (< 5 mmol / 12 hours) Note, unless there is anuria, KCl is added to the fluid regimes according to electrolyte results. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial CDiarrhoea which persists for more than 14 days. It most commonly occurs in an infant recovering from an acute episode.Possible causes include transient lactose intolerance or transient cows milk protein intolerance. Send stools for O+S, pH and reducing substances while taking ordinary milk.Try a low lactose or a lactose free milk for 6 weeks e.g. Pregestimil, Prejomin, Soya milk With Toddler s diarrhoea the infant is healthy and well. Vegetable matter can often be identified in the stool. Send stools for O+S, ova and cysts, pH and reducing substances.If normal and the child s weight is satisfactory, reassure that it is likely to resolve. Avoiding cold drinks and limiting snacks may help. With other causes of chonic diarrhoea it is likely that fairly extensive investigations will be necessary. Refer for an out-patient opinion. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial LConsider as a diagnosis with frequency, dysuria abdominal pain fever, anorexia, vomiting crying infant failure to thrive neonate with prolonged jaundice enuresis Confirmation of the diagnosis The diagnosis is confirmed if there is a pure growth of >10 bacteria / microlitre on the following specimens: -bladder tap ideal sample between 0 - 6 months) -clean catch in an infant -midstream sample in co-operative older child Any growth when a child is on antibiotics should be treated as a urinary infection. If any organisms are seen under direct microscopy of an urgent sample, begin treatment and await culture results for confirmation. N.B. A negative result from a uri - bag is reliable but a positve result should be confirmed by a bladder tap or clean catch. If this is not possible, aim to send 3 uri - bag specimens. Management 1. High fluid intake 2. Document blood pressure. 3. Therapeutic antibiotic therapy for 7 days (see Paediatric Prescriber) 4.Prophylactic antibiotics until follow -up investigations complete (see Paediatric Prescriber) Baseline investigations after first proven UTI (These guidelines are based on current consensus and current availability of follow-up investigations) At all ages Abdominal X-ray with any suggestion of calculi (renal colic, Proteus infection, haematuria, persistent infection) or any suspicion of neuropathic bladder All neonates and those under 2 years USS renal tract DMSA Scan Micturating cystogram All children aged 2 - 5 years USS renal tract DMSA Scan Micturating cystogram if abnormal DMSA scan Children over the age of 5 years a. with lower tract symptoms / cystitis USS renal tract b. with systemic symptoms USS renal tract DMSA scan Timing of investigations USS - at any stage. MCUG - when infection clear DMSA - at least 6 weeks after the infection Prophylactic antibiotics are generally used until investigations are complete until vesico ureteric reflux has resolved ( any grade) or until the age of 5 years Further management depends on the results of baseline investigations,the age of child and subsequent clinical course. Vesico ureteric reflux on MCUG + normal DMSA scan prophylactic antibiotics until the age of 5 DMSA scan every 2 years until the age of 5 Scar on DMSA scan but normal MCUG annual blood pressure checks and urinalysis for life (G.P. might check after the age of 10) no prophylaxis is needed Scar on DMSA scan and vesico ureteric reflux prophylaxis until the age of 5 regular blood pressure checks regular DMSA scans depending on the frequency of symptoms Normal investigations but recurrent infections a 6 month trial of prophylaxis may be helpful consider possibility of cystitis or irritable bladder Other points Repeat urine samples should be checked at any stage when symptoms arise Surgical advice may be helpful if infections are recurrent or are of increased severity despite prophylaxis Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial EProtein may be found in the urine of healthy children. The upper limit of normal protein excretion is approximately 60 mg / 24 hr. Proteinuria is commonly detected by the dipstick test. 1+ is approximately 30 mg / 100 ml. 2+ is approximately 100 mg / ml. Possible causes A. False positive e.g. chlorhexidine contamination, delayed reading of stick B. Non - renal e.g. febrile illness, exercise, postural C. Renal e.g. UTI, glomerulonephritis, polycystic disease Point in history recent exercise fever drugs family history of renal disease Points on examination blood pressure must be recorded Baseline investigations urine for microscopy and culture dipstick for haematuria / glycosuria single sample for protein / creatinine ratio (Normal value is < 20 mg protein / mmol creatinine) Management 1. Management depends on the clinical findings and degree of proteinuria. 2. Consult the guidelines on urinary tract infection and glomerulonephritis. 3. If there is no obvious cause for the proteinuria and the child is well, it is reasonable to review in 4. Nephrology referral is generally indicated for persisting, unexplained proteinuria. Further investigations Serum U+E, Creatinine, CO2 Serum complement C3 C4 Autoimmune profile Vasculitis profile Creatinine clearance USS renal tract Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial @ confirm with direct microscopy: > 5 red blood cells/mcl watch for false positives e.g. delayed reading, haemoglobinuria watch for false negatives e.g. vitamin C red urine has many causes e.g. beetroot, rifampicin, urates ( neonate) red cell casts and or proteinuria imply renal disease Some possible causes of haematuria Urinary tract infection Perineal irritation Glomerulonephritis Trauma Coagulopathy Stones Hypercalcuria Tumour Exercise induced Anatomical abnormalities Benign recurrent haematuria Haemolytic uraemic syndrome Points in the history age dysuria / frequency of micturition recent illness recent exercise drugs family history of renal disease family history of hearing problems Points on examination oedema evidence of pharyngitis anaemia blood pressure genital inflammation palpable kidneys or abdominal masses Baseline investigations 1. reagent strip for proteinuria 2. urine for microscopy and culture 3. urine examination for casts and red cell morphology 4. spot sample for protein / creatinine ratio Indications for admission oedema hypertension oliguria macroscopic haematuria with no obvious cause ( e.g. trauma, perineal irritation, coagulopathy ) Nephrology referral is indicated for microscopic haematuria persisting for more than a month. Meanwhile, organise USS renal tracts U+E, creatinine, CO2 complement C3, C4 coagulation screen ASO titre autoimmune and vasculitis screen single urine sample for calcium / creatinine and protein / creatinine ratio abdominal X ray throat swab Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial BGlomerular and tubular dysfunction co-exist. This may give rise to a nephritic syndrome or a nephrotic syndrome. In the nephrotic syndrome, the fluid retained is extravascular, so giving rise to oedema. Sometimes there is overlap between the two syndromes but the term nephrotic syndrome is generally used when oedema predominates. Haematuria can occur in either syndrome. Nephritic syndrome Nephrotic syndrome haematuria heavy proteinuria oliguria hypoproteinaemia hypertension hypercholesterolaemia mild facial oedema marked dependent oedema + / - ascites Arial Arial Arial Arial Arial Arial 'G(minimal change in 90% of European children) Investigations urine dipstix, direct microscopy and culture single urine sample for protein/ creatinine ratio (>200 mg / mmol for diagnosis of nephrotic syndrome) FBC, U+E, Creatinine, CO2 total protein, albumin cholesterol complement C3, C4 serum to virology for measles, chicken pox and hepatitis B status Management of nephrotic syndrome Record height, weight and surface area. Daily record of input / output, weight and urinalysis. Monitor blood pressure. Exclude added salt in the diet. Observe for abdominal pain which may be a symptom of peritonitis of hypovaleamia. Begin steroids at presentation.(see Paediatric Prescriber) Diuretics may be used to help manage oedema but only with extreme caution lest they precipitate hypovolaemia. If hypovolaemia occurs give plasma expansion using salt - poor 5 % albumin at 10 ml / kg over 2 hours. Signs of hypovolaemia include abdominal pain, decreasing blood pressure and urinary output, increasing heart rate, increasing haematocrit or urinary sodium < 10 mmol / l pre- frusemide. Infusion of 20 % albumin is sometimes necessary but it can be hazardous and it may be helpful to seek nephrology advice prior to its use. Remember to issue a steroid warning card prior to discharge. Relapse of nephrotic syndrome At discharge, advise parents to perform urinalysis daily until an early out - patient review. Urinalysis should continue most days for at least 6 months. Relapse is defined as ++ protein or more for three consecutive days and epeat steroid therapy is indicated. (see Paediatric Prescriber) Referral to a nephrologist is generally indicated with 2 or more relapses in 6 months or no initial response to steroids after one month. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial xIA sudden cessation in renal function. There may be a pre-renal, renal or post renal problem. It is important to differentiate between the three groups. Symptoms and signs of renal failure oliguria drowsiness oedema and fliud overload acidotic breathing Baseline investigations Urine : dipstix for protein and blood -microscopy and culture - urea, electroylytes, creatinine -osmolality, pH, specific gravity Blood : FBC, film for fragmented red cells, - U+E, creatinine, C02, -calcium, phosphate - serum osmolality - blood culture X-ray chest and abdomen USS renal tract Also consider micturating cystogram (to look for posterior urethral valves in infant) Pre renal failure oliguria .urinary sodium < 10 mmol / litre ( pre-frusemide) Urea urine / plasma concentration > 20 Creatinine urine / plasma concentration > 40 Management of pre-renal failure Dehydration is the commonest cause. 1. Consider catheterisation. 2. Give 20 ml /kg 0.9% saline over 30 - 60 minutes. 3. If necessary repeat, over 2-4 hours. 4. If still no response give 1 mg / kg frusemide intravenously. 5. If a response is obtained at any stage , continue rehydration. 6. If not , then consider that there is established renal failure. 7. Remember to check that any catheter is in situ and patent ! Renal or post renal failure oliguria and anuria urinary sodium 30 - 90 mmol / litre urea urine / plasma concentration ratio < 10 creatinine urine / plasma concentration ratio < 15 Management of renal failure 1. General Daily weight. Test all urine. Regular blood pressure 1- 4 hrly. 2. Fluids Catheterise. Record input / output each hour. Fluid restrict to 300 ml / m / day ( insensible loss) + previous day s output. 3. .Hypertension - due to fluid overload or increased rennin secretion. Firstly, review fluid balance. If unhelpful , anti-hypertensives are indicated. See Paediatric Prescriber. 4. Hyerkalaemia See Paediatric Prescriber 5. Drugs Avoid, if possible, drugs excreted by the kidneys. Indications for dialysis Severe heart failure / pulmonary oedema Anuria Uncontrolled hypertension Cerebral oedema Hyperkalaemia Severe acidosis Severe electroylyte imbalance Symptomatic uraemia Presence of dialysable toxin Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial QDRenal stones are rare, occurring in 1.5 children per million per annum. Predisposing factors include: infection -especially Proteus anatomical abnormalities metabolic problems - increased secretion of calcium, uric acid, cystine, xanthine or oxalate Points in the history immobilisation poor oral intake or dehydration diet drugs family history Symptoms and signs abdominal or loin pain renal colic haematuria may present as UTI Investigations If renal stones are suspected abdominal X-ray USS renal tracts urine for direct microscopy+ culture If stone disease is confirmed a nephrology referral is generally indicated. Meanwhile it will be helpful to organise urine pH (send to laboratory - do not rely on ward testing) oxalate / creatinine ratio ( send single sample in container with acid) calcium / creatinine ratio and urate / creatinine ratio( both can be done on single specimen ) urinary amino acids serum for renal and bone profile serum uric acid N.B. Urine samples are taken from the second voiding of the day. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial EThe manifestations of this disease are due to vasculitis of the small blood vessels and are generally seen in children aged 2 - 8 years. It may follow an upper respiratory tract infection or in some cases allergy and drug sensitivity may play a role. Manifestations malaise, low grade fever symmetrical rash (urticarial and / or purpuric) affecting extensor aspects of buttocks and forearms and anterior aspects of lower limbs swollen , painful joints especially ankles, knees, wrists and elbows microscopic or macroscopic haematuria proteinuria is an ominous sign abdominal pain, vomiting, blood in stools, intussuception hepatoslenomegaly and lymphadenopathy rarely, seizures, paresis and coma Baseline investigations 1. urinalysis 2. blood pressure 3. FBC, U+E, creatinine, CO2, coagulation studies Indications for admission abdominal pain severe arthritis haematuria / proteinuria Management as outpatient simple analgesia and rest weekly review with urinalysis and blood pressure until symptoms settle review at any stage if symptoms worsen Management in hospital simple analgesia and rest daily urinalysis and blood pressure monitor urinary output The management of a nephritic syndrome with Henoch Schonlein Purpura is considered under separate guidelines. Corticosteroids are generally indicated for CNS complications, GIT complications and nephritis but in each case it is likely that the appropriate specialist will have been consulted. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial @Possible causes A. Infection Part of febrile illness Sinusitis, otitis media, dental caries Meningitis, encephalitis B.Vascular Sub-arachnoid haemorrage Migraine Systemic hypertension C. Raised intracranial pressure Brain tumour or abscess Benign intracranial hypertension D.Muscle strain Tension Occular headaches A careful general and neurological examination is essential to look for focal signs and to detect raised intracranial pressure. Remember to check optic fundi and blood pressure. Seek advice re neuroimaging when headache is associated with any of the following neurological signs symptoms and signs of raised ICP (headache awakens child from sleep, occurs in early morning especially if associated with vomiting, is induced by exercise or cough) failure to return to normal between headaches not relieved by simple analgesia increasing frequency or severity of attacks slowing of physical / mental development,deteriorating school work or change in personality age < 6 years head circumference out of line with other growth parameters Headache syndromes Meningitis. The headache tends to be accompanied by neck stiffness.The onset is over hours and systemic illness is present. Encephalitis.Initially, this may resemble a non - specific viral illness with fever and headache. Suspect the diagnosis with any of the following - altered level of consciousness, emotional outbursts, convulsions, vomiting, bizarre movements, focal neurological signs.Neck stiffness may be present. Sinusitis. The frontal sinus is rarely a source of infection until > 6 years. Ethmoiditis can present in infancy. Suspect sinusitis if a seems more severe than usual or lingers for more than ten days. Look for oedema and tenderness( not common). Amoxycillin is a reasonable initial choice of antibiotic. Decongestants and antihistamines are not usually helpful. Seek an E.N.T. opinion if the therapy is unsuccessful Brain tumour or abscess.Focal neurological signs or signs of raised intracranial pressure are usually present. Sub-arachnoid Haemorrage. Classically, there is a very sudden onset of headache with neck pain and stiffness. In contrast to migraine, any neurological features appear during or after the headache. Confusion, seizures and focal neurological si0 gns may develop. Benign intracranial hypertension.This diagnosis can only be made when a space occupying lesion has been excluded. Papilloedema is often present. Ask about recent otitis media, viral illness or recent corticosteroid therapy. Systemic hypertension. This should not be forgotten as a reason for any kind of aheadache. Occular headaches.These result from constant muscular activity attempting to correct a latent squint or refractive error. Note, that children qualify for free eye testing by an optician. Migraine. This is defined as a paroxysmal headache with symptom free intervals and at least three of the following in association: 1. nausea or vomiting 2. throbbing in character 3. unilateral location 4. abdominal pain 5. relief following sleep 6. positive family history of migraine Common migraine does not have an aura.It usually lasts 1-3 hours although it can last up to 24 hours. Classic migraine has a pre-ceding aura - blurred vision/ scotoma/ distortion of body image/ perioral parasthesias and numbness in hands and feet. Management of migraine 1. Advise simple analgesia early in the course of the headache. Paracetamol or a non-steroidal antiinflammatory compound usually gives relief, especially followed by a brief rest in a darkened room. 2. Try to find any reason for the timing of the presentation as it may avoid unnecessary medications e.g anxiety re brain tumour. 3. For the few who continue to experience troublesome frequent attacks a prophylactic agent may be tried. Pizotifen is used as directed in the B.N.F. for a three month period initially. The need and effectiveness of continuining therapy should be reassed at intervals.There are alternative prophylactic agents e.g propranolol but at this stage consider asking for neurological advice. 4. Provoking factors include stress, fasting, food, fatigue, light and minor head trauma but they tend to be inconsistent in their effects .Watch out for such factors but there is no indication for routine food avoidance. Arial Arial Arial Swiss Arial Swiss Swiss Swiss Swiss Swiss Swiss Swiss Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial FHead circumference > 97 th centile.(Measure over forehead and occiput so maximum circumference is obtained) Possible causes familial hydrocephalus, brain tumour subdural effusion benign external hydrocephalus bony disorders e.g. achondroplasia, degenerative CNS disease. Macrocephaly may occur as a result of megalencephaly (brain substance is greater than normal) which may be an early sign of degenerative disease. Points in the history and on examination symptoms of raised intracranial pressure medication especially recent steroid therapy head size in parents, grandparents and siblings ask about developmental milestones ask to see the Parent Held Child Health Record card. An 8 week measurement is the best baseline. signs of raised ICP ( bulging anterior fontanelle, wide-spaced sutures, dilated scalp veins, sunsetting eyes) abnormal neurological or developmental features measure head circumferences of parents and, if possible, those of siblings and grandparents retinal examination ( looking for haemorrhages ) neurocutaneous stigmata Management 1. If the child is well and there are no abnormal clinical signs, measure head circumference fortnightly on two occasions and discharge if it is following centiles and the child remains well. 2. If child is unwell or there are abnormal clinical signs, urgent referral is appropriate. Neuroimaging may. be indicated. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial BHead circumference < 3 rd centile.( Measure over occiput so maximum circumference is obtained.) Possible causes A. Primary genetic syndromes familial cerebral malformations B. Secondary intrauterine infection intrauterine or perinatal hypoxic insults metabolic disorders craniosynostosis Points in the history details of pregnancy and birth family history Points on examination plot out all growth parameters dysmorphic features hepatomegaly / splenomegaly neurological features developmental milestones Invetsigations to consider TORCH titres ( up to 2 years) chromosomes (consider genetic referral) neuroimaging urine for CMV screen serum amino acids Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial 3EHypotonia is a diminished resistance to passive movement. Muscle power may be normal or weak. Hypotonia can be caused by central or peripheral problems or seen in a child with severe systemic illness or a chromosomal abnormality. Weakness is a prominent feature of peripheral hypotonia but not usually of central hypotonia. With systemic illness ( e.g. metabolic, endocrine, cardiac, renal, liver disease) weakness is variable. Detection of weakness can be difficult in a young child. Points in the history ask about pregnancy (e.g. fetal movements) and birth family history medical history ( seizures suggest a central cause) developmental milestones a fluctuating course may suggest metabolic disease Points on examination A thorough neurological examination is required to try to localise the lesion. Features of central hypotonia include microcephaly fisting scissoring brisk reflexes Features of peripheral hypotonia include muscle wasting muscle fasiculations weaknss sensory loss reduced reflexes Investigations should be tailored to the clinical picture. Creatinine kinase should be checked in all cases. Neuroimaging is appropriate in central hypotonia. It will be helpful to seek neurological advice re further investigation of peripheral hypotonia Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial }B1. Work of breathing respiratory rate recession (subcostal, sternal, suprasternal, indrawing, flaring alae, use of accessory muscles) respiratory noise - stridor = extra thoracic airways obstruction - wheeze = intra thoracic airways obstruction - grunt = pneumonia, pleural effusion or RDS (neonate) 2. Effectiveness of breathing air entry on auscultation degree of abdominal excursions N.B. A silent chest or disappearance or respiratory noise is an extremely worrying sign. 3. Adequacy of respiration colour mental status (agitation, drowsiness) heart rate N.B. Bradycardia is a pre - terminal sign. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial HDCauses A. Early childhood Viruses predominate (RSV, parainfluenza virus) but may co-exist with the pneumococcus or haemophilus type B. Staphylococcus aureus is rare but should be considered especially if pneumatocoeles present. B. Over the age of 5 years mycoplasma or the pneumococcus are more usual. Sympyoms and signs may follow an upper respiratory tract infection pyrexia, cough, tachypnoea, grunting reversal of the respiratory pattern (i.e. a pause after inspiration) often classical signs of consolidation (reduced air entry, dullness to percussion, bronchial breathing) a chest X-ray is essential for diagnosis Management 1. Oxygen may be required. 2. Give antibiotics oral or systemically depending on how ill the child is and whether vomiting is present. A. Under 5 years, use amoxycillin + / - flucloxacillin or augmentin or cefuroxime + / - flucloxacillin B. Over 5 years, use benzyl penicillin (lobar pneumonia) or erythromicin (mycoplasma pneumonia) or cefuroxime and erythromycin (bronchopneumpnia) Add metronidazole of aspiration suspected. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial CDefinition: Inspiratory crowing noise, worse with crying,usually due to extra thoracic airways obstruction. With a fixed severe obstruction there is an expiratory component. Some possible causes Laryngotracheobronchitis (viral croup Acute epiglottitis Bacterial tracheitis Foreign body Pressure on the brain stem - always look out for the child with stridor and V-P shunt in situ, especially those with spina bifida Laryngeal oedema, acute tonsillar enlargement , retropharyngeal abscesses, hypocalcaemia Superimposed acute infection plus laryngeal cysts or webs, haemangiomas, laryngomalacia and vascular rings REMEMBER - CALL THE AIRWAYS TEAM IF THE AIRWAY IS COMPROMISED OR EPIGLOTTITIS IS SUSPECTED. (The contact number is in RBHSC A/E.) In any conscious child with obvious airways obstruction allow him to maintain his own airway position meddling may make matters worse call for assistance Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial CAetiology: Haemophilus influenza type B. Occasionally streptococcal. Age: peak incidence is 3 - 6 years Signs and Symptoms Acute onset fever, often >38.5 degrees C. Sore throat ++++ Stridor is soft, usually no cough Worsening over 6-12 hours Tripod sign DROOLING, TOXIC Management Calmness and reassurance. Administer 100 % oxygen by face mask if tolerated Contact the airways team and anaesthetist. If conscious, let the child adopt whatever position he wants as he will naturally optimise his own airway. Intubation is required. THEN blood cultures and intravenous cefuroxime. Under NO CIRCUMSTANCES should you use a tongue depressor attempt to withdraw blood or establish intravenous access send the child for an X-ray adopt a wait and see approach Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial tHAetiology : Parainfluenza type 1 (also 2+3). Influenza A. RSV. Age:peak incidence is 3 months - 3 years Signs and Symptoms URTI for 1-2 days Harsh barking cough Hoarse voice, Worse at night If significant obstruction, then indrawing at rest Admit if age < 1 year stridor with indrawing cyanosis HR > 160 / min or RR > 60 / min inability to drink previous severe attack In mild cases Give 2mg of nebulised Budesonide as a single dose in A/E. If child settles quickly and shows , , discharge. Advise to return at once if symptoms recur. Management in hospital If very severe, initial management is as for acute epiglottitis (up to 5 % of croups require intubation) Monitor oxygen saturations. Humidification + / - oxygen when necessary (NOT steam tent). Admiister steroids as either (1)Nebulised budesonide 2mg all agesas a single dose followed by 1 mg 12 hrly until signs of airway obstruction have disappeared or (2) Dexamethasone 0.6 mg / kg, orally, IV or IM Note, nebulised adrenaline may tried with caution after budesonide in severe cases. Dose is 1-5 mls of 1 in 1000 adrenaline given with oxygen via a face mask, with continuous ECG and oxygen saturation monitoring. Repeat in 2 - 4 hrs. Tachycadia is common and rebound may occur.Children requiring this therapy should be closely monitored in a high dependency area. Consider need for intravenous fluids. Neither antibiotics or chest X-rays are routinely indicated. Recurrent spasmodic croup may be an allergic response to viral antigens.There are no coryzal symptoms and is managed as croup.Regular inhaled steroids may be helpful. Repeated episodes of croup may very rarely be caused by the presence of a vascular ring or subglottic stenosis. Consider sending these children for elective bronchoscopy. Foreign body Remember with sudden stridor. Seek urgent ENT advice.(Initial management as per epiglottitis) Laryngeal oedema If due to thermal or chemical injury seek urgent ENT advice. If part of an anaphylactic reaction, see guidelines on anaphylaxis. Retropharyngeal abscess May be seen on lateral x-xray of neck. Seek urgent ENT advice. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial ALaryngomalacia Onset of stridor at birth or weeks later. Stridor variable. Seek ENT advice. Subglottic stenosis Especially if pre-term and previously intubated Vascular compressions on trachea Larnygeal cysts , webs, haemangiomas and vocal cord paralysis Arial Arial Arial Arial Arial Arial Arial @As a general guideline, consider the possible diagnoses, look for the associated clinical signs and symptoms and investigate accordingly. Possible causes chronic lung disease (ask about prematurity) swallowing incoordination e.g cerebral palsy, gastro oesophaeal reflux cystic fibrosis asthma inhaled foreign body immunosupression - Ig A deficiency, Other immunoglobulin deficiencies, T cell deficiencies, neutropenic states, complement deficiencies tracheo oesophageal fistula vascular ring or congenital lun g malformation Consider the following baseline investigations FBC, Serum immunoglobulins with Ig G subclasses Chest X-ray if not performed recently Barium swallow Sweat test Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial 4BIn non emergency situations the child should be referred back to the local CF clinic. In emergency situations organise a chest x-ray if the child has not acquired Pseudomonas infection then the most likely organisms are Staphyloccocus or Haemophilus.Send sputum for culture and change the antibiotics from Flucloxacillin to Augumentin. If the child has acquired Pseudomonas infection then, as an emergency measure,send sputum for culture and commence oral Ciprofloxacin or intravenous Ceftazidime. Contact the CF clinic as soon as possible for advice. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial FThe child with abdominal pain may have a problem which is unrelated or related to cystic fibrosis. Therefore consider A. Possible causes related to cystic fibrosis constipation distal intestinal obstruction syndrome (meconium ileus equivalent) pancreatitis gallbladder disease intussusception and volvulus hypersplenism and portal hypertension (large spleen may cause abdominal pain) lower lobe pneumonia B. Possible causes unrelated to cystic fibrosis medical conditions e.g. urinary tract infections, gastroenteritis, hepatitis, mesenteric adenitis surgical conditionse.g. appendicitis, renal calculus, torsion of ovary or testis Initial management 1. Careful history and general examination 2. Palpate carefully for abdominal masses, particularly in the right iliac fossa. 3. Organise straight abdominal X-ray. Further management of abdominal pain with CF depends on the situation and underlying cause. If there is evidence of faecal loading refer to the CF clinic where oral gastrografin and,if necessary, gastrografin enema will be given.Instructions regarding the administration of gastrografin are available in a booklet on the ward. It is important that there is a clearing out in the early phase or the child can develop total obstruction.Careful attention must be given to hydration when gastrografin is used.Intravenous fluids may be necessary. Distal intestinal obstruction syndrome should be managed in the tertiary centre. Surgical ntervention should be avoided where possible.Management involves the use of gastrgrafin as above. A child with this syndrome reguires active medical intervention with extremely close monitoring. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Table1 Title: X-ref: &Keywords: Intro: &Protocol: Refs: Notes: ;D These guidelines have been compiled to help junior medical staff of the Royal Belfast Hospital for Sick Children with the management of common paediatric medical conditions.They reflect the current thinking of many medical consultants. Details of drugs mentioned in this handbook can be found in the Paediatric Prescriber. It is hoped that the Paediatric Prescriber and Paediatric Medical Guidelines can be used as sister handbooks. Guidelines can only be used to guide you as the clinician.They will not apply to every child you see and it is not anticipated that they will be adhered to rigidly in every case.Consultation with an experienced colleague remains a cardinal rule when managing a sick child. Paediatricians may differ in the fine details of management of certain conditions and it is right that this should continue but it is hoped that these guidelines reflect a consensus on the broader details of management. Some of the guidelines may change with time and, although efforts will be made to update them, this should be borne in mind. EThis booklet contains guidelines for the management of many common paediatric medical conditions and has been compiled with help from medical staff in the Department of Child Health and the Royal Belfast Hospital for Sick Children. I acknowledge with gratitude the contributions made by the following: Dr K Armstrong, Dr A Bingham, Dr B Bartholome, Dr D J Carson, Dr B Craig, Dr S I Dempsey, Dr E M Hicks, Dr A E Hill, Dr P Jackson, Dr M O Connor, Dr A E Redmond, Dr M Shields, Dr H Steen, Dr Moira Stewart, Dr C Thornton, Dr D Webb Special thanks are due to Dr Moira Stewart who has been closely involved in the compilation of the handbook form the outset and to the staff in the Department of Child Health. Dr Mary Claire McGovern (Senior Registrar, Community Paediatrics) This version (v1.0) has been converted to Psion Series 5 Data format by Dr Shane McKee. Many regimes incorporated here will differ from unit to unit, and what is presented here is in no way intended to be an authoritative protocol, but guidelines to good clinical practice. In all circumstances ensure that your clinical practice conforms with your locally-applied guidelines and your ethical obligations to your patients. Neither I nor any of the above take any responsibility for the accuracy, applicability, or currency of the information contained in this database. Anything you do to your patients remains your sole responsibility. Dr Shane McKee, April 1998 Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial BInflammation or necrosis of the myocardium due to infectious, toxic, connective tissue or idiopathic processes. Signs congestive heart failure (commonest manifestation) fever tachycardia out of proportion to fever arrhythmias distant heart sounds Investigations FBC, ESR, Blood cultures,Viral titres( paired) Mycoplasma titres, Cold agglutinins Cardiac enzymes - CPK, LDH Chest X-ray - cardiomegaly and pulmonary oedema ECG - sinus tachycardia, reduced QRS voltages, ST and T wave abnormalities Management Treat congestive heart failure (Paediatric Prescriber) Treat any arrythmias ( Paediatric Prescriber) Commence Erythromycin if mycoplasma suspected. Arial Arial Arial Arial Arial Arial Arial Arial Arial @A concentration of haemoglobin and/or red cells below the normal for age. Significant anaemia is always a manifestation of disease or nutritional deficiency. Possible causes Consider the headings of Haemorrhage Haemolysis Marrow failure due to hypoplasia or aplasia or infiltration Haematinic factor deficiency e.g iron, B12, folate Points in the history symptoms of acute or chronic blood loss presence of dark urine family history of anaemia, gallstones, jaundice drugs bruising, recurrent infections growth and developmental milestones dietary history including milk ingestion prematurity or twin births Points on examination jaundice - haemolysis skull bossing - haemolytic anaemia hepato / splenomegaly - haemolysis, malignancy purpura - malignancy, aplastic anaemia lymphadenopathy - malignancy bone tenderness - malignancy smooth tongue, koilonychia - iron deficiency growth parameters fundal haemorrhage - any anaemia Baseline investigations If a child is noted to be pale, a full blood count, blood film and iron studies should be performed. Contact Dr. Dempsey in the RBHSC at once if there are major abnormalities in the blood film. If the platelet count or the white cell count is abnormal, consider asking for haematological advice, even if the blood film is normal. Further investigations depend on clues from the history and indices on full blood count. Normal indices Hb MCV MCH g / dl fl pg / cell Birth 14.5 - 22.5 110 - 128 31 - 37 2 mths 9.4 - 13.0 6 - 24 mths 11.5 - 13.5 70 -85 25 - 31 2-6 yrs 11.5 - 13.5 75 - 90 24 - 30 6 - 12 years 11.5 - 15.5 78 - 95 25 - 33 All ages Platelets 150 - 400 x 10 6 / litre MCHC 30 - 36 g Hb/ dl Reticulocytes 0.5 - 2.5 % Macrocytic anaemia If the patient is Caucasian, suspect B12 / Folate deficiency, haemolysis or liver disease. Check serum B12, plasma folate, reticulocyte count, liver function, plasma haptog` lobins. Test urine for urobilinogen.If reticulocytes are raised, ask for haematological advice. Hypochromic anaemia Suspect iron deficiency. Rarer causes are lead poisoning or sideroblastic anaemia. Thalassaemia is rare in N.I. but commoner in parts of Britain. Normocytic anaemia Suspect chronic infection, chronic renal disease or autoimmune disease. Management of iron deficiency anaemia A therapeutic trial of oral iron without further investigation is justified in the pre-school child. Poor compliance is the commonest cause of failure to respond. 1. Dietary advice is essential. 2. Commence oral iron in a dose of 3 mg / kg of elemental iron /day. 3. Repeat Hb in 1-4 weeks depending on the severity of the anaemia to check that it is rising. 4. If so, continue oral iron for three to six months. 5. If a compliant patient on an adequate dosage of iron fails to respond, then investigate further. Consider: barium swallow, pH studies for oesophagitis, faecal occult bloods, coeliac antibody screen, technetium scan for Meckel s diverticulum. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial hPVVDt BT>ZF^P1 Autopsy procedures (RBHSC)* Eczema, atopic, Eczema herpeticum. Napkin dermatitis0 Impetigo2 A Toxic Epidermal Necrolysis (TEN)4 A+Staphylococcal Scalded Skin Syndrome (SSSS)6 Scabies8 Herpetic Whitlow: Warts< Erythema Multiforme> A Urticaria@ Urticarial vasculitisB Drug eruptionsD **General Info9 Arial Arial Arial Arial Arial Anaemia LAtaxia is an inability to co-ordinate voluntary movement. It may result from lesions in the cerebral hemispheres, cerebellum, vestibular apparatus, posterior columns and spinocerebellar tracts in the spinal cord, peripheral nerves or muscles. Ataxia may be acute, progressive or chronic. Possible causes A. Acute intoxications - e.g. phenytoin, alcohol, lead posterior fossa tumours, abscess, haemorrage acute cerebellar ataxia - often occurs 2-3 weeks after a viral illness such as varicella, coxsackie or echovirus and is thought to be due to an autoimmune response to the viral agent affecting the cerebellum. Occurs especially in pre-school children. acute labryinthitis epilepsy - ataxia and drooling may be a post ictal phenomen or may be a manifestation of minor epileptic status B. Progressive metabolic disease - e.g. abetalipoproteinaemia, Hartnup disease, arginosuccinic aciduria, maple syrup urine disease degenerative CNS disease - e.g. Friedeich s ataxia vitamin E deficiency ataxic telangiectasia demyelination C. Chronic cerebral palsy congenital CNS malformations N.B. pseudo ataxia can occur.Co-ordination is normal but weakness or hypotonia can be mistaken for ataxia. Points in the history with acute ataxia access to drugs or toxins recent change in drug therapy headaches or vomiting preceding viral or other illness Points on examination A thorough general and neurological examination is required to localise any lesion. Signs of cereballar disease include past pointing intention tremor nystagmus disdiadochokinesis dysarthria pendular reflexes Signs of peripheral neuropathy include sensory loss distal weakness positive Rhomberg arreflexia Investigations in acute ataxia In acute ataxia admit and consider the following urine and blood for toxin screen drug levels FBC + slides, blood cultures, paired viral titres, cold agglutinins, mycoplasma titres. Second titre is taken 10 -14 days after the first.) serum amino acids urine for organic acids and amino acids. Urine should be saved as soon as possible and frozen if necessary CSF for protein, cells, glucose, culture and virology stools for viral culture CT scan brain or MRI brain Further investigations may be required in some cases of acute ataxia. Extensive investigations may be required in chronic ataxia.It will be helpful seek neurological advice in these situations. Non - acute investigations may also be required in some cases. It may be helpful to discuss individual cases with a neurologist at this stage. cholesterol + lipid profile (beta lipoprotein level creatinine kinase (immunoglobulins alpha fetoprotein (thyroxine and TSH uric acid (male) (chromosome analysis fasting lactate , pyruvate and ammonia copper and caeruloplasmin Vitamin E levels ( with lipid profile) phytanic acid white cell enzymes(esp. ArylSulphatase and Galactocerebrosidase) white cell irradiation E.E.G. Opthalmology opinion - VER and ERG B.S.A.E.R. Muscle biopsy E.C.G. Nerve conduction velocities ( x - ray spine (This page not in handbook) Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial FSome children bruise more easily than others and most of them are normal. Investigate those who bruise spontaneously or have prolonged bleeding following cuts, dental extraction and surgery. Points in the history recent trauma previous similar episode family history of bleeding disorders drugs general wellbeing - fever or recurrent infections Points on examination distribution of bruising evidence of NAI haemarthroses joint laxity lymphadenopathy , hepato/splenomegaly bone tenderness or a limp Baseline investigations Full blood count and film Coagulation screen Possible diagnoses 1. Consider leukaemia with abnormal full blood count,neutropenia or abnormal white cells on the film. Contact Dr. Dempsey. 2. Consider aplastic anaemia with an abnormal FBC. Typically there is a pancytopenia. Contact Dr. Dempsey. 3. Consider Idiopathic Thrombocytopenic Purpura when there is a grossly reduced platelet count with a normal haemoglobin and a white cell count. Check the differential white cell count on blood film. 4. Consider haemophilia A and B in a male with normal platelet count, normal prothrombin time and raised PTTK . Consider Von Willebrand s disease in a male or female with a normal platelet count, normal prothrombin time and normal or slightly prolonged PTTK. Assay for Factor 8c, V Wag antigen, Vwag activity, Factor 9 should be diagnostic for Haemophilia A,B, and VW disease. 5. Consider Haemorrhagic Disease of the Newborn with bleeding or bruising in a baby up to three months old. Prothrombin time and PTTK are prolonged and the platelet count is normal. 6. Consider Henoch-Schonlein purpura when the platelet count is normal. (See guidelines on HSP) Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial R~hFVZbJHXXNLdA Bruisingm A)Idiopathic Thrombocytopenic Purpura (ITP)L LymphadenopathyN A%Meningitis, Meningococcal septicaemiaP Herpetic GingivostomatitisR A PertussisT Diarrhoea (acute)V Diarrhoea (chronic)X Urinary Tract InfectionZ Proteinuria\ Haematuria^ Glomerulonephritis` Nephrotic Syndromeb Renal Failured Renal Stonesf Henoch-Schonlein Purpurah @Aetiology : Respiratory syncitial virus (95% once epidemic started), parainfluenza, adenovirus. 90% of those affected are 1 - 9 months of age. Clinical features < 4 weeks Bubbly nasopharyngeal secretions causing feeding difficulties + / - apnoea. Clinical features > 4 weeks temperature rarely > 38 degrees (C cyanosis or pallor, 1-2 days coryza, irritating cough, tachypnoea, recession, hyperinflated chest, fine expiratory crackles, expiratory wheeze, feeding difficulties. Remember, bronchiolitis is especially severe with pre-existing lung disease. It is a differential diagnosis for the collapsed infant Likely to require admission are those at high risk of severe disease (congenital heart disease, cystic fibrosis, bronchopulmonary dysplasia or immune deficiencies) marked respiratory distress Sa O2 < 92 % room air apnoeic spells inability to feed Remember to isolate. Investigations on admission Chest X-ray Pulse oximetry Nasopharyngeal secretions for RSV status and O+S Management (all drug doses are in the Paediatric Prescriber) Monitor O2 saturation. Humidified O2 to keep SaO2 > 92 %. Intravenous fluids for those infants who are so breathless that oral feeding is not safe. Suction of nasopharyngeal secretions. Salbutamol nebulisation should be tried. If there is no improvement, then there is little point persisting. If there is a partial response, consider adding regular ipatropium nebulisation. Use a flow of oxygen of 6 - 8 l / minute. Aminophylline infusion is worth a trial in more severe cases (do not use routinely). Antibiotics should not be prescribed as a routine measure but may be required depending on clinical severity and chest X-ray findings. There is little experience of adrenaline nebulisation in bronchiolitis as yet but in severe cases it may be helpful to try this with ECG monitoring. The dose is 1 - 3 mls of 1 in 1000 adrenal. ine made up to 3 mls with normal saline. Ventilatory support is required in 1 - 5 % of cases. Ribovarin is occasionally used. It must be used early for maximun effect. Due to the high cost and very limited evidence of any benefit it is usually restricted to high risk infants or not used at all. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial D@LLjrNFBZy Th|ZA Headachek AtaxiaG Macrocephalyo Microcephalyq Hypotonia & muscle weaknesss Respiratory Failure: Assessmentu BronchiolitisJ A Pneumoniay Stridor{ Epiglottitis, Acute Tracheitis, Bacterial Aetiology: Staph. aureus. Streptococcus. Haemophilus Influenzae type B. Signs and Symptoms as for acute epiglottitis but cough often present Management: as for epiglottitis A-Croup, viral (acute laryngotracheobronchitis) Stridor, chronic Chest infection, recurrent A$[CF] Exacerbation of chest infection [CF] Abdominal Pain yJPain, difficulty or delay in defaecation. Possible causes Poor food, fluid or fibre intake Fear of painful defaecation because of previous painful episode or anal fissure Impacted faecal mass in rectum Hirschprung s disease (rare) Other anal abnormalities Often seen in children with cerebral palsy, learning difficulties (mental handicap) and cystic fibrosis Points in history dietary history passage of meconium at birth( delay of > 24 hours) associated vomiting consider psychological factors Points on examination failure to thrive( suggests Hirschprung s Disease) abdominal distension inspect anal region for fissure, infection N.B. rectal examination is not always necessary but may help in some cases Investigations none in mild cases abdominal X-ray is often useful - at first presentation - to assess treatment - in the presence of abdominal pain or distension perianal skin swab with inflammation / purulent exudate barium enema and rectal biopsy if Hirschprung s disease suspected or poor response to treatment ( consult surgeons) N.B. Serum calcium and thyroid function are not routine investigation in the absence of other symptoms Management A. Evacuation of retained faeces B. Establishing regular and effective defaecation C. Supporting the child and family A. Soften retained stools by giving Docusate or Lactulose for 2-3 weeks. N.B. During this time overflow soiling may occur. Then, to evacuate softened stools, try (1) Senokot syrup or Senna tablets (2) if no response, try Sodium Picosulphate (3) if no response, try Polyethylene Glycol , orally or by NG tube Enemas may be required at the onset, especially with abdominal symptoms, but should not be a matter of routine. (doses for enemas at end of section, doses for laxatives in Paediatric Prescriber ) Increase dietary fibre - diet sheets available on handout Use regular bulk laxative - Lactulose or Methylcellulose or Ispaghula Also use regular stimulant laxative - e.g. single dose of Senna or Bisacodyl with additional Picosulphate at weekends if necessary. C.Parents and chidren should be informed that medication may be needed for at least one year. Rectal preparations Obstructive lesions must be excluded prior to their use. The following are guidelines as precise information is difficult to obtain. < 1 month - one glycerol suppository 1-6 months - one Micralax or one Relaxit enema 6 months - 3 years - try a Micralax or Relaxit enema. If unsuccessful, use a Phosphate enema - approx. 3 ml / kg 3 - 13 years - use a Phosphate enema - 3 ml / kg to a maximun of 128 mls. Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial Arial ZZNJLBTJLZ\>TDVJA **AcknowledgementsF ECG - a quick guide Heart Failure Myocarditis Pericarditis Murmurs Kawasaki Disease Tachycardia Constipationw Crying (persistent) Enuresis (nocturnal) Fever Febrile Seizures! Vomiting# Failure to Thrive% Child abuse' KConsultant paediatric pathologists Dr.Claire Thornton and Dr. Denis O Hara should be contacted as soon as it is practical as they will give advice about how to proceed with arranging the autopsy. They are available by phone throughout the week and over the weekend at the following numbers. Dr. C. Thornton Dr. M.D.O RVH: Ext. 2625 RVH: Ext. 2518 If the pathologists are unavailable at the above numbers, call their mobile phone. (Number available from Switchboard) General information There are two forms of autopsy - the Coroner s autopsy and the hospital autopsy. The Coroner s autopsy is requested by the Coroner when the death falls into one of the following catagories 1. sudden, unexpected death ( at home or in hospital) 2. unnatural cause of death 3. anaesthetic death 4. when there is a possibility of litigation Parental consent is not required in these cases and the family cannot prevent the autopsy. If the death falls in to one of the above catagories, telephone the Coroner s office (01232 743040) and give the Coroner or his officer a short summary of the clinical history. Remember that both paediatric and forensic pathologists do autopsies for the Coroner so ask which pathologists are to perform the autopsy. If the paediatric pathologists are to carry out a Coroner s post mortem, this will be done in the RVH mortuary. If the forensic pathologists carry out the autopsy the body may be transferred to the Belfast City mortuary at Forster Green. When the Coroner requests an autopsy, the police are required to take a history from the family and you should let the parents know that this will happen. A clinical summary and the case notes are also required. The pathologist gives preliminary details of the cause of death to the Coroner who then issues a burial order to enable the funeral to take place. The completed autopsy report is sent to the Coroner who may then wish to hold an inquest. He ultimately provides the death certificate although this may happen weeks or months later. A hospital autopsy is requested by the clinicians and requires written consent forn the next of kin of the deceased. The autopsy will be performed by the paediatric pathologist or by their junior staff in the RVH mortuary. For a hospital autopsy, the pathologist requires the writen consent form and the clinical summary on a completed request form. When the autopsy is complete, the pathologist will telephone the ward with the result and a death certificate can be issued if this has not already been done. A provisional summary is issued the following day by the pathologist and the final report is sent to the consultant clinician severral weeks later. When the patient has been under the care of the paediatric neurologists or neurosurgeons, the autopsy, whether Coroner s or hospital in type, is generally caried out by the neuropathologists. When an autopsy is being arranged, please inform the RVH mortuary staff at RVH extension 3860 / 3855. Arial Arial Arial Arial hPVVDt BT>ZF^P1 Autopsy procedures (RBHSC) Eczema, atopic, Eczema herpeticum. Napkin dermatitis0 Impetigo2 A Toxic Epidermal Necrolysis (TEN)4 A+Staphylococcal Scalded Skin Syndrome (SSSS)6 Scabies8 Herpetic Whitlow: Warts< Erythema Multiforme> A Urticaria@ Urticarial vasculitisB Drug eruptionsD **General Info9 Arial Arial Arial Arial Arial Anaemia