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Clinical Manifestations of Kawasaki Disease: Comparison
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Please note this is a comparison between Version 3 by Conner Chen and Version 2 by Conner Chen.

Kawasaki disease is a systemic idiopathic febrile vasculitis that often affects children under 5 years [1]. In Japan back in 1961, KD was initially reported and subsequently recognised based on the profiling of 50 patients with a similar phenotype by Dr Tomisaku Kawasaki in 1967 [2]. Kawasaki disease was then identified as the most common cause of acquired heart disease in paediatric populations as it would subsequently result in coronary artery aneurysms if left untreated [1,2].

  • Kawasaki disease
  • intravenous immunoglobulin
  • coronary artery aneurysm
  • vasculitis
  • acute febrile mucocutaneous lymph node syndrome

1. Diagnostic Clinical Features of KD

Kawasaki disease is diagnosed through a constellation of classic clinical features, which have remained in use and was hardly changed since its first description 50 years ago. Based on the current guideline by McCrindle et al., patients with a high-grade fever (more than 39 degrees Celsius) for at least 5 days; coupled with at least 4 out of 5 classic features are diagnosed with Complete KD (Typical KD), while those who do not fulfil the mentioned clinical criteria are categorised as incomplete KD (Atypical KD). The classical features of KD include: (i) erythema and cracking of lips, strawberry tongue, erythema of oral and pharyngeal mucosa; (ii) bilateral bulbar conjunctival injection without exudates; (iii) diffuse maculopapular rash eruptions; (iv) painful erythema and oedema of the hand and feet; (v) unilateral cervical lymphadenopathy. If more than 4 principal clinical criteria are present, especially through redness and swelling of the hands and feet, the diagnosis can be established earlier with only 4 days of fever [1]. This current list of classic criteria remains to be the gold standard of the diagnostic tool for KD.
The presence of fever, although it is originally described to be high grade with a temperature of more than 39 degrees Celcius lasting more than five days; in the real clinical setting, may not always be the case, especially in younger infants [2]. The KD rash is mainly described to be manifested as diffused maculopapular rash eruptions that occur within the onset of a febrile period in the published diagnostic criteria, although various other descriptions of cutaneous manifestations had been reported [1]. The typical KD rashes usually start to become visible on the trunk and start to spread outwards to the extremities as the illness progresses [3]. The other KD skin manifestations may include: (i) diffuse scarlatiniform erythroderma [1] (ii) erythema multiforme-like rashes [4][5] (iii) erythema and oedema of the hand and feet [1][3]. Erythema multiforme usually appears as targetoid lesions, predominantly affecting the torso and extremities [4][5]. During the acute onset of KD, the palms and the soles can appear erythematous, whereas the dorsum of the hand and feet will be oedematous and tender. This will be followed by desquamation which usually starts in the periungual areas 2 to 3 weeks during the subacute phase of KD and subsequently, the appearance of Beau lines during the resolution phase of KD [1][3]. Other KD dermatological features may include: (i) urticarial or fine micro pustular eruptions which mainly involve the trunk and extremities [1]; and (ii) palmoplantar psoriatic eruption with plaques and pustular lesion [1][6][7]. KD associated psoriasiform rashes had been observed to resolve earlier when compared to conventional psoriasis [7]. Interestingly, several studies have also demonstrated a higher risk of developing atopic dermatitis among patients with KD observed during their follow-up [8][9].
Being one of the classic features of KD, cervical lymphadenopathy usually appears unilaterally distributed within the anterior cervical triangle, measuring more than 1.5 cm in diameter [1]. It is very crucial to pay attention that some KD patients may have fever and lymphadenopathy as their sole features. However, there was an insignificant association between patients who presented with only fever as well as lymphadenopathy, with the prognosis of coronary artery aneurysm or IVIG resistance [10]. KD-related lymphadenopathy (LKD) can be distinguished from bacterial cervical lymphadenopathy (BCL) by imaging procedures such as ultrasound or contrast-enhanced computed tomography (CT) [1][11]. LKD usually affects multiple lymph nodes of various sizes, whereas abscesses, phlegmon or a solitary lymph node with a hypoechoic core are more commonly present in BCL [1][12]. The absence of abscesses on CT, at a younger age, and a raised C-reactive protein (CRP) are helpful to differentiate (LKD) from BCL [11]. LKD was found to be affecting more older children and usually presented with more severe inflammatory reactions than KD patients without lymphadenopathy [13], with a higher possibility of developing the life-threatening Kawasaki Shock Syndrome (KDSS) [14].
There was a significant number of reported KD cases presented with severe oral manifestations. These include changes on the lips and in the oral cavity which may be presented as erythema, dryness, fissuring, peeling, vertical cracking, and bleeding of the lips; a strawberry tongue with erythema and prominent fungiform papillae; and diffuse erythema of the oropharyngeal mucosa. This can be seen when the patient’s lips were grossly swollen, and eroded with haemorrhages, leading to marked difficulty to open the mouth [11][15]. In another case, the patient was presented with red and cracked lips, coupled with diffused pharyngeal hyperemia without any exudate resulting in microstomia, which required reconstructive lip surgery with bilateral commissuroplasty [15].
Bilateral nonexudative conjunctivitis is one of the features with a lesser variation in its association with KD, although some reports had documented other ocular manifestations. Bilateral nonexudative conjunctivitis and anterior uveitis are the most common eye manifestations in KD while the involvement of the posterior segment is rare [16]. The manifestation of anterior uveitis in KD is mild and bilateral, sometimes associated with precipitate keratitis [17]. According to a study conducted by Choi et. al, anterior uveitis is a significant ocular sign to help with the diagnosis of Incomplete KD, as the study observed that out of 110 patients with KD, 32 patients presented with anterior uveitis, giving an incidence rate of 29% [18]. It is also noted that the manifestation of anterior uveitis among KD patients is associated with older age groups and the presence of neutrophilia [18]. Other ocular signs that had been associated in patients with KD may include punctuated keratitis, retrodescemetic precipitates, vitritis, bilateral optic disc swelling with papillitis, bilateral iridocyclitis and subconjunctival haemorrhage [18][19][20].

2. Other Clinical Manifestations of KD

Interestingly, Kawasaki may also manifest with some additional clinical manifestations, or in some cases with atypical presentation. These manifestations are helpful to provide an additional certainty in the establishment of the diagnosis of KD. These clinical manifestations involve the cardiovascular [1], gastrointestinal [1][21][22], neurological [1][21][23], genitourinary [1][24], musculoskeletal [21][25], and respiratory systems [1][26][27], which are described below.

2.1. Cardiac Manifestation of KD

Cardiovascular manifestations are specifically associated with KD and are widely reported all over the world (Table 1). They are recognised as the foremost reason for long-term morbidity and mortality. The cardiovascular abnormalities of KD may include coronary artery abnormalities, aneurysm of medium-sized non-coronary arteries, aortic root enlargement, pericarditis, myocarditis, endocarditis and valvular regurgitation [1]. Non-coronary cardiac features such as mitral regurgitation and aortic root dilation developed in 27% and 8% of the KD patients, respectively [28]. The acute stage of KD manifests pericarditis and myocarditis, while coronary artery aneurysm can only be seen in the second week of the illness [29]. Coronary artery abnormalities in KD include dilation only or aneurysm of various sizes, numbers, and characteristics. Thus, 2-dimensional (2D) echocardiography should be performed in patients suspected of KD. The prevalence of coronary artery lesions detected during the initial echocardiography was 3.6% in Japan [30], with a majority of the affected patients were having coronary artery dilation [30][31][32][33][34][35][36]. The major risk factors of coronary artery lesions may include the incomplete KD diagnosis, IVIG unresponsiveness, and a longer duration of fever [36]. Apart from these, coronary artery lesions were apparentamongst patients who had delayed hospital visits (≥7 days from onset of symptoms) [32]. In Malaysia, about 10% of the patients have developed coronary artery aneurysms and the non-IVIG treated patients (19%) have formed a larger proportion than those who were given IVIG (9%) [21]. This is supported by another study which indicated that around 15% to 25% of the children who were not treated adequately for KD eventually had coronary artery aneurysm or ectasia [37]. The majority of the patients who were diagnosed with coronary artery aneurysms are younger than 5 years old [32][38].
Table 1. Summary findings of cardiac manifestation from different studies *.
Authors Saundankar et al. (2014) [39] Sanchez-Manubens et al. (2014) [29] Ae et al. (2021) [30] Pinto et al. (2017) [32] G. B. Kim et al. (2017) [33] Xie et al. (2020) [34] Son et al. (2020) [35]
Country (n sample) Australia

n = 281		 Spain

n = 398		 Japan

n = 3714		 Italy

n = 470		 South Korea

n = 12,269		 China

n = 4442		 Vietnam

n = 167
Coronary artery dilation/ecstasia #, n (%) 47 (16.7) N/A 3343 (90) N/A 1328 (10.8) 231 (5.2) N/A
Coronary artery aneurysm/small aneurysm #, n (%) 14 (5.0) 53 (13.3) 316 (9) 40 (8.5) 207 (1.7) N/A 49 (29.2)
Medium aneurysm, n (%) N/A N/A N/A N/A N/A 118 (2.7) 60 (9.6)
Large/giant aneurysm, n (%) 5 (1.8) N/A 49 (1) N/A 19 (0.16) 31 (0.7) N/A
Myocarditis, n (%) N/A 4 (1) N/A N/A N/A N/A N/A
Pericarditis, n (%) N/A 9 (2.3) N/A 18 (3.8) N/A N/A N/A
Valvular lesion, n (%) N/A 28 (7) N/A 2 (0.4) N/A 653 (14.7) 2 (1.2)
N/A: Not Available. * Cardiovascular findings include those diagnosed during hospitalisation and follow up. # Coronary artery aneurysm and dilatation were determined in accordance with the Japanese Ministry of Health (JCS Joint Working Group, 2014; Research Committee on Kawasaki Disease, 1984).

2.2. Gastrointestinal System

It is undeniable that some patients with atypical KD are frequently presented with gastrointestinal symptoms which may include abdominal pain and distention, diarrhoea, vomiting, jaundice, gallbladder hydrops, pancreatitis, pseudo-obstruction, paralytic ileus and haematemesis [40][41][42]. Diarrhoea, vomiting, abdominal pain, hepatitis, and gallbladder hydrops are the most frequent gastrointestinal symptoms of KD while pancreatitis and jaundice are less prevalent [1]. 4.6% of the patients with KD that came in with the signs and symptoms of acute abdomen, high fever, and jaundice, mostly suggested the presence of gallbladder hydrops [29]. In Iran, the incidence rate of gastrointestinal presentation in KD patients was 38%, with gallbladder hydrops seen in 1% of those patients [22]. It was far higher when compared to a retrospective study done in Malaysia, where only 6% of KD patients have presented with gastrointestinal symptoms [21]. Kawasaki disease patients with abdominal symptoms have a higher risk of being resistant to IVIG as well as developing coronary aneurysms [42]. Apart from that, the likelihood of patients who are less than one year old to have gastrointestinal symptoms and subsequently coronary artery aneurysm is higher [43]. In terms of pseudo-obstruction, the incidence is unusual to occur [44]. Haematemesis as a clinical presentation of KD is rare and caused by hemorrhagic duodenitis. However, haematemesis can also be seen in other vasculitides, thus diagnosis of KD is often delayed [42].

2.3. Genitourinary System

KD is a systemic vasculitis disease. As such, it may involve the kidneys and the urinary tract. The clinical manifestations involving the genitourinary system may include pyuria, prerenal acute kidney injury (AKI), renal AKI caused by tubulointerstitial nephritis (TIN), renal AKI associated with either KD shock syndrome, hemolytic uremic syndrome (HUS), immune-complex mediated nephropathy [45]. Renal abnormalities from ultrasound imaging study TIN will either show normal kidney size or increase in size of kidney as well as hyperechogenicity due to infiltration of the inflammatory cells, as it is the common renal disease in KD [45][46]. Pyuria, being one of the commonest genitourinary manifestations, was reported in 30–80% of the KD patients with those below one-year-old being more likely to be affected [25]. TIN is typically the cause of acute kidney injury among patients with KD, which is the main pathogenesis due to abnormal T-cell activation, causing dysregulated immune responses in the renal tubules [47]. Urethritis is a common finding in KD, whereas hydrocoele and phimosis rarely occur [1]. In terms of renal abnormalities observed through imaging study, renal sonographic findings of increased cortical echogenicity, enlarged kidneys, and enhanced corticomedullary differentiation are common associations with KD, and are mostly due to vasculitis involving the kidney that causes cellular infiltration leading to ischemia and oedema [37].

2.4. Musculoskeletal System

KD also affected the musculoskeletal system with arthralgia and arthritis as the most prevalent conditions reported with KD [1]. Around 3% of patients in Southern Malaysia had musculoskeletal manifestations whereas 11% of patients with KD in China had arthritis [25][48]. Older children seem to be more likely to have arthritis when compared to those who are younger [25][43]. This is most probably due to a better understanding and communication skills among the older patients, who complain about their pain better than the younger patients [26]. Patients with arthritis have been associated with amplified risk of progressing toward a coronary artery aneurysm [25]. Several studies have found a small proportion (0.2–0.5%) of KD patients who subsequently developed systemic-onset juvenile idiopathic arthritis (sJIA) [49][50]. Interestingly, Kanemasa et al. has reported that KD-related arthritis involved both interval-type (KD-reactive) and continued-type (true sJIA) requiring biologics, may have a similar immunopathology with sJIA as there were overlapping clinical features between KD and sJIA [51]. There were cases where the KD patients have presented with myositis with a normal or mild elevation of the muscle enzymes, which causes proximal muscle weakness that requires the use of glucocorticoid as a treatment [52][53][54].

2.5. Respiratory System

The presence of cough, sputum production and rhinorrhoea are considered common symptoms in patients diagnosed with KD [26]. In a prospective study conducted in Taiwan, 69% of the KD patients had cough while 58% of these patients have subsequently developed rhinorrhoea [27]. In Korea, respiratory symptoms were also observed among KD patients as cough, rhinorrhoea and sputum production accounted for 46%, 31% and 15%, respectively [26]. The chest radiographs of patients with KD may reveal peribronchial and interstitial infiltrates, while nodular infiltrates were only seen in rare cases [1]. These findings resonate with He et al. [55] who found that peripheral consolidation was the predominant feature in the chest radiographs of KD patients. Umezawa et al. also mentioned that 129 acute KD patients manifested some abnormalities in the chest X-ray, with the most common finding being the reticulogranular pattern (89.5%), followed by peribronchial cuffing (21.1%), pleural effusion (15.8%), atelectasis (10.5%), and air trapping (5.3%) [56]. According to Lee et al., 51.8% of patients with KD from their cohort has concurrent Mycoplasma pneumoniae infection, evidenced by high titre of anti-M.pneumoniae antibody [57].These patients additionally presented with chest X-ray abnormalities, which include findings such as focal reticulonodular lesions, atelectasis and hilar lymphadenopathy [57]. Patients with pulmonary manifestations have a heightened risk of getting coronary artery abnormalities. This was possibly due to the delayed diagnosis of KD as the initial treatments were focusing on the misdiagnosis of pulmonary causes [58]. There are also other pulmonary manifestations observed in KD, including bronchopneumonia [59], hydropneumothorax [60] and pleural effusion [61]. In this regard, patients with pulmonary manifestations are often delayed in the diagnosis of KD as it is uncommon and atypical, thus physicians who encounter patients with difficult-to-treat bronchopneumonia should think of Kawasaki disease.

2.6. Neurological System

The neurological symptoms of KD include aseptic meningitis and severe irritability beyond that seen in other febrile diseases. Temporary unilateral peripheral facial nerve palsy (FNP) and sensorineural hearing loss (SNHL) had been observed in KD patients [1]. SNHL was reported as early as 1988 by Suzuki et al. from Japan, and 33–36% of children with KD were noted to present with some degree of SNHL after the disease onset [24][62]. In comparison, only approximately 2.8–5% of the KD patients were reported to develop neurological symptoms, including SNHL in Malaysia and Iran, probably due to the lack of awareness and screening of the neurological manifestations [21][63]. Given the increasingly reported incidences of SNHL, some studies have strongly urged the inclusion of audiology screening for patients with KD as SNHL can contribute to delayed development in cognitive and speech domains, if it is not diagnosed and remains untreated [62]. Unusual manifestations, such as ataxia and facial nerve palsy, had also been reported in KD patients [64][65][66]. Most of the patients who developed facial nerve palsy were below 20 months in age and IVIG treatments have shown to assist in its resolution [65]. Though rare, clinicians should be well-informed of FNP as an association with KD, as it was noted to be remarkably interrelated with an elevated risk of coronary artery lesions [65][66]. All the clinical features of KD are summarized in Figure 1.
Figure 1. A summary of the clinical features of KD.

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