appointments for the child. Inform the parents that the police will visit them as a matter of course. \200 Finally, c onsider yourself and your colleagues. Staff have feelings too All staff involved with the child and family (ambulance staff, poli ce, GP, nurses and doctors \200\224 including you) will be traumatized by the experience. Those who are themselves parents with young children may be particularly distressed. At the very least, a debrie \201 ng session over a cup of coffee will be required. \200\230Near miss sudden infant death syndrome \200\231 (apparently life- threatening even t) Refer to the pediatrician for admission and monitoring any infant whose parents report a n apparently life-threatening event ( \200\230ALTE \200\231): apnoea, color change, tone ch ange, cyanosis, choking, gagging. The patient may appear well at the time of presentation. Liaise with the pediatric team and take blood (to include FBC, U&E, glucose, calcium, magne sium, phosphate) and admit for apnoea monitoring. The differential diagnosis includes arrhythmias and congenital heart disease, child abuse, gastro-oesophageal re \202 ux, meningitis and sepsis, seizures and metabolic disorders. In 50 % of cases, no cause is found. Despite parental anxiety, short apnoeic episodes (<15sec ) may, in fact, be entirely normal. Theophylline, home monitoring devices, and counseling h ave all been used for infants believed to be at risk. 660 CHAPTER 15 Pediatric emergencies Problems of neonates and infants Neonatal cephalhaematoma This haematoma results from birth trauma and overlies a single skull bone (usually parietal). It resolves spontaneously: do not attempt to aspirate. Umbilical cord sepsis The dried cord separates at 1 week. If the stump develops signs of in fection (becoming moist and red), refer to the pediatrician. Breast swelling Neonatal breasts commonly swell, due to exposure to maternal hormones. Occa sionally, these breasts lactate ( \200\230witch \200\231s milk \200\231) and very occasiona lly become infected, requiring parenteral antibiotics. Neonatal jaundice Jaundice within 24hr of birth is highly abnormal. Neonates who develop ja undice after 24hr mostly have \200\230physiological jaundice \200\231 (typically in the \201 rst week, especially premature babies) or \200\230breast milk jaundice \200\231 (typi cally in second week: self-limiting, breast feeding can usually continue). Refer all patien ts to exclude serious underlying disorders: Rhesus haemolytic incompatibility; congenital s pherocytosis; glucose-6- disease; ABO phosphate dehydrogenase (G-6-PD) de \201 ciency; CMV infection; hypothy- roidism; biliary atresia. The pediatrician will check: serum bilirubin (including ratio of conjugated: unconjugated), FBC; blood \201 lm; U&E; LFTs; direct ant iglobulin test; TFTs; and infection screen. Neonatal conjunctivitis A watery/sticky eye in the \201 rst few days of life may be due t o an unopened tear duct, or occasionally to gonococcal or chlamydial infection acquired fro m the mother \200\231s genital tract. Therefore, take a swab for Gram staining for gonococc i and culture for chlamydia. Refer the baby and mother if organisms are demonstrated, other wise arrange GP follow-up. Sepsis Potentially life-threatening sepsis (eg meningitis) may present in a non- speci \201 c manner in infants (this is especially true of neonates). Classic presen- tations are replaced by: feeding problems, irritability, drowsiness, jaundice, hypotonia, poor weight gain, petechiae or skin rash, apnoea, bradycardia, and cyanotic episodes. Neonates at i ris k are those with low birth weight, those previously ventilated and those with congenital ab normalities. Treatment Give O 2 and IV \202 uids (20mL/kg). Refer for admission and urgen t investigation: BMG, urine culture, FBC, blood cultures, TORCH screen (Toxoplasma, Rubella , CMV, Herpes), CXR, abdominal X-ray (if necrotizing enterocolitis suspected), LP. Commence \200\230blind \200\231 antibiotics (see BNFC ). 661 PROBLEMS OF NEONATES AND INFANTS Crying babies It is quite normal for babies to cry. The amount of crying varies enormously, as does the ability of parents to cope with it. With more acute onset of irritability and crying exclude an acute cause (eg otitis media, incarcerated hernia, testicular torsion, in tussusception, fractured limb), before reassuring and counseling the parents. Parents who a re driven to despair may bene \201 t from a self-help group (eg CRY-SIS 020 7404 5011 www. cry-sis.com ) or follow-up with a pediatrician. Feeding dif \201 culties Parents bring their babies to the ED with a variety of feeding pr oblems. The underlying causes vary widely and range from acute life-threatening sepsis to c hronic parental anxiety or overfeeding. Obtain a careful feeding history and watch the baby feed. Babies normally require at least 15mL of milk/kg/day at day 1, increasing to (cid:12 4) 150mL/kg/day by day 7. Plot weight, height, and head circumference on centile charts. Ta ke weight loss or failure to satisfactorily gain weight seriously \200\224 it may be due t o a signi \201 cant underlying disorder (eg pyloric stenosis). Remember that newborn babie s lose up to 10 % of their birth weight in the \201 rst week, but should regain it by 2 w eeks. Arrange for the health visitor to advise. Refer chronic feeding problems to GP or ped iatrician. Bilious vomiting Occasionally neonates and infants present with bilious vomiting, a sign of serious pathology. The most important differential diagnosis is intestinal malrotation (vo lvulus) secondary to peritoneal bands, which requires emergency laparotomy to avoid total s mall bowel infarction ( b Abdominal pain in children, p.698). Consult a pediatric surgeon u rgently. Other differential diagnoses include an obstructed hernia, Hirschsprung \200\231s disease or sepsis. Metabolic diseases (inborn errors of metabolism) Occasionally neonates present to the ED da ys after birth with coma or seizures with no obvious cause (infection, trauma, hypoglycaemi a, etc.). These infants may have an inborn error of metabolism (e.g. maple syrup urine dise ase, urea cycle disorders, and hyperammonaemia) and they require urgent specialist pediatri c care, often at a tertiary children \200\231s hospital. If an older child presents to the ED with a previously diagnosed metabolic disease, seek expert advice by referring to the pe diatricians early. Remember the parents will know more about the disease than you. Treatmen t Give O 2 and IV \202 uids (20mL/kg) and treat hypoglycaemia, and sepsis. Refer for admi ssion and urgent investigation by a pediatrician. Emergency treatment protocols for this ch allenging group of patients are available at the British Inherited Metabolic Disease Group website ( http:// www.bimdg.org.uk/protocols/documents.asp?o=1&tid=1 ). 662 CHAPTER 15 Pediatric emergencies Skin problems in infants Minor skin problems are common in infants. The combination of a sk in rash and an ill infant should arouse suspicion of serious illness (eg b Meningococcal di sease, p.666) and prompt urgent referral. Do not discharge an infant with an undiagnosed ra sh \200\224 obtain an expert opinion. Neonates Multiple tiny white papules ( milia ) seen on the face of neonates are super- \201 cial epidermal inclusion cysts. Erythematous lesions with central white vesicles are c ommon in the \201 rst days of life \200\224 erythema toxicum ( \200\230neonatal urticari a \200\231). Both are harmless and disappear spontaneously within days. Peeling skin Peeling skin is a common feature of post-mature babies and should be dis- ting uished from scalded skin syndrome and Kawasaki disease ( b p.672). Scalded skin syndrome ( \200\230toxic epidermal necrolysis \200\231) This staphylococcal in fection results in red peeling skin, sometimes with blistering. Refer for admission and IV antibiotics. Eczema Usually managed most appropriately by GP and outpatient department with emollients topical corticosteroids, but if very severe, refer for a period of inpatient treatment. S ometimes the scratched skin becomes secondarily infected, requiring admission for IV antibi otics. Impetigo Any breach in the skin (eg eczema, nappy rash, scabies) may develop impetigo. Stap hylococcal or streptococcal infection results in an ulcera- tive erythematous area, which f orms a golden brown crust that spreads rapidly. If the infection is localized and the child is well, treat with topical fucidic acid (if extensive \200\224 oral penicillin and \202 ucloxacillin), arrange GP follow-up and advise the parents to isolate the child from o ther children until it has resolved. If the child is unwell, refer for IV antibiotics. Nappy rash ( \200\230ammoniacal dermatitis \200\231) Erythema with some ulceration in the n appy area, but sparing the \202 exures, is usually the result of excessive moisture conta ct with the skin. Treat by exposure to fresh air as much as practicable and frequent changi ng of nappies. Consider barrier creams (see BNFC). Monilial infection Nappy rash may become infected with Candida albicans , leading to erythe ma of the \202 exures. Give nystatin cream and advise regular changing. Seborrhoeic dermatitis This erythematous greasy rash commonly involves the nappy area, the occipital region and behind the ears. It may become infected with Candida albicans \200 \224 treat with nystatin and refer to GP. 663 THE FEBRILE CHILD The febrile child Febrile illness is extremely common in childhood and many parents will br ing their child to the emergency department, rather than to a primary care team for assessm ent, particularly when they feel the child is very unwell. Primary care teams will also ref er febrile children to hospital for assessment when the child is seriously ill or the diagn osis is in doubt. Approach \200 Assess the airway, breathing and circulation of the child to identify and t reat life-threatening problems as they are found in order to maintain vital functions befor e disease speci \201 c therapies are started ( b Primary assessment and resuscitation of t he sick child, p.634). Involve senior ED staff, PICU, and senior pediatric staff as soon as you suspect the child is critically unwell. Measure and record the temperature (electronic thermometer in axilla if <4 weeks old, can a lso use tympanic thermometer if older than 4 weeks). Speci \201 cally look for an impaired conscious level and lack of recognition of parents/carers. Check BMG in all sick children. Early recognition and treatment of respiratory failure and shock is essential to avoid cardiorespiratory arrest. \200 Administer oxygen to maintain SpO 2 > 9 4 % . \200 Give a bolus of IV/IO 0.9 % saline 20mL/kg if any signs of shock (tachy- cardia, CRT > 2sec, mottled skin, purpuric rash, d conscious level). If there is any suspicion or sign of meningococcal disease, administer parenteral benzylpenicillin or cefotaxime as soon as possible. If the child is <3 months old, check FBC, blood cultures, CRP and urine; if unwell, or WCC <5 or > 15 \227 10 9 /L, or <1 month old, perform lumbar puncture (LP) and give parenteral antibiotics. If <1 month old, add ampicillin to cover Listeria . If the child is > 3 months old, check FBC, blood cultures, CRP and urine; get CXR if T > 39 C or WCC > 20 \227 10 9 /L or clinically unwell. Check U&E, ABG, and lactate if clinically unwell or drowsy. \200 Consider LP if clinicall y unwell and febrile at any age, especially <1 year. \200 If drowsy or d conscious level, consider adding IV acyclovir to cover possibility of herpes simplex encephalitis. Resuscitate aggressively with repeated IV \202 uid boluses, inotropes and early ventilation for children with d conscious level. In older children, do not forget rarer causes of fever and impaired conscious level, includ ing illicit drugs such as MDMA ( \200\230Ecstasy \200\231) or other amphetamines, or ketami ne. Get a detailed history of the illness from parents and carers at the earliest opportunity; remember the vaccination history and any recent travel, or recent illness in the child \200 \231s family or school. 1 See the \200\230 NICE Guidance on Feverish Illness in Children \200\231. Available at: http://www.nice.org.uk/ nicemedia/live/11010/30524/30524.pdf 664 CHAPTER 15 Pediatric emergencies Purpuric rashes The development of a purpuric rash in a child is often greeted with conside rable and understandable parental alarm, due to the well- publicized association with menin gococcal disease. History, examination, and FBC will help to identify the cause. Causes of purpuric lesions \200 Meningococcal disease. \200 Henoch \200\223Sch nlein purpura. \200 Thrombocytopenia. Idiopathic thrombocytopenic purpura; \200 Leukemia; \200 Septic shock; \200 Aplastic anemia. \200 Some viral illnesses. \200 Trauma. \200 Forceful coughing or vomiting ma y cause petechiae of the face. Meningococcal disease (see b p.666) Presume that an ill chil d (particularly an infant) who develops a purpuric rash has meningococcal meningitis/septic aemia and treat urgently for this. Henoch \200\223Sch nlein purpura This vasculitic proces s affects small arteries in the kidneys, skin, and GI tract. It is relatively common in 4 \200\22311-year olds and appears to follow a viral or bacterial infection. Erythematous mac ules develop into palpable purpuric lesions, which are characteristically concentrated over the buttocks and extensor surfaces of the lower limbs, although the distribution can be at ypical in younger children. Associated symptoms include abdominal pain, testicular pain and joint pains (arthritis in ankles and knees). Nephritis may occur, producing micro- or macr oscopic haematuria, proteinuria. Very occasionally, this progresses to renal failure. Check BP, urinalysis, urine microscopy, FBC (platelets are normal), U&E. Refer to the pediatrici an. Idiopathic thrombocytopenic purpura Probably results from autoimmune reaction to preced ing viral infection. Presents with a purpuric rash, mucous membrane bleeding, conjunctival hemorrhage and occasionally, GI bleeding. Check FBC (platelets are <30 \227 10 9 /L). Refe r for investigation and follow-up. In the presence of lymphadenopathy or splenomegaly, cons ider alternative diagnoses. Treatment is usually expectant, since the natural course is for most cases to resolve spont aneously over 3 months. Occasionally, life-threatening hemorrhage occurs: obtain expert hel p, resuscitate with O 2 and IV \202 uids and give platelets. Acute leukemia This may pres ent acutely to the ED with purpura associated with throm- bocytopenia. Look for hepatomegal y, splenomegaly and lymphadenopathy. FBC/blood \201 lm reveals anemia with blast cells, d platelets, and i WBC). Refer for admission. This page intentionally left blank 666 CHAPTER 15 Pediatric emergencies Meningococcal disease See algorithm Fig. 15.10 b p.668 \200\2239. Meningococcal disease is unpredictable. Most children present acutely febrile and may not have a rash in the early s tages. Septicaemia Children presenting with septicaemia may have: \200 A history of fever/rigors but be afebrile at the time of presentation. \200 Isolated severe limb pain in the absen ce of any other physical signs. \200 Abdominal pain, diarrhea and vomiting are common in septicaemia. \200 Alertness until late in the illness. Patients presenting in septic shoc k without meningitis have the worst prognosis. Meningitis Young children may present with fever, vomiting, irritability and confusion. Tho se aged <2 years are less likely to have neck stiffness or photophobia. Take parental conce rns about a child \200\231s responsiveness and alertness seriously. Older children typicall y present more classically with fever, vomiting, headache, stiff neck and photophobia. Teen agers may present with a change of behavior (eg confusion, aggression), which may be falsel y attributed to alcohol or drugs. Rash Underlying meningococcal disease may be very advanced by the time a rash appears. This may initially be blanching, macular, or maculopapular. Children without a rash or with a b lanching rash can still have meningo- coccal disease. The classic rapidly evolving petechia l or purpuric rash may be a very late sign and can carry a poor prognosis. Urgent treatment and experienced help are essential. CT scanning of the brain should be und ertaken if there is impaired conscious level or focal neurological signs or signs of i ICP. CT scans must not delay treatment. LP has no immediate role in the ED care of the critical ly ill child and can be fatal. LP is contraindicated if there is extensive purpura, shock, impaired consciousness, coagulopathy, local infection or i ICP on CT or clinically. Give an tibiotics (IV ceftriaxone or cefotaxime) immediately to: \200 All children with a fever a nd petechial/purpuric rash. \200 Children in shock with or without a rash. \200 Childre n with clinical meningitis, but LP contraindicated. Take any haemorrhagic rash in a febrile child very seriously. Although many children with fever and petechiae have viral illnesses , there is no room for complacency. Ensure that all have their vital signs measured, and ar e carefully checked for signs of meningitis or septicaemia. 667 MENINGOCOCCAL DISEASE Airway and ventilation Intubate and ventilate: \200 If impaired conscious level or i ICP clinically. \200 Prior to CT scanning if critically ill. \200 If \202 uid resuscitati on requirement is > 40mL/kg. Seek expert help for rapid sequence induction/intubation (RSI) \200\224 haemodynamic collapse is common. Consider using IV ketamine for induction if expe rienced in its use. Fluid resuscitation Vast quantities of IV \202 uids are required in meningococcal septica emia \200\224 often up to 100mL/kg. Many UK authorities recommend 4.5 % human albumin solut ion (HAS) for \202 uid resuscitation, but give crystalloid (0.9 % saline) if HAS is not i mmediately available. Inotropes \200 Dopamine or dobutamine at 10 \200\22320mcg/kg/min. Make up 3 \227 weight (kg) mg in 50mL 5 % glucose and run at 10mL/hr = 10mcg/kg/min. These dilute solutions can be used via a peripheral vein. \200 Start adrenaline via a cen tral line only (seek expert help) at 0.1mcg/kg/min. Make up 300mcg/kg in 50mL of saline at 1mL/hour = 0.1mcg/kg/min. Hypoglycaemia (glucose <3mmol/L) 5mL/kg 10 % glucose bolus IV and then glucose infusion at 80 % of maintenance requirements over 24 hrs. Correction of metabolic acidosis (pH <7.2) 1mmol/kg NaHCO 3 IV = 1mL/kg 8.4 % NaHCO 3 over 20min or 2mL/kg 4.2 % NaHCO 3 in neonates. If K + <3.5mmol\L Give 0.25mmol/kg KCl diluted i n saline or glucose over 30min IV with ECG monitoring. Caution if anuric. If total calcium <2mmol/L or ionized Ca 2 + <1.0mmol/L Give 0.1mL/kg 10 % calcium chloride (0.7mmol/mL) over 30min IV (max 10mL) or 0.3mL/kg 10 % calcium gluconate (0.22mmol/mL) over 30min (max 20mL) . If Mg 2 + <0.75 mmmol/L Give 0.2mL/kg of 50 % MgSO 4 over 30min IV (max 10mL). See: Meningitis Research Foundation ( www.meningitis.org ) and \200\230NICE Guidance on Ba cterial meningitis and meningococcal septicaemia \200\231 . Available at: http://www.nice.o rg.uk/nicemedia/ live/13027/49341/49341.pdf RECOGNITION May present with predominant SEPTICAEMIA (with shock), MENINGITIS (with raised ICP) or both. Purpuric/petechial non-blanching rash is typical. Some may have neither shock nor meningitis. Rash may be atypical or absent in some cases. Bacterial meningitis algorithm www.meningitis.org Call consultant in Emergency Medicine, Pediatrics, Anesthesia or Intensive Care Initial ass essment looking for shock/raised ICP Do not perform Lumbar Puncture Give IV ceftriaxone (80 mg/kg od) without delay Do not use ceftriaxone at the same time as calcium-containing solutions: in this situation use cefotaxime (50 mg/kg qds) SIGNS OF SHOCK? RAISED INTRACRANIAL PRESSURE? Reduced (GCS \211 8) or \202uctuating level of consciousness Relative Bradycardia and Hy pertension Focal neurological signs Abnormal posture or posturing Seizures Unequal, dilated or poorly responsive pupils Papilloedema (late sign) Abnormal \200\230doll \200\231s eye \200\231 movements Tachycardia Capillary re \201ll time >2 seconds Cold hands/feet; pale or blue skin Respira tory distress/ oxygen saturation <95% in air Altered mental state/decreased conscious level Decreased urine output (<1ml/kg/hr) Hypotension (late sign) Hypoxia on arterial blood gas Base de \201cit (worse than -5 mmol/l) Increased lactate (>2 mmol/l) NO YES YES NO YES Do not perform Lumbar Puncture; Nil by mouth Do not perform Lumbar Puncture; nil by mouth ABC and Oxygen (minimum 10 l/min) by face mask Measure glucose. Give Mannitol (0.25g/kg) bo lus or 3% Saline (3 ml/kg) over 5 minutes Treat shock if present ABC & High \202ow Oxygen (minimum 10 l/min) by face mask Measure glucose. Insert 2 large i.v. cannulae (or intraosseous); Take bloods, see CLINICAL FEATURES OF MENINGITIS? VOLUME RESUSCITATION Call anesthetist and contact PICU Immediate bolus of 20ml/kg of 0.9% Sodium Chloride over 5 \200\22310 minutes and reassess i mmediately If shock persists immediately give second bolus of 20ml/kg of 0.9% Sodium Chlori de or of 4.5% human Albumin over 5 \200\22310 minutes and reassess immediately Observe clos ely for response/deterioration Intubate and ventilate to control PaCO2 (4 \200\2234.5 kPa) Urinary catheter and monitor ou tput, NG tube Consider urinary catheter to monitor output NO NEUROINTENSIVE CARE 30 \232 head elevation, midline position Avoid internal jugular lines Repeat Mannitol or 3% Saline if indicated Sedate (muscle relax for transportation) Cautious \202uid resuscitat ion (but correct coexisting shock) Monitor pupillary size and reaction Avoid hyperthermia O nce patient is stabilized, consider CT scan to detect other intracranial pathology if GCS \211 8, \202uctuating conscious level or focal neurological signs NO After 40ml/kg \202uid resuscitation STILL SIGNS OF SHOCK? Repeated review YES WILL REQUIRE URGENT ELECTIVE INTUBATION AND VENTILATION Call anesthetist and contact PICU Close monitoring for signs of Immediate bolus of 20ml/kg of 0.9% Sodium Chloride or 4.5% Human Albumin over 5 \200\22310 minutes and reassess immediately; Continue boluses if necessary with repeated clinical and laboratory assessments including blood gas measurements. Raised ICP Shock Perform LP if no contraindication DO NOT DELAY ANTIBIOTICS Start peripheral inotropes (Dopamine); if IO access start Adrenaline ET Tube (Cuffed if pos sible) and CXR Anticipate pulmonary oedema (ensure PEEP) Central venous access Urinary cath eter to monitor output, Nasogastric tube Start Adrenaline infusion (central) if continuing need for Volume resuscitation and Inotropes Do not restrict \202uids unless there is evidence of: Raised intracranial pressure, or Increased antidiuretic hormone secretion For warm shock (warm peripheries, bounding pulses and low diastolic pressure) give Noradren aline (central) or Dopamine (peripheral) If \202uid and inotrope resistant shock discuss with pediatric intensivist. STEPWISE TREATMENT OF SEIZURES i.v. Lorazepam (0.1 mg/kg) or Midazolam (0.1 mg/kg) bolus Consider Paraldehyde (0.4 ml/kg P R) Phenytoin (18mg/kg over 30 min i.v. with ECG monitoring) Anticipate, monitor and correct: If persistent seizures: Thiopental (thiopentone) 4mg/kg in intubated patients (beware of hypotension) Midazolam/Thi opental infusion Hypoglycaemia Acidosis Hypokalaemia Hypocalcaemia Hypomagnesaemia Anemia Coagulopathy (Fres h Frozen Plasma 10ml/kg) Repeated Review Children with MD can deteriorate rapidly. Deterioration detected? Perform delayed LP when stable and no contraindications GO TO BACTERIAL MENINGITIS ALGORITHM Transfer to Intensive Care by Pediatric Intensive Care Retrieval Team Notify public health Fig. 15.10 Management of meningococcal disease in children and young people. Reproduced wit h kind permission from the Meningitis Research Foundation www.meningitis.org Take blood for glucose, FBC, coagulation screen, U&E, Ca 2 + , Mg 2 + , PO 4 3 \200\223 , blood cultures , ABG, lactate, cross-match, and PCR for N. meningitidis. 670 CHAPTER 15 Pediatric emergencies How to perform a lumbar puncture \200 Take senior advice before performing a LP. \200 C on \201 rm that there is no contra-indication to LP (eg prolonged or focal seizure, focal neurological signs, purpuric rash, GCS<13, pupillary dilatation, impaired oculocephalic re \202 exes, abnormal posture, hypertension, bradycardia, coagulopathy, papillodema). Prepare parents, set up equipment, and enlist help from an experienced nurse. Position the child on their side, curled up into a ball (Fig. 15.11 ). \200 Mark the skin with a pen in the midline at level of iliac crests. \200 Scrub and don sterile gown and gloves. \200 Clean the skin with antiseptic solution and cover with sterile drapes. \200 Consider LA for the skin with 1 % lidocaine solution. \200 Slowly insert the 21G lumbar puncture needle aiming towards the umbilicus. If this causes much pain, withdraw needle and use more lidocaine LA (but <3mg/kg \200\224 b Analgesia in speci \201 c situations, p.280). If no CSF is obtained, withdraw needle and reassess its direction, then try again. Collect 4 drops of CSF in each of 3 bottles and send for: microscopy and Gram stain, cultur e and sensitivity; cell counts; glucose and protein. If bloody tap is obtained, send the clearest sample for cell counts. Fig. 15.11 Positioning for a lumbar puncture. This page intentionally left blank 672 CHAPTER 15 Pediatric emergencies Skin lesions in multisystem disease The appearance of the skin may provide a valuable clue to an under- lying disease process. If suspected, refer all of the following diseases to a pediatrician. Kawasaki disease (mucocutaneous lymph node syndrome) This disease, believed to be related t o a viral infection, was \201 rst reported in Japan in 1967 and has now spread worldwide. Most cases affect chil- dren <5 years. Extensive skin and mucosal changes occur, including an erythematous rash, which may affect palms and soles and desquamate. Conjunctivitis, uve itis, \201 ssured lips, and a strawberry tongue may be seen. Other features: fever, acute cervical lymphadenopathy, arthritis, and diarrhea. Coronary ar tery aneurysm (and subsequent thrombosis) is a signi \201 cant complication. If Kawasaki disease is suspected check FBC, erythrocyte sedimentation rate (ESR), and viral titres, and refer to a pediatrician. Dermatitis herpetiformis This is the skin manifestation of coeliac disease. Vesicles and pa pules occur over the knees, elbows and buttocks. The lesions are very itchy and produce muc h scratching. Dapsone is effective treatment: refer to a pediatrician. Erythema multiforme Target lesions often with pale blistered centers are symmetrically dist ributed, particularly over the extensor surfaces of the limbs, sometimes including the hand s and feet. The skin lesions combined with fever, systemic illness, oral and genital ulcera tion comprise the Stevens \200\223Johnson syndrome. Causes include infection (herpes, mycoplasma, tuberculosis TB) and drugs (sulphonamides, ba rbiturates). Erythema nodosum Painful red skin nodules or plaques on the anterior surfaces of both shins with associated fever, lethargy and arthralgia. It may be due to strepto- coccal infection , TB, sulphonamides, ulcerative colitis, or sarcoid. Erythema marginatum A transient erythematous rash with raised edges occurs in 20 % of cases of rheumatic fever ( b p.496). Rheumatic fever is an autoimmune disease which follows infe ction with group A streptococci. Once common, it is now unusual in the UK. Diagnose using the revised Duckett \200\223Jones criteria (2 or more major; or 1 major and 2 minor, plus evidence of preceding streptococcal infection eg throat swab, i ASO titre): M ajor criteria Erythema marginatum, carditis, polyarthritis, Sydenham \200\231s chorea, subc utaneous nodules. Minor criteria Fever, arthralgia, i ESR, i WBC, previous rheumatic fever, prolonged PR interval. 673 SKIN LESIONS IN MULTISYSTEM DISEASE Erythema chronicum migrans (see b Infestations, p.230) The characteristic skin rash of Lyme disease begins as a red papule, which spreads to produce erythematous lesions with pale ce nters and bright edges. Lyme disease is a multisystem disorder resulting from tick-borne in fection. It initially manifests with one or more of a variety of symptoms, including fever, headache, malaise, arthralgia, myalgia. The rash is present in most cases. The diagnosis c an be elusive, but consider it if there has been any history of travel to an affected area. Identifying skin lesions (Table 15.4 ) Description \200 Impalpable colored lesion <1cm di ameter = macule. \200 Impalpable colored lesion > 1cm diameter = patch. \200 Palpable l ump <0.5cm diameter = papule. \200 Palpable lump > 0.5cm diameter = nodule. \200 Palpab le \202 uid- \201 lled lesion <0.5cm diameter = vesicle. \200 Palpable \202 uid- \201 lled lesion > 0.5cm diameter = bulla Table 15.4 Skin lesions and possible causes Feature Causes Peeling skin Toxic epidermal necrolysis ( \200\230scalded skin syndrome \200\231), Kawasaki disease. Streptococcal infection Blistering lesions Staphylococcus (impetigo and toxic epidermal necrolysis), scabies, chickenpox, herpes zoste r, herpes simplex, Stevens \200\223Johnson, pompholyx, coxsackie A16 (hand, foot and mouth disease), dermatitis herpetiformis, epidermolysis bullosa, drugs Coxsackie A16, Kawasaki disease, erythema multiforme, scables, pompholyx Lesions on palms and soles Pruritis Eczema, urticaria, psoriasis, chickenpox, scabies, lice, insect bites, dermatitis herpetifo rmis 674 CHAPTER 15 Pediatric emergencies Pediatric ENT problems Background Due to frequent infections and large concentrations of ac tive lymphoid tissue, certain ear, nose, and throat (ENT) problems are very common in pedia tric practice. For example, acute suppurative otitis media ( b Earache, p.550) has an incid ence of 20 % amongst pre-school children; secretory otitis media ( \200\230glue ear \200 \231) has a prevalence of 5 % amongst all children. Rhinorrhoea from coryza and rhinitis is even more common. Approach Although many ENT diseases are usually considered as primary care problems, childr en often present to the ED suffering from them. It is obviously important to examine the ea rs and throat of any child presenting with a fever. Remember, however, that the ill, septic child with large red tonsils may also have a signi \201 cant septic focus elsewhere (eg m eningitis or pneumonia). Examination Examination of the ears and throat is generally disliked by children and as a r esult, can prove to be rather a struggle. It is therefore sensible to leave this part of th e full examination of a child until last. Parental help can be invaluable in allowing exami nation of the slightly uncooperative toddler or younger child. Sit the child on a parent \200\231s lap for examination of the ears and throat, as shown in Fig. 15.12 . The dif \201 cult examination Despite various maneuvers, it can be very dif \201 cult to adequately visualize the throat of a child who adamantly refuses to open their mouth. A use ful trick is to draw the face of a \200\230Smiley Man \200\231 on the end of a wooden spat ula. The child may then consent to the \200\230Smiley Man \200\231 having a look at their throat (preferably with the ink side up!). Presentation and treatment The presentation, diagnosis and treatment of speci \201 c ENT d iseases in both children and adults are described in Chapter 12. \200 b Ear, nose, and th roat foreign bodies, p.546. \200 b Earache, p.550. \200 b Epistaxis, p.552. \200 b Na sal fracture, p.553. \200 b Sore throat, p.554. 675 pediatric ENT PROBLEMS Examining a child \200\231s ear In an infant pull the pinna back and down (rather than up) for the best view. Fig. 15.12 Examining a child \200\231s throat. 676 CHAPTER 15 Pediatric emergencies Stridor: upper respiratory infections The upper airway is a tube which may be blocked by: d istortion (eg tongue falling back in coma), extrinsic compression (eg haematoma), swelling of its wall (eg burns, croup, epiglottitis, diphtheria), or FB within. Signs of upper airwa y obstruction Stridor, marked dyspnoea, drowsiness, subcostal/suprasternal recession, drool ing of saliva, dif \201 culty speaking, and cyanosis. Any of these warn of impending obstr uction. Stridor is a high pitched inspiratory noise. It occurs in croup, acute epiglottitis , inhaled FB, laryngeal trauma, laryngomalacia ( \200\230congenital laryngeal stridor \200 \231), angioneurotic oedema. See Table 15.5 . Acute croup (laryngotracheobronchitis) Viral in origin (para-in \202 uenza virus in > 80 % ). Common between 6 months, and 5 years of age. Spring and autumn epidemics occur. Illness lasts 8 3 \200\2235 days. Coryzal symptoms usually precede harsh stridor, a barking cough ( \200\230seal \200\231s bark \200\231) with hoarseness i over several days. Temperature (T ) * is only mildly i . Leave the child in a comfortable position preferably in the arms of the parent, who can hold an O 2 mask near the child. Look for signs of signi \201 cant air way obstruction, but do not examine the pharynx as this may precipitate laryngospasm or obs truction. If any of these signs are present, or if SpO 2 <92 % in air refer urgently \200 \224 intubation may be required. Use the modi \201 ed Westley croup score by adding indivi dual values as follows: \200 Stridor : none = 0, only when upset or agitated = 1, at rest = 2. \200 Retractions : mild = 1, moderate = 2, severe = 3. \200 Air entry : normal = 0, mild decrease = 1, marked decrease = 2. \200 SpO 2 <92 % on air : none = 0, with agita tion = 4, at rest = 5. \200 Level of consciousness : normal = 0, altered conscious level = 5. Children with moderate (score 3 \200\2235) or severe croup (score 6 \200\22311) and im pending respiratory failure (score > 11) require admission to hospital. Give oral dexametha sone 0.15mg/kg or nebulized budesonide (1 \200\2232mg in 5mL 0.9 % saline) if vomiting or s evere respiratory distress and refer to the pediatric team. If severe (score > 5), consider nebulized adrenaline driven by O 2 at 8L/min (0.5mL/kg of 1:1000, max 5mL; repeat as requi red). Refer severe cases to PICU (<1 % of croup is severe). Many children with mild croup ( score 0 \200\2232) can be safely discharged from the ED after a brief period of observation . This decision should be taken by an experienced emergency physician or pediatrician. Disc harge in the evening may be inadvisable, since croup can worsen overnight. Diphtheria Although rare in the UK, the exotoxin of Corynebacterium diphtheriae may produce serious organ damage (especially myocarditis) and upper respiratory tract obstruction. The non-immunized child may present with pyrexia, sore throat, and dysphagia due to an adheren t pharyngeal exudate. Cervical lymphadenopathy causes a \200\230bull neck \200\231 appeara nce. (Note that infectious mononucleosis may present similarly \200\224 b p.241). Treat wi th O 2 , obtain ECG and venous access, send blood for FBC, blood culture, and obtain a thro at swab. Refer for antitoxin (20,000U IM after a test dose) and IV erythromycin. 677 STRIDOR: UPPER RESPIRATORY INFECTIONS Acute epiglottitis Increasingly uncommon, due to widespread Hib vaccination. Rapidly progre ssive airway obstruction may result. Children aged 2 \200\2237 years are most usually invol ved, although it does occur in older children and adults. Unlike croup, stridor is usually soft and may even be absent. Onset is typically acute. The child is systemically unwell wit h pyrexia > 38.5 * C, but little or no cough. In severe cases, the child may be ominously q uiet, unable to speak, sitting upright drooling saliva in a \200\230snif \201 ng position \200\231. Management Do not attempt to visualize the throat as this may precipitate total airway obstruction. Let the child adopt the most comfortable position, give humidi \201 ed O 2 and call urgently for anesthetic, ICU and ENT help. Nebulized adrenaline (0.5mL/kg of 1:1000, max 5mL) may \200\230buy time \200\231. Defer doing blood tests (FBC, blood cultur es) and treatment with IV cefotaxime until an anesthetist has assessed the child. Lateral n eck X-rays are unnecessary and potentially hazardous. Intubation, if required, may be very dif \201 cult to perform. A safe approach is for an experienced anesthetist to use a gaseo us induction in the presence of a surgeon who is prepared for a surgical airway. Airway swe lling may require a smaller than expected diameter (and thus uncut) ET tube. Let the anesth etist know the number of adrenaline nebulizers given, as halothane induction could precipit ate arrhythmias. If visualization of the tracheal ori \201 ce is dif \201 cult at laryngo scopy due to oedema, ask an assistant to squeeze the chest and look for an air bubble emerg ing from the trachea. Loss of the airway \200\224 if this happens, summon help and attempt to ventilate with O 2 using bag and mask. If ventilation proves impossible, obtain a surgical airway (needle cri cothyroidotomy if <12 years, surgical cricothyroidotomy if \211 12 years) \200\224 see b p.326. Bacterial tracheitis May be due to Staph. aureus, Strep. , or H. in \202 uenzae . The pres entation of \200\230croup \200\231, plus moderate/severe pyrexia, and production of copiou s secretions suggests the diagnosis. If suspected, refer and treat as for acute epiglottiti s (intubation is often required). Bacterial tracheitis can cause rapid onset of septic shoc k. Table 15.5 Clinical presentations of upper airway obstruction Croup Epiglottitis Bacterial tracheitis Foreign body Age 1 \200\2232 years 2 \200\2236 years Throughout childhood Throughout childhood Onset 1 \200\2232 days <24hr <24hr <24hr History Coryza, barking cough Sore throat, dysphagia Rattling cough, sore throat Afebrile, non-toxic T > 38.5 toxic, mucopurulent secretions, soft/ absent stridor T > 38.5 toxic, upright position Signs T <38.5 non-toxic, harsh stridor, hoarseness 678 CHAPTER 15 Pediatric emergencies Severe acute asthma in children Assess conscious level, degree of breathlessness, degree of agitation, use of accessory muscles, amount of wheezing, pulse rate and respiratory rate. Attempt to measure peak \202 ow if age > 5 years (See Fig. 15.13 for normal peak \202 o w). Follow the 2011 British Thoracic Society/Scottish Intercollegiate Guidelines Network (BTS/S IGN) Guidelines based on age and severity ( http://www. sign.ac.uk/pdf/sign101.pdf ). Inves tigations, including blood gas estimations, rarely alter immediate management. Cautions Chi ldren with severe asthma attacks may not appear distressed. Wheeze and respiratory rate cor relate poorly with severity of airway obstruction. Increasing tachycardia denotes worsening asthma, a fall in heart rate in life-threatening asthma is pre-terminal. Assessment in the very young (<2 years) may be dif \201 cult \200\224 get expert help. Normal peak expiratory \202 ow in children aged 5 \200\22318 years. 600 2SD Boys and girls ) n m 500 i Mean / s e r t i l ( w o 400 l f y r o t a r i p x e \200\2232SD 300 k a e P 200 100 110 120 130 140 Height (cm) 150 160 170 Fig. 15.13 679 SEVERE ACUTE ASTHMA IN CHILDREN