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Kawasaki disease: Complications

Kawasaki disease: Complications
Literature review current through: Jan 2024.
This topic last updated: Aug 11, 2023.

INTRODUCTION — Kawasaki disease (KD, also called mucocutaneous lymph node syndrome) is one of the most common vasculitides of childhood [1]. KD also occurs rarely in adults. It is typically a self-limited condition, with fever and manifestations of acute inflammation lasting for an average of 12 days without therapy [2]. However, complications such as coronary artery aneurysms, depressed myocardial contractility and heart failure, myocardial infarction, arrhythmias, and peripheral arterial occlusion may develop and lead to significant morbidity and mortality (table 1). Noncardiac complications may also affect children with KD.

The complications of KD are discussed in this topic review, with long-term cardiovascular sequelae of KD reviewed in greater detail separately. The epidemiology, etiology, clinical manifestations, diagnosis, and treatment of KD, refractory KD, and incomplete (atypical) KD are also presented separately. (See "Cardiovascular sequelae of Kawasaki disease: Clinical features and evaluation" and "Kawasaki disease: Epidemiology and etiology" and "Kawasaki disease: Clinical features and diagnosis" and "Kawasaki disease: Initial treatment and prognosis" and "Refractory Kawasaki disease" and "Incomplete (atypical) Kawasaki disease".)

SHOCK — KD shock syndrome (KDSS), defined as sustained systolic hypotension (decrease in blood pressure greater than 20 percent from baseline) or clinical signs of poor perfusion, is a potentially life-threatening complication of KD [3,4]. It may be accompanied by multiple organ dysfunction syndrome (MODS), with MODS seen in 8 of 11 patients with KD and shock in one series [5].

It is important to distinguish patients with KDSS from those with other causes of severe hypoperfusion since aggressive use of intravenous immune globulin (IVIG), which is essential for the successful control of KDSS, is not typically used in other types of shock. Features that may help distinguish KDSS from other types of shock (see "Initial evaluation of shock in children") include the following:

Thrombocytosis – Thrombocytosis is a characteristic finding in KDSS, whereas thrombocytopenia is more common in other types of shock (eg, toxic shock syndrome [TSS] and septic shock). However, in one study of 13 children with KDSS, 7 (54 percent) had thrombocytopenia with a mean platelet nadir of 54.3 cells/microL, potentially complicating the distinction between KDSS and other types of shock [3].

Younger age – Patients with KDSS are typically younger than those with TSS (mean age approximately three years versus nine years, respectively) [6].

Echocardiographic abnormalities – Coronary artery abnormalities (CAAs), when present, are highly suggestive of KD. Additional echocardiographic abnormalities including valvulitis, mitral regurgitation, and impaired left ventricular systolic function are more prevalent in KDSS than in KD patients who are hemodynamically stable.

In one case series from a single institution, 13 of 187 consecutive patients with KD (7 percent) presented with KDSS between 2003 and 2007 [3]. All patients with KDSS received fluid resuscitation, and seven also received inotropic agents. Patients with shock syndrome were more likely than KD patients who were hemodynamically stable to have consumptive coagulopathy and cardiac abnormalities. In addition, patients who presented with shock had higher C-reactive protein (CRP) levels than those with uncomplicated KD. Most importantly, children with KDSS were also less responsive to initial IVIG therapy and more commonly required additional treatment for their KD.

CARDIAC COMPLICATIONS — The major complication of KD is coronary artery abnormalities (CAAs), which can include dilation, aneurysm, and/or stenosis (table 2). Patients also can develop depressed ventricular function in the acute phase, valvular regurgitation, and pericardial effusions. Late cardiovascular complications include progressive coronary artery stenosis or occlusion, myocardial infarction, and arrhythmias. These late complications are generally limited to patients who had CAAs in the acute phase. Acute myocardial infarction (AMI) is the main cause of death in KD. The risk of AMI is highest in children with giant CAA aneurysms. (See "Cardiovascular sequelae of Kawasaki disease: Clinical features and evaluation".)

Coronary artery abnormalities — CAAs are the most serious complication of KD (movie 1 and movie 2 and movie 3). The frequency of CAAs in KD and the associated mortality have decreased dramatically as a result of intravenous immune globulin (IVIG) therapy [7]. Patients treated with IVIG within the first 10 days of illness have an approximately 75 percent decrease in the risk of developing coronary artery aneurysms and a more than 95 percent decrease in mortality. While CAAs occur in approximately one-quarter of KD patients in the IVIG era, most of these patients have small, reversible coronary artery dilatation, not true aneurysms. (See "Kawasaki disease: Initial treatment and prognosis", section on 'Intravenous immune globulin'.)

CAAs are classified based upon Z-score (the number of standard deviations below or above the population mean coronary diameter adjusted for sex and body surface area) (table 2). CAAs typically increase over the first four to six weeks after illness onset, and approximately one-half regress to normal lumen diameter over the subsequent two years. The likelihood that an aneurysm will regress to normal lumen diameter (Z-score <2) is most strongly related to its maximum diameter. Giant aneurysms (defined as Z-score >10, typically ≥8 mm internal diameter in children under five years of age) are least likely to regress. They are associated with the highest risk of morbidity and mortality. Up to 50 percent of such aneurysms become obstructed, leading to myocardial infarction, arrhythmias, or sudden death. A far larger percentage of children KD have subtle and often transient coronary artery changes. The acute evaluation, treatment, natural history, and long-term monitoring of coronary artery aneurysms are discussed in detail separately. (See "Cardiovascular sequelae of Kawasaki disease: Clinical features and evaluation".)

Factors associated with increased risk of CAAs that are most consistently reported in the available studies include the following [8-10]:

Late diagnosis and delayed treatment with IVIG

Age younger than one year or older than nine years

Male sex

Fever ≥14 days

Serum sodium concentration <135 mEq/L

Hematocrit <35 percent

White blood cell count >12,000/mm3

Additional risk factors are discussed in greater detail separately. (See "Cardiovascular sequelae of Kawasaki disease: Clinical features and evaluation", section on 'Risk factors'.)

Ventricular dysfunction — Evidence of mild to moderate ventricular dysfunction is commonly seen on echocardiography during the acute phase of KD. Rarely, function is severely depressed. Depressed ventricular function during the acute phase may manifest as an S3 gallop that becomes more prominent with hydration. In rare cases, it may progress to heart failure. Depressed ventricular function may be caused by direct myocardial inflammation (ie, myocarditis) or from indirect negative inotropic effects of the systemic inflammatory response. Treatment with IVIG usually restores normal ventricular function rapidly [11]. On the other hand, lymphocytic infiltrates or fibrosis are sometimes noted on endomyocardial biopsy even years after the acute illness, especially in children who do not receive IVIG [12]. In addition, ischemic cardiomyopathy may occur in patients with coronary artery aneurysms after myocardial infarction. (See "Cardiovascular sequelae of Kawasaki disease: Clinical features and evaluation", section on 'Ventricular dysfunction'.)

MACROPHAGE ACTIVATION SYNDROME — Macrophage activation syndrome (MAS, also called secondary hemophagocytic lymphohistiocytosis [HLH]) is characterized by activation and proliferation of macrophages and T cells. This may lead to severe complications including disseminated intravascular coagulopathy, cytopenias, and thrombosis. MAS may complicate a variety of infections, rheumatologic conditions, and malignancies. It has been described rarely in children with KD who have persistent and sustained fever after intravenous immune globulin (IVIG) treatment [13-21]. A small number of children with secondary HLH have mutations of perforin or other genes that are more typically associated with congenital HLH [22]. The clinical features of HLH and the diagnosis and treatment of MAS are reviewed in greater detail separately. The primary medications chosen for treatment of MAS are guided by the underlying disease. Thus, IVIG and systemic glucocorticoids are the first choice medications for MAS in children with KD. (See "Systemic juvenile idiopathic arthritis: Course, prognosis, and complications", section on 'Macrophage activation syndrome' and "Clinical features and diagnosis of hemophagocytic lymphohistiocytosis", section on 'Clinical features' and "Treatment and prognosis of hemophagocytic lymphohistiocytosis".)

A retrospective review of 719 Chinese patients with KD found that slightly more than 1 percent had MAS [23]. Cases with MAS were characterized by hepatosplenomegaly, cytopenias, hypofibrinogenemia (<1.5 g/L), and hyperferritinemia, findings not usually seen in uncomplicated cases of KD. However, hemophagocytosis was evident in only three cases, and commonly used criteria for the diagnosis of HLH [24] correctly identified only one case of MAS complicating KD. The preliminary MAS diagnostic guidelines (Ravelli criteria) were more accurate in identifying patients with MAS in this setting [25]. Seven of eight patients with MAS were nonresponders to IVIG, two developed coronary artery ectasia, and one of the eight died. Thus, early recognition of MAS as a complication of KD is crucial, both in order to optimize treatment for KD and to administer potentially lifesaving therapy for the MAS.

NONCORONARY VASCULAR INVOLVEMENT

Types of arteries involved — KD has a definite but unexplained predilection for coronary arteries, although virtually any vascular bed may be affected. Medium-sized muscular arteries (eg, axillary, iliac, brachial, and mesenteric) are the most commonly involved. While small arteries, veins, and visceral vessels are relatively spared [26], vascular changes may uncommonly occur in peripheral and visceral arteries.

Peripheral vascular involvement — Peripheral arterial obstruction can lead to ischemia and gangrene. This complication generally accompanies other manifestations of severe disease, such as giant coronary artery aneurysms and aneurysms in peripheral arteries [27].

Visceral vascular involvement — KD can affect the vasculature in numerous organ systems other than the heart, but clinically significant vasculitis is unusual. Among the rare extra-cardiac presentations of KD are cases involving the gastrointestinal tract, kidneys, and central nervous system. Other diagnoses, especially systemic vasculitides such as Takayasu arteritis and polyarteritis nodosa, should be considered when the presenting features are atypical. (See "Kawasaki disease: Clinical features and diagnosis", section on 'Differential diagnosis'.)

Urinary abnormalities and kidney disease — With the exception of sterile pyuria, urinary abnormalities and kidney disease are uncommonly associated with KD. Among the kidney complications noted in selected cases are acute interstitial nephritis, mild proteinuria, and acute kidney injury (AKI) [28-30]. AKI is a rare complication, and the underlying pathologic processes vary in different patients. Hemolytic uremic syndrome, immune complex-mediated glomerulonephritis, and acute interstitial nephritis, for example, have each been reported in a handful of cases [29,30]. As with all unusual manifestations of KD, other diagnoses must be seriously entertained when organs other than the heart are involved. (See "Acute kidney injury in children: Clinical features, etiology, evaluation, and diagnosis" and "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children" and "Intravenous immune globulin: Adverse effects", section on 'Complications affecting the kidney'.)

Gastrointestinal abnormalities — Children with KD may present with a wide variety of gastrointestinal manifestations. Hydrops of the gallbladder is a common finding during the acute phase of KD. It may persist in untreated cases but generally resolves rapidly after intravenous immune globulin (IVIG). A case series from Italy reported 10 children with gastrointestinal symptoms that were not immediately recognized as due to KD. There were five patients with gallbladder hydrops and cholestasis, three with paralytic ileus, one with appendicular vasculitis, and one with hemorrhagic duodenitis [31]. Other reports document KD presenting as gastrointestinal obstruction [32] or pseudoobstruction [33,34], intussusception [35], pancreatitis [36,37], and bile duct stenosis [37]. In such atypical cases, consideration must be given to alternative diagnoses, such as macrophage activation syndrome (MAS), polyarteritis nodosa, immunoglobulin A (IgA) vasculitis (Henoch-Schönlein purpura [HSP]), and infections. (See "Kawasaki disease: Clinical features and diagnosis", section on 'Differential diagnosis'.)

Musculoskeletal complications — The most common musculoskeletal complications in KD are arthralgia and arthritis, occurring in 4.6 to 17.6 percent of patients in historical cohorts and 20 percent in one retrospective case series of patients with refractory KD [38]. Arthritis can occur during the acute (early-onset) or subacute (late-onset) phase. Patients with early- versus late-onset arthritis tend to be older (4.9 versus 2.8 years, respectively). Additionally, polyarticular involvement of the upper extremities (elbows and fingers, especially the proximal interphalangeal joints) is predominant in early-onset arthritis, whereas involvement of large joints of the lower extremities (knees, ankles, and hips) is more common with a late-onset presentation. Patients with arthritis and KD may have somewhat higher acute phase reactants than those with KD alone, but the arthritis is not associated with more severe KD or more coronary artery abnormalities (CAAs). The arthritis typically is self-limited, rarely persisting for longer than two weeks. However, most patients with persistent arthritis require treatment, usually with nonsteroidal antiinflammatory drugs (NSAIDs) and, in some cases, a short course of glucocorticoids.

Uncommonly, patients with KD can present with a juvenile dermatomyositis-like picture (myositis with normal or mildly elevated muscle enzymes and proximal muscle weakness that requires treatment with glucocorticoids [39]) or clinical features consistent with systemic juvenile idiopathic arthritis (sJIA) [40].

Central nervous system — In general, direct vasculitic effects on the brain in KD are unusual, and autopsy studies before the introduction of IVIG treatment showed minimal central nervous system involvement [26]. Irritability is a feature of the acute illness and is thought to be related to the cerebral spinal fluid pleocytosis seen in up to 40 percent of children with KD. Data regarding potential long-term behavioral problems are variable.

A retrospective study of 65 patients reported an increase in long-term behavioral problems in children following KD when compared with hospital- and sibling-matched controls [41]. In contrast, an earlier study showed no effects on the incidence of attention, behavior, or learning problems in 110 children with KD compared with a general population sample. Parents of children who had KD did express more concern about potential cardiac problems, even when their children had completely normal cardiac evaluations. Similarly, some parents reported a higher proportion of anxiety issues in their children [42].

Sensorineural hearing loss — Sensorineural hearing loss can occur during the acute illness, but it rarely persists. Thus, hearing tests are only performed when there is a clinical suspicion of hearing loss.

A series of 40 patients seen between 2005 and 2007 was evaluated for hearing loss within the first 30 days of disease and six months later [43]. Initial evaluation included acoustic immittance measurement and brainstem-evoked response audiometry. Those found to have hearing disability also underwent otoacoustic emissions analysis. Hearing loss was identified in 55 percent of patients within the first 30 days, and 30 percent still had hearing loss six months later. Most subjects developed conductive hearing loss; persistent sensorineural hearing loss was associated with delayed use of IVIG and prolonged thrombocytosis, anemia, and an elevated erythrocyte sedimentation rate (ESR). An earlier study in which inflammation due to KD was successfully controlled with IVIG demonstrated a similar early incidence of auditory abnormalities, but these resolved over several months in the vast majority of cases [44].

Ocular complications — The primary ocular feature of KD is bulbar conjunctivitis. Ocular complications of KD include anterior uveitis as well as iridocyclitis, vitreous opacities, papilledema, and subconjunctival hemorrhage [45,46]. These ocular complications are usually successfully managed with local or systemic treatment of inflammation. Vision loss or other serious complications are rare. Management of uveitis is discussed in greater detail separately. (See "Kawasaki disease: Clinical features and diagnosis", section on 'Conjunctivitis' and "Uveitis: Etiology, clinical manifestations, and diagnosis" and "Uveitis: Treatment".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Kawasaki disease".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Kawasaki disease (The Basics)")

SUMMARY

Overview – The primary complications of Kawasaki disease (KD) are cardiac sequelae, although noncardiac complications also may occur (table 1). Most children with KD have thrombocytosis, while low platelet counts are more common in infectious conditions. When KD and thrombocytopenia do occur simultaneously, careful evaluation for dangerous complications such as KD shock syndrome (KDSS) or macrophage activation syndrome (MAS) is necessary. (See 'Introduction' above.)

Shock – KDSS, defined as sustained systolic hypotension or clinical signs of poor perfusion, is a potentially life-threatening complication. (See 'Shock' above.)

Macrophage activation syndrome – MAS is a rare and potentially life-threatening complication of KD that should be considered in patients with persistent fever after intravenous immune globulin (IVIG) therapy. (See 'Macrophage activation syndrome' above and "Clinical features and diagnosis of hemophagocytic lymphohistiocytosis", section on 'Rheumatologic disorders/MAS'.)

Cardiac sequelae – The major complication of KD is coronary artery abnormalities (CAAs; including dilatation, aneurysm, and/or stenosis). However, other cardiac sequelae can occur, including depressed ventricular function, valvular regurgitation (primarily mitral valve involvement), and pericardial effusion. Acute myocardial infarction (AMI) is the main cause of death in KD. (See 'Cardiac complications' above and "Cardiovascular sequelae of Kawasaki disease: Clinical features and evaluation".)

Noncoronary vascular involvement – Virtually any vascular bed may be affected by KD, and vascular changes may occur in peripheral and visceral arteries. (See 'Noncoronary vascular involvement' above.)

Peripheral arterial obstruction can lead to ischemia and gangrene. (See 'Peripheral vascular involvement' above.)

Urinary abnormalities and kidney disease, with the exception of sterile pyuria, are uncommonly associated with KD. (See 'Urinary abnormalities and kidney disease' above.)

Children with KD may present with a wide variety of gastrointestinal manifestations, rarely including acute abdominal catastrophes. (See 'Gastrointestinal abnormalities' above.)

Direct vasculitic effects on the brain in KD are unusual. (See 'Central nervous system' above.)

Sensorineural hearing loss, usually transient and asymptomatic, may develop following KD. (See 'Central nervous system' above.)

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Topic 15688 Version 23.0

References

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