Introduction
Obstructive colonic cancer is a common presentation of colonic cancer, and it is the
major presenting symptom in 8 to 29% of patients with colorectal cancer (CRC), and
85% of emergency colorectal surgery for cancer is for colonic obstruction. However,
obstructive colitis (OC), or extensive ischemic colitis, proximally to an obstructive
colonic cancer is an uncommon condition. [1 ]
[2 ] In addition, obstructive CRC may be complicated by perforation, electrolyte disturbance,
bacterial translocation, and sepsis.[1 ] OC refers to ulcero-inflammatory lesions occurring in the colon proximal to a completely
or partially obstructing lesion. This is in contrast to true ulcerative colitis complicated
by colon cancer, where there are inflammatory lesions proximal and distal to the neoplasm.[3 ] Rarely, OC can progress to acute necrotizing colitis. Only few cases of acute necrotizing
colitis due to colon cancer are reported in the literature.[4 ]
In this case report, we present a 72-year-old man who manifested two separate ischemic
bowel events secondary to an obstructing sigmoid adenocarcinoma. The first event was
small bowel necrosis; the second event was large bowel ischemia that occurred few
days later despite colonic decompression. To the best of our knowledge, there is no
reported similar case in the literature.
Case Report
A 72-year-old male patient with a history of smoking (>100 pack years), coronary artery
disease, hypertension, dyslipidemia, diabetes mellitus type 2, and a family history
of colon cancer (first-degree relative, age of onset >50 years old) presented for
2 days history of gradually worsening abdominal pain and distension, associated with
nausea, vomiting, and constipation of several days duration. He had a 2-months history
of gradual weight loss reaching 10 kg, poor appetite, abdominal bloating, and change
in bowel habits with decreased stool caliber. His physical examination on admission
revealed: blood pressure 123/68 mmHg, pulse 105 bpm, respiratory rate 17/min, temperature
37.3°C, oxygen saturation 97%, positive bowel sounds, distended abdomen with diffuse
tenderness, and no guarding or rebound tenderness. Laboratory results showed increased
inflammatory markers: leukocyte count 20,500 cells/μL, 85% neutrophils, C-reactive
protein 1 mg/dL initially, hemoglobin 17.3 mg/dL, blood urea nitrogen 20 mg/dL, creatinine
0.79 mg/dL, lipase 25 u/L, and normal electrolyte levels. Abdominal pelvis enhanced
computed tomography (CT) showed diffuse dilatation of the large bowels proximal to
a transition zone in the proximal sigmoid measuring around 3 cm in length, mild wall
thickening, and mild fat stranding raising the suspicion of a malignant lesion. A
highly suspicious intrahepatic mass was also seen ([Fig. 1 ]).
Fig. 1 Abdominal enhanced computed tomography scan showing: (A ) highly suspicious intrahepatic mass; (B ) diffuse dilatation of the large bowels; (C ) transition zone in the proximal sigmoid showing mild wall thickening with mild fat
stranding raising the suspicion of a malignant lesion.
Diagnosis of obstructive sigmoid tumor was done. A nasogastric tube was placed, intravenous
(IV) hydration and antibiotics started. Rectal tube was not attempted. The patient
deteriorated few hours later, with worsening abdominal pain and increased distension,
and emergency laparotomy was decided. After induction, the patient became unstable
and was started on vasopressors. Intraoperative findings were sigmoid colon severe
stenosis, proximal dilation without perforation, and mild ascites. The small bowels
were dilated proximally and black colored from the ileocecal valve up to 2 meters,
proximal to the terminal ileum, suggesting acute ischemia without major vessel occlusion.
The colon was dilated but viable ([Fig. 2 ]).
Fig. 2 Macroscopic view of the dilated large bowels and necrotic small bowels.
A Pezzer tube was inserted in the cecum to drain and decompress the colon. We performed
a resection of 2 meters of ischemic small bowel from the ileocecal valve including
the appendix and an end ileostomy was created ([Fig. 3 ]). Omental and peritoneal lesions were also biopsied and sent to pathology. Final
pathology result showed ischemic enteritis, mostly mucosal, with metastatic deposit
of adenocarcinoma on proximal appendiceal serosa. Both surgical margins showed ischemic
mucosa and transmural inflammation with edematous yet viable submucosa and muscularis
propria. Omental and peritoneal lesion returned positive for metastatic adenocarcinoma
consistent with the primary tumor of colonic origin.
Postoperatively, the patient was transferred to the incentive care unit, intubated,
ventilated, sedated, on vasopressors, and on broad-spectrum IV antibiotics.
The patient's general condition was controlled initially, on minimal vasopressors
dose. On postoperative day 5, an abdomen pelvis CT scan without enhancement was done
for persistent fever, worsening acute kidney injury (AKI), and increasing Creatine
phosphokinase (CPK) level to 7,363 IU/L. CT scan showed findings of right colitis
of infectious or ischemic origin that cannot be determined due to lack of IV contrast
([Fig. 4 ]). IV antibiotics were empirically escalated.
Fig. 3 Specimen removed.
Fig. 4 Nonenhanced abdominal computed tomography scan showing right colitis.
On postoperative day 6, patient was still febrile with temperature at 39.5°C, now
anuric, volume overloaded, creatinine increased to 10.02 mg/dL, and CPK to 117,66
IU/L. Decision was taken to go for urgent dialysis for volume overload due to renal
failure secondary to rhabdomyolysis, followed by emergency exploratory laparotomy
that showed an ischemic descending colon proximal to the sigmoid mass. Total colectomy
(sparing of the rectal vault for possible later anastomosis) was done ([Fig. 5 ]). Pathology results reported pT3N0M1c, showing a 2 × 2 cm moderately differentiated
adenocarcinoma of the sigmoid colon, completely obstructive with invasion of the serosa,
rare vascular emboli, no metastatic lymph nodes (0 out of 16), and ischemia of all
the colon with neoplastic thrombosis of the inferior mesenteric vein.
Fig. 5 Colonic ischemia proximal to the sigmoid mass.
After the second surgery, endotracheal extubation was delayed for 1 week due to recurrent
episodes of desaturation secondary to pneumonia-related mucous plugs. Abdominal cultures
grew Enterococcus faecium , Escherichia coli , Candida albicans , and Stenotrophomonas maltophilia . His infected abdominal fluid was continuously drained in the surgical drain bag,
and the infection was treated with wide antibiotics and antifungal coverages. Rectal
pouch leakage was diagnosed on imaging fluoroscopy and abdomen-pelvis CT scan. The
contrast was identified from the rectal vault surgical clip and up to the right anterolateral
draining tube in the abdomen. Management was conservative and the pouch resolved with
no surgical intervention. AKI improved after resolution of septic shock and rhabdomyolysis.
Gradually, the patient improved, was weaned off pressors and mechanical ventilation,
extubated, switched to specialized PO diet for short bowel syndrome, and transferred
to a regular floor. On postoperative day 37 from the first operation, he was discharged
home on daily Loperamide and Cholestyramine, with close follow-up, vitamins replenishment,
good hydration, and low carbohydrate diet for short bowel syndrome.
Discussion
CRC is the third most common tumor in men and the second in women, accounting for
10% of all tumor types worldwide. CRC is the fourth most common cancer-related cause
of death. The mortality rate is 15–20/100,000 in males and 9–14/100,000 in females.[5 ]
[6 ]
In total, 20% of patients with CRC are diagnosed with colonic obstruction, mostly
on the left side.[5 ] Colonic obstruction may lead to multiple complications such as perforation, electrolyte
disturbances, sepsis from bacterial translocation, OC, and bowel ischemia.[2 ]
In addition, 0.3 to 3.1% of CRCs are associated with OC.[7 ] OC is defined as a nonspecific inflammatory lesion of the colon, such as erosion
and ulceration, proximal to a completely or partially obstructive lesion. It can become
fulminant, which is then known as acute necrotizing colitis.[8 ]
In patients with acute colonic obstruction due to malignancy, there are different
strategies to decompress colonic obstruction. It can be with nonsurgical approaches
such as balloon dilatation, or placement of a rectal tube, or with a surgical approach
such as low hole enterostomy and resection of the tumor with or without colostomy.[2 ] In some cases, resection of the cancer may not be possible because of concomitant
medical disease or hemodynamic instability.[9 ] In our case, due to rapid deterioration of the patient, surgical management was
the best option.
For left colon obstruction, two types of surgical approaches can be used. The first
is synchronous treatment of carcinoma and obstruction by primary anastomosis. The
second is Hartmann procedure, which is the treatment of the obstruction by staged
resection. The benefits of staged operation are less surgical trauma, which is significant
in patients whose general condition is precarious, and reduction of the risk of contamination
due to unprepared bowels.[2 ] Our patient was hemodynamically unstable post-induction and he was started on vasopressors.
We decided to go for a staged operation to reduce operating time and to prevent short
bowel syndrome and extensive ileal resection.
Malignant large bowel obstruction can be complicated by an ischemic episode in 5%
of the cases.[7 ] Various etiologies were suggested for this condition: hypovolemic states, systemic
diseases like vasculitis and hypercoagulable states, mechanical obstruction, atherosclerosis,
bacterial proliferation, therapeutic drug effect including pressors use, and infection.[9 ] Our patient had multiple factors from these suggested etiologies: hypovolemic states,
hypercoagulable states due to malignancies, mechanical obstruction, and bacterial
proliferation in the initial ischemic episode. Therapeutic drug effects including
pressors use and infection were added on the subsequent ischemic events.
To further explain these possible causes, colon distension from malignant colon obstruction
may reduce the blood supply to the bowel wall leading to hypoperfusion and ischemia
and colonic gangrene. When endoluminal pressure exceeds 35 cmH2 O, intramural perfusion decreases. Once the endoluminal pressure is sustained over
40 cmH2 O, there will be irreversible ischemic lesions of the mucosa. The ischemia affects
predominantly the hypoxia-sensitive mucosal and submucosal layers. Creation of a decompressed
colostomy in malignant colon obstruction can help with the elevated intra-luminal
pressure.[2 ]
Earlier surgical intervention may have mitigated the progression to secondary ischemic
events in the first presentation considering hypovolemic states, mechanical obstruction,
and bacterial proliferation as possible causes of the first ischemic event. But despite
decompression and hemodynamic support, our patient has a second episode of distal
colon ischemia.
First, histopathologically, OC is characterized by either an erosion or a shallow
ulcer confined to the mucosa or submucosa. The most common microscopic findings of
OC are necrosis of the mucosa with denudation of epithelial cells, hemorrhage, congestion,
and prominent neutrophilic infiltration. The serosa and muscular layer better resist
the pressure and preserve their normal aspect. In many cases, the diagnosis is made
at exploratory laparotomy.[9 ]
[10 ] Therefore, even severe ischemic lesions may occasionally be difficult to notice
in the course of laparotomy. Frequently, the colon has a normal appearance during
the surgery. If the surgeon does not have a clinical suspicion of OC, the anastomosis
is made through the involved segment of colon with consequent complications, up to
25%. Complications include peritonitis, perforation, bleeding of the remained ulcerative
lesion, and breakdown of anastomoses made through involved segments of colon. Awareness
of the features and incidence of OC should help physicians avoid these diagnostic
and therapeutic problems by applying a thorough approach while inspecting the mucosal
and submucosal layers of the bowels.[11 ]
Second, bacterial proliferation in the obstructed bowel may lead to massive bacterial
reflux into the ileum from the colon that may cause capillary vasoconstriction of
the bowels, causing ischemia. Hypoxia stimulates the germination of spores and bacterial
growth, which progresses rapidly to produce exotoxins that destroy the surrounding
tissue, leading to rapid spread of the disease.[7 ]
Third, our patient had multiples comorbidities that can result in atherosclerosis
and chronic ischemia of the bowels.[7 ] He was elderly, hypertensive, diabetic, dyslipidemic, and had coronary artery disease.
The use of vasopressors can be an additional factor, decreasing blood supply to the
already compromised circulation.
Moreover, colonic ischemia is difficult to diagnose preoperatively due to its occasionally
mild and transient clinical presentation, and the symptoms are not specific. The most
common presentation is the obstructive syndrome associated with peritonitis. Common
clinical symptoms are abdominal pain, tenderness, constipation or watery diarrhea,
hematochezia, nausea, vomiting, and fever.[3 ]
It was difficult to diagnose colonic ischemia in this patient suspected to have colonic
obstruction due to a distal colon cancer. In the initial presentation of the patient,
we opted for emergency surgery because our patient was deteriorating rapidly. Enhanced
CT scan did not change the final management and might simply have delayed the operation.
Relying on radiologic findings to diagnose ischemia can be misleading in most cases.
In a series of seven patients reported by Chang et al[1 ], the radiologic findings of the abdominal CT of the six cases were compatible with
colon or rectal cancer and distention of the proximal bowel without ischemic changes.
There was only one case where proximal colonic ischemia was diagnosed with abdominal
CT prior to surgery.[3 ]
Of note, the surgeon should pay attention to whether the dilated colon is viable or
not before creating an anastomosis.[8 ] During the first operation, we confirmed that the colon proximal to the obstruction
was viable. A staged operation was done to reduce surgical trauma. Resection of all
ischemic small bowels and cecal decompression were performed. However, he deteriorated
again after 5 days, with rhabdomyolysis and septic shock. Lack of IV contrast made
our diagnosis of colonic ischemia difficult on repeat CT scan, yet we had a high clinical
suspicion for bowel ischemia. Our suspicion was confirmed by the findings of the second
operation.
Equally important, the gross finding of OC is large, irregular ulceration with mucosa
covered by a hemorrhagic and purulent exudate. The margins of the ulcers are frequently
sharply defined with intact intervening mucosa. The wall of the diseased colon is
usually thickened, stiff, and friable. The mucosa of the colon distal to the malignant
lesion is normal grossly and microscopically. Frequently, 2 to 6 cm proximally to
the carcinoma is usually free of ulceration and inflammation. The rest of the proximal
colon will have varying degrees of inflammation and ulceration.[3 ] Most necrotizing enterocolitis involves a single bowel segment (50%), but some cases
may involve multiple segments. The terminal ileum is the most common site of necrotizing
enterocolitis, followed by the large intestine. About 44% of necrotizing enterocolitis
cases occur in both the large and small intestines. Yet, this case is the only one
reported to have a stepwise presentation of small and then large bowel ischemia, to
the best of our knowledge. Pan-necrotizing enterocolitis or necrotizing enterocolitis
totalis is fulminant necrotizing enterocolitis characterized by necrosis of more than
75% of the intestine. As many as 19% of all cases of necrotizing enterocolitis treated
with surgery and necrotizing enterocolitis causing death were pan-necrotizing enterocolitis.[9 ]
Conclusion
OC is an uncommon yet lethal condition that is confined to the mucosa or submucosa
making it difficult to be identified during the laparotomy as the serosal surface
of the colon may be normal. The surgeon must examine the removed colonic segment to
exclude an ischemic process in the area of the anastomosis. Hence, the treatment for
patients with suspected colonic obstruction should be an emergency operation with
long abdominal incision to allow careful and detailed inspection of the whole small
and large bowels.
Because the involved segments of the colon appear externally normal during laparotomy,
it is important to open the resected bowel in the operative field and inspect the
mucosal surface of the dilated and thickened bowel to exclude any inflammatory or
ischemic process.
