Keywords acute necrotizing pancreatitis - sinistral portal hypertension - splenomegaly - colonic obstruction
Schlüsselwörter akute nekrotisierende Pankreatitis - sinistrale portale Hypertension - Splenomegalie - Kolonobstruktion
Introduction
Acute necrotizing pancreatitis (ANP) can cause various regional complications due to necrosis and exudation of the pancreatic parenchyma and peripancreatic tissue. The close anatomical connection between the pancreas, spleen, and transverse colon often results in combined spleen or colon involvement in ANP cases. Sinistral portal hypertension (SPH) refers to regional portal hypertension caused by compression and distortion of the splenic vein, inflammatory wall thickening or luminal narrowing and blockage, venous thrombosis, and impaired blood return. SPH accounts for less than 5% of all patients with portal hypertension [1 ]. Among the causes of SPH, pancreatitis is the most common, accounting for about 60% of all reasons. The incidence of colonic complications in acute pancreatitis is approximately 11%, including paralytic intestinal obstruction, segmental necrosis, and colonic fistula [2 ]. However, mechanical obstruction of the colon caused by pancreatitis is much more rare. Herein, we report a patient with ANP combined with SPH who had a sudden acute mechanical obstruction of the colon during treatment. We also analyzed the relationship between pancreatitis and colon obstruction and SPH, as well as the choice of treatment measures.
Case presentation
The patient, a 37-year-old male, was admitted to our hospital with ”epigastric pain for more than three months and fever for 20 days”. The patient was diagnosed with “acute pancreatitis” at a local hospital three months prior and received anti-inflammatory treatment and abdominocentesis. Twenty days before admission, the patient developed intermittent abdominal pain with a high fever after the drainage tube of the abdominal puncture was removed and transferred to our hospital. The patient was in good health and had no food or drug allergies history. Abdomen CT plain scan on admission ([Fig. 1 ]
A–C ) showed ANP with peripheral infection, gas accumulation, and abdominal effusion. The spleen was enlarged and less uniform in density. The splenic flexural wall of the colon was thickened. After admission, patients were treated with fasting, gastrointestinal decompression, active infection control, nutrition support, and acid inhibitor and ulinastatin.
Fig. 1 The clinical data of the case. (A )–(C ) CT scan of the whole abdomen on admission. The spleen is obviously enlarged.Pancreatic enlargement with an accumulation of necrotic material and gas density shadow visible in the tail of the pancreas and splenic hilum area, considering infection. (D ) and (E ) Enhanced CT of the whole abdomen shows splenic vein stenosis, locally indistinct. Coronal view: stenosis of splenic vein shown by the arrow. (F ) and (G ) Intestinal wall thickening in the splenic region of the transverse colon with proximal colonic obstruction. (H ) and (I ) Colonoscopy showed that intestinal mucosa edema caused by splenic curvature of the colon was obvious. (J ) the transanal decompression tube consists of a lateral suction port and a balloon at the front and a balloon filling port, a recharge port and a drainage port from top to bottom at the rear. (K ) Percutaneous puncture and drainage were performed under CT, and the drainage tube was placed in the left pararenal anterior space, and the shadow of the transanal decompression tube in the descending colon was visible.
On the 6th day of admission, the patient had sudden onset of full abdominal distension and pain without defecation. Enhanced CT of the whole abdomen showed ([Fig. 1 ]
D–G ) an enlarged pancreas with uneven density, increased density in the surrounding fat space, a patchy high-density shadow, a gas density shadow with the tail of the pancreas being prominent, multiple tortuous vascular shadows in the splenic portal area, and a thickened wall in the splenic region of the transverse colon with incomplete obstruction of the proximal colon, not excluding occupying lesions. After a multidisciplinary discussion, it was considered that the patient had developed mechanical colonic obstruction. Subsequently, the patient underwent transanal decompression tube placement via colonoscopy to relieve the obstructive symptoms. Colonoscopy showed significant mucosal edema in the colonic splanchnic lumen resulting in luminal stenosis ([Fig. 1 ]
H–I ), and the tube was fixed at the proximal end of the obstructed intestine through the stenotic segment, draining a large amount of feces. After 10 days, the patient was drained by a CT-guided percutaneous puncture, and a drainage tube was placed in the left pararenal anterior space through the left abdomen ([Fig. 1 ]
K ), and the drainage fluid was purulent. After 20 days, minimally invasive removal of pancreatic necrotic tissue was performed. After the operation, the patient was given continuous saline flushing through the drainage tube and continued symptomatic treatment. The patient was discharged after two months with improvement of symptoms.
Discussion
The pathogenesis of SPH by ANP is that infected necrosis of the pancreas causes damage to the intima of the splenic vein adjacent to the pancreas and vasospasm, leading to luminal narrowing and hemodynamic disturbances, which in turn cause thrombosis of the splenic vein [3 ]. Generally speaking, the main clinical manifestations of SPH are the formation of gastroesophageal varices, ascites, and splenomegaly. In terms of treatment, most scholars believe that in patients with simple splenomegaly not combined with gastrointestinal bleeding, the risk of splenectomy is higher, even higher than the risk of gastrointestinal bleeding due to SPH, so prophylactic splenectomy is not recommended, and active management of the primary disease and regular follow up is required [4 ]. In this case, the patient only presented with spleen enlargement and had a good prognosis after active treatment of the primary disease.
Mechanical obstruction of the colon caused by pancreatitis is rare. We considered two possible reasons for the patient’s colonic obstruction in this case. Firstly, the enlargement of the spleen due to pancreatitis may compress the wall of the colon, as T. Sommer reported in a case of colonic obstruction due to progressive splenomegaly in a patient with hematological disease [5 ]. Secondly, a large amount of peripancreatic necrotic material in patients can form external pressure on the colon or irritate the colon wall and peri-colonic fatty tissue leading to peri-colonies and causing colonic stricture.
Most of the previously reported cases of colonic obstruction due to pancreatitis were treated with colonic surgery, for example, M. Pascual et al. [6 ] performed subtotal colectomy for a preoperative misdiagnosis of colonic obstruction secondary to pancreatitis as a splenic flexure tumor of the colon. Mohiuddin et al. [7 ] performed left hemicolectomy and splenectomy in patients presenting with colonic splenic flexure obstruction after three months of conservative treatment for severe pancreatitis. In a recent report, colonic stents were used to treat colonic strictures secondary to acute pancreatitis [8 ]. In Eastern countries such as Japan and China, a transanal decompression tube is often used as an alternative to emergency surgery for malignant large bowel obstruction [9 ]. To date, no cases of transanal decompression tubes being used for colonic obstruction due to pancreatitis have been seen.
In this case report, we emphasize that the primary focus in addressing adjacent organ complications in patients with ANP involves the drainage and elimination of peripancreatic necrotic tissue. For patients experiencing ANP along with a reversible mechanical obstruction of the colon, utilizing a transanal decompression catheter can be a preferable treatment option, potentially averting the need for additional surgical intervention.
