Complicated caecal volvulus with intestinal malrotation in a 20-year-old: a call for heightened diagnostic suspicion: case report

¹Department of Surgery, Consolata Hospital Nkubu, Nkubu, Kenya

^&Corresponding author
Derrick Omoga Oloo, Department of Surgery, Consolata Hospital Nkubu, Nkubu, Kenya

Introduction    

Cecal volvulus (CV) is the second most common cause of volvulus, accounting for 10-15% of volvulus cases [1]. While it predominantly afflicts middle-aged females, the presence of supervening congenital factors may account for an earlier presentation [2]. Congenital CV has been associated with developmental abnormalities such as a highly movable cecum, persistent transverse colon, absent ascending colon, and mesenteric abnormalities of midgut development [3]. Cecal volvulus (CV) often presents as an acute abdomen and carries up to 40% of mortality. Despite diagnostic and therapeutic advances, outcomes remain discouraging owing to late diagnosis and interventional delays in resource-limited settings [3]. Data on cecal volvulus in Kenya is scarce, owing to the rarity of the condition, coupled with underdiagnoses and poor reporting [4]. Nevertheless, in atypical cases, clinical suspicion and timely imaging aid in prompt diagnosis, hence averting complications incidence, and poor outcomes[4]. Sylvester et al. noted the increased perioperative mortality (31%) and hospital stays in patients with a gangrenous or perforated bowel [5]. Thus, a high index of suspicion is essential in atypical demographics with nonspecific image findings for timely diagnosis and intervention.

Patient and observation     

Patient Information: a 20-year-old previously healthy male with sudden-onset periumbilical pain, accompanied by non-bilious vomiting, abdominal distension, and constipation but passing flatus. There was no report of fevers, right lower quadrant pain, dyspepsia, recent alcohol intake, or prior surgery.

Clinical findings: examination revealed a sick-looking, dehydrated, afebrile patient without pallor or scleral icterus. Vital signs: blood pressure 120/79, pulse 79, saturation 97% on room air, T: 36.9°C, respiratory rate 14/minute. His abdomen was symmetrically distended, with visible bowel loops and marked periumbilical tenderness. Hernial orifices were clear, and a digital rectal examination revealed an empty rectum. Cardiovascular, neurological, and respiratory systems were normal.

Diagnostic assessment: an erect abdominal x-ray showed large bowel distension without air-fluid levels (Figure 1), findings that were later confirmed on abdominal computed tomography (CT) scan (Figure 2). Right renal agenesis was also noted on the scan. Initial complete blood count (CBC), lipase levels, and renal function tests were normal. An assessment of partial bowel obstruction was made.

Therapeutic intervention: he was initiated on conservative management with intravenous hydration (IV Ringer's at 125mls/hr), analgesia (IV paracetamol 1gm TID), antiemesis (IV Ondansetron 8mg TID), a nasogastric tube (NGT), flatus tube, nil-per-oral, and input-output charting. Forty-eight hours later, there was worsening abdominal distention, borderline fevers (37.5°C), and increasing NGT output (800mls to 1100mls). Other systems and hemodynamic status were normal. He was also developing acute kidney injury (urea 9.3mmol/L), suspected tubular necrosis evidenced by hypercalcemia (2.61mmol/L) and hypermagnesemia (2.92mM), and a left shift on CBC. Broad-spectrum antibiotics were initiated (IV ceftriaxone 2gm OD, IV Metronidazole 400mg TID), and an emergent exploratory laparotomy was performed after consent. Intraoperative findings revealed gross peritoneal soiling with foul-smelling peritoneal fluid. Also noted was type 2 cecal volvulus with extensive necrosis involving the terminal ileum to the mid-transverse colon, cecal perforation, and small bowel ischemia. There was intestinal malrotation, marked by a leftward mesentery, a displaced duodenojejunal flexure (DJF), and right renal agenesis (Figure 3, Figure 4, Figure 5). Damage control surgery (DCS) involving resection of the necrosed segment and stump creation was done. Post abdominal washout and temporary closure, he was noted to be desaturating (85-88% room air) and hypotensive (85/54mmHg, pulse-89/minute), and was admitted to the intensive care unit (ICU).

Further care and follow up: the patient was on vasopressor support for twenty-four hours (norepinephrine 1.5mcg/kg/min, titrated to maximum of 2mcg/kg/min), along with oxygen supplementation (5mls/min via non-rebreather mask), fluids (IV saline alternating 5% dextrose at 150mls/hour), antibiotics(IV Meropenem 500mg 8 hourly, IV Metronidazole 400mg 8hourly), other medications (IV Omeprazole 40mg 24hourly, IV paracetamol 1g 8hourly, IV Ketorolac 30mg 12 hourly), and parenteral nutrition per calorie demands. On day one post-DCS, there was an interval worsening of kidney injury, mentation, positive fluid balance, and septicaemia (Table 1), likely due to sepsis-related evolution. In the subsequent 24 hours, gradually, renal, neurologic, and respiratory functions improved, and confusion and septicemia resolved. He was weaned off oxygen, and vasopressors were stopped. Hypermagnesemia, hypercalcemia, respiratory alkalosis, and elevated lactate levels would resolve much more slowly (Table 1). The patient consented to relook surgery, and intraoperatively, the small bowel was noted to be viable, and an end-to-side ileotransverse anastomosis was done. Post the relook surgery, lactate levels normalized, respiratory alkalosis resolved, and bowel function returned after 72 hours post-relook surgery. Graduated feeding was initiated, and thereafter management was de-escalated to the general ward until his discharge on full feeds and normal clinical and laboratory parameters 16 days later. Subsequent fortnight follow-ups demonstrated good adjustment and resumption of normal activities, and he is faring well 3 years later.

Patient perspective: He appreciated the promptness of surgical intervention when conservative care failed, and the subsequent intensive care.

Informed consent: Patient consented to the case publication, and consent details can be availed on request.

Discussion     

CV is rare before 30 years [5], owing to the role of acquired risk factors such as colonic malignancy, adhesions, chronic constipation, pregnancy, and psychotropics [6]. While a hypermobile mesentery of ascending colon and cecum is a major predisposition to volvulus development, only 11% of individuals with hypermobility develop CV, underscoring the role of acquired factors [7]. In our case, the presence of intestinal malrotation with a leftward mesentery, right renal agenesis, and a displaced duodenojejunal flexure (DJF) suggested the likelihood of a congenital etiology. Those findings were interesting since up to85% of malrotation cases are diagnosed within 2 months of life, and rarely do they persist undetected to adulthood [8]. Further, it is established that the coexistence of congenital malrotation also heightens the risk for other obstructive events, and thus identification and communication prevent delayed diagnosis in possible future presentation [8]. Save for recreational khat use, the patient had no other acquired risk factors for CV.

The definitive diagnosis of cecal volvulus is an intraoperative finding. Imaging, such as abdominal ultrasound and erect x-ray, suffer from poor negative predictive value and user dependence, as was in this case [5]. The CT scan, while used as a gold standard, has a sensitivity of 90% [7,9]. Importantly, imaging does not preclude operative intervention in unstable patients, such as in our case, since the timing of intervention is critical in averting the attendant complications [6]. Further, surgical approaches and outcomes rely on the preoperative hemodynamic stability and clinical severity of the condition [4], and bowel viability guides the extent of surgery, impacts recurrence risk, and perioperative morbidity [9,10]. As in our patient, DCS involved ileocolectomy with stump creation, generous abdominal washout and closure, followed by secondary anastomosis 48 hours later. In DCS, the torted segment was not untwisted to avoid reperfusion injury and resultant overwhelming toxemia.

Mortality in these patients is predominantly sepsis-related and rises as high as 40% in complicated cases. As in our case, necrosis with overwhelming septicemia and multiorgan dysfunction necessitated intensive care for hemodynamic and respiratory support. Hydration, vasopressor use, and oxygenation were prerequisites, even as aggressive fluids and drug options faced the hurdle of one functioning kidney. Further, with interval deterioration in renal function and incipient pulmonary edema, fluid demands were carefully regulated, and NSAIDs were also avoided to prevent further renal injury. The case also encountered some limitations. It is noteworthy that the case was likely beset by delays in surgical intervention, due to initial unspecific imaging and clinical findings. These occasioned the bowel complications noted, intensive care, and extended hospital stay. Further, the suspicion of congenital etiology lacked objective confirmation and was purely based on intraoperative findings and clinical information.

Conclusion     

In summary, cecal volvulus is a rare but emergent diagnosis. Atypical disease presentation raises a likelihood of delays in diagnosis or intervention, thereby adversely affecting outcomes. Accordingly, attempts at improving outcomes should be hinged on heightened clinical suspicion, investigation, and early surgical intervention.

Competing interests     

The authors declare no conflict of interest.

Authors' contributions     

DO. Lead author, conceptualization, compilation, and final review. DO, SO, CSL, CO. Manuscript writing and review. CSL, CO, SO. Approval seeking, manuscript writing, ethical adherence, and review. All the authors have read and agreed to the final manuscript.

Table and figures     

Table 1: evolution of key parameters

Figure 1: erect abdominal radiograph with dilated bowel loops

Figure 2: computed tomography scan showing non specific colonic distension

Figure 3: intraoperative image of necrosed bowel segment before resection

Figure 4: intraoperative image of necrosed bowel segment after resection

Figure 5: bowel examination after laparotomy

References