Journal of Vascular Medicine & Surgery

Kawasaki Disease with Intestinal Ischemia/Mucous Membrane Necrosis in a 16 Months Old Boy: A Case Report and literature Review

Xiao-Zhe Cui and Hong Wang^* Department of Pediatric, Shengjing Hospital of China Medical University, Shenyang, China
^*Correspondence: Hong Wang, Department of Pediatric, Shengjing Hospital of China Medical University, Shenyang, China, Email:

Received: 01-Sep-2022, Manuscript No. JVMS-22-17914; Editor assigned: 05-Sep-2022, Pre QC No. JVMS-22-17914 (PQ); Reviewed: 19-Sep-2022, QC No. JVMS-22-17914; Revised: 26-Sep-2022, Manuscript No. JVMS-22-17914 (R); Published: 06-Oct-2022, DOI: 10.35248/2329-6925.22.S10.476

Abbreviations

KD: Kawasaki Disease; IVIG: Intravenous Immunoglobulin; ASA: Acetyl Salicylic Acid; CRP: C-Reactive Protein; ESR: Erythrocyte Sedimentation Rate; PCT: Procaicitonin; ALT: Alanine Aminotransferase; AST: Aspartate Aminotransferase; TBIL: Total Bilirubin; D-BIL: Direct Bilirubin; CSF: Cerebrospinal Fluid; DR: Digital Radiography; CT: Computed Tomography; HIV: Human Immunodeficiency Virus; EBV: Epstein-Barr Virus; HSV: Herpes Simplex Virus; MP: Mycoplasma Pneumonia; CP: Chlamydia Pneumonia; HAV, HBV, HCV, and HEV: Hepatitis A, B, C, and E Virus.

Introduction

Kawasaki Disease (KD) is a common vasculitis in children, characterized by inflammation in medium-sized arteries, with involvement of almost all systems. It is the most common cause of acquired heart disease in the developed countries [1]. The prevalence of KD in China is gradually increased. KD mainly affects children younger than 5 years old, most in boys, without any definite causes [2].

The prevalence of digestive system involvement in KD is 2.3% [3]. Clinical aspects are reported to include nausea, vomiting, diarrhea, hypoproteinemia, liver dysfunction, cholestasis, cholecystitis, pancreatitis, limited peritonitis, and intussusception and so on [4- 6]. However, KD with intestinal necrosis has been never reported. Here we report a case of 16 months old boy who was diagnosed with KD and developed intestinal mucous membrane necrosis. The patient recovered completely, neither with surgical intervention to remove affected segment of intestine nor with coronary artery damages.

Case Presentation

A 16-months-old previously healthy boy presented with fever for five days, along with rashes, congestive conjunctiva, red and cracked lips, left cervical lymphadenopathy, edema on hands and feet for one day. He had vomiting, progressed abdominal distension, along with poor mental state and irritability for 2 days. He had no family medical history and no history of allergies.

Physical examinations

His body temperature was 38℃ and his vital signs were stable. There were scarlet rashes on his trunk and legs. He had congestive conjunctiva without purulent discharges. His lips were red and cracked, and he had strawberry tongue. Ultrasound revealed a left lymphadenopathy about 1.8 cm × 0.7 cm. His abdomen was distended and his bowel movement sounds were weakened. He had edema on hands and feet. Neck rigidity was observed. Other systems were normal.

Laboratory results

A normal blood routine results (PLT 283 × 10⁹/L), elevated C-Reactive Protein (CRP) 85.2 (<8 mg/dl), Erythrocyte Sedimentation Rate (ESR) 94 (<15 mm/h), Procalcitonin (PCT) 3.26 (<0.05 ng/ml), Interleukin-6 (IL-6) 477.3 (<1.72 pg/ml). Hepatic function tests revealed elevation in Alanine Aminotransferase (ALT) 80 (0-40 U/L), Aspartate Aminotransferase (AST) 40 (5-34 U/L), Total Bilirubin (TBIL) 86.1 (3.4-20.5 umol/L), Direct Bilirubin (D-BIL) 74.3 umol/h (0-8.6 umol/L). Albumin was decreased to 29.8 g/L. Potassium was 2.7 mmol/l. D-dimer was 4810 (252 ug/L), and NT pro-BNP was 3524 (<300 pg/ml). Renal function test was normal. In the examination of Cerebrospinal Fluid (CSF), pressure was 90 drops/min, protein, glucose, chloride and the amount of cells were normal. Pathogen tests were negative. Abdominal Digital Radiography (DR) showed there was gas at left abdominal intestine (Figure 1). Abdominal Ultrasound revealed pneumatosis in the liver (Figure 2a), red arrow located around portal vein (Figure 2a), green arrow, partially dilated intestinal tube (Figure 2b), red arrow, enlarged gallbladder (Figure 2c), red arrow, and stasis bile in gallbladder (Figures 2a-2d). Pathogen tests were negative for Human Immunodeficiency Virus (HIV), Syphilis, Epstein-Barr Virus (EB virus), Herpes Simplex Virus (HSV), Mycoplasma Pneumonia (MP), Chlamydia Pneumonia (CP), Hepatitis A, B, C, and E Virus (HAV, HBV, HCV, and HEV).

Figure 1: Abdominal DR showed the intestine is flush with fluid and gas most at left abdomen on Day 5 of illness.

Figure 2: Abdomen ultrasound showed pneumatosis in liver. 2A: (red arrow), around portal vein (green arrow), dilated intestine (B), enlarged gallbladder (C), and stasis bile in gallbladder (D) on Day 5 of illness.

Treatments

He was treated with intravenous infusion of immunoglobulin (1 g/Kg) for 2 days, and second generation of cephalosporin. He was given oral aspirin at 30 mg/kg/day, divided into 3 times, and metronidazole and gentamicin suppositories as soon as KD was diagnosed after he was admitted. Meanwhile, potassium and albumin were infused. Meanwhile he was maintained on a liquid diet.

Disease progression

He continued to have fever on Day 7 of illness. His abdominal distension was worse, and bowel movement sounds diminished. Enhanced CT of the abdomen revealed hydronephrosis in the left kidney (Figure 3a), red arrow, dilated intestinal tube, pneumatosis, and hydrocele (Figure 3b), green arrow (Figures 3a and 3b). There was air accumulated in the small intestine wall (intestinal wall necrosis) at the middle and lower abdomen (Figure 3b), yellow arrow (Figure 3b). The rectal wall was slightly thickened and there was mild interstitial edema around portal vein. Echocardiography showed normal coronary arteries. Electrocardiogram result was normal.

Additional treatments and examinations

He was on water intake restriction, gastrointestinal decompression, and parenteral nutrition. He was given intravenous infusion of methylprednisolone (2 mg/Kg for 2 days and 1 mg/Kg for one day). About 67 hours later after fasting, abdominal distension diminished and bowel movement sounds recovered. On Day 10 of illness, repeated abdominal CT showed the same hydronephrosis in the left kidney (Figure 3c), red arrow, but almost normal intestines (Figures 3c and 3d). His fever subsided on Day 12 of the illness. On Day 13 of illness, there was skin peeled around fingernails. On Day 15 of illness, he was discharged after CRP subsided.

Figure 3: Abdominal enhanced CT showed hydronephrosis of left kidney (A), dilated intestinal tube. 3B: (green arrow) and pneumatosis (yellow arrow) at middle-lower abdomen intestinal wall on Day 7 of illness. Abdominal CT showed hydronephrosis of left kidney (C) and almost normal intestine (D) on Day 10.

Follow up

We have followed up with this patient routinely for 2 years. At about 2 months of illness, a deep transverse groove was developed across his finger nails (Beau’s lines). Echocardiography repeatedly showed normal coronary arteries. He stopped taking oral aspirin at 2 months.

Results and Discussion

The boy met the criteria of classic KD. In addition, he presented with vomiting, progressive abdominal distension. His symptoms and radiography results indicate intestinal ischemia or mucous membrane necrosis. It has been shown that portal or mesenteric venous gas strongly suggests the presence of bowel infarction and necrosis [7,8]. Superior mesenteric artery infarction or mesenteric vein thrombosis can result in the intestinal ischemia, presented with detectable gas. KD is essentially inflammation-mediated small vasculitis. Despite the mechanism difference behind intestinal complication, the bowel gas accumulation in KD patients is also considered a manifestation of intestinal mucosal necrosis. A persistent and significant elevation of D-Dimer level could also suggest cardiac infarction or intestinal necrosis [9]. Recovery is possible as long as there is no occurrence of transmural necrosis (intestinal gangrene) and perforation of the intestine. For this patient, the surgeon recommended conservative treatment rather than surgical removal of the ischemic or necrotic bowel segments due to KD related intestinal arteritis.

In our center, it is common to see KD patients with digestive system involvement. Clinical aspects include abdominal pain and/or distension, hepatic dysfunction, gallbladder wall edema, and other forms of gastrointestinal involvement such as intussusception, ischemic colitis, hepatic necrosis, splenic infarct, intestinal obstruction, colitis, and colon edema but much less frequently. Hypoproteinemia, a high risk factor for coronary aneurysms, can occur during fever due to KD-related vasculitis that causes plasma albumin leaking. Thus, if possible, we monitor food intake in these patients, and keep them at least on liquid food. However, in the case of intestinal paralysis and incomplete intestinal obstruction, food intake may result in intussusception or food retention in the expanded intestinal cavity, thus facilitates bacteria growth in intestine, aggravates intestinal paralysis, and, as a result, leads to intestinal necrosis.

Therefore, it requires clinicians to monitor the scale of food intake in patients. When KD children develop abdominal distension, hypokalemia caused by poor feeding should be concerned at first. Once confirmed, intravenous potassium supplementation must be applied as soon as possible. Based on the concentration limit of potassium supplementation, oral potassium is also a good supplement choice. However, with added potassium, if abdominal distension is not relieved or continues to progress, the toxicity of intestinal paralysis should be considered, and the relevant examinations should be performed, including tests for blood amylase, lipase, urinary amylase and abdominal DR and ultrasonic imaging. Once the diagnosis of intestinal paralysis is established, antibiotics for gram-negative bacteria and anaerobic bacteria need to be used in treatment. If above treatments for anti-inflammatory, fluid, potassium supplementation and albumin supplementation fail to improve the abdominal distension, along with lack of the intestinal movement sound, clinicians should consider possibilities of the intestinal obstruction and/or intestinal necrosis.

Abdominal ultrasound is the first choice for non-invasive examination of cholecystitis, pancreatitis and intussusception, and abdominal enhanced CT is the first choice for evaluating intestinal necrosis diagnosis. Whether diagnosis of intussusception or intestinal necrosis is established, patients must be on fasting and given nutrition intravenously. The most important part is to give albumin to KD children, because they have higher risk for IVIG-resistance and coronary aneurysm development [10]. As for hydronephrosis, it occurred before the patient had KD. As the result of comprehensive treatment, this patient did not develop damages in coronary arteries, which is the key outcome measurement for a long-term quality of life in pediatric KD patients.

We input key words “Kawasaki Disease and intestinal or gastrointestinal” when searching in PubMed. In recent 20 years, there are 34 cases of KD with intestinal involvements, including 9 girls, 23 boys, and 2 with unknown gender [11-37]. About 44.1% (15 cases) of these patients had coronary artery involvements, 20.6% (7 cases) with coronary artery aneurysm, 8.8% (3 cases) with both left and right coronary arteries lesion. One 7 months old child with coronary artery aneurysm developed complete occlusion 2 years later [26]. Six of them recovered in the follow-up. Total 7 cases (20.6%) had pericardial effusion, and all recovered in one month of the illness. The incidence of coronary artery lesion in KD with intestinal involvement is 43.8% (21/48), which is much higher than the average incidence of 0.3%-5.3% in KD [38,39].

This is mainly due to the leakage of proteins caused by intestinal arteritis and obstruction to protein absorption and utilization due to inflammatory edema in intestinal walls. In consequence, hypoproteinemia leads to coronary artery edema and exacerbates coronary artery lesion. According to these case reports, some of patients presented intestinal symptoms at first as primary symptoms, which may result in delaying diagnosis of KD in these patients. Among the 34 reported cases with intestinal involvement, there were 13 with intestinal obstruction, and the most common complication in patients was pseudo-obstruction. 7 with abdominal effusion, 2 with intestinal wall edema, 2 with ischemic intestinal stenosis, 2 with limited peritonitis, 2 with cholestasis, 1 with intestinal dilatation, 1 with intussusception, 1 with descending duodenal perforation, 1 with pancreatitis, 1 with appendicitis, and 1 with sigmoid colitis. Though their inflammation and lesion were relatively limited, without prompt IVIG treatment, these patients tend to develop coronary artery complications. This patient presented with vomiting, progression of abdominal distension.

Physical examination found his abdomen was distended and his bowel movement sounds were weakened and eventually diminished after treatment. Laboratory test showed significantly increased levels of inflammatory markers. Abdominal ultrasound showed dilated intestinal tubes. Enhanced abdominal CT revealed dilated abdominal intestinal tubes, pneumatosis, and gallbladder wall edema. There was extensive air accumulated in the small intestine wall (intestinal ischemia or mucosal necrosis) at the middle and lower abdomen, along with slightly thickened rectal wall and mild interstitial edema around portal vein. Test results showed that D-Dimer level was 4810 ug/L (<252 ug/L) at admission and continued to increase to 7384 ug/L five days later. After treatment, D-Dimer level decreased to 1423 ug/L (Figure 4). Thus, he met the criteria for intestinal ischemia/necrosis [8,40].

Figure 4: The dynamic changes of D-Dimer.

In this case, enhanced CT revealed necrotic gas accumulation in the wall of the large area in small intestine. If the patient did not receive timely treatment, the intestine involvement could progress to necrotic enterocolitis. In that case, the necrotic intestine would need to be surgically removed, which may lead to short bowel syndrome. Therefore, timely diagnosis combined with appropriate comprehensive treatment is the keys to noninvasively treat the intestinal complication in KD patients.

Conclusion

In our center, we have seen significant number of KD patients who have complication in digestive system. In cases with mild symptoms, once KD patients were treated timely, the mild symptoms diminish. However, in cases with severe complications, patients need comprehensive treatment. When a child presents with remittent fever, rashes, hypoproteinemia, intestinal symptoms, especially with pseudo-ileus observed in radiography examination, a diagnosis of KD with intestinal complication should be considered. If intestinal necrosis is limited to the mucosal layer, prompt diagnosis and proper comprehensive treatment can prevent complication progressing.

Declarations

Ethics approval and consent to participate

We have submitted a statement on ethics approval and consent.

Consent for Publication

Written informed consent for the publication of this case report and figures was obtained from the parents.

Availability of Data and Materials

All data generated or analyzed during this study are included in this published article.

Competing Interests

The authors declare that they have no competing interests.

Fundings

No

Author´s Contributions

XZ C, the case observation, data collection, manuscript editing. H W*, the case diagnosis, treatment, and the main points discussed. All authors have read and approved the manuscript.

Acknowledgements

Not applicable.

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