Cardiovascular Emergencies in The Pediatric Patient

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Emerg Med Clin N Am 23 (2005) 1233–1249

Cardiovascular Cardiovascul ar Emergen Emergencies cies in the Pediatric Patient William A. Woods, MDa,*, Michael A. McCulloch, MDb a

Departments of Emergency Medicine and Pediatrics, University of Virginia Health System, PO Box 800699, Charlottesville, VA 22908, USA b Department of Pediatrics, University of Virginia Health System, PO Box 800386, Charlottesville, VA 22908, USA

Children with heart disease may present to the emergency department (ED) in many stages of life. They can present with undiagnosed congenital heart disease with their disease undiagnosed, after a temporizing procedure has bee been n per perfor formed med or after after defi definit nitive ive rep repair air.. The pra practi cticin cing g eme emerge rgency ncy physician needs to be prepared to make the diagnosis of congenital heart disease and to recognize complications common after a surgical correction of heart disease. Children can also present at any stage of life with syncope or che chest st pai pain; n; the theref refore ore,, emerge emergency ncy phy physic sician ianss mus mustt als also o be comfor comfortab table le with wi th the the mo most st co comm mmon on ty type pess of hear heartt dise diseas asee asso associ ciat ated ed with with thes thesee symptoms. The purpose of this article is to describe the physiology and presentation of undiagnosed congenital heart disease, to describe the complications that can occur after a staged or definitive repair, and to discuss acquired heart disease in children. Evaluation of the child who has suspected congenital heart disease

The first step in recognizing a previously undiagnosed congenital heart disease is being familiar with the common presentations. In general, patients with significant congenital heart disease present with signs and symptoms of  congestive heart failure (CHF), cyanosis, or shock. Infants manifest CHF as feeding difficulty, tachypnea, fussiness, or agitation. Physical examination

* Corresponding author. E-mail address:   [email protected] [email protected] ia.edu (W.A.  (W.A. Woods). 0733-8627/05/$ - see front matter     2005 Elsevier Inc. All rights reserved. doi:10.1016/j.emc.2005.07.003  

emed.theclinics.com

 

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may reve may reveal al a mu murm rmur ur,, ta tach chyp ypne nea, a, di diap apho hore resi sis, s, feed feeding ing into intoler leran ance ce,, or hepatomegaly. In this setting, any murmur, especially if present in diastole, must be addressed. If a murmer is benign, it is imperative the emergency physician seek reassurance from the primary physician or a consultant. Cent Ce ntra rall cy cyan anos osis is re refe fers rs to exce excess ssiv ivee diss dissoc ocia iate ted d he hemo moglo globi bin n an and d is [1].. Data suggest that classically visible in the lips and mucous membranes  membranes   [1] 3 to 5 g/dL of dissociated hemoglobin are necessary before central cyanosis becomes visible [2–4] visible [2–4].. Peripheral cyanosis, by comparison, is a manifestation of poo oorr peri rip pher eral al perf rfu usi sion on.. In th this is situ situat atio ion, n, a dec ecre reas ased ed flo flow w of  oxyg ox ygen enat ated ed bl bloo ood d to th thee pe peri riph pher ery y exis exists ts with with an incr increa ease sed d ox oxyg ygen en extraction at the end organs. Often the lips and mucous membranes are spared spa red.. Th Thus, us, per periph ipheral eral cya cyanos nosis is can occ occur ur wit withou houtt hyp hypoxi oxia. a. Affe Affecte cted d children can present with central and peripheral cyanosis. This combination can be seen when children with hypoplastic left heart syndrome (HLHS) or critical coarctation of the aorta present in shock. The second step in identifying congenital heart disease is classifying the lesion. Significant congenital heart disease can be broken down into two groups: mixing and obstructive lesions. Mixing lesions can result in a left-toright shunt (oxygenated blood mixes with deoxygenated blood and exits the heart into the pulmonary system) as in atrial or ventricular septal defects. These patients can present with pulmonary edema, heart failure, inadequate peripheral perfusion, and peripheral cyanosis. Mixing lesions can also result in a right-to-left shunt (deoxygenated blood mixes with oxygenated blood and an d ex exit itss the the he hear artt in into to th thee sy syst stem emic ic ci circ rcula ulati tion on)) as in a teen teenag ager er with with pulmonary hypertension as a result of an undiagnosed atrial septal defect. RightRig ht-toto-lef leftt les lesion ionss may pre presen sentt wit with h cen centra trall cya cyanos nosis is and pro progre gress ss to peripheral cyanosis, as seen in children having hypercyanotic episodes (‘‘Tet spells’’). Symptomatic obstructive lesions can be a result of intracardiac obstruction (eg, valvular atresia or stenosis) or extracardiac obstruction caused by atrectic vasculature (eg, pulmonary atresia). Obstructive lesions may present after closure of the ductus arteriosis, as in coarctation of the aorta. These patients often demonstrate peripheral cyanosis signs and symptoms of  CHF or shock. Severe CHF may result in hypoxia with secondary central cyanosis. Obstructive lesions that present in the ED are typically caused by closure of the ductus arteriosis. Other forms of obstruction lesions are usually identified in the nursery. Ductal dependent lesions typically become symptomatic within the first two weeks of life; however, reports of children up to 6 weeks old presenting with HLHS or coarcation are not uncommon. This Th is clas classifi sifica catio tion n sc sche heme me is no nott pe perf rfec ect. t. Fo Forr exam example ple,, the the ch chil ild d wh who o develops HLHS may return home from the nursery with a mixing lesion balanced to keep them asymptomatic. When the ductus arteriosis closes the infant develops an obstruction to peripheral flow. This obstruction results in peri pe riph pher eral al cy cyan anos osis is,, yi yiel eldi ding ng an in infa fant nt in sh shoc ock. k. Al Alth thou ough gh no nott pe perf rfec ect, t,

 

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thin thinki king ng of co cong ngen enit ital al he hear artt di dise seas asee in thes thesee term termss he help lp the the trea treati ting ng emergency physician manage the patient until able to reach definitive care. No matter how complicated the congenital heart disease lesion, stabilizing treatment depends only on considering mixing and considering obstruction to flow; therefore, further attempts at classifying the lesions are unnecessary. Further description of cardiac lesions are not presented here. The reader is referred to standard texts   [5,6]   if interested and is urged to consider this classification system to deal with the lesions not listed in the standard texts, the proverbial ‘‘scrambled heart.’’ One lesion poorly suited for this categorization is transposition of the great vessels. Children with this condition have a mixing lesion until the ductus closes, typically within the first 3 days of life. After closure, children sudden sud denly ly develo develop p sev severe ere cen centra trall cya cyanos nosis is due to sign signific ificant antly ly dec decrea reased sed mixing between the pulmonary and systemic circulations. The third step in identifying children with undiagnosed congenital heart disease is the diagnostic evaluation in the emergency department. The initial diagnostic evaluation is the attempt at classification done by the history and physical examination. Further workup should be done to verify this suspicion. Blood pressures in all four extremities can identify an obstructive ductal duc tal de depen penden dentt les lesion ion pre presen sentin ting g aft after er clo closur suree of the ductus ductus art arterio eriosis sis.. Blood pressures higher in the arms than the legs suggest a lesion becoming sy symp mpto toma mati ticc wit with h cl clos osur uree of th thee du duct ctus us arte arterio riosi sis. s. Re Reco cord rdin ing g ox oxyg ygen en satura sat uratio tions ns in prepre- and pos postdu tducta ctall ext extrem remiti ities es also also ass assist istss in ide identi ntifyi fying ng a ductal dependent lesion. If blood pressures are adequate and comparable in all four extremities but oxygen saturations are lower in the legs, then right to left shunting is occurring at the ductus arteriosus after the takeoff of the head and neck vessels. The child, thus, has an open ductus arteriosis with a right to left shunt. Chest Che st radiog radiograph raphy y can identi identify fy a partic particula ularly rly abn abnorm ormal al he heart art siz sizee or shape. Radiography can also assist with determining the degree of pulmonary blood flow. A child who has a ventricular septal defect with mixing left left-t -too-ri righ ghtt may may ha have ve pulm pulmon onary ary edem edema a pr pres esen entt on ch ches estt radi radiog ogra raph ph.. Conv Co nver erse sely ly,, a ch chil ild d who who ha hass deve develo lope ped d a ve vent ntri ricu cula larr se sept ptal al de defe fect ct and and pulmonary atresia may have central cyanosis from right-to-left mixing across the defect, and that child may have a paucity of pulmonary vascularity on chest radiograph. Similar to adults with shortness of breath, in children it may be difficult to determine if hypoxia is caused by a pulmonary or cardiac problem. The hyperoxygenation test may assist the physician in making this distinction. Arterial oxygenation should be greater than 150 mm Hg if a child is allowed to breath 100% oxygen for 10 minutes and there is a respiratory cause for the hypoxia. Values less than 100 mm Hg suggest congenital heart disease with a mixing lesion as the cause for the hypoxia   [4] [4].. No diagnostic evaluation of the child who has suspected congenital heart diseas dis easee is com comple plete te withou withoutt the con consid sidera eratio tion n of altern alternativ ativee dia diagno gnoses, ses,

 

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such as de such dehy hydr drat atio ion, n, se seps psis is,, in intr trac acra rani nial al he hemo morrh rrhag age, e, pneu pneumo monia nia,, an and d hypoglycemia. Thee fin Th final al ste step p when when identif identifyin ying g ch child ildren ren who have have und undiag iagnos nosed ed con con-genital heart disease is to initiate ED therapy. The aggressiveness of the initial therapy is determined by the classification of the lesion, the tempo of  presentation, and the severity of the child’s clinical condition. Mixing lesions typica typ ically lly pre presen sentt wit with h gra gradua duall ons onset et of sym sympto ptoms, ms, unl unless ess an ass associ ociate ated d obstructive ductal dependent lesion also exists. Left-to-right mixing lesions may worsen from supplemental oxygenation if pulmonary edema is present. Thee pu Th pulmo lmonary nary vas vascul culatu ature re diff differs ers from from the system systemic ic vas vascul culatu ature re in tha thatt oxyg ox ygen en is a va vaso sodi dila lato tor; r; th ther eref efor ore, e, su supp pple leme ment ntal al ox oxyg ygen en may may ca caus usee a decr decrea ease se in pulm pulmon onar ary y ar arte tery ry pr pres essu sure re wi with th a re resu sult ltan antt incr increa ease se in pulmonary pulmo nary edem edema a and worse worsening ning central cyano cyanosis. sis. Alte Alternativ rnatively, ely, posit positive ive press pr essur uree ven venti tila lati tion on may may im impro prove ve th thee sh shun untt frac fractio tion. n. Th Thee incr increa ease se in pulmonary artery pressure with positive pressure ventilation may decrease pulm pu lmon onar ary y bloo blood d flo flow w (w (whi hich ch is al alre read ady y ex exce cessi ssive ve)) an and d re redu duce ce ce cent ntra rall cyanosis (improve oxygenation). Righ Ri ghtt-to to-le -left ft le lesi sion onss may may im impr prov ovee with with ox oxyg ygen enat atio ion. n. Ag Again ain,, ox oxyg ygen en decreases pulm decreases pulmonary onary vascular vascular resis resistance tance,, lessening lessening the rightright-to-le to-left ft shunt and improving oxygenation. Supplemental oxygen has a minimal effect on arterial oxygenation unless the shunt fraction alters because the inadequate flow of blo blood od thr throug ough h the pul pulmon monary ary vascul vasculatu ature re enters enters the lef leftt atr atrium ium 100% saturated with oxygen. Conversely, positive pressure ventilation may increase pulmonary vascular resistance, worsening the shunt fraction and worsening arterial oxygenation. Intravenous (IV) fluid administration may be beneficial in these children and should be considered. In the case of a hypercyanotic episode, or ‘‘tet spell,’’ a child with the tetralogy of Fallot has an acute worsening of the right-to-left shunt after an increase in the intracardiac obstruction or decrease in systemic vascular re resis sista tanc nce. e. In th this is ca case se,, pl plac acin ing g th thee ch chil ild d in the the kn knee ee ches chestt po posit sitio ion n or [7] increases  increases systemic vascular resistance compressing the abdominal aorta  aorta   [7] and may acutely decrease the right-to-left shunt. Acut Ac utee ob obstr struc ucti tive ve le lesio sions ns pr pres esen entin ting g in the the ED typi typica cally lly do so afte afterr closure of the ductus arteriosis. Infusion of prostaglandins may open the ductus, relieving the obstruction, and allowing the child to stabilize until they they ar aree ab able le to re reac ach h defin definit itive ive car care. e. Co Comp mpli licat catio ions ns of pr pros ostag tagla land ndin in infusion include apnea, a mild decrease in systemic vascular resistance and Althou ough gh un unst stud udie ied, d, co conv nven enti tion onal al nonpatholo nonp athologic gic hyper hypertherm thermia ia   [8,9]. [8,9]. Alth teac teachin hing g is that that th thee ris risk k fo forr ap apne nea a in incr crea ease sess wi with th high higher er infu infusio sion n rate rates. s. Initi In itial al infu infusi sion on rate rate is co cont ntro rove vers rsia ial. l. So Some me clin clinici ician anss pr pref efer er to star startt at a higher dose (0.10–0.20   mg/kg/min) and decrease the dose after the ductus reopens. Other investigators prefer to start at a lower dose (0.05   mg/kg/min) and increase the dose every 15 to 20 minutes until an effect is achieved. Although there is concern that starting prostaglandins in a child who has se sepsi psiss an and d no nott co cong ngen enit ital al he hear artt di dise seas ase, e, ma may y wo wors rsen en re resu susci scita tati tion on an and d

 

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outcome as a result of the decrease in systemic vascular resistance, no data support or refute this concern. Careful administration of a bolus of IV fluids may be beneficial in these children.

Corrected congenital heart disease

ED ca care re of th thee chil child d wh who o has has co corr rrec ecte ted d co cong ngen enit ital al he heart art dise disease ase ha hass received little attention in the emergency medicine literature; however, care of these children also can follow simple principles, allowing the emergency physician a starting place until consultation can be obtained. Once a child is diagnosed with congenital heart disease, they may be discharged home with medical management until they grow large enough, whic wh ich h de decr crea ease sess th thei eirr surg surgic ical al mo morta rtali lity ty risk risk.. Th They ey may may also also unde underg rgo o a temporizing or initial surgical repair. Finally, children undergo definitive repa repair ir.. Th They ey ma may y pr pres esen entt to th thee ED wi with th a wi wide de vari variat atio ion n in or orig igin inal al anatomy in various stages of surgical repair. Fortunately for the emergency physician, a few principles apply to these repairs. Onee co On comm mmon on pr prob oble lem m acro across ss al alll su surg rgic ical al re repa pair irss is sten stenos osis is at the the extraca ext racardi rdiac ac surgica surgicall ana anasto stomos mosis. is. In this this situat situation ion,, the chi child ld resort resortss to presur pre surgic gical al phy physio siology logy be becau cause se whatev whatever er repair repair perfor performed med to enc encour ourage age flow has become stenotic, resisting additional flow. Consider, for example, a child who has had a repair of coarctation of the aorta. If stenosis develops at the ana anasto stomos mosis, is, the chi child ld pre presen sents ts with with sym sympto ptoms ms of an obs obstru tructi ctive ve lesion. Peripheral cyanosis in the lower extremities with decreased pulses resu results lts.. An Anot othe herr exam exampl plee is th thee ch chil ild d wh who o had had a Bl Blal aloc ock-T k-Tau auss ssig ig sh shun untt plac placed ed af afte terr di diag agno nosis sis wi with th tr tric icus uspi pid d valv valvee atre atresia sia wi with th an asso associ ciat ated ed hypoplastic right ventricle and pulmonary artery stenosis. Blood exits the ri righ ghtt at atri rium um di dire rect ctly ly in into to th thee le left ft at atri rium um.. A Bl Blal aloc ockk-Ta Taus ussi sig g sh shun untt is ty typi pica call lly y a go gort rtex ex gr graf aftt fr from om th thee ri righ ghtt su subc bcla lavi vian an arte artery ry to the the righ rightt pulmon pul monary ary artery artery.. Thi Thiss shu shunt nt is a tem tempor porizi izing ng pro proced cedure ure,, whi which ch cre create atess a left-t left-to-r o-righ ightt shu shunt, nt, allowi allowing ng adequa adequate te mix mixing ing unt until il the chi child ld gro grows. ws. If  st sten enos osis is de deve velo lops ps at th thee an anas asto tomo mosi sis, s, the the ch chil ild d ma may y de deve velo lop p less lessen enin ing g pulm pu lmon onar ary y bl bloo ood d flow flow (w (whi hich ch may may be visi visibl blee wi with th co comp mpar aris ison on ches chestt radiographs) with an increase in central cyanosis. The result is the child’s preoperative physiology. Another common complication in postsurgical patients is arrhythmias. Practi Pra ctical cally ly all pat patien ients ts tha thatt hav havee und underg ergone one sur surgery gery for con congen genital ital hea heart rt disease are at increased risk for sudden death from a presumed ventricular arrhythmia. Those procedures that do not increase the risk for sudden death are an atrial septal defect repair and patent ductus arteriosis ligation. Box ligation.  Box 1 provides a list of common procedures associated with an increased risk for sudden sud den dea death. th. No chi child ld who has und underg ergone one the these se proced procedure uress sho should uld be discha dis charge rged d fro from m the ED aft after er pre present sentati ation on wit with h sync syncope ope or palpit palpitati ations ons unless thoroughly discussed with the child’s cardiologist.

 

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Box 1. Corrected congenital heart disease lesions associated with sudden death High Risk  Tetralogy of Fallot Aortic stenosis Transposition of the great arteries Coarctation of the aorta Atrioventricular septal defect Pulmonary Pulmon ary stenosi stenosis s Anomalies that undergo the Fontan procedure Low Risk  Ventricular septal defect

Because of the increased atrial pressures present before and sometimes after surgery, many of these patients are also at increased risk for atrial arrhythmias. Arrhythmias can also arise from the cardiac chamber manipulated during surgery. For example, a suture in the ventricular septal defect repair can be a focus of ventricular arrhythmia. The final group of complications includes those specific to a particular surgical repair. The Fontan repair is the procedure with the longest list of  1)) is typically performed in the case serious complications. The Fontan (Fig. (Fig. 1 of sin single gle ven ventri tricle cle phy physio siolog logy. y. Th Thee mos mostt effe effecti ctive ve ven ventri tricle cle become becomess the systemic ventricle, whereas the superior and inferior vena cava drain directly 2 contains  contains a list of the most common into the right pulmonary artery.  Box 2 complications of a Fontan procedure presenting after discharge from the hosp ho spit ital al.. Th Thro romb mboe oemb mboli olism sm ca can n oc occu curr in the the pu pulm lmon onar ary y or sys syste temi micc circulation. Thrombotic complications occurred in 25% of patients within 4 years after surgery in one study  [10]  [10].. Twenty-five percent of these thrombi wer eree in the syst system emic ic art arter eria iall cir ircu cula lati tion on,, wh wher erea eass 75 75% % we were re in the pulmonary pulmo nary circu circulation lation   [10] [10].. Ma Many ny of the the comp compli lica cati tion onss aris arisee from from the the pers pe rsis iste tent nt incr increa ease sed d ce cent ntra rall ve veno nous us pr pres essu sure re that that de deve velo lops ps to dr driv ivee fene nest stra rate ted d Fo Font ntan an is pe perf rfor orme med, d, pulm pu lmon onar ary y bloo blood d flow flow   [11,12]. [11,12].   If a fe a ‘‘pop-off ‘‘pop-off valve’’ exists between the inferior vena cava and the right atriu atrium. m. Becau Be cause se of th thee fe fene nest stra ratio tion, n, it is po poss ssib ible le for for thes thesee ch chil ildr dren en to de deve velo lop p cyanosis with a significant right to left shunt across the fenestration. The Blalock-Taussig shunt is a temporizing procedure whereby the right subclavian artery is anastomosed to the right main pulmonary artery. In addi ad diti tion on to th thee ri risk skss fo forr st sten enos osis is at th thee anas anasto tomo mosis sis,, thes thesee sh shun unts ts may may thrombos when a child is dehydrated. Additionally, the ipsilateral vertebral ar arte tery ry ma may y ha have ve be been en in inte tent ntio iona nall lly y liga ligate ted d to pr prev even entt a ba basi sila larr stea steall phenomenon. The long-term risks of this ligation are unknown.

 

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Fig. 1. Fenestra Fig. Fenestrate ted d Fontan Fontan in repair repair of tri tricus cuspic pic atresi atresia a with with result resultant ant hypopl hypoplast astic ic right right ventri ven tricle cle.. Inferi Inferior or vena vena cava cava and superi superior or vena vena cava cava drain drain into into rig right ht pulmon pulmonary ary artery artery.. Fenestration into the right atrium from the inferior vena cava.

Surgical repair of coarctation of the aorta carries another set of postoperative risks. One recent series details the complications of 383 patients available for follow-up of 580 patients who had repair. Aneurysmal dilation at the sight of the coarctation occurred in 2% of patients. Two patients had massive mas sive hem hemopt optysi ysiss fro from m an aort aortobr obronc onchial hial fist fistula ula.. Int Intrac racard ardiac iac ste stenos nosis is requiring surgery occurred in three patients, and one patient had a rupture of  a sinus of Valsalva aneurysm [13] aneurysm  [13].. Heart transplantation

Childr Chi ldren en pre present senting ing to the ED aft after er orthot orthotop opic ic heart heart transp transplan lantat tation ion have ha ve co comp mpli lica cati tion onss th that at di diffe fferr fr from om ot othe herr child childre ren n wh who o ha have ve co corr rrec ecte ted d

Box 2. Complications that may occur after a Fontan procedure Thromboembolism Thrombosis Increased central venous pressure Ascites Pulmonary Pulmon ary effusio effusion n Pericardial Pericar dial effusion Protein-losing enteropa Protein-losing enteropathy thy Atrial arrhythmia Sudden death

 

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congenital heart disease and require separate attention. These children may present to the ED with an invasive infection, acute/chronic rejection or with posttransplant lymphoproliferative disorder. Infectious complications in transplant recipients may be caused by viral, bacterial, protozoan, or fungal infections. Most bacterial infections occur within the first month after transplant. Viral infections predominate over the foll follow owin ing g mo mont nth. h. Th Thro roug ugho hout ut th thee life life of the the tran transp spla lant nt re reci cipi pien ent, t, an  [14].. increasing risk for protozoan or fungal infections exists  [14] In a re revi view ew of 74 ou outp tpat atie ient nt fe febr bril ilee epis episod odes es in 22 pe pedi diat atri ricc he hear artt transplant patients, 22 of 74 (30%) were considered serious and required inpatient therapy [15] therapy  [15].. Three episodes were pneumonia, two were caused by cytomegalovirus (CMV) infections, and two were caused by streptococcic infection. One child in the series died. No data are available to reassure the emergency physician that clinical presen pre sentat tation ion or acu acute te lab labora orator tory y eval evaluat uation ion can exc exclud ludee the pre presen sence ce of  bact ba cter eria iall illn illnes esss in th thee tr tran ansp spla lant nted ed pa pati tien entt wh who o ha hass an ac acut utee illne illness ss.. In a small series, pneumococcal bacteremia occurred in 9 of 80 patients (11%) at 3 to 48 months posttransplant [16] posttransplant  [16].. Of those 9 children, 3 had pneumonia, 2 presented with otitis media, and 1 child had petechiae and purpura. Most of thes thesee ch chil ildr dren en,, but but no nott al all, l, ha had d a te temp mper erat atur uree high higher er than than 101 101 F at presentation. Pneumocystis carinii pneumonia (PCP) can present with symptom durations from 1 to 2 days to 2 weeks [17] weeks  [17].. In this small series, all 10 patients had tachypnea and room air oxygen saturations less than 95%. CMV is a recognized cause of morbidity in the transplant recipient [18] recipient  [18].. CMV infections can present as a mononucleosis-type syndrome, an interstitial pneumonitis, a hepatitis, or as a gastrointestinal disease. The symptoms are typically nonspecific and include headache, myalgias, abdominal pain, and diarrh diarrhea. ea. CMV-monon CMV-mononucleo ucleosis sis differ differss from Epste Epstein-Ba in-Barr rr Virus 

(EBV) mononucleosis because it does not include pharyngitis, tonsillitis, or splenomegaly. Acut Ac utee reje reject ctio ion n has has be been en de defin fined ed as the the clin clinic ical al de deci cisi sion on to inte intens nsif ify y immunosuppression in association with histopathology or dysfunction [19] dysfunction  [19].. The distinction between acute and chronic rejection does not refer to the time of onset after transplantation. Acute rejection is a more fulminant process than chronic rejection. Children may be asymptomatic or present in cardiogenic shock. Common symptoms include fever, myalgias and vomiting. Chest pain may occur, but is uncommon. The electrocardiogram may show sh ow a de decr crea ease sed d R wave wave am ampl plitu itude de an and d an incr increa ease sed d QR QRS S du dura rati tion on;; ho howe wever ver,, these findings are not sensitive. Laboratory findings are not helpful. There is no data to suggest that cardiac enzymes are reliably elevated with acute rejection. Elev rejection. Elevated ated hepat hepatic ic transa transaminase minases, s, altho although ugh nons nonspecifi pecificc for acute rejection, always suggest an invasive complication in the transplant recipient. Chro Ch ronic nic reje reject ctio ion n di diffe ffers rs micr micros osco copi pica cally lly from from ac acut utee re reje ject ctio ion. n. Th Thee clinic cli nical al man manife ifesta statio tion n of chroni chronicc rej reject ection ion is acc accele elerat rated ed athero atheroscl sclero erosis. sis.

 

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Sympto Symp toms ms ar aree ca caus used ed by is isch chem emia ia or infa infarc rcti tion on and and us usua uall lly y incl includ udee decrea dec reased sed exercis exercisee tol tolera erance nce or malaise malaise.. Pat Patien ients ts may als also o pre presen sentt after after syncope or sudden death. As with acute rejection, no specific laboratory, or ECG findings exist to secure this diagnosis. Posttransplant lymphoproliferative disorder (PTLD) is typically a B-cell [20,21].. Th Thee ca caus usee is mo most st like likely ly lymphoma lympho ma ass associ ociate ated d with with tra transp nsplan lantt pat patien ients ts [20,21] a resu result lt of EB EBV. V. Pre Prese sent ntin ing g sy symp mpto toms ms incl includ udee feve fever, r, ma mala lais ise, e, a mo mono no-nucleosis-type syndrome, palpable lymphadenopathy, or mass effect from tumor location. The most common location of the masses are (in descending order): abdomen, thorax, head and neck, and brain [21] brain  [21].. Abdominal PTLD may present with abdominal pain, hepatomegaly, splenomegaly, an abdominal mass, gastrointestinal bleeding, anemia, intussusception, diarrhea, or a protein-wasting enteropathy [21] enteropathy  [21].. In caring for the transplant recipient with an acute illness, the emergency physician physi cian should perform several steps. steps. A caref careful ul histo history ry allows the treat treating ing phys ph ysic ician ian to iden identif tify y a cl clin inic ical al sy synd ndro rome me cons consist isten entt wi with th a se self lf-l -lim imit ited ed or mo more re aggressive illness. Noncompliance with the immunosuppressive regimen and PCP prophylaxis increases the risk for acute rejection   [22]   or acute PCP infection  [17]..  After a careful physical examination, a chest radiograph and infection [17] ECG should be obtained in all children who experience an unclear symptom complex. A comparison ECG is necessary because changes including right bundle branch block, left atrial enlargement, and right ventricular hypertrophy are not associated with clinical deterioration   [23]. [23]. Laboratory studies should include a complete blood count with differential, serum electrolytes, hepatic transaminases, and blood cultures. The admission recommendations are unclear for children who develop an obvi ob viou ouss et etio iolog logy y fo forr th thei eirr sy symp mpto toms ms.. Th Thee em emer erge genc ncy y ph phys ysic icia ian n sh shou ould ld consider cons ider admission for any child who experien experiences ces a significant significant fever or feve feverr history. histor y. Children with vomit vomiting ing without a history history clear clearly ly sugge suggestive stive of acut acutee viral gastroenteriti gastroenteritiss are also a conce concern. rn. Dehydration Dehydration shoul should d be treat treated ed more aggressively in transplant recipients because of the nephrotoxicity of their immunosuppressive regimens. Infective endocarditis

Infective endocarditis refers to a condition in which an organism infects the the va valv lves, es, en endo doca card rdiu ium, m, or ot othe herr ca card rdiac iac stru struct ctur ures es.. Th Thee term term ac acut utee bacterial endocarditis refers to a fulminant illness whereby death can occur within weeks. Subacute bacterial endocarditis refers to an indolent course evol ev olvin ving g ov over er mo mont nths hs.. The The mo most st co comm mmon on bact bacter eria iall ca caus uses es of infe infect ctiv ivee endocarditis are  Staphylococcus aureus,  Streptococcus pyogenes   and   Streptococcu toc occuss viri viridans dans. Th Thee mo most st comm common on symp sympto toms ms in pa pati tien ents ts who who ha have ve infective endocarditis are fever, malaise, chest and abdominal symptoms, and arthralgias. Physical findings may include embolic events, a changing or new murmur, splenomegaly, and petechiae. The classically described findings of 

 

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Roth spots, Osler’s nodes, Janeway lesions, and splinter hemorrhages are uncommon. The most common laboratory abnormalities in patients who havee inf hav infect ective ive end endoca ocardi rditis tis are ele elevate vated d erythr erythrocy ocyte te sed sedime imenta ntatio tion n rat ratee (ESR), anemia, hematuria, and positive blood cultures. Children who have congenital heart disease are at an increased risk for bacterial endocarditis. Surgical manipulations of the aortic valve or aorta are the highest risk anomalies. Surgically corrected septal defects or rightsided lesions are at a low risk. The cause of the initial bacteremia leading to endo en doca card rditi itiss is fr freq eque uent ntly ly un unkn know own. n. In the the mo most st comp compre rehe hens nsiv ivee se seri ries es available, a precipitating event could be identified in only 87 of 214 cases of   [24]..  Of these 87, endocarditis in patients who had congenital heart disease  [24] 42 cases were associated with dental procedures and 10 were associated with skin ski n inf infect ection ions. s. Int Intere eresti stingly ngly,, pat patien ients ts rec receiv eived ed app approp ropria riate te end endoca ocardi rditis tis prophylaxis in one half of the cases occurring after dental procedure  [24].  [24].  [24] does  does not list any cases of  The extensive series by Li and Somerville  [24] bacterial endocarditis occurring after traumatic injury. Current recommendations do not suggest endocarditis prophylaxis for cases of traumatic injury [25,26]. Invest estiga igator torss sta state te tha thatt prophy prophylaxi laxiss is not ind indicat icated ed for ure urethr thral al [25,26].   Inv catheteri cathet erizat zation ion wit withou houtt infect infection ion or for end endotr otrach acheal eal int intuba ubatio tion n   [25,26]; [25,26]; however, one investigator recommends prophylaxis for urethral catheterization in the face of a urinary tract infection [26] infection  [26].. Endoc En docard arditi itiss pro prophy phylax laxis is is ind indica icated ted for all pat patien ients ts with with con congen genita itall heart disease. Prophylaxis is not indicated for patients at least 6 months from a surgically repaired ventricular septal defect or patent ductus arteriosis without residual defect. Patients with an isolated atrial septal defect do not req requir uiree pro prophy phylax laxis is be befor foree rep repair air or 6 mon months ths aft after er comple complete te repair repair [25,26]. Bo ox 3   detai details ls th thee cu curr rren entt dosin dosing g re regi gime men n re reco comm mmen ende ded d by the the [25,26].   B American Heart Association for infective endocarditis prophylaxis. Arrhythmias or congestive heart failure in children

Not all cardiac causes of acute illness in children are a result of congenital heart disease. Children may present to the ED with syncope, palpitations, chest pain, or shortness of breath. The following section describes the most common pathologic cardiac conditions that may result in ED presentation. Befo Be fore re st start artin ing g th thou ough gh,, it is ne nece cess ssar ary y to ha have ve an un unde ders rsta tand ndin ing g of the the normal age-related progression of the pediatric ECG. Normal changes in the pediatric ECG

The pediatric ECG is an evolving process, changing on a nearly weekly basis bas is as pul pulmon monary ary vascul vascular ar res resista istanc ncee (PV (PVR) R) dec decrea reases ses,, left left ven ventri tricu cular lar (LV) mass increases relative to right ventricular mass (RV), and various other changes occur in the developing cardiovascular system. Though the basic premises are unchanged, physicians must be familiar with these age-

 

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Box 3. Endocarditis prophylaxis recommendations Dental, oral, respiratory tract, or esophageal procedures  Give 1 hour before procedure: Amoxicillin (50 mg/kg with a maximum of 2.0 g) by mouth. No follow-up dose recommended. Genitourinary or gastrointestinal procedures in high risk patients Give within 30 minutes of starting procedure: Ampicillin (50 mg/kg with a maximum of 2.0 g) and Gentamicin (1.5 mg/kg not to exceed 120 mg) IV. Give 6 hours after the procedure: Ampicillin or amoxicillin (25 mg/kg with a maximum of 1.0 g). For more information see:   Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease. Prevention of bacterial endocarditis: recommendations by the

American Heart Association. JAMA 1997;277:1794–1801; Circulation 1997;96:358– 66; JADA 1997;128:1142–50.

related variations associated with pediatric ECG to correctly interpret its data. This discussion focuses on this and anatomic variations specific to the pedi pe diat atri ricc po popu pula latio tion n fr from om bi birt rth h to 2 mont months hs of ag agee to he help lp phys physic ician ianss accurately detect anomalies during this critical period. Most of the age-related variations demonstrated in the pediatric ECG are because of the changes in the ratio of LV to RV mass. As PVR continues to decrea dec rease se rel relati ative ve to system systemic ic vascul vascular ar res resist istanc ancee (SV (SVR), R), RV do domin minance ance ra rapi pidl dly y wa wane ness fr from om an LV/R LV/RV V ra rati tio o of 0.8 0.8 to 1.5 1.5 by 1 mo mont nth h of ag age. e. Concurrent with these changes is a gradual decrease in the severity of the right QRS axis deviation. The precordial R/S ratios also change, increasing and decreasing in the left and right precordial leads, respectively. As a point of reference, the newborn ECG may demonstrate a complete reversal of the adult R/S progression, but by 1 month of age, the R/S ratio is typically greater than 1 in V6 and between 1–6 months of age, the R/S ratio in V2 also approaches appro aches 1. Durin During g this last age range range,, it is not uncommon uncommon to erron erroneous eously ly suspect bilateral ventricular hypertrophy based on the large precordial QRS deflections. T waves are typically dynamic during the first week of life. At birth the T waves are upright in V1 and V6 with the vector anterior and to the left. Within a few days the vector changes rightward leaving flattened or inverted T waves laterally. By the end of the first week of life, the T wave axis changes posterior and leftward, producing inverted T waves in lead V1 and upright T waves in lead V6. The inverted T wave in V1 may not turn upright until late adolescence.

 

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Supraventricular tachycardia

Pediat Pedi atri ricc arr arrhy hyth thmi mias as in th thee fir first st 2 mont months hs are are rare rare but but ca can n beco become me hemodynamically significant. The most commonly experienced arrhythmia in this age group is supraventricular tachycardia (SVT), generally producing narrow nar row complex complex hea heart rt rat rates es gre greate aterr than than 240 bea beats ts per minut minute. e. At these these rates, P waves (if present) are often buried in the preceding T waves making it difficult to differentiate an atrial from a nodal focus. SVT is not, however, always associated with a heart rate greater than 240. An inappropriately elevated heart rate in an otherwise calm or sleeping infant is SVT until proven otherwise. Any infant found to have an initial episode of SVT should be thoroughly evaluated by a pediatric cardiologist to rule out problems, such as SVT-induced CHF, anatomic anomalies (ie, Ebstein’s anomaly), or a reen reentra trant nt/a /abe berr rran antt pathw pathway ay as wi with th Wo Wolff lff-P -Par arkin kinso sonn-Whi White te (W (WPW PW)) syndro syn drome. me. Th Thee progno prognosis sis for infan infants ts wit with h SVT is exc excell ellent ent with 60% to 90% of patients experiencing complete remission of symptoms by 6 to 12 months of age.

Wolff-Parkinson-White syndrome

WPW syndrome is associated with ventricular pre-excitation by way of  an acc access essory ory pat pathwa hway y bet betwee ween n the atr atria ia and ven ventric tricles les.. The These se access accessory ory pat athw hway ayss do not dem emon onst stra ratte th thee obli obliga gato tory ry pa pau use as se seeen in the the atrioventricular node. As a result, ventricular pre-excitation is responsible for the short PR interval and delta waves frequently detected on ECG. WPW typ typica ically lly occurs occurs spo sponta ntaneo neously usly;; ho howev wever, er, fam familia iliall clu cluste sters rs hav havee been described. Pre-excitation can be intermittent, making true prevalence in the the po popu pula lati tion on di diffic fficul ultt to defin define. e. WP WPW W freq freque uent ntly ly co coin inci cide dess wi with th congenital cardiac abnormalities, including Ebstein’s anomaly, hypertrophic cardiomyopathy, and atrial septal defects. Thee WP Th WPW W sy synd ndro rome me re refe fers rs to a pa pati tien entt wi with th sym sympt ptom omss of tach tachya yarrrhyth rh ythmi mias as in th thee fa face ce of ECG ECG ev evid iden ence ce of prepre-ex exci cita tati tion on.. Th Thre reee ECG ECG features are described: (1) short PR interval (!0.12 seconds), (2) a prolonged QRS duration (O0.12 seconds), and (3) a delta wave or a slow gradual upsl up slop opee lead leadin ing g in into to th thee QRS QRS co comp mple lex. x. Th Thee degr degree ee of pr pree-ex exci cita tati tion on detected on the ECG depends on the relative conduction times between the atrioventricular node and the accessory pathway. Measures to slow conduction tio n thr throug ough h the atr atriove ioventr ntricu icular lar no node de may mak makee an acc accesso essory ry pat pathwa hway y more prominent. Described methods include Valsalva or vagal maneuvers and adenosine therapy. Not all patients with ECG evidence of pre-excitation are symptomatic. Most of tho Most those se wit with h sympto symptoms ms are limite limited d to che chest st dis discom comfor fort, t, diz dizzin ziness ess,, syncope, or shortness of breath [27] breath  [27].. The most common arrhythmias in this population are atrial fibrillation and orthodromic reciprocating tachycardia. Orthodromic reciprocating tachycardia is a type of paroxysmal supraven-

 

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tricular tachycardia that allows antegrade conduction down the atrioventricular node and retrograde conduction in the accessory pathway. Episodes of the less common antidromic tachycardia place the patient at higher risk  [28].. for ventr ventricula icularr fibrill fibrillation ation [28] Although atrial fibrillation is common in patients who have WPW, its occurrence in the presence of rapid conduction across an accessory pathway may pre predis dispos posee a pat patien ientt to ven ventric tricula ularr fibrill fibrillati ation on   [29,30] [29,30].. Medications Medications that slow conduction across the atrioventricular node should not be used in patients who develop atrial fibrillation and WPW syndrome. Agents, such as digoxi digoxin, n, cal calciu cium m cha channe nnell blo blocke ckers, rs, bet beta-b a-bloc locke kers, rs, and ade adenos nosine ine,, may increase incre ase the risk for ventr ventricula icularr fibrill fibrillation ation.. Proc Procainamid ainamidee or amiod amiodarone arone are drugs of choice for rate control in this situation. Anomalous coronary artery

Ano nom mal alou ouss or orig igin in of a co coro rona nary ry ar arte tery ry,, alt althou hough a rare rare for orm m of  congen con genita itall hea heart rt dis disease ease,, can cau cause se myo myocar cardia diall isc ischem hemia ia in the inf infant ant or sy sync ncop opee in the the yo youn ung g ad adul ult. t. Ma Many ny ty type pess of co cong ngen enit ital al co coro ronar nary y arte artery ry abnormalities are described [31] described  [31];; however, the two most common variations that cause symptoms are discussed here. The left main coronary artery may arise from the pulmonary artery. This rare lesion occurs in 1 of 300,000 children  [32].  [32]. Infants with this anomaly pres pr esen entt af afte terr in infa farc rcti tion on or wi with th an angi gina na.. Ch Chil ildr dren en wi with th an angi gina na ma may y be diagnosed with colic due to inconsolable crying, especially after feeding. In Mahle’s series  [33]  [33],,  the most common finding in the 11 children identified [32].. The were cardiomegaly on chest radiography and ischemia on ECG   [32] classic ECG finding are deep Q waves in leads I and aVL with poor R-wave progression across the precordium [31] precordium  [31].. If the left coronary artery originates from within the right coronary sinus or from the right coronary artery, syncope and sudden death may occur in adol ad oles esce cenc nce. e. Sy Sync ncop opee an and d sudd sudden en de deat ath h are are most most comm common on if the the left left coro co rona nary ry ar arte tery ry cour course sess be betw twee een n th thee pulm pulmon onary ary arte artery ry and and ao aort rta. a. Le Left ft coronary artery blood flow may be asymptomatic until, classically, flow is impair imp aired ed by ext extern ernal al compre compressi ssion on fro from m the aor aorta ta and pu pulmo lmonary nary art artery ery lead leadin ing g to isch ischem emia ia,, ar arrh rhyt ythm hmia ia,, or su sudd dden en de deat ath. h. Th This is oc occu curs rs du durin ring g exertion when cardiac output increases causing a mild dilation in diameter of the aortic and pulmonary artery roots. Detection of this lesion requires diagnosis of acute ischemia or clinical suspicion confirmed by echocardiography or catheterization. Kawasaki Kawasa ki Diseas Diseasee

Kawasaki Kawasa ki Dis Diseas easee (KD), (KD), for former merly ly des descri cribe bed d as muc mucocu ocutan taneou eouss lym lymph ph node syndrome, was originally defined by Kawasaki in a series of 50 cases in 1967   [34] [34].. KD is an acute febrile syndrome of childhood of uncertain

 

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etiolo etio logy gy that that is al also so th thee le lead adin ing g ca caus usee of ac acqu quir ired ed he hear artt dise diseas asee an and d myocardial infarction (MI) in children in the United States. Eighty percent of all cases occur in children less than 5 years old. KD is rare in infants less than 4 months old and in adults. Diagnostic criteria for KD include fever of at least 5 days, and four of the following five findings: (1) nonpurulent bilateral bulbar conjunctivitis, (2) polymorphous exanthema, (3) cervical lymphadenopathy, (4) involvement of the the ex extr trem emit itie ies, s, an and d (5 (5)) ch chan ange gess in the the lips lips and and or oral al ca cavi vity ty (inj (injec ecte ted d pharynx or lips, fissured lips or strawberry tongue). The polymorphous rash is typically truncal without vesicles. Lymph nodes must be at least 1.5 cm in diameter. Extremity involvement includes edema and erythema of the hands and feet followed by periungual desquamation. Other findings in children who hav havee Kaw Kawasa asaki ki Dis Diseas easee may inc includ ludee extrem extremee irritab irritabilit ility, y, art arthri hritis, tis, gallbladder hydrops, mild hepatitis, uveitis, urethritis, aseptic meningitis, or myocarditis. Laboratory abnormalities may include thrombocytosis (usually in the second and third weeks of illness), elevated sedimentation rate, sterile pyur py uria ia,, an and d pr prot otei einu nuri ria. a. At it itss pe peak ak,, the the plat platel elet et coun countt ma may y ex exce ceed ed 1, 1,00 000,0 0,000 00.. EC ECG G ch chan ange gess th that at ma may y be dete detect cted ed duri during ng the the ac acut utee ph phas asee incl includ udee PR pr prol olon onga gati tion on,, co corr rrec ecte ted d QT prol prolon onga gati tion on,, an and d TT-wa wave ve flattening. Children may have symptoms of myocarditis or pericarditis during the acute phase; this is typically self-limited. Aneurysms of the coronary arteries may ma y de deve velo lop p du durin ring g th thee se seco cond nd an and d th third ird we week ekss of illn illnes ess. s. Th Thos osee wi with th aneurysms may suffer acute MI. While occurring in less than 3% of patients, MI ty typi pica call lly y oc occu curs rs with within in 1 ye year ar of on onse sett of symp sympto toms ms an and d freq freque uentl ntly y within 3 months of onset of symptoms. MIs may be silent, or the child may present with abdominal pain, vomiting, or crying. Treat reatm men entt in th thee ac acut utee phas phasee of Kaw awas asak akii Di Dise seas asee in the ED is supportive suppo rtive.. Intra Intravenou venouss fluids are typic typically ally requ required ired beca because use the children have had poor oral intake with increased insensible losses. Aspirin therapy and intravenous gamma-globulin have been shown to decrease complication ra rate tes; s; ho howe weve ver, r, th thes esee th ther erap apie iess woul would d no nott typi typica cally lly be star starte ted d wi with thou outt appropriate consultation. Myocarditis

Myocarditis refers to an inflammatory disease of the myocardium that is not cau caused sed by acu acute te isc ischem hemia. ia. Myocar Myocarditi ditis, s, the then, n, is a cli clinic nico-p o-path atholo ologic gic diagnosis, which does not refer to a specific etiology. While most myocarditis in the United States is viral, the cause can be bacterial, rickettsial, protozoal, parasitic, fungal, autoimmune or pharmacologic [35,36] pharmacologic  [35,36].. Coxsackie B virus, an en ente tero rovi viru rus, s, an and d aden adenov ovir irus us ar aree th thee mo most st comm common on vira virall ca caus uses es of  myocar myo cardit ditis. is. Whi While le new newbor borns ns are par partic ticula ularly rly sus suscep ceptib tible le to cox coxsac sackie kie B myocarditis, all ages are at risk. Presenting symptoms include fever, poor appetite, irritability, sudden death, diaphoresis, pallor, and congestive heart

 

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failure. failur e. Old Older er chi childr ldren en may not pre presen sentt un until til dil dilate ated d car cardio diomyo myopat pathy hy is already present. Older patients are more likely to present with a gradual onset of congestive heart failure, or atrial or ventricular arrhythmias. The electrocardiogram may demonstrate sinus tachycardia, low-voltage QRS complexes, and inverted or low-voltage T waves. Wide Q waves and ST-segment changes may also be apparent. The chest radiograph typically shows a dilated heart and pulmonary edema. Treatment is supportive until the the ch chil ild d ca can n be tr tran ansf sfer erre red d to a ce cent nter er wher whereb eby y ag aggr gres essi sive ve diag diagno nost stic ic evaluation and therapy can be performed.

Hypertrophic cardiomyopathy

Hypertrop Hypert rophic hic car cardio diomyo myopat pathy, hy, in thi thiss sectio section, n, ref refers ers to the idi idiopa opathi thicc cond co ndit itio ion n so some meti time mess re refe ferr rred ed to as id idio iopa path thic ic hy hype pert rtro roph phic ic su suba baor orti ticc stenosis or familial hypertrophic subaortic stenosis. Hypertrophic cardiomyop my opat athy hy ca can n al also so be a de desc scri ript ptiv ivee diag diagno nosi siss that that incl includ udes es card cardia iacc conditions secondary to obstructive congenital heart disease (aortic stenosis) or an inborn error of metabolism (glycogen storage disease). The lef leftt ven ventri tricul cular ar hyp hypert ertrop rophy hy in hyp hypert ertrop rophic hic car cardio diomyo myopat pathy hy is variably asymmetric and, at the cellular level, myocardial cells are organized in a bizarre fashion. Commonly, this condition is a result of mutations in the cardiac myosin heavy-chain gene. A familial component commonly exists to this disorder. Clinic Cli nical al manife manifesta statio tions ns are typ typica ically lly cau caused sed by obs obstru tructi ction on of flow or arrhythmias. The disorganized contraction of the hypertrophic section of  vent ve ntri ricl clee resu results lts in su suba baor orti ticc ou outfl tflow ow ob obst stru ruct ctio ion n du duri ring ng syst systol ole. e. Th Thee increased ventricular pressure required to overcome this obstruction results in increased myocardial-wall stress and oxygen demand. Arrhythmias may result from this ischemia or may result from the arrhythmogenic foci of the bizarrely arranged myocardial fibers. Phys Ph ysic ical al ex exam amina inati tion on of th thee ch child ild wh who o ha hass de deve velo lope ped d hy hype pert rtro roph phic ic cardiomyopathy may reveal a systolic murmur exacerbated by a Valsalva maneuver or by standing. The murmur is best detected at the left lower sternal boarder or at the apex. A prominent left ventricular lift may exist on palp pa lpat atio ion. n. EC ECG G fr freq eque uent ntly ly re reve veal alss le left ft ve vent ntri ricu cula larr hy hype pert rtro roph phy y an and d ST-seg STsegmen mentt and T-wave T-wave cha change nges. s. Che Chest st radiog radiograp raph h is typ typica ically lly nor normal. mal. Treatment at presentation is limited to supportive therapy for the patient’s clinical condition. Consultation is necessary even in children who experience only mild symptoms.

Summary

Although the myriad of congenital heart lesions and their surgical repairs can seem overwhelming, ED evaluation and care of children who experience

 

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these conditions requires the practitioner to understand a few principles. A so solid lid un unde ders rsta tand ndin ing g of th thee ph physi ysiol olog ogy y of cy cyan anosi osiss he help lpss the the clin clinic icia ian n dete de term rmin inee the the ap appr prop opri riat atee di diag agno nosti sticc stud studie iess an and d inte interp rpre rett the the re resu sult lts. s. Remember Reme mbering ing common common patterns patterns of postsurgic postsurgical al comp complicat lications ions allow allowss the physic phy sician ian to ini initia tiate te tre treatm atment ent in the chi child ld who has sur surgic gically ally cor correc rected ted congenital heart disease, even if the family cannot relate the surgical history to the physician. Finally, reviewing the common pathologic cardiac causes of CHF and syncope should allow the physician to appropriately exclude a pathologic cause of syncope or palpitations in a child.

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