ICU Management & Practice, Volume 16 - Issue 3, 2016

Is Enteral Feeding Feasible Early After Abdominal Crisis?

The enteral route is commonly accepted as the first choice for providing ‏nutrition to patients in the ICU with stable haemodynamics and a functional ‏gastrointestinal (GI) tract. However, there is wide uncertainty ‏regarding safe enteral nutrition in patients with critical pathology in the ‏abdomen. In the current review we address different abdominal conditions ‏in critically ill patients where safety and feasibility of enteral nutrition ‏might be questioned. We discuss respective pathophysiological ‏mechanisms, existing evidence and practical aspects.

 

Enteral nutrition (EN) prevents loss of ‏physical and immunological barrier ‏function (Kudsk 2002; McClave 2009). ‏Early EN reduces infections and is recommended ‏in critically ill patients with stable haemodynamics ‏and functional gastrointestinal (GI) tract ‏(Taylor et al. 2016).

 

Feeding in the Early Phase of Critical ‏Illness

 

Even if feeding is started early, a negative energy ‏balance in the first acute phase of critical illness ‏is generally unavoidable. New insights show ‏that early hypocaloric nutrition may even be ‏preferred (Casaer and Van den Berghe 2014) ‏because of an inflammation-induced endogenous ‏energy production and nutrition-induced ‏inhibition of autophagy. Therefore early EN ‏should be started at a low rate in the acute ‏phase and be slowly increased towards target. ‏This is especially true in patients with, or after, ‏abdominal crisis, with continuing vulnerability ‏of GI tract.

 

Based on common sense, EN is considered ‏harmful in the case of the clinical syndrome ‏called “acute abdomen”, in case of obvious gut ‏ischaemia, mechanical obstruction or perforation, ‏and in cases with no continuity of GI tract. ‏In most other abdominal pathologies initiation ‏of EN remains a matter of “try and see”, e.g. ‏starting low dose EN and evaluating feeding ‏tolerance/intolerance.

 

Feeding intolerance (FI) is not uniformly ‏defined; gastric residual volumes (GRV) have ‏been mainly used for assessment of FI (Reintam ‏Blaser et al. 2014). Some authors suggest ‏abandoning GRV measurements all together ‏(Reignier et al. 2013). We suggest that GRVs ‏may still be useful to avoid gastric overfilling ‏in the initial phase of EN or in the presence of ‏abdominal symptoms (e.g. abdominal distension ‏or pain). Evaluation of gastric filling with ‏ultrasound may offer a good alternative to GRV ‏(Gilja et al. 1999).

 

Enteral Nutrition in Specific Abdominal ‏Conditions

 

In critically ill patients with severe abdominal ‏pathology, both abdominal pathology and ‏systemic disease may contribute to GI dysfunction ‏(Table 1). GI function will usually recover ‏if haemodynamics and gut perfusion improve, ‏fluid resuscitation-induced gut oedema resolves ‏and analgo-sedation can be reduced. On the ‏contrary, a patient with persisting severe ‏general condition is prone to complications. ‏Thus EN should be initiated at a low rate and ‏slowly increased under careful monitoring of ‏abdominal symptoms to avoid dilatation of the ‏stomach, bowel distension and increasing intraabdominal ‏pressure (IAP) (Figure 1).

 



Emergency Gastrointestinal Surgery

 

Direct injury of the GI tract due to trauma or ‏surgery and/or infection/inflammation leads ‏to gut oedema and dysmotility. Denervation, ‏discontinuation of spinal reflexes and ‏resection of enterochromaffin cells producing ‏motilin may add to gut paresis. In emergency ‏GI surgery, gut hypoperfusion due to shock, ‏bowel oedema and intra-abdominal hypertension, ‏exacerbated by inflammation and massive ‏fluid resuscitation, is often evident. Therefore, ‏major factors to consider for recovery after ‏emergency GI surgery (if bowel continuity is ‏restored) are: bowel perfusion, bowel oedema ‏and bowel distension. The intraoperative evaluation ‏of bowel viability is important; therefore ‏good communication with surgeons is crucial. ‏If a stoma is created and bowel cranial to stoma ‏has normal appearance, low dose EN can usually ‏be started within 24 hours. In elective surgery, ‏performed anastomoses will likely heal better with EN than without (Boelens et al. 2014). ‏The risk of anastomotic leak is much higher if ‏an anastomosis is performed during emergency ‏surgery, but there is no evidence on harmfulness ‏of early EN in this situation. A positive effect of ‏early EN regarding infections after emergent ‏GI surgery has been shown in one randomised ‏controlled study (Singh et al. 1998).

 

Damage control surgery enables postponement ‏of restoration of bowel continuity until ‏hypoperfusion, oedema and distension are ‏resolved. Still, trophic EN might already be ‏considered if a diverting stoma is present and ‏the next surgery is not planned within the next ‏24 hours.

 

In patients with prolonged abdominal sepsis ‏requiring multiple interventions and clearly not ‏reaching their energy and protein targets with ‏EN, supplemental PN should be considered after ‏a couple of days, while avoiding overfeeding. ‏Supplemental PN should also be considered ‏if such patients have severe diarrhoea with ‏impaired absorption of nutrients. ‏

 

Open Abdomen

 

Patients with open abdomen often require ‏multiple surgeries and have increased risk for ‏fistula formation. A few studies have shown that ‏EN is feasible in patients with open abdomen ‏and is associated with a higher rate of abdominal ‏closure and a lower incidence of ventilatorassociated ‏pneumonia (Collier 2007; Byrnes ‏et al. 2010; Dissanaike 2008). ‏

 

EN should be applied early, as soon as ‏bowel continuity is confirmed or restored ‏and haemodynamic and tissue perfusion goals ‏can be reached with or without vasopressors/ ‏inotropes. Continuing need for fluid resuscitation ‏may refer to unsolved abdominal pathology, ‏whereas losses due to the open abdomen ‏need to be taken into account.

 

See Also: What’s the Benefit of Enteral Nutrition? Updated Review


Abdominal Aortic Surgery

 

Rupture of the abdominal aorta and associated ‏surgery carry a risk of massive bleeding and transfusion, retroperitoneal haematoma ‏formation and impaired gut perfusion, which ‏might be an argument for delaying EN in these ‏patients. The major adverse event after abdominal ‏aortic surgery is colonic ischaemia (CI), ‏which occurs in about 2% of patients after ‏elective surgery for aneurysm, and 10% in case ‏of rupture (Björck et al. 1996; Van Damme et al. ‏2000), somewhat less in endovascular repair ‏(Becquemin et al. 2008). Presumed causes of ‏CI are ligation or obstruction of supply arteries ‏(inferior mesenteric artery, hypogastric arteries, ‏meandering mesenteric arteries), non-occlusive ‏ischaemia due to shock or vasopressor drugs, ‏and (micro) embolisation (Steele 2007).

 

Length of operation, aneurysm rupture ‏and renal insufficiency are independent risk ‏factors of CI (Becquemin et al. 2008). Surgical ‏details (reimplantation of inferior mesenteric ‏artery, intraoperative assessment of blood flow ‏by Doppler flowmetry, large bowel viability, ‏etc.) should be carefully recognised. The main ‏clinical symptoms of CI are early diarrhoea, ‏haematoschisis (Björck et al. 1996) and ileus ‏(Valentine et al. 1998). Colonoscopy remains ‏the method of choice to detect ischaemic ‏lesions of colonic mucosa, but its routine ‏application is not supported (Steele 2007). ‏Whether and how the endoscopic findings can ‏guide EN is not clear. Circulating biochemical ‏markers such as intestinal fatty acid-binding ‏protein may facilitate the recognition of CI ‏(Vermeulen Windsant et al. 2012), but whether ‏this information can be used for feeding ‏decisions remains unknown.

 

Taking the relatively low incidence of CI, ‏it is not rational to delay EN in all patients ‏routinely for several days after abdominal ‏aortic surgery. Instead, EN should be initiated ‏with low dose under careful monitoring of ‏abdominal symptoms, IAP and signs of CI, and ‏increased gradually (van Zanten 2013). In overt ‏bowel ischaemia, EN should be withheld.

 

Abdominal Trauma

 

Abdominal trauma is a complex injury, ‏where a multidisciplinary approach has made ‏non-operative management increasingly ‏feasible and effective (Prachalias and Kontis ‏2014). Early EN may be well integrated in this ‏approach. However, obstacles such as GI tract ‏discontinuity, compromised gut perfusion ‏and/or abdominal compartment syndrome ‏may necessitate delay of EN. At the same ‏time, some older RCTs using needle catheter ‏jejunostomy have shown benefit of early EN ‏over early PN (Kudsk 1992) and over delayed ‏EN (Moore 1986) regarding infectious complications. ‏We suggest starting EN early after ‏abdominal trauma if continuity of GI tract is confirmed/restored, and abdominal compartment ‏syndrome and bowel ischaemia excluded.

 

Abdominal Compartment Syndrome

 

Abdominal compartment syndrome (ACS), ‏defined as IAP above 20 mmHg along with ‏new or worsening organ failure, is an immediately ‏life-threatening condition, where prompt ‏measures to reduce IAP are needed. These ‏measures include decompression of GI tract ‏and avoidance of adding any volume into the ‏abdomen (Kirkpatrick et al. 2013), thereby ‏excluding EN. Moreover, splanchnic perfusion ‏is severely jeopardised during ACS.

 

EN should be considered at elevated IAPs ‏between 12 and 20 mmHg without ACS, but ‏high incidence of feeding intolerance has ‏been described (Reintam et al 2008). Further, ‏EN itself may cause an increase in IAP. We ‏suggest incorporating IAP measurements into ‏standard monitoring of critically ill patients ‏with abdominal pathologies in the initial phase ‏of EN, and cessation of feeding to be considered ‏if worsening of clinical status is possibly ‏attributed to increasing IAP.

 

Severe GI Bleeding

 

Patients admitted to the ICU due to acute GI ‏bleeding require immediate diagnostics and ‏intervention to localise and stop bleeding. EN ‏might be considered when the bleeding has ‏been stopped endoscopically or surgically. The ‏main rationale to withhold EN after stopping ‏active bleeding is disturbed visibility if a ‏new endoscopy is needed; therefore delaying ‏enteral intake for at least 48 hours in case of ‏high risk of rebleeding has been suggested ‏(Hébuterne and Vanbiervliet 2011). Such a ‏time frame is not well justified nor supported ‏by the evidence. We suggest that when upper ‏GI bleeding has been stopped and there are no ‏signs of rebleeding, low dose EN can be started ‏within 48 hours. In case of lower GI bleeding ‏EN could be started immediately.

 

Bowel Ischaemia

 

EN increases gut perfusion (Matheson 2000), ‏but only if the vasculature is intact and the ‏systemic haemodynamics sufficient. There is ‏broad consensus to withhold EN in patients ‏with suspected small bowel ischaemia. ‏This condition requires optimisation of the ‏circulation and, if symptoms of ischaemia ‏persist, a surgical or radiological intervention. ‏In addition, continuous thoracic epidural ‏anaesthesia may increase splanchnic blood ‏flow by blocking afferent sympathic reflexes ‏(Holte 2000). Local mucosal ischaemia of the ‏colon has a tendency to heal when the general ‏condition of the patient improves. Therefore ‏EN should be considered in patients with ‏colonic mucosal ischaemia without bowel ‏distension. Bowel distension may possibly be ‏aggravated by EN and lead to further impairment ‏of bowel wall perfusion. We suggest that ‏EN should not be started if transmural bowel ‏ischaemia is confirmed or suspected or signs ‏of local mucosal ischaemia are seen in severely ‏distended bowel.

 

Bowel Obstruction

 

Bowel obstruction leads to obstructive ileus, ‏with initial hypermotility (be warned: presence ‏of bowel sounds is misleading) to force ‏bowel contents through the obstruction and ‏subsequent bowel distension above the obstruction. ‏Bowel obstruction requires a surgical or ‏endoscopic intervention to restore passage of ‏bowel contents or to create a proximal stoma. ‏EN should be withheld in case of obstructive ‏symptoms, but can be carefully initiated as soon ‏as passage is restored or a proximal stoma has ‏been created. It may take a couple of days before ‏bowel distension and paresis are resolved and ‏EN can be increased.

 

Bowel Paralysis

 

EN itself promotes motility and has beneficial ‏effects regarding the physical and immunological ‏gut barrier, whereas prolonged enteral ‏fasting will aggravate dysmotility and should ‏be avoided. Since gastroparesis is often more ‏pronounced than small intestinal paralysis, ‏the use of prokinetics and postpyloric feeding ‏should be considered early in case of gastric ‏intolerance to EN. However, paralytic ileus is ‏often encountered in patients with peritonitis. ‏Inflammation-induced dysmotility is mediated ‏by cytokines and nitric oxide produced by ‏locally activated macrophages in the muscular ‏layer, and by neuronal pathways (Schmidt et ‏al. 2012). Non-abdominal sepsis may also be ‏associated with bowel paresis, due to the release ‏of nitric oxide, which causes bowel relaxation, ‏oxidative stress and the systemic release of ‏tumour necrosis factor (TNF), which inhibits ‏the central vagal pathways (Emch et al. 2000). ‏Furthermore, many conditions and therapies ‏in critically ill patients (e.g. hyperglycaemia, ‏hypokalaemia, acidosis, use of dopamine, ‏opioids, clonidine and dexmedetomidine) ‏may contribute to bowel paralysis.

 

In rare cases, isolated large bowel distension ‏mainly in the caecum region occurs called Ogilvie’s syndrome seu colonic pseudoobstruction. ‏This condition carries high risk of ‏bowel ischaemia and perforation due to distension, ‏and should be promptly recognised and ‏managed (Oudemans-van Straaten 2011; De ‏Giorgio and Knowles 2009) with intravenous ‏neostigmine (van der Spoel et al. 2001; Valle ‏and Godoy 2014), endoscopic decompression ‏or temporary coecostomy. Early start of lactulose ‏or polyethylene glycol (van der Spoel et al. ‏2007) and neostigmine, if defaecation does not ‏occur, may help to prevent Ogilvie’s syndrome. ‏In less severe cases of bowel paralysis, there are ‏no confirmed contraindications to start a trial ‏of low dose EN under careful monitoring of ‏symptoms and promotion of defaecation with ‏laxatives and neostigmine.

 

Acute Colitis with Toxic Megacolon

 

Acute colitis as a cause of diarrhoea in intensive ‏care is a rare condition that is mostly caused by ‏a Clostridium difficile infection. Sometimes severe ‏enterocolitis is caused by chemotherapy for ‏haematological disorders. In most severe cases ‏toxic megacolon—a severe and life-threatening ‏condition associated with systemic toxicity— ‏may develop (Oudemans-van Straaten 2011). ‏Colitis requires specific therapy, including ‏antibiotics, discontinuation of motility ‏impairing drugs, replacement of intravenous ‏fluids, electrolytes, trace elements and vitamins ‏(Dickinson 2014; Oudemans-van Straaten ‏2011). In rare cases of toxic megacolon, total ‏colectomy becomes necessary for the patient’s ‏survival. In most patients with colitis, there is ‏no contraindication for EN, because the small ‏intestine is intact. However, EN should probably ‏not be applied to patients with toxic megacolon.

 

Conclusions

 

In most patients EN should be considered early ‏after initial management of abdominal crisis, ‏when continuity of GI tract is confirmed or ‏restored, and bowel ischaemia and abdominal ‏compartment syndrome are excluded. However, ‏EN should be started at a slow rate under careful ‏monitoring of GI symptoms and IAP.

 

Conflict of interest

 

Annika Reintam Blaser declares that she has no ‏conflict of interest. Heleen M. Oudemans-van ‏Straaten declares that she has no conflict of ‏interest. Joel Starkopf declares that he has no ‏conflict of interest.

 

Abbreviations
 

ACS abdominal compartment syndrome

CI colonic ischaemia

EN enteral nutrition

FI feeding intolerance

GRV gastric residual volume

IAP intra-abdominal pressure

TNF tumour necrosis factor

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