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Critical care dysmotility: abnormal foregut motor function in the ICU/ITU patient
  1. E M M Quigley
  1. Correspondence to:
    Professor E M M Quigley
    Alimentary Pharmabiotic Centre, Department of Medicine, Clinical Sciences Building, Cork University Hospital, Cork, Ireland;

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While aspiration and feeding difficulties are well known challenges in the intensive care unit, their pathophysiology has been poorly understood. New information suggests that the critically ill are subject to profound alterations in motor and sensory function of the oesophagus, lower oesophageal sphincter, stomach, and duodenum which go some way to explaining their propensity to reflux and gastroparesis, with their attendant risks

As medicine changes so should all aspects of medical care and knowledge; as more and more patients are subjected to surgical procedures of increasing complexity and risk and as survival rates from catastrophic illness rise, due to advances in surgery, anaesthesia, and intensive care, one would expect an associated growth in awareness of, and research into, the effects of critical illness on gut motor function. However, motor function and dysfunction, in this context, have received scant attention and have remained, for the most part, poorly understood. While a high prevalence of such phenomena as gastro-oesophageal reflux and gastroparesis are assumed, their true rates of occurrence have been scarcely documented. Similarly, while potential consequences of these entities, such as aspiration, oesophagitis, nosocomial pneumonia, feeding difficulties, and even gastric perforation are well known and, justifiably, feared, the effects of critical illness on oesophageal and gastric motor function have been little investigated. There are, it must be conceded, many reasons for this. Several factors, intrinsic to any intensive care (or therapy) unit (IC/TU) patient population, deter the clinician-scientist from embarking on the investigation of these subjects and confound the interpretation of any studies completed.

First and foremost, this is, by definition, a heterogeneous population. Depending on the nature of a particular unit, it may include among its patients a wide range of ages as well as a diverse catalogue of precipitating illnesses and events. Among the latter, prior surgery, raised intracranial pressure, intra-abdominal or systemic sepsis, cranial, abdominal, or spinal trauma, and such conditions as acute pancreatitis and intestinal ischaemia will directly influence gut motor function. Within each of these categories further heterogeneity prevails; ileus following surgery being especially prevalent in relation not only to extensive abdominal procedures but also to abdominal aortic, cardiac, and spinal surgery.1 Pre-existing illnesses, such as diabetes, will also influence the response to acute stress and the likelihood of motor dysfunction. Electrolyte abnormalities are common in the critically ill and can influence the function of excitable tissues, including intestinal nerve and muscle.

Secondly, these patients are prey to a host of iatrogenic influences on gut motor function. The typical ICU patient receives significant sedation and analgesia, typically requires mechanical ventilation, is administered adrenergic agents for circulatory support, and relies on ether total parenteral (TPN) or enteral nutrition: all can influence foregut motor function. Administration of TPN, together with the metabolic effects of acute stress, may result in significant fluctuations in blood sugar levels with their attendant effects on the gut and, especially, gastric motility. Hyperglycaemia, for example, can profoundly suppress gastric motility and delay gastric emptying.2

Finally, these patients are critically ill and rarely fully conscious. Symptoms cannot be expressed, thereby ensuring that the consequences of motor dysfunction will be, for the most part, silent. These same factors may give rise to difficulties in relation to consent and ability to cooperate with research protocols.

Given this daunting background those who have endeavoured to answer crucial questions in this context are to be lauded and none more so than the Adelaide group which has recently presented us with two seminal works in this area.3,4 Taking advantage of the latest advances in technology, they have boldly gone where few have previously dared to tread and, in so doing, have provided us with some real progress in this area. Taken together, these studies provide some striking and clinically important observations on foregut motility in the critically ill. The first of these studies addressed oesophageal function, the second gastroduodenal; when combined they provide a frightening scenario which goes some way to explaining the prevalence of feeding intolerance and aspiration in this patient population.

Turning firstly to the study of oesophageal motor function.3 Among 15 mechanically ventilated patients they documented some striking abnormalities. Lower oesophageal sphincter (LOS) pressure was virtually non-existent (averaging just 2.2 mm Hg!) and the motor response to reflux (secondary peristalsis) was strikingly impaired. Not surprisingly, reflux was frequent and often prolonged; in some patients, pH was below 4 for the entire six hour study period. The median percentage of time that pH was below 4 was 39% during fasting and 32% following nutrient administration. Reflux events were related either to absent LOS pressure or the occurrence of straining, on a background of marked LOS hypotension. Of considerable clinical relevance, most episodes of straining were precipitated by coughing, in turn usually provoked by endotracheal tube suction, a familiar scenario in any ICU. The ICU patient is clearly at extreme risk for acid reflux whose prevalence must have been greatly underestimated in the past if these data are in any way representative of the general ICU/ITU population. Acid may not be the only risk factor. This study incorporated motility, pH, and impedance measurements; the latter detecting many non-acid reflux events. In the ICU, parenteral acid suppression has become the norm; in this hypo- or achlorhydric environment bacterial overgrowth may occur in the stomach5 and could, through non-acid reflux events such as those described, lead to the development of aspiration pneumonia. It must be conceded that evidence for an increased incidence of nosocomial pneumonia in relation to acid suppression, in this context, has remained, for the most part, elusive.6,7 Nevertheless, given the findings of Nind and colleagues,3 one could speculate that therapy directed at the LOS or oesophageal body function may ultimately prove to be more appropriate than, or should be administered in addition to, acid suppression in the ICU.

In the second study, in this issue of Gut,4 efforts were exerted further “south”, in the stomach and duodenum, but the findings were equally alarming (see page 1384). Fifteen mechanically ventilated ICU patients were subjected to antro-pyloro-duodenal manometry and gastric emptying in the fasted state and following intragastric and intraduodenal nutrient infusion at the very modest rate of 1 kcal/min. The most striking finding was the profound inhibition of antral motility which resulted from either intragastric or intraduodenal nutrient installation; a similar rate of nutrient infusion to healthy volunteers had no effect on this parameter of gastric motor function. Intraduodenal nutrient also provoked isolated pyloric pressure waves and augmented pyloric tone, phenomena which would serve to further impair gastric emptying. Gastric emptying, was, not surprisingly, delayed. Taken together, these findings indicate a profound “upregulation” of the feedback loop which normally regulates the gastric emptying of nutrients and guarantees the steady delivery of 2–3 kcal/min to the small intestine, thus ensuring optimal digestive function. In the ICU patient, this very same mechanism appears to be preventing the egress of gastric contents in response to a duodenal nutrient delivery rate of just 1 kcal/min, an observation that may go some way towards explaining the frequency of intolerance to enteral nutrition in this population. To add insult to injury, duodenal motility was disrupted with a failure to convert to a fed pattern and a persistence of burst activity, hardly the ideal accompaniment for the digestive process.

In both of these studies, the investigators were careful to control for some of the factors that have bedevilled prior investigations; nevertheless, the pathophysiology of these oesophageal and gastric motor changes remains unclear and the relative contributions of such factors as underlying illness, mechanical ventilation, or hypotension remain unresolved. The Chapman study, by invoking an abnormality in the intestinal sensing of nutrient, does indicate that, in terms of gastric function, the primary abnormality may not be simple “pump” failure, as has been described by others in the critically ill,8,9,10 but rather a hypersensitive intestino-gastric feedback loop.4

Regardless of the pathogenesis of these findings, everyone who cares for these patients must be aware of the triple jeopardy to which these patients are prone: LOS hypotension, oesophageal body dysmotility, and gastroparesis (fig 1). When combined, these factors expose the ICU patient to an extreme risk of aspiration of acid or, alternately, pathogen enriched, acid depleted gastric juice. These findings demand that we pay much more attention to motor dysfunction11 and the delivery of enteral nutrition to a highly vulnerable patient population. Here we are presented with a dramatic example of the need for ever greater emphasis on the “organic” manifestations of gastrointestinal myoneural pathology.12

Figure 1

 Abnormalities of oesophageal and gastric motor function in the intensive care unit patient. The “double jeopardy” of gastric and oesophageal motor dysfunction which conspire to promote reflux, aspiration, and feeding intolerance in the critically ill. IPPWs, isolated pyloric pressure waves; LOS, lower oesophageal sphincter, GOR, gastro-oesophageal reflux.

While aspiration and feeding difficulties are well known challenges in the intensive care unit, their pathophysiology has been poorly understood. New information suggests that the critically ill are subject to profound alterations in motor and sensory function of the oesophagus, lower oesophageal sphincter, stomach, and duodenum which go some way to explaining their propensity to reflux and gastroparesis, with their attendant risks


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  • Conflict of interest: None declared.

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