Dog Has to Have Intestonal Surgery Again
Vet Sci. 2021 May; eight(5): 83.
Small-scale Bowel Obstruction Induced past Concurrent Postoperative Intra-Abdominal Adhesions and Modest Bowel Fecal Materials in a Young Canis familiaris
Jae-Eun Hyun
1Department of Veterinarian Internal Medicine, Konkuk Veterinary Medical Teaching Hospital, Konkuk University, Seoul 05029, Korea; rk.ca.kuknok@nuyhnueeaj
Hyun-Jung Han
iiDepartment of Veterinary Emergency Medicine, Konkuk Veterinarian Medical Teaching Hospital, Konkuk University, Seoul 05029, Korea
Dong-In Jung, Academic Editor, DoHyeon Yu, Academic Editor, and Tomohiro Yonezawa, Bookish Editor
Received 2021 Apr 2; Accepted 2021 May eleven.
Abstract
A 7-month-old neutered male poodle dog presented with full general deterioration and gastrointestinal symptoms after two carve up operations: a jejunotomy for minor-intestinal strange trunk removal and an exploratory laparotomy for diagnosis and treatment of the gastrointestinal symptoms that occurred 1 month after the first surgery. The domestic dog was diagnosed equally having small-bowel obstruction (SBO) due to intra-abdominal adhesions and small-bowel fecal material (SBFM) by using abdominal radiography, ultrasonography, computed tomography, and laparotomy. Nosotros removed the obstructive adhesive lesion and SBFM through enterotomies and applied an autologous peritoneal graft to the released jejunum to forestall re-adhesion. Afterward the surgical intervention, the dog recovered apace and was healthy at 1 year after the surgery without gastrointestinal signs. To our knowledge, this study is the outset report of a successful handling of SBO induced past postoperative intra-abdominal adhesions and SBFM after laparotomies in a dog.
Keywords: dog, small-bowel obstacle, postoperative intra-abdominal adhesion, pocket-sized-bowel fecal sign, anastomosis, autologous peritoneal graft
1. Introduction
Postoperative intra-abdominal adhesions (PIAs) are inevitable complications of major abdominal surgery in both humans and animals, with various extents of adhesion formation depending on the patient [one,two,3]. Among man patients, up to 93% develop intra-abdominal adhesions postoperatively, and up to 10% who underwent laparotomy presented with adhesions related to complications such every bit small-bowel obstruction (SBO) [iv]. On the other mitt, in modest animals, PIA rarely causes serious clinical problems because the active fibrinolytic system in dogs and cats usually prevents adhesion germination, which causes clinical issues after laparotomy [ane]. All the same, if the dogs and cats nowadays clinical and imaging signs of gastrointestinal obstruction subsequently laparotomy, PIAs should be also considered as a differential diagnosis of bowel obstruction in spite of the small possibility [ane].
With computed tomography (CT), small-bowel fecal material (SBFM) was first described in humans every bit "small-scale-bowel fecal signs (SBFSs)"; particulate thing was shown to exist mixed with gas bubbles in the lumen of dilated small-bowel loops [five]. SBFM was characterized by the accumulation of undigested thing in the small intestine that resembled the fecal content in the large intestine equally a result of delayed transit through the abdominal tract [6]. SBFSs are mainly observed in patients with SBO, simply can also occur in patients with metabolic or infectious diseases that cause abnormalities in the small intestine [seven]. SBO can upshot from a variety of causes, such as ingestion of foreign materials, infection, intussusception, postoperative adhesions, or neoplasia. Although abdominal radiography and ultrasound still have loftier diagnostic value, abdominal computed tomography (CT) is a useful tool for confirmation of obstacle, localization of the site and level, and detection of strangulation and the cause of obstruction [eight].
This case study describes the successful surgical treatment of and preventive measures against SBO induced by two unusual postoperative complications, PIA and SBFM, in a young dog. To the best of our knowledge, this is the first report to describe the treatment and consequence of concurrent PIA and SBFM occurring subsequently laparotomies in a dog.
2. Instance History
A seven-month-onetime neutered male poodle dog with a body weight of 3.0 kg was presented with anorexia, weight loss, and no defecation at the Konkuk Veterinary Medical Teaching Hospital. According to the referring veterinarian, the dog had been diagnosed with a small-intestinal foreign body (earmuff), which was removed via jejunotomy with 3-0 polyglyconate (Maxon®, Davis and Geck, Danbury, CT, Us) 2 months earlier referral. Ane month after the operation, the constant diarrhea, vomiting, and anorexia had not improved with symptomatic handling, including fluid therapy, antiemetics, and antibiotics. Imaging examinations, including radiography and abdominal ultrasonography, showed no foreign bodies, only showed decreased gastrointestinal move. Equally the owner suspected that the dog might have eaten foreign bodies again, the referring veterinarian performed another exploratory laparotomy and reported jejunal adhesions and dilatation without whatever foreign bodies. Afterward the second laparotomy, the dog'south condition deteriorated chop-chop, with persistent gastrointestinal signs, including anorexia, vomiting, and weight loss from 3.nine to 3 kg. The dog did not defecate from that point on.
A physical test on presentation revealed decreased appetite, depressed mentation, mild abdominal hurting on palpation, hyperthermia (39.8 °C), and viii% dehydration. The dog's perfusion parameters were within the normal limits. Hematology revealed normocytic normochromic anemia (packed cell volume (PCV), 28.3%; reference range, 37–55%), leukocytosis (28.83 × xnine/L; reference range, 6.0–17.0 × 109/50), and neutrophilia (24.36 × 109/50; reference range, 3.0–eleven.five × 10nine/L), with some toxic changes and reactive lymphocytes. A biochemical assay, gas analysis, and coagulation test revealed no abnormalities except the elevated C-reactive protein (CRP) level (iii.6 mg/dL; reference range, <1.0 mg/dL). Abdominal radiography revealed loss of serosal particular and pocket-size-abdominal dilation, with the ratio betwixt the maximal modest-intestine (SI) diameter and the summit of the fifth lumbar vertebral body (L5) increasing to 2.24. Abdominal ultrasonography revealed a severe dilation with intraluminal intestinal contents and accumulation of fluid in well-nigh the whole jejunal segment, with its largest bore existence eighteen mm, likewise as jejunal lymph node enlargement. Markedly reduced gastrointestinal motility was generally shown, just remarkable pathological changes were not identified in other gastrointestinal segments except for the jejunum. No foreign material was identified in any segment. A minor amount of peritoneal effusion around the urinary bladder and balmy hyperechoic change in the mesentery were idea to be due to the previous operation. To identify the cause of the severe jejunal dilatation and the presence and level of the obstruction, a CT scan (LightSpeed; GE Medical Arrangement, Milwaukee, WI, USA) was obtained under full general anesthesia. The imaging protocols were 120 kVp, 200 mAs, 512 × 512 matrix, and 0.6 rotation fourth dimension with a 1.25 mm slice thickness. For a contrasting CT examination after the plain CT scan, iohexol (Omnihexol 300; Korea United Pharmaceutical, Seoul, Korea) was manually injected at 600 mg iodine/kg into the cephalic vein. All CT images were transferred to a workstation using a commercially available DICOM imaging assay software (Osirix viewer; Pixmeo, Los Angeles, CA, USA). The abdominal CT browse revealed generalized gastrointestinal dilatation with abrupt narrowing of the jejunal segment and SBFS (Figure 1). The small-scale intestines were plicated and tortuous, and the jejunal segment was abruptly narrowed to a iv.0 mm diameter. The stomach, duodenum, and jejunal loop proximal to the narrowed lesion were moderately to severely dilated, representing a jejunum with a 21.nine mm maximal diameter. The jejunum distal to the narrowed lesion was commonly to mildly dilated, inside 8.vii mm in diameter. An SBFS consisting of intraluminal particulate-like materials mixed with gas bubbles was observed within the dilated jejunal segments distal to the narrowed lesion and entire ileum. The lumen of the dilated stomach contained food residues, but there were no remarkable changes in wall thickness or patency. The large intestines, including the cecum, colon, and rectum, were complanate without fecal contents. A small quantity of free fluid effectually the dilated jejunal segment and a diffusely hyper-adulterate mesentery were identified. On the basis of the imaging findings, the dog was diagnosed every bit having SBO of the jejunal segment acquired by the stenotic jejunal lumen. The SBO was estimated to be of high form, with >50% discrepancy between the proximal and distal minor-bowel luminal calibers based on the previously reported human being classification organisation [9]. No causes that could induce SBO, such as strange bodies or other intestinal wall abnormalities, were identified.
Postcontrast dorsal (A,East), transverse (B,C), and sagittal (D) computed tomography images of the abdomen of the dog with severe dilatation of the overall small intestines. The breadbasket and overall jejuna are markedly dilatated, and the proximal jejuna are plicated at an acute angle, causing a stenotic lumen (B, blackness arrowhead). The small-bowel fecal signs evidence hyper-attenuated fecal-like materials mixed with gas bubbling from the dilated jejunal segments to the entire ileum (A,C,D, white arrows). The large intestines from the ileocecocolic junction to the rectum are collapsed, with little gas and no fecal contents (C–East, blackness arrows).
To identify and right the cause of the SBO, an exploratory laparotomy was performed. The canis familiaris was premedicated with cefazolin (30 mg/kg intravenously (Four)), butorphanol (0.two mg/kg Four), midazolam (0.one mg/kg IV), and maropitant (one mg/kg SC). General anesthesia was induced with propofol (4 mg/kg IV) and maintained with isoflurane in oxygen afterwards endotracheal intubation. After an abdominal midline incision was made, diffuse fibrous adhesions were identified throughout the overall jejunum and between the jejunum and peritoneal wall. Bowel plication was identified between the proximal jejunums, adhering to the serosal layers with loops positioned at acute angles, causing the narrowing of the lumen. The jejunal loop proximal to the narrowed lesion was markedly distended and hyperemic, and the distal jejunum and ileum distal to the narrowed lesion were obstructed with hard intestinal contents that could not be squeezed (Figure twoA). The large intestines distal to the obstructed ileum were totally collapsed with no palpable contents. Adhesiolysis was performed using blunt dissection and electrotomy. Afterwards the adhesiolysis, a stenosed jejunal lesion was identified, with a fibrinous adhesive strand tightly encircling the narrowed jejunum, inducing a SBO (Figure iiB). The near-complete obstacle of the lesion led to a wide difference between the proximal and distal jejunal calibers with lack of luminal patency. The stenosed jejunum was removed and anastomosed using a previously described sutured anastomosis [10]. The resected abdominal segment was grossly inspected. The antimesenteric edge was advisedly incised to find the adhesive stenosed lesion that caused the SBO, and a potent, thick, gristly tissue that formed between the next abdominal serosa was identified to markedly reduce the jejunal lumen (Figure twoC). No other obvious gross abnormalities were observed in the affected jejunum. By direct observation and palpation, it was confirmed that there were no pathological changes or impaired patency of the stomach or other intestinal segments. Cytology and bacterial civilization using a small corporeality of intestinal effusion and agglutinative peritoneum revealed no bacterial growth, just a histopathological assay of the resected intestine was non performed because it was a financial brunt to the owner.
Intraoperative photographs of a dog that presented with postoperative small-bowel obstruction with small-bowel fecal signs in computed tomography images. (A) The proximal jejuna were adhered, inducing plication at acute angles (white arrowheads); they were too markedly dilated and hyperemic. The distal jejunum and ileum were mildly dilatated and contained hard intestinal contents that could not exist moved or crushed (black arrowheads). (B) Afterwards the release of the entrapped jejunal segments, a fibrinous adhesive strand was observed to have tightened the eye region of the jejunum, inducing jejunal stenosis (white arrow). A large discrepancy in the intestinal lumen was identified between the proximal and distal jejunum to the stenosed lesion. (C) Thick, fibrous agglutinative tissue developed betwixt the adjacent serosa and reduced the abdominal lumen (black arrows).
The hardened fecal-like contents were removed via the enterotomies that were made over the distal end of the jejunum and ileum and were identified every bit hard and dry fecal thing respective to a fecal score of one. The enteronotomy sites were closed with iii-0 polydioxanone (PDS) in a simple interrupted pattern. After securing the intestinal patency and confirming that at that place was no leakage, the serosal surfaces of the entire modest intestine were closely examined, and a remarkable serosal injury of 7 cm in length was identified in the proximal jejunum where the adhesion was separated (Figure 3A). To prevent re-adhesion of the damaged serosa, an autologous peritoneal graft (APG) was transplanted to embrace the entire damaged lesion. Equally an APG, viii × one.5 cm of the parietal peritoneum was harvested at the eye of the left-side of the abdomen (Effigy 3B). The APG was expanded over the injured serosal surface and attached with several simple interrupted sutures using 3-0 PDS Two (Ethicon, Somerville, NJ, USA; Figure 3C). The margin of the excised parietal peritoneum was apposed past a uncomplicated continuous suture using 4-0 PDS 2 (Ethicon). The belly was fully lavaged with warm saline and closed routinely.
Intraoperative photographs representing the damaged serosal surface of the jejunum after adhesiolysis in a dog. (A) The proximal jejunum, which was released later on adhesiolysis, represents the damaged serosal surface of approximately 7 cm in length (white arrows). (B) A parietal peritoneum (8 × 1.v cm rectangular shape) was harvested from the left side of the abdominal wall. (C) The excised peritoneal graft was attached to the injured serosal surface with simple interrupted sutures to cover the entire damaged serosa.
Postoperatively, the dog recovered from anesthesia uneventfully. He was serenity, alarm, and responsive, and he maintained normal vital signs and normotension. His postoperative medication included continuous infusion of fentanyl (4 μg/kg/h) and lidocaine (50 μg/kg/h) for the start 24 h, followed by carprofen (2.2 mg/kg orally twice daily) and tramadol (v mg/kg orally twice daily) for 5 days, maropitant (0.one mL/kg subcutaneous once daily) for 4 days, and misoprostol (5 μg/kg orally twice daily) for 5 days. As intestinal supplements, probiotics were administered for 2 weeks subsequently the operation. During hospitalization after the surgery, the dog showed no airsickness, regained his appetite, started to defecate (fecal score: 5/vii) from postoperative day 2, and was discharged on postoperative day four.
Postoperative follow-up examinations, including radiography, ultrasonography, and claret test, showed no dilatation, obstruction, or plication, with normal motion of the overall intestines. Regenerative anemia, mild hypoalbuminemia, neutrophilic leukocytosis, and elevated CRP levels were identified immediately after surgery, merely returned to inside the reference ranges in 2 weeks. Throughout the one-twelvemonth telephone follow-upwards, the dog remained healthy without any clinical signs associated with gastrointestinal disease. Considering the history of two separate previous operations, the confirmation that there were no other obvious pathological changes, including foreign bodies, and the fact that there was no recurrence subsequently resecting the obstructive jejunum, this patient was tentatively diagnosed with SBO induced by PIA.
3. Discussion
PIA occurs when the balance between fibrin deposition and fibrinolysis, which gain normally in the case of peritoneal injury, is disrupted by specific causes. The peritoneum has powerful coagulation and fibrinolytic capacity, which normally exceeds coagulation; thus, abdominal adhesion does not ordinarily occur under normal conditions [11]. As the integrity of the mesothelial layer constituting the peritoneum promotes fibrinolytic activity, mesothelial damage is considered to accelerate peritoneal adhesion germination by reducing the fibrinolytic chapters to lower than the coagulation part of the peritoneum [12,13].
In homo medicine, PIAs are the near frequent causes of SBO, of which adhesions business relationship for 50–75% of SBOs, which occur after surgery in 80% of all cases [8]. Early postoperative SBOs acquired by PIAs occur within 30 days after surgery [14,15]. This is a familiar simply challenging complication for surgeons, with an incidence of approximately 1–12% in human patients undergoing abdominal surgery [fourteen,15]. As PIA-induced SBO can be difficult to distinguish from functional ileus, which typically occurs afterwards abdominal surgery, CT could exist beneficially used to confirm the adhesive obstacle while checking for other causes of mechanical obstacle and localizing the site and level of the obstacle [eight,16,17]. The widespread use of CT and awareness of the high incidence of PIA-induced SBO tin can help surgeons recognize early postoperative SBOs and establish appropriate treatment strategies, especially if the apparent causes of mechanical SBOs could not be identified in patients with a history of prior surgery [sixteen]. Compared with several human being studies [18,xix,20], studies in veterinary medicine have paid little attention to PIAs and associated SBOs, and studies of PIA-induced SBOs in small animals are defective. In the nowadays case, a PIA-induced SBO was highly suspected due to the dog's history and CT scans, and it was confirmed on the footing of the gross morphology during the surgery. The dog presented with persistent gastrointestinal signs and markedly reduced gastrointestinal move on ultrasonography later on the laparotomies, so a typical postoperative functional ileus was initially considered. Withal, marked dilatation of the small bowel without obvious causes of an SBO, such as foreign bodies or tumors, was identified, and the CT revealed like images of PIA-induced SBOs in man studies, including mechanical SBOs with no obvious causes, proximal dilated loops of the small bowel, and an undilated distal bowel with a transition zone [8]. With this history and CT findings, the typically occurring postoperative functional ileus and other causes of mechanical SBO could exist excluded. PIA, which was suspected to have resulted from the two inexperienced open intestinal surgeries, was considered as the main cause of the SBO in this dog.
Human patients with PIA-induced SBOs ordinarily improve with non-surgical handling, and eighty–100% of patients experience alleviation of their clinical signs inside two weeks of the symptoms' onset after non-surgical treatment [15,21]. On the other paw, a significant number of patients with PIA-induced SBOs (fourteen%–58%) withal require surgical handling because of clinical and radiological symptoms that indicate intestinal strangulation or obstruction [xv,xvi]. In addition, the duration of non-surgical treatment and nature of the index performance also impact the conclusion for surgical treatment [16]. Equally fibroblast contents increase two weeks after surgical injury, thus inducing the maturation of adhesion [16,21], surgical handling may become more invasive after two weeks of the injury. In a previous homo study, patients who underwent late surgery (>13 days after surgical peritoneal injury) had a college enterotomy rate of 17%, whereas those who underwent surgery before 13 days presented a 5% charge per unit [22]. On the basis of these homo studies, in small animals with suspected PIA-induced SBOs, surgical handling may be fully considered as a valid option if symptoms do not improve within 2 weeks in spite of not-surgical direction. Moreover, an operator should be mindful that the surgery may become hazardous every bit time passes, especially if information technology is to be performed after more than than 2 weeks after the previous surgery. In this domestic dog, a relatively long fourth dimension—over 1 month—had passed before surgery was performed for the management of the PIA-induced SBO. Consequently, the astringent agglutinative lesions that induced the irreversible jejunal stenosis were identified; thus, jejunal resection and anastomosis had to be performed to regain the abdominal patency. If the domestic dog had been surgically treated a little earlier, before the adhesion maturation had progressed further, the invasiveness of the surgery could have been reduced. Unfortunately, the clan between PIA and SBO in canine patients has non been reported as much as that in humans. Therefore, further studies are needed on the prevalence and pathological period of PIA-induced SBOs in dogs.
Furthermore, SBFSs were identified in the CT results of the dog, and hardened fecal materials in the distal jejunum and ileum were confirmed during surgery. This was first described in man beings in 1995 [v], but no study has reported SBFSs in the field of veterinary medicine. SBFSs are mainly due to the SBO inducing stagnation of the intestinal contents, which causes gradual fluid absorption across the bowel wall, leaving undigested fecal matter to accumulate in the SI [six]. In homo patients with SBOs due to adhesions, the prevalence of SBFSs ranged from 37.1% to 55.ix% [9,23,24,25], despite the earliest written report reporting an SBFS prevalence of 7.iv% among SBO cases [five]. Due to the high prevalence, routine CT examination is recommended to identify SBFSs in man patients with SBOs [23]. In this canis familiaris, the SBFS was identified in the distal jejunum and ileum distal to the stenotic lesion in CT images and surgery. In this dog, the SBFS was located distal to the transition zone, which indicated a region undergoing a radical change in intestinal luminal diameter due to the obstructed lesion, whereas it is usually (93%) identified immediately proximal to the transition zone [23]. The reason for this divergence was estimated to be the reduced overall intestinal motility and decreased corporeality of water in the abdominal contents distal to the stenotic lesion. In this dog, the distal jejunum and ileum were not expected to have severe intestinal stasis due to the mechanical obstruction because they were distal to the stenotic lesion; however, postoperative functional ileus might take more than probable induced the SBFM in this canis familiaris in that markedly reduced intestinal motion could lead to overall intestinal stasis, resulting in increased fluid assimilation across the bowel wall. In addition, as the intestines distal to the stenosis were non severely distended, the corporeality of water in the intestinal contents was not as much every bit that in the severely distended intestine proximal to the stenosis; thus, the drying and hardening of fecal matter might have occurred relatively quickly. The degree of SBO in the domestic dog of this study was assessed using a human grading system based on the discrepancy betwixt the proximal and distal small-bowel luminal calibers. Further research is needed to plant an imaging occlusion grading system for diagnosis and prognosis of canine SBO patients [ix].
The clinical significance of SBFSs in human medicine remains unclear. Although the relevance of correlation between SBFSs and diagnosis of SBO remains controversial in patients with acute abdominal pain, it has been reported that SBFSs are useful signs for localization of transition zones in SBO patients on account of their tendency to be near prominent in the transition region from the dilated intestinal loop to the collapsed bowel [9]. SBFSs do non independently support the prediction of successful treatment or progression of lesions such equally ischemia [23]. However, as in this dog, hardened fecal matter in the SI could crusade mechanical obstacle and boosted intestinal damage, such every bit ischemia, which would require surgery. Therefore, surgical removal of the SBFM may exist necessary for the management of SBO in dogs. A model for criteria to predict the demand for operative intervention was presented in human medicine, and was too demonstrated to exist proportional to the morbidity and mortality [26]. In this model, patients with mesenteric edema, lack of an SBFS, and obstipation were strongly recommended for early operative exploration. Further studies are needed to establish criteria for the presence and timing of surgery in canine SBO patients.
PIA-induced SBO has been considered as a high-hazard recurring problem subsequently surgical correction in human studies (B), which reported overall recurrence rates ranging from 8.vii% to 53% [19,27,28,29,xxx], while related studies in pocket-size animals are lacking. The previously reported gamble factors for increasing re-adhesion included the magnitude of the surgical trauma in both the parietal peritoneum and abdominal serosa, decreased intraperitoneal fibrinolytic activity, and early patient historic period [eleven,31,32,33]. Owing to this high prevalence of recurrence, extensive research for preventing re-adhesion has been conducted, merely no clinical standard has been established for any preventive modalities, either surgical or pharmacological [xiii,34]. As one of these preventive modalities, barriers, which are a kind of a membrane or gel adult to separate the damaged serosal surfaces from the adjacent organs [three,20], have been demonstrated to be constructive in animal models and clinical trials [3,twenty,34]. Virtually recently, APG was demonstrated to take a preventive effect on peritoneal adhesion by transplanting mesothelial cells and rapid reperitonealization [34]. Mesothelial cells grade the thin basement membrane of the peritoneum and are supported past a submesothelial layer consisting of a connective tissue stroma [35]. The mesothelial cells maintain the serosal integrity, and their progenitor cells could play an of import office in peritoneal remodeling [35]. Thus, preservation of functional mesothelial cells is a necessary cistron for adhesion prevention, and an APG can provide mesothelial reconstruction and preserve the function of the transplanted mesothelial cells [34]. In addition, this autologous barrier has other benefits, including minimizing adverse biological reactions, availability, and economic feasibility, as compared with synthetic barriers [34]. In this dog, a meticulous surgical technique, including careful tissue handling to avert desiccation and ischemia, was established as the first step to prevent re-adhesion. Moreover, the significant serosal impairment in the released jejunum was covered with an APG to separate the damaged serosa from the other side by side intestines to prevent re-adhesion. On the ground of the study past Bresson et al. [34], the mesothelial layer of the graft should exist exposed to the abdominal crenel during transplantation considering the appropriately positioned polarity of the mesothelial cells is important for preserving functional mesothelial cells [33]. They reported that the mesothelial cells were detected 14 days after APGs were transplanted with the mesothelial cell side exposed to the abdominal cavity, but were not detected when the submesothelial layer was exposed to the intestinal cavity [34]. Although the preventive effect of APGs on serosal re-adhesion has been proven in human patients and in rat and mouse models [3,20,34], an boosted randomized, prospective study is necessary in club to establish the evidence of the prophylactical application of APGs in canine patients.
4. Conclusions
This study describes the first reported case of PIA and obstructive SBFM-induced SBO in a young dog. These ii rarely occurring postoperative complications were diagnosed on the basis of the dog's history and CT results and were successfully treated with meticulous surgical techniques for resection of the obstructive agglutinative lesion and removal of the obstructive SBFM via enterotomies. The deperitonealized lesion of the released jejunum was completely covered with autologous peritoneal graft to foreclose re-adhesion.
Author Contributions
Conceptualization, J.-Eastward.H. and H.-J.H.; methodology, H.-J.H.; investigation, J.-East.H. and H.-J.H.; writing—original draft preparation, J.-E.H. and H.-J.H.; writing—review and editing, J.-E.H.; visualization, J.-E.H. and H.-J.H.; supervision, H.-J.H. Both authors have read and agreed to the published version of the manuscript.
Funding
This research was funded by the National Research Foundation of Korea (NRF) grant funded by the 261 Korea authorities (2020R1A2C101378712).
Institutional Review Lath Statement
The ethical review and approval were waived for this study, as in that location was no interference with animal wellbeing.
Informed Consent Argument
An informed consent statement was obtained from the dog's owner.
Data Availability Statement
Data sharing is not applicative.
Conflicts of Interest
The authors declare no conflict of involvement.
Footnotes
Publisher's Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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