Non-traumatic ruptured splenic abscess presenting with pneumoperitoneum in an immunocompetent patient: a diagnostic dilemma

Abstract

Splenic abscess is a rare life-threatening clinical entity. There are only a handful of reported cases of spontaneous splenic abscess rupture with pneumoperitoneum. Rupture of splenic abscess associated with gas-producing pathogens may lead to pneumoperitoneum. We hereby report the case of a ruptured splenic abscess with pneumoperitoneum in a young immunocompetent woman masquerading as hollow viscus perforation peritonitis. Ruptured splenic abscess should be kept in mind for treating surgeons as a differential diagnosis of pneumoperitoneum or peritonitis, particularly for immunocompromised patients.

Background

Splenic abscess is a rare clinical entity with ~600 reported cases with incidence rate of 0.2%–0.7% in autopsy series.¹ The reported mortality rate of this condition in different series vary from 0% to 47%.¹ Presentation of the splenic abscess is often vague and insidious including left upper quadrant abdominal pain, fever and chills.² Additionally, these patients may present with leucocytosis, left upper quadrant mass and pleural effusion on chest X-ray. It generally occur in patients with underlying comorbidities, which commonly include neoplasia, immunodeficiency, trauma, metastatic infection, splenic infarct or diabetes. Pneumoperitoneum is considered almost always secondary to perforated hollow viscus organ until proven otherwise. However, splenic abscess may be considered as one of the differential diagnosis for pneumoperitoneum or peritonitis particularly in immunosuppressed state.

Case presentation

A 62 year-old non-diabetic woman was brought to the emergency department of a tertiary care hospital in Delhi, north India with complains of upper abdominal pain and high-grade fever with chills and rigour for last 1 week, followed by gradually progressive abdominal distention, multiple episodes of non-bilious vomiting and obstipation for last 5 days. Pain was sudden in onset, severe in intensity, initially localised to the upper abdomen and gradually involved whole of the abdomen. There were no aggravating factors and the pain was relieved with medications.

On general physical examination, she was dehydrated and hypotensive (90/56 mm Hg) with tachycardia (pulse rate 120/min). Abdominal examination revealed gross abdominal distension with diffuse tenderness with marked guarding and rigidity. Shifting dullness, obliteration of liver dullness and absent bowel sounds were noted on further examination. On the basis of clinical examination and radiological imaging, a provisional diagnosis of duodenal ulcer perforation peritonitis was made.

Investigations

Routine blood investigation revealed anaemia (haemoglobin 8.8 g/L), leucocytosis (white blood cells (WBC) count 30.5×10⁹/L) with normal platelet count (322×10⁹/L), serum amylase (110 IU/L) and renal function test. Further evaluation with X-ray abdomen erect revealed free gas under right hemidiaphragm (figure 1). However, CT scan of the abdomen could not be performed due to haemodynamic instability of the patient.

Figure 1.

X-ray abdomen erect showing free gas under right hemidiaphragm.

Differential diagnosis

Duodenal/gastric perforation, perforated diverticulitis/appendicitis, enteric ileal peroration, perforated bowel malignancy, acute pancreatitis and strangulated intestinal obstruction.

Treatment

Patient remained haemodynamically unstable after initial intravenous fluid resuscitation and ionotropic support was started. Patient was taken up for emergency exploratory laparotomy for suspected duodenal perforation peritonitis under general anaesthesia after proper counselling and consent. On exploration, 500 mL of frank pus was noted in the peritoneal cavity. Much to our surprise, thorough exploration of the stomach, duodenum, small and large gut did not reveal any hollow viscus perforation. Evaluation of the solid viscera revealed ruptured and severely damaged spleen with features of inflammation (figure 2). Splenectomy along with peritoneal lavage was performed and left paracolic and pelvic drains were placed. In the immediate postoperative period, patient was shifted to the intensive care unit (ICU) for intensive monitoring in view of intraoperative blood loss and decreased respiratory efforts. Postoperative period was uneventful. Pus culture from splenic abscess was positive for Klebsiella pneumoniae and anaerobe Prevotella intermedia, for which appropriate antibiotics were started. Abdominal drains were removed on the 5th postoperative day and patient was discharged on the 10thpostoperative day.

Figure 2.

Intraoperative specimen image showing severely damaged and congested spleen after spontaneous rupture of splenic abscess.

Outcome and follow-up

She received vaccination for prevention of overwhelming postsplenectomy infection including Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae. At 3-month follow-up, she was doing well with no fever or pain abdomen.

Discussion

Splenic abscess is an uncommon and life-threatening condition with an incidence of 0.14%–0.7% in some series.^1–3 However, recent literature demonstrate that splenic abscesses are increasingly being identified, possibly due to widespread use of imaging modalities, and increasing prevalence of immunodeficiency state like AIDS. The reported mortality rate of this condition in different series vary from 0% to 47%. It is commonly associated with neoplasia, trauma, metastatic infection, immunodeficiency, splenic infarction or diabetes.⁴ Infective sources include typhoid, paratyphoid, malaria and so on. Abscess can arise from the following.

1. Haematogenous spread to a previously normal spleen, for example, in immunocompromised patients, patients with septic endocarditis.

2. Haematogenous spread to a diseased spleen, for example, in patients with single or multiple splenic infarcts or bacteremia with splenic colonisation.

3. Contiguous spread, that is, direct spread from pancreatic abscess, gastric or colonic perforations or subphrenic abscess.

The signs and symptoms of splenic abscess are non-specific and remains a diagnostic challenge.⁵ The most common clinical features of splenic abscesses are high-grade fever and exclusively localised left upper quadrant abdominal pain. The classical triad of fever, left upper quadrant pain and splenomegaly is seen in only one-third of patients. The most common cause of splenic rupture in clinical practice is trauma, which accounts for 30% of patients undergoing exploratory laparotomy for blunt abdominal trauma. However, spontaneous rupture of spleen is suspected in case of acute abdomen and signs of haemodynamic compromise in a background of sepsis, malignancy, acute viral infections, haematological disorders and immunosuppresion.⁶

Peritonitis resulting from spontaneous splenic abscess rupture has been reported in handful of cases.^{7 8} Pneumoperitoneum as a result of splenic abscess rupture is even rarer clinical entity with <10 cases reported until.⁹ Pneumoperitoneum is considered almost always secondary to perforated hollow viscus organ (like gastric or duodenal ulcer perforation, Ileal perforation, diverticular perforation and appendicular perforation) until proven otherwise. However, certain other clinical entities which may also lead to pneumoperitoneum include postoperatively (laparoscopy/laparotomy), ruptured liver abscess, pneumatosis cystoides intestinalis, pneumocholecystitis, thoracic cause (ruptured emphysematous blebs, pleuroperitoneal or bronchoperitoneal fistula) and so on.

The most common organisms isolated on bacteriological culture is case of splenic abscess are Gram-negative bacilli (K. pneumoniae, Escherichia coli) and Gram-positive cocci (Staphylococcus aureus), although a vast variety of microorganism have been described.^{10 11} Due to presence of gas-producing organisms in the splenic abscess, may cause pneumoperitoneum after burst into the abdomen.^{11 12} We also noted presence of gas-producing organism as a cause of pneumoperitoneum in our case.

Due to non-specific clinical presentation, ruptured splenic abscess remains a diagnostic challenge. Multidetector CT scan is the diagnostic modality of choice to establish the presence of splenic abscess or associated rupture in the peritoneal cavity.⁵ With the recent development of minimal invasive techniques and percutaneous ultrasound or CT-guided procedures, the placement of drains has resulted in resolution of the abscess in a high percentage of cases with low morbidity and negligible mortality. Percutaneous drainage is indicated for solitary unilocular or bilocular abscess or for patients with high-surgical risk.¹⁰ While, multiple or loculated splenic abscesses may sometimes respond to antibiotics alone but splenectomy is the preferred treatment. In general, failure to respond to antibiotics with or without percutaneous drainage necessitates the splenectomy. Splenectomy is the final definitive management for ruptured, severely damaged spleen or in cases not responding to percutaneous drainage.^{5 12}

Learning points.

• Splenic abscess is a rare fatal clinical entity with ~600 reported cases and spontaneous rupture is even rarer condition.

• Rupture of splenic abscess associated with gas-producing pathogens may lead to pneumoperitoneum and mimics hollow viscus perforation peritonitis.

• Ruptured splenic abscess should be kept in mind as a differential diagnosis of pneumoperitoneum or peritonitis, particularly for immunocompromised patients.

• Splenectomy is the final definitive management for ruptured splenic abscess, when other measures fail.