Gastrointestinal complications in Kawasaki disease are described in the literature as case reports similar to those observed in Henoch-Schönlein purpura, such as: intestinal obstruction,[1] colon swelling,[2] intestinal ischemia,[3] intestinal pseudo-obstruction,[4] and acute abdomen.[5]
Ophthalmologic changes associated with KD have been described since the 1980's, being found as uveitis, iridocyclitis, conjunctival hemorrhage,[6][7][8] optic neuritis,[9] amaurosis and ocular artery obstruction.[10]
Kawasaki disease can also be found as necrotizing vasculitis, progressing into peripheral gangrene.[11]
The neurological complications per central nervous system (CNS) lesion are increasingly reported.[12] The neurological complications found are meningoencephalitis,[13] subdural effusion,[14][15] cerebral hypoperfusion,[16] cerebral ischemia and infarct,[17] cerebelar infarction,[18] manifesting with seizures, chorea, hemiplegia, mental confusion, lethargy and coma,[9] or even a cerebral infarction with no neurological manifestations.[17]
Other neurological complications from cranial nerve involvement are reported as ataxia,[9] facial palsy,[19] and sensorineural auditory loss.[20]
The first description for hearing loss in KD was made by Suzuki et al.35 in Japan in 1988. In 1992, Sundel et al.36 assessed 40 patients by standard audiometry and BERA (Brainstem Evoked Response Audiometry) in patients who could not undergo an audiometry. Seven patients (17.5%) had a sensorineural auditory loss and 14 patients had an inconclusive result. In 2001, Knott et al.37 reported another study where they performed an audiological assessment in 62 patients over the first thirty days of KD; from these, 13 had a sensorineural auditory loss and two patients kept the sensorineural auditory deficit in a second audiological assessment 10 days later.
Behavioral changes, such as attention deficits, learning deficits, emotional disorders (emotional lability, fear of night and night terrors) and internalization problems (anxious, depressive or aggressive behavior).[21][22]
Valvular insufficiencies, particularly of mitral or tricuspid valves, are often observed in the acute phase of Kawasaki disease due to valvulitis or myocarditis-induced myocardial dysfunction, regardless of coronary involvement.[23] These lesions mostly disappear with the resolution of acute illness,[24] but a very small group of the lesions persist and progress.[25] There is also late-onset aortic or mitral insufficiency caused by thickening or deformation of fibrosed valves, with the timing ranging from several months to years after the onset of Kawasaki disease.[26] Some of these lesions require valve replacement.[27]
Another issue that raises concerns is vascular abnormalities other than those involving coronary arteries. Several reports indicated abnormal changes in systemic vascular physiology in Kawasaki disease patients with persistent or regressed coronary lesions, including increased wall thickness and decreased distensibility of carotid arteries131,132 and increased stiffness of central and peripheral arteries with enhanced wave reflections.132–134 Patients with Kawasaki disease free of coronary involvement have been reported to have abnormal endothelium-dependent brachial artery reactivity135 and stiff conduit arteries, as demonstrated by high pulse-wave velocity,133,136 although this finding remains controversial.137 In addition, children with Kawasaki disease, with or without coronary artery complications, may have a more adverse cardiovascular risk profile, such as high blood pressure, obesity, and abnormal serum lipid profile.132,133,138 Whether these abnormalities predict clinically relevant morbidities awaits future investigation.
Cardiac complications
editKD is the main cause of heart disease acquired in childhood in the USA and in Japan.[29] Coronary artery aneurysms occur as a sequela of the vasculitis in 20-25% of untreated children.[30] it is first detected at a mean of 10 days of illness and that the peak frequency of coronary dilatation or aneurysms occurs within 4 weeks of onset.[31] aneurysms are classified into small (internal diameter of vessel wall <5mm), medium (diameter ranging from 5-8mm), and giant (diameter > 8mm).[29] Saccular and fusiform aneurysms usually develop between 18 and 25 days after the onset of illness.[32] Even when treated with high-dose IVIG regimens within the first ten days of illness, 5% of children with Kawasaki disease develop at the least transient coronary artery dilation and 1% develop giant aneurysms.[33][34][35] Death can occur due either to myocardial infarction secondary to thrombosis of a coronary artery aneurysm or to rupture of a large coronary artery aneurysm. Death is most common 2 to 12 weeks after the onset of illness.[32]
Many risk factors predicting coronary artery aneurysms have been identified.[36] include persistent fever after IVIG therapy,[37][38] low hemoglobin concentrations, low albumin concentrations, high white-blood-cell count, high band count, high CRP concentrations, male sex, and age less than one year.[39] Thus, laboratory evidence of increased inflammation combined with demographic features (male sex, age less than six months or greater than eight years) and incomplete response to IVIG therapy create a profile of a high-risk patient with Kawasaki disease.[40][39]
Coronary artery lesions resulting from Kawasaki disease change dynamically with time.[41] Coronary artery lesions resulting from Kawasaki disease change dynamically with time. Resolution one to two years after the onset of the disease has been observed in half of vessels with coronary aneurysms.[23][42] The likelihood that an aneurysm will resolve appears to be determined in large measure by the initial size of the aneurysm, in which the smaller aneurysms have a greater likelihood of regression.[43][44] Other factors that are positively associated with the regression of aneurysms include being younger than a year old at the onset of Kawasaki disease, fusiform rather than saccular aneurysm morphology, and an aneurysm location in a distal coronary segment.[42]
Stenosis, which occurs as a result of the healing process of the vessel wall, often leads to significant coronary obstruction and myocardial ischemia.[23] and eventually can lead to Myocardial infarction.[23] The highest rate of progression to stenosis occurs among those who develop large aneurysms.[41] The worst prognosis occurs in children with giant aneurysms.[45] This severe outcome may require further treatment such as percutaneous transluminal angioplasty,[46] coronary artery stenting,[47] bypass grafting,[48] and even cardiac transplantation.[49]
Myocardial infarction caused by thrombotic occlusion in an aneurysmal, stenotic, or both aneurysmal and stenotic coronary artery is the principal cause of death from Kawasaki disease.[50] The highest risk of myocardial infarction occurs in the first year after the onset of the disease.[50]
Myocardial infarction in children presents with different symptoms from that in adults. The main symptoms were shock, unrest, vomiting, and abdominal pain; chest pain was most common in older children.[50] most of these children, had the attack occurring during sleep or at rest, and around one third of attacks were asymptomatic.[32]
Lipid profiles following KS have yielded conflicting results. Although these profiles are clearly abnormal during acute KS, they may be altered during many acute infectious and inflammatory processes as part of the acute-phase response. Further study is required to determine whether any consistent lipid abnormalities are present in the long term in individuals following KS (60, 81).
However, it is useful for the clinician to be aware of some of the features that suggest a poorer prognosis: duration of fever for more than 16 days, recurrence of fever following an afebrile period of at least 48 h, arrhythmias other than first-degree heart block, male gender, age younger than 1 year, cardiomegaly, and low platelet count, hematocrit, and albumin level in serum at presentation (6, 58a, 83, 87).[32]
2
editThe key non-invasive high sensitivity and specificity test to detect abnormalities of proximal segments of coronary arteries is echocardiography (level of evidence C). Echocardiogram is essential in the assessment of children with fever and other KD findings. The exam may show perivascular enhancement, ectasia or narrowing of coronary arteries that represent coronary arteritis before the formation of aneurysm, which is rarely seen before the disease has been in place for at least 10 days. Reduction of myocardial contractility of left ventricle, regurgitation of mitral valve and pericardial effusion are frequent echocardiographic findings in patients with KD in acute phase.
To cases without cardiac impairment, echocardiogram should be performed at the moment of diagnosis, on week 2 and on week 6-8 after onset of manifestations.
It is important to recognize the limitations of echocardiogram in visualizing thrombosis and stenosis of coronary distal segments 2,42. There are other diagnostic options such as magnetic resonance imaging (MRI), angioresonance, high resolution computed tomography, and angiography that are used according to their availability, advantages, severity and indications in each case. Both MRI and angioresonance are capable of detecting aneurysms in the distal branches of the coronary, and the latter can be useful in early stages of the disease even in children < 6 months 49. Recently, high resolution computed tomography has been recommended rather than transthoracic echocardiogram or MRI. It has the advantage of detecting calcifications on the arterial wall, quick acquisition of images and it simplifies the interpretation of the images, whereas MRI requires prolonged anesthetic time in children for collection of images 2,50,51. The objective of the exams is to primordially detect the heart affections to detect risk stratification for appropriate therapeutic management 51.
Angiography is the gold standard to assess heart impairment, but it is an invasive test and has obvious risks, requiring specific indications of use. In patients with medium and spindle shaped aneurysms visualized by echocardiography and showing tendency to regression, there is no indication of this exam. The indications to angiography depend on the abnormalities seen in non-invasive tests such as signs of myocardial ischemia in stress echocardiogram, failure in visualizing the distal branches of coronary arteries, multiple aneurysms, giant aneurysm, coronary stenosis and follow up after myocardial revascularization (level C of evidence) 6. The ideal time for performing the test varies depending on the hospital Center; however, it is normally recommended after 6-12 weeks of the disease and after resolution of the acute inflammatory process (level of evidence C).
A review estimated the incidence of myocardial acute infarction in pregnant women in 1: 10.000.52 There are few studies about pregnancy and delivery in pregnant women with coronary disease caused by KD. A study of 13 pregnant women with KD in childhood and coronary lesion showed that none of the patients presented coronary thrombosis by using low doses of aspirin, which is considered safe for pregnancy and delivery. Nine pregnant women had vaginal delivery, with epidural anesthesia and no cardiac complications. Analgesia is indicated in the delivery of women with heart disease because it maintains the hemodynamic function and reduces the cardiac activity during labor. In symptomatic cases, a C-section may be considered 53.[29]
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