A rare cause of spleen abscess

Full Text

BACKGROUND

Splenic abscess as an independent disease accounts for no more than 1% of all acute surgical diseases of the organs of the abdomen [1]. The major pathogenetic mechanism of development of primary splenic abscesses is the septicopyemia type generalization of the bacterial infection. In most cases, the splenic abscess is developing acutely on the background of bacterial endocarditis, moreover, there were reports of its development against severe COVID-infection, leukoses, and primary spleen lymphoma [2–5]. A much rarer clinical manifestation is subacute splenic abscess, which develops following a severe infection [6] or in the setting of autoimmune diseases [7]. Splenic abscesses have also been described as a result of suppuration of traumatic hematomas and hydatid cysts [2, 8].

The infectious agents are usually the bacteria of the coliform group; however, specific infection cases have been described, viz. brucellosis [9], tuberculosis [10].

Clinical manifestations of the splenic abscess comprise symptoms of general infectious syndrome, often with organ dysfunction of various severity and local symptoms that present clinically as pains in the left hypochondrium with irradiation to the left part of the chest, enlarged spleen, and pleural exudate [2–4]. In the subacute course, the disease is accompanied by minimal symptoms and low-grade fever [11].

Clinical diagnostics of the splenic abscess is complicated and thus necessitates instrumental methods. Ultrasound diagnostics, Ct and MRI all have sufficient sensitivity and specificity; however, most authors consider it necessary using ultrasound diagnostics as the screening method and CT and MRI as the confirming methods [2–4, 12]. Cases have been reported when differential diagnosis took several months because splenic abscess was progressing masked by splenic lymphoma or hemorrhagic vasculitis [4]. Diagnostics of splenic abscess is especially complicated in the presence of immunodeficiencies [13].

The pathology can be treated conservatively, which is effective in 30% of observations [2–4], and surgically, which includes the traditional splenectomy or puncture drainage. In the cases of bacterial endocarditis, most authors prefer the traditional splenectomy [2, 3, 11]. In some cases, first the transcutaneous drainage is performed, and splenectomy follows relief of sepsis symptoms [11]. Laparoscopic splenectomy is not performed due to the presence of adhesion and hazard of rupture of the abscess into the free peritoneal cavity [2–4, 11].

It is to be mentioned that only a few authors give preference to transcutaneous drainage as the main treatment method justifying it by preserving the spleen as an immunocompetent organ. At the same time, they admit that the removal of the residual cavity and the time of its drainage last for several weeks [14]. There have been individual reports of open organ-preserving operations [15, 16].

Mortality in cases of splenic abscess remains high, up to 50% [3]. It stems, however, not from the splenic abscess proper but from the generalization of the infection, i.e. from sepsis.

This article presents a clinical observation of a successful treatment of splenic abscess without the primary focus of sepsis in an old age female patient against a severe cardiovascular pathology and justifies our refusal from low-invasive treatment methods.

DESCRIPTION OF CLINICAL CASE

Female patient N., 79 years old, urgently admitted in a moderately severe condition with complaints of temperature rising to 38.4°С and feeling generally unwell. She had been ill for about 4 weeks, when the feeling unwell set on and the temperature would rise to 37.3°С in the evenings, that the patient herself considered manifestations of a respiratory infection. Gradually, the fever became hectic (up to 38.4°С in the evenings). She had no chills. She denied pains in the stomach or dyspeptic symptoms.

For more than 20 years, the patient had coronary heart disease. Six years prior she had a myocardial infarction, following which a permanent form of atrial fibrillation with ventricular tachysystole developed. For three years after, she received Clopidogrel. Then, she stopped taking antiaggregant drugs of her own accord; she did not receive any anticoagulants. Before the infarction, she had surges of blood pressure up to 160/90 mmHg. After the infarction, she had no BP surges.

In the course of outpatient examination, pneumonia was excluded. Ultrasound examination revealed mild increase in the spleen size (area: 72 cm2). The greater part of the organ was occupied by a large (D=84 mm) homogenous echo-negative mass. The patient was urgently handed over to the surgical hospital with a referral diagnosis of “Splenic abscess”. The laboratory tests only included total blood count and urine analysis (revealing mild leukocytosis (11.2·1012) and biochemical blood assay (no abnormalities found).

Hospital-based examination pronounced the patient’s condition as moderately severe. Normal consciousness. Body temperature 36.4°С. Respiratory rate 16 per minute, vesicular breathing. HR 92–106 bpm, arrhythmic pulse of 82–96 bpm. BP 125/75 mmHg. The tongue is moist. The abdomen is soft, with slight tenderness on palpation in the left hypochondrium; the liver and spleen are not palpable. Soft pitting edema of the lower legs and feet is present and does not resolve overnight. Appetite is reduced. The patient has a tendency to constipation, with bowel movements occurring after laxative use. Urinary output is preserved.

Considering the temperature reaction and ultrasound examination data, the patient was preliminarily diagnosed with “Splenic abscess”. In order to verify the diagnosis, CT of the abdominal cavity was performed with intravenous bolus contrast enhancement. Spleen dimensions: 118×96×109 mm. The greater part of the organ is occupied with a hypodense homogenous mass of irregular shape, size: 110×78×84 mm, density: 28–32 HU, weak and non-homogenous hyperdense amplification of the walls to the arterial phase (Fig. 1–3). The blood flow in the splenic artery and vein is preserved.

 

Figure 1. CT scan of patient N. Coronal projection.

Рисунок 1. Компьютерная томография больной Н. Корональная проекция.

 

Figure 2. CT scan of patient N. Axial projection.

Рисунок 2. Компьютерная томография больной Н. Аксиальная проекция.

 

Figure 3. CT scan of patient N. Sagittal projection.

Рисунок 3. Компьютерная томография больной Н. Сагиттальная проекция.

 

EchoCG was performed to stratify surgery and anesthesiologic risk that revealed the following: thickening of the walls of the ascending aorta and of the aortic valve leaflets, as well as the mitral valve leaflets, with grade 2 regurgitation; signs of pulmonary hypertension; reduced left ventricular systolic function with an ejection fraction of 33%. No thrombi were detected in the atria. Transesophageal echocardiography was not performed due to the severity of the patient’s condition and the presence of indications for emergency surgical treatment.

Laboratory tests reported mild anemia (hemoglobin 116 g/L, RBC 3.7·1012; mild elevation of nitrogenous waste (creatinine 107 µmol/L, urea 8.1 µmol/L). Homeostasis values within reference range (INR 1.05, aPTT 32 seconds, platelets 205·109). The absence of a leukocyte reaction was notable (4.5·109) as was the change in the leukocyte formula (rod nuclear cells 4%; segmental leukocytes 62%; lymphocytes 28%; monocytes 4%; eosinophils 2%). C-reactive protein concentration was mildly elevated (8.1 mg/L), fibrinogen and D-dimer levels were not studies due to a short preoperative period.

Based on the medical history, platelet response and CT findings, the diagnosis of splenic abscess was confirmed. On the third day after admission, the patient underwent splenectomy via an upper midline laparotomy. Upon exploration, a cicatricial adhesive process was found in the left subphrenic space. The liver was slightly enlarged, firm, and smooth in texture. Examination of the remaining abdominal organs revealed no obvious pathological changes. After the adhesions were divided, the body and the upper pole of the spleen were exposed. A large, thin-walled, fluctuant mass was palpated in the lower pole. The splenophrenic ligament and the vascular pedicle were ligated and divided, with separate handling of the artery and the vein; the vessel lumens were free. Subsequently, the spleen was separated from the splenic flexure of the colon. During dissection, the abscess ruptured, and up to 150 mL of thick, gray-brown, odorless pus mixed with splenic detritus was evacuated (Fig. 4).

 

Figure 4. Separation of the splenic-colon ligament. The moment of opening of the spleen abscess.

Рисунок 4. Разделение селезеночно-ободочной связки. Момент вскрытия абсцесса селезенки.

 

Specimens were taken for bacteriological examination. The abscess capsule was dissected free from the colon. The avascular splenorenal ligament was divided. The spleen was removed. The subphrenic space was irrigated until clear and drained through two counter-incisions in the left flank using two tubular drains. The wound was closed in layers.

The postoperative period was free from complications. On the third postoperative day, flatus began to pass. No fever was observed. During the first postoperative day, up to 100 mL of intensely colored hemorrhagic exudate was drained, with the amount progressively decreasing. The drains were removed on the 5th and 6th postoperative days. The wound healed by primary intention. The patient was discharged on the 12th postoperative day.

Postoperatively, the patient received enoxaparin 10,000 anti-Xa IU/mL, 0.4 mL subcutaneously twice daily; cefoperazone-sulbactam 1.0 g + 1.0 g in 250 mL of 0.9% sodium chloride solution intravenously twice daily; ketorolac 3%, 1 mL in 10 mL of 0.9% sodium chloride solution intravenously three times daily; and omeprazole 40 mg in 500 mL of 0.9% sodium chloride solution intravenously once daily.

Histological examination of the abscess wall revealed neutrophilic infiltration with areas of vascular thrombosis. The histological diagnosis was splenic abscess. Examination of the remaining splenic tissue showed no pathological changes.

Bacteriological analysis of the pus from the abscess cavity identified a high concentration of Enterococcus faecalis (106 CFU).

Final clinical diagnosis. Main diagnosis: splenic abscess. Complications: none. Secondary diagnosis: CHD. Postinfarction cardiosclerosis. Permanent atrial fibrillation with ventricular tachysystole. Grade 2 mitral valve insufficiency. Cerebral atherosclerosis. Grade 2 dyscirculatory encephalopathy.

DISCUSSION

The first specific feature of this observation is the pathogenetic mechanism of splenic abscess. It follows from literature that a typical mechanism of abscess development is hematogenous dissemination in case of presence of a primary septic focus [2–4]. The emboly of branches of the splenic artery with subsequent abscess formation in the infarction area is indicated as the probable but rare mechanism of abscess development [11, 12]. We were not able to find any clinical observations of the actual implementation of this mechanism.

Usually, hematogenous dissemination develops on a background of an initially severe septic disease. In the case under observation its history revealed neither a clinical manifestation of the infectious process nor the potential primary septic focus. Considering the presence of atrial fibrillation and ventricular tachysystole, the most likely pathogenic mechanism was the emboly of the splenic artery with development of infarction of the spleen with further formation of abscess of the necrosis zone.

With atrial fibrillation present, the main source of thromboembolism are the atria. Echocardiography did not confirm the presence of atrial thrombi; however, exclusion of atrial thrombosis can be most reliably achieved using transesophageal echocardiography [16], which was not performed.

Regretfully, over the past several years the patient did not receive either antiarrhythmic or antithrombotic therapy, which was indicated for her condition [7] and might potentially have prevented the development of splenic abscess. At the same time, there was no history of pain syndrome, characteristic for the massive emboly of the splenic artery, without which the development of an infarction of the organ is not possible that would be sufficient for the formation of the abscess. Smaller infarctions of the spleen organize, in the majority of cases [2, 11]. Thus, it is not possible to form a well-justified opinion on the pathogenic mechanism of the development of splenic abscess in this particular observation.

The second specific feature of this observation is the symptomatic landscape of the splenic infarction. Usually, it comprises general symptoms of a severe endogenous intoxication and local symptoms of organ damage. While the patient had the first group of symptoms, she had none from the second. There was no abdominal pain, no tenderness on palpation, and no dyspeptic manifestations. The reason for such a clinical course is unclear. It may be related to the patient's advanced age, or possibly to the localization of the abscess in the upper pole of the spleen, which to some extent isolated the abscess from the free peritoneal cavity.

The third special feature of this clinical case is the choice of treatment method. With the abscess of such dimensions, conservative treatment has no prospects, and surgical treatment was clearly indicated for the patient. Our clinic has sufficient experience in puncture drainage surgeries under ultrasound and CT-assisted navigation. We also perform laparoscopic splenectomy and laparoscopic fenestration of splenic cysts. In this particular case we made a deliberate choice of not using minimally invasive treatment methods since the time of disease led to believe a manifested adhesive process was in place that would preclude a laparoscopic surgery. The lack of a clear demarcation and formation of a dense wall of the abscess results in a necessity of a long-time drainage of the cavity and unjustified extension of treatment time, which is not advisable for old age patients with limited self-care capacity. The data of intraoperation revision and histological study of the resected organ confirmed our suppositions.

CONCLUSION

Splenic abscess is a rare pathology; therefore, most surgeons have, at best, experience with only isolated cases of this condition. The clinical condition of patients with splenic abscess is generally quite severe.

These circumstances necessitate the following: first, the immediate use of the full available range of additional instrumental examinations to establish an accurate topographic diagnosis and, second, a rational approach to selecting the method of surgical treatment. Modern minimally invasive treatment modalities certainly have significant advantages. In some cases, however, their benefits are completely offset either by increased risk or by an unpredictable duration of patient rehabilitation after surgery.

 

ADDITIONAL INFORMATION	ДОПОЛНИТЕЛЬНАЯ ИНФОРМАЦИЯ
Study funding. The study was the authors’ initiative without external funding.	Источник финансирования. Работа выполнена по инициативе авторов без привлечения финансирования.
Conflict of interest. The authors declare that there are no obvious or potential conflicts of interest associated with the content of this article.	Конфликт интересов. Авторы декларируют отсутствие явных и потенциальных конфликтов интересов, связанных с содержанием настоящей статьи.
Contribution of individual authors. Makarov I.V.: concept and design of the study, analysis and interpretation of data, editing of the article. Grachev B.D., Lopukhov E.S.: writing and editing of the text. All authors gave their final approval of the manuscript for submission, and agreed to be accountable for all aspects of the work, implying proper study and resolution of issues related to the accuracy or integrity of any part of the work.	Участие авторов. Макаров И.В.: концепция и дизайн исследования, анализ и интерпретация данных, редактирование статьи. Грачев Б.Д., Лопухов Е.С.: написание текста и его редактирование. Все авторы одобрили финальную версию статьи перед публикацией, выразили согласие нести ответственность за все аспекты работы, подразумевающую надлежащее изучение и решение вопросов, связанных с точностью или добросовестностью любой части работы.
Consent for publication. Written consent was obtained from the patient for the depersonalized publication of relevant medical information and all of accompanying images in the journal.	Информированное согласие на публикацию. Авторы получили письменное согласие пациентки на публикацию в журнале медицинских данных и фотографий в обезличенной форме.
Statement of originality. No previously published material (text, images, or data) was used in this work.	Оригинальность. При создании настоящей работы авторы не использовали ранее опубликованные сведения (текст, иллюстрации, данные).
Data availability statement. The editorial policy regarding data sharing does not apply to this work.	Доступ к данным. Редакционная политика в отношении совместного использования данных к настоящей работе не применима.
Generative AI. No generative artificial intelligence technologies were used to prepare this article.	Генеративный искусственный интеллект. При создании настоящей статьи технологии генеративного искусственного интеллекта не использовали.
Provenance and peer review. This paper was submitted unsolicited and reviewed following the standard procedure. The peer review process involved 2 external reviewers.	Рассмотрение и рецензирование. Настоящая работа подана в журнал в инициативном порядке и рассмотрена по обычной процедуре. В рецензировании участвовали 2 внешних рецензента.

 

About the authors

Igor V. Makarov

Samara State Medical University

Author for correspondence.
Email: i.v.makarov@samsmu.ru
ORCID iD: 0000-0002-1068-3330

MD, Dr. Sci. (Medicine), Professor, Head of the Department of General Surgery and Surgical Diseases.

Russian Federation, Samara

Boris D. Grachev

Samara State Medical University

Email: b.d.grachev@samsmu.ru
ORCID iD: 0000-0002-4778-9518

MD, Cand. Sci. (Medicine), Associate professor, Surgeon at the Surgical Department No. 1 of the Propaedeutic Surgery Clinic.

Russian Federation, Samara

Evgenii S. Lopukhov

Samara State Medical University

Email: e.s.lopuhov@samsmu.ru
ORCID iD: 0009-0001-5894-3197

MD, Cand. Sci. (Medicine), PhD, Associate professor, Head of the Surgical Department No. 1 of the Propaedeutic Surgery Clinic.

Russian Federation, Samara

References

Supplementary files