The Seventh Organ-Gastrointestinal Tract: Neglect at Your Own Peril!

How to cite this article: Kulkarni AP, Govil D, Gupta S. The Seventh Organ-Gastrointestinal Tract: Neglect at Your Own Peril!. Indian J Crit Care Med 2020;24(Suppl 4):S143-S145.

Charak Samhita, an ancient Hindu medical text, written in 4th to 2nd century BCE, is a testimony, that the Ayurveda practitioners understood the importance of the process of digestion quite well.[1] Ayurveda goes beyond caloric intake and contains detailed description of classification general properties of food, and dietary regulations.[2]

In comparison, the anatomists and physicians of medieval age seemed to think that stomach was an unclean organ and was therefore separated by nature with diaphragm to protect the important organs and the site of reason and of the mind.[3] Some descriptions from this period seem exotic from today's perspective. “The stomach has the liver below it like a fire underneath a cauldron; and thus the stomach is like a kettle of food, the gall-bladder its cook, and the liver is the fire”.[4]

The gut manages between 8 and 10 L of fluid and vast amounts of electrolytes [sodium (800 mEq), chlorides (700 mEq), and potassium (100 mmol)] every day. This contains nearly 3.5 to 4.0 L of secretions containing innumerable important enzymes and factors.[5]

Critical care literature is full of organ support therapies directed at managing respiratory failure, shock, renal, hepatic, and central nervous system dysfunction. The realization that gut dysfunction can initiate, propagate, and amplify critical illness and worsen the patient outcomes is relatively new in the critical care literature. The search for term “Gut dysfunction in Critically ill” in PubMed yields only 276 citations.

Mutlu et al. described the complex interactions between mechanical ventilation and gut dysfunction.[6] Due to concomitant presence of gut dysfunction and critical illness, it is difficult to pinpoint mechanical ventilation as a sole cause of gut dysfunction. However, mechanical ventilation can certainly worsen gut function primarily by reducing the splanchnic circulation by decreasing mean arterial pressure and increasing resistance of the gut vasculature. Furthermore, the gut is at a distinct disadvantage due to its lack of inability to autoregulate the blood flow and possibility of persistent splanchnic vasoconstriction, even when global hemodynamics are optimized. The hematocrit of blood in gut vessels is barely 10%, owing to dilution caused by absorption of nutrients and fluid from intestinal lumen and finally the tips of gut villi still remain vulnerable to hypoxia due to shunting of blood. This affects all parts of gut leading to multiple complications, such as stress ulcers, gastroparesis, feed intolerance, paralytic ileus, and diarrhea, not forgetting the worsening of hepatic and pancreatic function. In a multicenter prospective study of 337 patients from 40 ICUs, presence of 3 more GI symptoms on day 1 of ICU stay was associated with increased 28-day mortality (62.5 vs 28.9 %, p = 0.001).[7] Innumerable problems with gut function may be seen in the critically ill patients, which escape the radar of the intensivists, unless they are the presenting problems, such as acute pancreatitis or fulminant hepatic failure. Acute mesenteric ischemia, a problem seen mainly in the elderly, is seen in 0.1% of all hospital admissions in the USA.[8] This is not often seen in countries with lower life expectancy and is liable to be missed easily, since it may resolve spontaneously. However, low index of suspicion will worsen the outcomes in these patients. In a narrative review, Reintam Blaser et al. stated that gastrointestinal symptoms and signs were common in critically ill patients.[9] Diffuse or localized pain though common in acute abdominal emergencies, this may be difficult to elicit in sedated or obtunded patients. Other common problems at presentation or during ICU stay may be vomiting, diarrhea, abdominal distension, high gastric volumes, and upper and lower gastrointestinal bleeding. Many underlying pathologies causing these signs and symptoms may lead to delayed enteral feeding, feeding intolerance, increased ICU length of stay and costs, and increased mortality (Table 1).

Table 1

Gastrointestinal complications in critically ill patients

Complications	Incidence (%)	Risk factors
SRMD (on endoscopy)[6]	74	MV >48 hours
	100	TBI, coagulopathy, corticosteroids
Upper GI bleeding[16–18]	0.1
	25
Delayed gastric emptying[19,20]	50	Sedation, opioids, TBI, hypoxia, hypercapnia, hyperglycemia
	80
Paralytic ileus[21,22]	2550	Sepsis, peritonitis, pancreatitis, opioids, hypoxia, hypokalemia, hypercapnia, hyperglycemia, hypothermia
Diarrhea[23,24]	11.9–23.1	Infective (C. difficile, norovirus, etc.)
	5.3(6.5 infective)	Laxatives, enemas, feed intolerance
Constipation[6,25]	15 (Mutlu)51.9	MV, opioids, sedation, neuromuscular blocking agents, enteral nutrition, vasopressors
	83
IAH (ACS)[26,27]	50.5 (8.2)30–49	Retroperitoneal hemorrhage, penetrating and blunt abdominal injury, massive ascites, pancreatitis, liver transplant, circumferential burns
	(1.6–6.1)

SRMD, stress-related mucosal damage; MV, mechanical ventilation; TBI, traumatic brain injury; IAH, intra-abdominal hypertension; ACS, abdominal compartment syndrome

The Working Group on Abdominal Problems of the European Society of Intensive Care Medicine standardized the terminology, definitions, and management.[10]

Piton and Capellier reviewed the biomarkers of enterocyte damage and dysfunction leading to failure of barrier function of the gut leading to bacterial translocation and worsening of patient outcomes in ICU. Citrulline, an amino acid produced by small bowel enterocytes. Reduced plasma levels of citrulline indicate reduced mass of enterocytes, suggesting possible intestinal failure. Intestinal fatty acid-binding protein (I-FABP) is present in cytosol of mature enterocytes and is not normally seen in plasma or urine. Elevated levels of I-FABP in either plasma or urine, thus indicate necrosis of enterocytes.[11] A recent review by Longhitano et al. details the use of biomarkers in altered gastrointestinal function in patients with septic shock.[12]

Point of care ultrasound (POCUS) is increasingly being in ICUs. e-FAST is now an established part of assessment and management patients with abdominal and thoracic trauma. Ultrasonography has also been used to aid the placement of the naso/orogastric tube along with placement of endotracheal tube. Similarly, it was found to be useful in assessing gastric residual volume and peristalsis.[13,14] Perez-Calatayud et al. proposed the gastrointestinal and urinary tract sonography (GUTS) protocol for the evaluation of gastrointestinal dysfunction in critically ill patients. They suggested that POCUS should be used to gain anatomical and functional information about the gastrointestinal injury, as defined by the European Consensus Definition of acute gastrointestinal injury (AGI), by looking at the four parameters like diameter, mucosal thickness, peristalsis, and blood flow (using Doppler).[15] Subsequently, Gao et al. used POCUS daily for 1 week in 116 critically ill patients to assess the intestinal thickness, diameter, folds, and peristalsis and stratification of the intestinal wall and calculate the acute gastrointestinal injury ultrasonography (AGIUS) and the GUTS score. They concluded that trans-abdominal USG could be used for evaluating gastrointestinal injury in the critically ill patients.[14]

Sequential organ failure assessment (SOFA) score is commonly used for evaluating progression of the organ dysfunction of six organ systems. It is time we started paying the gastrointestinal tract its due; and find a way to integrate its assessment as the seventh and equally important organ. This approach will certainly improve outcomes of our critically ill patients.