Case Ileus 1

Case Ileus

Allison Kliewer

Baptist Health System Dietetic Internship

March 28, 2013

Case Ileus 2

Case Ileus

Life expectancy in developed countries has almost doubled within the last 100 years and

now ranges from 76-80 years (Hiranyakas, 2011). The population aged over 65 years is

predicted to increase from 40 million in 2010, to 55 million in 2020 which is a 38 percent

increase since 2000 (Hiranyakas, 2011). This increase in the elder population will by necessity,

increase the number of surgical procedures and number of hospital stays. Elderly patients have

a higher complication of disease and have an increased need for more complicated and invasive

procedures which increase length of stay at the hospital and increase cost (Kuy, 2011). It is

important that these patients are properly cared for and given the best healthcare in order to

reduce hospital length of stay, costs to the patient, and related morbidity and mortality. The

following reading will discuss current literature and the clinical care of an elderly woman who

presented with ileus and associated complications.

Patient Profile

The 77 year old female was admit to North East Baptist Hospital on the twenty-fifth of

January, 2013. The patient stayed in the hospital for 13 days and was pronounced dead on the

sixth of February, 2013. She was brought to the hospital by her friend for vomiting blood. The

patient had been vomiting all night and felt weak. She complained of mid-epigastric abdominal

pain and generalized weakness. The patient had a remarkable past medical history of

cerebrovascular accident, sacral fracture, hypertension, dyslipidemia, coronary artery disease,

osteoporosis, and deconditioning. The patient had a past surgical history of hernia repair,

hysterectomy, diskectomy, exploratory surgery and pyloroplasty from duodenal ulcer in 2007, a

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cholecystectomy in 2007, and a recent sacroplasty in October of 2012. Family history includes

mother deceased at age 86 from a massive myocardial infarction, and father deceased from

metastatic prostate cancer. The patient experiences hallucinations when taking hydrocodone,

but is able to tolerate Tylenol with codeine, so it is not a true allergy, per se. Patient denies

history of melena, syncopal episodes, easy bruising or bleeding, chest pain, shortness of breath,

and history of bright red blood per rectum or hemorrhoids. The patient takes Ecotrin daily at

325 mg for her heart condition, codeine for body aches, and is a chronic aspirin user. She lives

in independent living and does not drink, smoke, or use drugs. She has two daughters and a

friend. The patient was underweight upon admittance with a body mass index of 16.8, at a

height of 66 in and 47.3 kg. Her ideal body weight (IBW) was 59 kg and she was at 80 percent of

IBW.

Course of Treatment

On day one of admission the impression of the patient’s condition was that of an acute

upper gastrointestinal tract bleed with associated hematemesis coffee ground in nature. The

bleed was considered to possibly be related to aspirin use. The patient was put on a nil by

mouth (NPO) status with IV fluids, proton pump inhibitors, and Protonix twice daily. The aspirin

regimen was discontinued, as well as, the Fosomax which the patient was taking for

osteoporosis. Fosomax was discontinued because it can cause additional gastrointestinal upset.

Other medications were continued for urinary retention, Baclofen, Claritin, and Codeine for

pain. Within the next two days of stay the patient had an endoscopy and she was found to have

an upper gastrointestinal bleed secondary to erosive induced gastritis and esophagitis. The

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patient tolerated the procedure well but continued with nausea and vomiting while feeling

weak and dizzy. The patient was tolerating a clear liquid diet but did not have an appetite. The

patient developed fever and following fever workup was found to have left lobe pneumonia

and was started on Levequin. On the fourth day of stay the patient was advanced to a full liquid

diet while still experiencing nausea and vomiting.

The patient continued on the fifth day with loss of appetite and was evaluated for a

skilled nursing facility (SNF), but the patient refused to go to a SNF. It is important to note that

the patient had previously refused SNF placement following a cholestectomy. Kuy and colleges,

(2011) found that following a cholecystectomy, a large portion of elderly patients required

home health care support, institutional short-term rehabilitation, and nursing home care

following discharge, which may increase the risk of post-discharge mortality. On the sixth day of

stay the patient was noted to need full assisted living and nutritional supplements. The patient

was not able to tolerate an oral diet.

A dietary consult was received on the seventh day of the patients stay for nutritional

supplements. The patient continued with feculent vomiting and was nauseated. She was put on

Zofran for nausea and vomiting and Megace to increase her appetite. The patient had been

receiving medication for nausea but the medication was not working, therefore, Zofran was

added to the medication list. The patient was given an enema for constipation.

Early in the morning on the eighth day of stay the patient developed respiratory distress

and was transferred to the intensive care unit (ICU) and put on BIPAP. She had been

experiencing an increased occurrence of vomiting. After assessment in the ICU the patient was

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diagnosed with erosive esophagitis and gastritis, aspiration pneumonia, ileus, sepsis secondary

to pneumonia, hypoxia, hypokalemia, hypophosphatemia, hypomagnesaemia, and leukopenia.

Her antibiotics were broadened to include Zosyn and Levaquin and the patient was also started

on pressors for hypertension. Sepsis was treated along with fluid replacement as hypertension

was likely related to volume depletion given the high amount of vomit. For hypoxia, the plan

was to begin her on a high flow system as opposed to BIPAP which she would possibly tolerate

better. The ileus is considered to be multifactorial and related to decreased mobility and low

electrolytes. The patient was given a PICC line and speech therapy was consulted for a swallow

evaluation.

The patient was seen by a gastrointestinal doctor when in the ICU, and dietary received

a consult for total parenteral nutrition (TPN). The patient’s primary diagnosis was ileus, rule out

obstruction, and the patient met the ASPEN guidelines for TPN with the following: patient does

not have functioning bowel, and patient has a nonfunctional gastrointestinal tract with

expected need for parenteral nutrition for at least seven days.

On the eighth day of stay, the patient passed her swallow evaluation and was given a

regular diet with thin liquids. Although the swallow function was working properly, the patient

was still unable to tolerate oral feeds and was put on TPN. At this point the patient began to

experience altered blood glucose, and insulin was added to her medications. Over the next four

days the patient was increased from level I sliding scale insulin to level III and insulin was

increased in her TPN as well. Significant lab values can be viewed in Table I. The patient’s

respiratory failure continued along with sepsis, ileus, and a new diagnosis of small bowel

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obstruction. On the eleventh day of stay the patient was intubated and sedated due to her

decreasing respiratory status.

The twelfth day of stay was remarkable to the beginning of trophic feeds while

continuing on TPN. On the final day of life the patient failed another trial to extibate on BIPAP,

and possibly developed acute respiratory failure. After discussion with the family, the patient

was put on supportive comfort care and declared do not resuscitate (DNR). The patient

deceased at 15:37 on February sixth, 2013.

Sepsis

The term sepsis is used when a patient has an infection and an identifiable organism

(Wilker and Malone, 2008). Sepsis leads to the release of cytokines, proteolytic enzymes, or

toxic oxygen species and activate the inflammatory cascade (Wilker and Malone, 2008). Sepsis

further complicates ileus by worsening gut dysfunction. The alterations in the intestinal gut

barrier function in association with malnutrition are thought to occur through weight loss and

villous atrophy (Wilker and Malone, 2008).

Intensive Care Unit

Patients enter the ICU due to cardiopulomonary diagnosis, intraoperative or

postoperative complication, multiple traumas, burn injury, or sepsis (Wilker and Malone, 2008).

Critical illness is associated with catabolic stress state most commonly demonstrated with

systemic inflammatory response and complicated with infectious morbidity, multi-organ

dysfunction, prolonged hospitalization, and disproportionate mortality (McClave, 2009). The

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Table I

Significant Lab Values

25-Jan 26-Jan 27-Jan 28-Jan 29-Jan 30-Jan 31-Jan 1-Feb 2-Feb 3-Feb 4-Feb 5-Feb 6-FebGlucose 140 H 141 H 173 H 261 H 357 H 177 H 133 H 122 HWBC 13.47 H 22.89 H 28.60 H 15.33 H 16.01 HLipase 16 LPotassium 3.3 L 3.0 L 3.2 L 3.1 L 2.8 L 2.9 L 5.2 H 3.1 LRed Blood Cells 3.73 L 3.48 L 2.82 L 2.87 L 2.50 L 3.33 LHemoglobin 11.2 L 10.5 L 8.5 L 8.6 L 10.4 L 9.8 LHematocrit 33.1 L 26.1 L 26.8 L 31.4 L 29.9 LChloride 111 H 112 H 114 HCarbon Dioxide 23 L 19 L 21 L 22 L 19 L 32 HCalcium 7.3 L 7.6 L 7.7 L 7.0 L 7.0 L 8.3 L 7.8 LAlbumin 2.5 L 2.6 L 2.5 L 1.9 L 1.7 L 1.4 L 1.5 L 1.3 L 1.5 LPhosphorus 1.3 L 1.9 L 2.1 L 1.1 L 7.5 H 4.6 HBlood Urea Nitrogen 8 L 7 L 34 H 42 HMagnesium 1.7 L 1.5 L

Creatine 0.46 L

Note: Values are displayed as the actual value with an H for high values and L for low values. All cellsthat are blank indicate values within normal limits or absent lab values.

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ICU patients often have numerous catheters for intravenous fluids and invasive hemodynamic

monitoring, as well as, tubes for drainage of body fluids (Wilker and Malone, 2008). Nutritional

assessments in the ICU do not follow traditional methods and require more time and attention,

mostly due to the patient’s condition and inability to provide dietary history. Weight values may

be erroneous after fluid resuscitation, and anthropometric measurements are not easily

attainable, nor are they sensitive to acute changes (Wilker and Malone, 2008). Serum albumin

may be altered as a result from the effects malnutrition and the severity of illness or the

underlying disease and other plasma proteins can be altered due to the inflammatory response

and shifts in body fluid (Wilker and Malone, 2008). The difficulty in conducting a nutrition

assessment requires clinical judgment when deciding on nutrition support. The ICU nutrition

assessment focuses on the preadmission, preoperative, or preinjury nutrition status, the

presence of any organ dysfunction, the need for early nutrition support, and options for enteral

or parenteral access (Wilker and Malone, 2008). Laboratory data is used in the critically ill

patient to design the nutrition prescription, rather than define or determine nutrition status

(Wilker and Malone, 2008).

Practice in ICU patients worldwide shows a significant underfeeding with hospital

nutrition protocol despite observational research that shows the amount of energy and protein

received during the early stages of ICU admission impacts patient mortality (Heyland et al,

2010). The goals for nutrition support in the ICU is to minimize starvation, prevent or correct

specific nutrient deficiencies, provide adequate calories to meet energy needs while minimizing

metabolic complications, and manage fluid and electrolytes for adequate urine output and

homeostasis (Wilker and Malone, 2008). Nutrition support should begin as soon as the patient

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is hemodynamically stable, which includes; stabilized vital functions, balanced fluid,

electrolytes, and acid-base, and adequate tissue perfusion to allow transport of oxygen and fuel

(Wilker and Malone, 2008).

Small Bowel Obstruction

Scarring from GI surgeries may partially or completely obstruct the GI tract of result in

dysfunctional segments (Beyer, 2008). When sections of the GI tract are partially obstructed or

are not moving appropriately, obstructions from food may occur causing prolonged bloating,

abdominal distention, pain, nausea and vomiting (Beyer, 2008). Some intestinal obstruction

may require clear liquids or total restriction of food and parenteral nutrition with fluid may be

needed (Beyer, 2008).

Coffee Ground Emesis

In the United States there are over 300,000 cases of hospital admissions for upper

gastrointestinal bleeds (Bou-Abdallah, 2012). Blood loss from the GI tract is manifested as

hematemesis or bloody coffee grounds (Bou-Abdallah, 2012). The treatment and initial

management of acute upper GI bleed is identical regardless of the mode of presentation and

usually involves stabilization of hemodynamic status (Bou-Abdallah, 2012). A recent case report

by Bou-Abdallah and colleagues (2012) found six patients admit for coffee ground emesis led to

other more severe complications including new-onset atrial fibrillation, ICU admits, pulmonary

emboli, ileus, and small bowel obstruction. The study showed that diagnosis and management

of the other complications were delayed due to the standard management given to patients

diagnosed with acute upper GI bleed (2012). Despite early endoscopy that has shown to have

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an impact on hospital admission, length of hospital stay, and transfusion requirements, in

patients presenting with coffee ground emesis, endoscopy does not predict further

complications (Bou-Abdallah, 2012).

Ileus

Ileus refers to the partial or complete blockage of the small and/or large

intestine due to impaired peristalsis or because of a mechanical obstruction (Madl and Druml,

2003). There is no standardized definition of ileus for diagnosis and is often difficult to

distinguish between a small-bowel obstruction (SBO) radiologically (Allen et al, 2012).

Diagnostic imaging studies and abdominal X-rays are most commonly used to diagnose and

help differentiate ileus from bowel obstruction (Allen et al, 2012). Symptoms caused by altered

bowel function are characterized by lack of bowel sounds, abdominal distention, accumulation

of gas and fluids in the bowel, decreased or absent defecation, nausea, vomiting, decreased GI

passage, and discomfort (Allen et al, 2012; Madl and Druml, 2003). Ileus is multifactorial in

origin and causative factors include neurogenic, inflammatory, hormonal, and pharmacologic

influences (Senagore, 2010). The neurogenic component relates to pain induced neural reflexes

which result in sympathetic hyperactivity and inhibition of gastrointestinal activity (Sengagore,

2010). Surgical manipulation can cause ileus by activating a number of inflammatory cascades,

which further exacerbate the effects of exogenous opiod analgesics given for analgesia, and

inhibit bowel function (Sengagore, 2010). Hormonal influence on ileus is mediated as a

response to trauma and pain medication may further impair GI motility (Sengagore, 2010).

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Ileus itself is not life-threatening but can lead to other complications, increased hospital

length of stay and healthcare resource utilization cost (Sengagore, 2010). Treatment usually

includes nasogastric decompression, diet reversal for symptom relief, hydration, antiemetics,

and restoring electrolyte balance (Allen et al, 2012). The abdominal distention increases the risk

of hernia formation and wound dehiscence, and nausea and vomiting impacts the possibility of

feeds and increases the risk for malnutrition and impaired wound healing (Sengagore, 2010).

Prolonged venous access and the need for nasogastric decompression inhibit ambulation and

can increase rates of pulmonary complications and thromboembolus (Sengagore, 2010).

Increased length of stay at hospitals also places a burden economically and raises issues with

hospitals of limited beds and high inpatient demand (Sengagore, 2010).

Gastric motility impaired by ileus can last over five days, and may required total

parenteral nutrition or TPN (Wilker and Malone, 2008). However, because of the demonstrated

benefits of enteral nutrition (EN), tube feeds can often be administered simultaneously with

TPN at low rates to maintain gut intergrity and preserve intestinal mucosa while providing

adequate nutrition (Wilker and Malone, 2008).

Pathophysiology

Ileus has been described as a chaotic activity of individual cells with a loss of

synchronization and impaired peristalsis (Madl and Druml, 2003). The associated increased in

luminal pressure can lead to gut wall ischemia and cause increased intra-abdominal pressure

(Madl and Druml, 2003). Intra-abdominal hypertension has been found in up to 20 percent of

critically ill patients and may lead to multiple complications including cardiovascular, hepatic,

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pulmonary, renal, and neurological dysfunction (Madl and Druml, 2003). Gastrointestinal

dysmotility may result in increased luminal pressure with intestinal dilatation, releasing nitric

oxide which is a known inhibitor of smooth-muscle tone (Madl and Druml, 2003). During

inflammation neutrophils invades the muscle layer of the gut wall and damages the muscle by

releasing proteolytic enzymes and cytokines (Madl and Druml, 2003). The inflammatory

response leads to the release of nitric oxide in the intestinal muscle layer, paralyzing the muscle

cells and aggravation the intestinal dilatation (Madl and Druml, 2003). The amount and activity

of nitric oxide synthase directly correlates to the severity of intestinal dilatation, and

consequently the severity of gut ischemia (Madl and Druml, 2003). Gut ischemia leads to an

uptake of cytokines and other inflammatory mediators which contribute to the systemic

symptoms of ileus and correlate with the severity of ileus (Madl and Druml, 2003).

Etiology

There is not one known cause of ileus and it can be due to a blockage in the small or

large intestine, as well as, a mechanical or paralytic bowel obstruction (Madl and Druml, 2003).

Disorders associated with a mechanical bowel obstruction can be located outside the gut wall,

within the gut wall, or intraluminal (Madl and Druml, 2003). A paralytic ileus may affect all parts

of the GI tract and is one of the most common complications in critically ill patients (Madl and

Druml, 2003). The cause of a paralytic ileus may be an adverse consequence of a surgical

procedure, use of opiods or catecholaminces, intraperitoneal of retroperitoneal infection,

edema or ascites secondary to massive fluid resuscitation during septic shock, or toxic shock

with capillary leakage, acute bacterial or parasitic intestinal infection, toxic megacolon, arterial

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or venous injury, intra-abdominal hematomas, or metabolic disturbances (Madl and Druml,

2003). In the critically ill, the degree of impairment of intestinal motility is tightly correlated to

the severity of illness and mortality (Madl and Druml, 2003).

Systemic Consequences

Aspiration

Impaired motility of intestinal contents promotes reflux of intestinal juice of the small

intestine back into the stomach and increases gastric residuals (Madl and Druml, 2003). This

allows for colonization of intestinal bacteria and ascension of microorganisms into the

esophagus, pharynx, and tracheobronchial tree (Madl and Druml, 2003). This along with

vomiting and aspiration increases the risk of evolution of pneumonia (Madl and Druml, 2003).

Hypovolemia

Distention, increased intraluminal pressure, and increased intra-abdominal pressure

impair microcirculation and ultimately result in fluid sequestration into the intestinal wall and

intestinal lumen (Madl and Druml, 2003). The fluid sequestration into the third space can result

in hypovolemia and circulatory impairment and can further aggravate various systemic

consequences of ileus (Madl and Druml, 2003).

Bacterial Overgrowth and Translocation

Ileus is associated with alterations in intestinal flora with an overgrowth of bacteria

(Madl and Druml, 2003). The impaired protective mucosal layer may allow microorganisms

and/or endotoxins/exotoxins to invade the mucosa, cause mucosal inflammation, and increase

Case Ileus 14

mucosal perfusion and hypersecretion (Madl and Druml, 2003). Medication has an impact on

bacterium and can promote bacterial selection and overgrowth resulting in antibiotic-induced

diarrhea or colitis, and can promote bacterial translocation (Madl and Druml, 2003).

Bacterial translocation refers to the permeation of viable microorganisms, fragments of

microorganisms, or macromolecules through an intact or injured intestinal wall into the

lymphatic system and/or intestinal venous circulation, such as the liver, spleen, kidney and

bloodstream (Madl and Druml, 2003). Intestinal bacteria is important to mature the immune

system and prompt the proper inflammatory responses but can become compromised when

there is an overgrowth of abnormal bacteria and/or the barrier function of the intestinal wall is

impaired (Madl and Druml, 2003). Bacterial overgrowth, increased permeability in the

intestinal mucosal barrier, and deficiencies in host immune defenses synergistically promote

the spread of indigenous translocation bacteria to cause lethal sepsis (Madl and Druml, 2003).

When the mucosal epithelium is damaged, indigenous bacteria translocate intercellularly

between the epithelial cells to directly access the blood. Sepsis can result with a spillover of

microorganisms into the lymphatic system via the vena cava superior into the circulation and

the lung, and/or spillover into the portal circulation promoting evolution of systemic infections

and septicemia (Madl and Druml, 2003).

Bacterial overgrowth, inflammation and impairment of barrier function of the intestinal

wall, and impairment of systemic immunocompetence are the three determinants of

translocation involved with ileus (Madl and Druml, 2003). Mucosal functions are further

compromised with a reduced mesenteric blood flow and increased intra-abdominal pressure

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(Madl and Druml, 2003). Therefore, treatment should be aimed particularly at preserving

intestinal functions in intensive care patients (Madl and Druml, 2003).

Pulmonary

Raised intra-abdominal pressure results in increased intrathoracic pressure and affects a

broad pattern of respiratory functions (Madl and Druml, 2003). Increased intra-abdominal

pressure can drop pulmonary residual capacity and may affect lung mechanics and decrease

lung compliance which promotes development of atelectasis and increased intrapulmonary

shunt (Madl and Druml, 2003). Increased pressure can negatively affect breathing and

significantly increased alveolar pressure and influence gas exchange (Madl and Druml, 2003).

Nutrition Therapy

Adequate hydration status is important to support cardiovascular function with ileus

(Madl and Druml, 2003). Maintenance of intestinal motility is a goal for a critically ill patient

with ileus and can be managed by prophylactic measures, motility medications, and early EN

(Madl and Druml, 2003). Early EN, even low in low or minimal amounts has been shown to

maintain intestinal functions, perfusions, motility, and barrier functions (Madl and Druml,

2003). Enteral diets containing dietary fiber can promote motlility, formation of short-chain

fatty acids through fermentation by bacteria, and reduce translocation (Madl and Druml, 2003).

Enteral diets including prebiotics has been shown to support intestinal barrier functions, to

reduce mucosal inflammation by inhibiting the adherence of pathological microorganisms to

the mucosal surface, and to prevent antibiotic-induced intestinal complications (Madl and

Druml, 2003).

Case Ileus 16

Feedings

After being NPO for a period of time, many patients do not have an appetite, suffer from

dry mouth, experience taste alterations, are too tired or weak to eat, are in an uncomfortable

position in bed, are in pain, and may require EN to meet their nutritional needs (Klos).

Psychological factors may influence a patient’s willingness to eat, such as stress caused by being

in a hospital and the fear of returned intestinal pain that might occur after the reintroduction of

oral food (Klos). Medications are also the cause of additional nausea, diarrhea, constipation, dry

mouth, and altered appetite that can influence a patients will to eat (Klos).

Enteral nutrition is the preferred route of nutrition support, with PN reserved for

patients whom adequate EN is not possible (Sriram, 2009). Enteral nutrition has been shown to

decrease infectious complications and is more cost effective when compared to PN (Sriram,

2009). Parenteral nutrition should be used only when the GI tract is not anatomically adequate

or not functional, the GI tract cannot be accessed, or when nutritional requirements cannot be

completely met with EN (Sriram, 2009).

When a patient receives parenteral nutrition (PN), the ultimate goal is to transition back

to enteral nutrition (EN) or oral feeds (Klos). Parenteral nutrition is used when the

gastrointestinal tract is nonfunctional or cannot be accessed, such as small bowel resection,

radiation enteritis, high output enterocutaneous fistula, and paralytic ileus (Klos). Mucosal mass

and function of the ileum and jejunum significantly decrease, as well as, intestinal digestive

enzyme activity and exocrine pancreatic function during total PN (Klos). After a period of time

Case Ileus 17

on NPO, the return of the GI function is slow and requires time and effort to resume tolerance

to a normal diet (Klos).

Enteral nutrition has been shown to support intestinal structure and function, prevent

increased permeability, bacterial translocation, and systemic inflammation (Rice et al, 2011).

Enteral nutrition has also been shown to attenuate hypermetabolism of critical illness, decrease

infectious complications, and shorten ICU stays compared to PN, and reduce mortality (Rice et

al, 2011). Overall, EN stimulates epithelial cell growth and proliferation, maintains mucosal

mass and microvilli height, preserves tight junctions between epithelial cells, and promotes

blood flow; all of which are absent with ileus (Rice et al, 2011).

Trpohic feeds refers to small volume enteral feeds in order to stimulate the GI tract by

improving gastrointestinal enzyme activity, hormone release, blood flow, motility, and

microbial flora (Mishra et al, 2007).

Literature

Rice and colleagues (2011) conducted a randomized, open-label study to test the hypothesis

that initial trophic feeds would decrease episodes of gastrointestinal intolerance/complications

and improve outcomes as compared to initial full-energy EN in patients with acute respiratory

failure. The study included 200 patients with acute respiratory failure expected to require

mechanical ventilation for at least 72 hours who randomly received either trophic feeds at 10

ml an hour, or full energy EN for the initial six days of ventilation. Primary outcome measures

included; ventilator-free days to day 28, ICU-free days, mortality, episodes of diarrhea, and

episodes of elevated gastric residual volumes. Rice found that initial trophic EN resulted in

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similar clinical outcomes in mechanically ventilated patients with acute respiratory failure as

early full-energy EN but with significantly fewer episodes of gastrointestinal intolerance (2011).

The National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome

Clinical Trials Network (2012) conducted a very similar randomized open-label design study

with 1000 adults across 44 hospitals that within 48 hours of developing acute lung injury

required mechanical ventilation. The purpose was to determine if initial trophic feedings would

increase ventilator-free days and decrease gastrointestinal intolerances compared with initial

full EN. Outcomes measures included; ventilator-free days to day 28, 60-day mortality,

infectious complications, vomiting, gastric residual volumes, constipation, plasma glucose

values and insulin administration. It was concluded that trophic feeds did not improve

ventilator-free days, 60-day mortality, or infectious complications but was associated with less

gastrointestinal intolerance (2012).

There is a lack of conclusive evidence regarding the caloric dose required for the critically ill.

The two studies show that more research is needed to determine the role of trophic feeds in

ventilated patients and possibly challenge hospital nutritional standards for the critically ill

patient.

Nutrition Care Process

The patient was consulted on January 31, 2013 after a referral from a nurse because the

patient was not eating. The patient was found with limited appetite because she could not keep

her food down. At that time the patient only had an appetite for a milkshake. That day the

patient was given different medications for nausea and vomiting because the other medications

Case Ileus 19

seemed to be ineffective. The patient was at 80 percent IBW had a BMI of 16.8, and met

guidelines to be clinically underweight. The patient was receiving adequate fluids with normal

saline at 75 ml per hour. She was assessed for weight gain and her calculated needs were 1420

to 1655 calories per day at 30 to 35 calories per kilogram actual body weight, and 56-71 grams

protein per day at 1.2 to 1.5 gram per kilogram actual body weight. Her nutrition status was

severely compromised with inadequate oral food intake related to her current condition as

evidence by intake record, BMI, and albumin lab values. Dietary intervention was to send

meals, snacks and supplements, and Mighty Shake was recommended twice daily to

supplement oral intake. The outcome set for the patient was to meet over 95 percent of

estimated nutritional needs (ENN), maintain lean body mass, protein profile to trend towards

normal, and to maintain skin integrity.

On the first of February the patient was referred from a physician for TPN assessment.

The patient met ASPEN criteria for TPN with a nonfunctional GI tract (ileus). It was

recommended the patient begin feeds at 85 grams protein, 275 grams dextrose, and 40 grams

of lipids to provide a total of 1675 calories, 85 grams of protein with a 2.3 glucose infusion rate

(GIR). The GI doctor was to write daily TPN orders.

The final nutrition assessment was made on the fifth of February for a follow up

evaluation. The patient had been receiving TPN of 100 grams protein, 300 grams dextrose, and

40 grams of lipids. As discussed previously with the GI doctor on the case, the patient was to

begin trophic feeds. The doctor ordered Pulmocare at 20 ml an hour in addition to the TPN

feeds and would hold for nasogastric residuals over 200 ml. Calculated needs were adjusted

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and needs were set at 1298 to 1593 calories at 22 to 27 calories per kilogram IBW and 88 to 118

grams protein at 1.5 to 2.0 grams per kilogram IBW. The nutrition status of the patient

remained severe due to an altered GI function related to ileus as evidence by PN and EN. The

nutrition intervention was requesting prealbumin and recommending trophic feeds with Vital

AF 1.2 at 20 ml an hour to help manage inflammation and promote GI tolerance. Outcomes

were that all forms of nutrition will meet over 95 percent of ENN, and that the patient would

tolerate EN feeds.

Reflection

As the patient was ultimately ventilated, it was appropriate in her case to begin trophic

feeds in hope to improve gut integrity, and to improve ileus status. Despite an unfortunate

outcome, the patient’s case provided means for an edifying research of the literature and

prevalent research questions. Effective nutritional support for critically ill patients represents a

difficult aspect of care with the complexity of the clinical status. With new research published

daily, there is a need to challenge commonly used nutritional support practices and to

individualize patient care with an evidence-based approach to achieve optimal nutrition

therapy.

Case Ileus 21

Reference

Allen, A. M., Antosh, D. D., Grimes, C. L., Crisp, C. C., Smith, A. L., Friedman, S., Mcfadden, B. L.,

Gutman, R. E., & Rogers, R. G. (2012). Management of ileus and small-bowel obstruction

following benign gynecologic surgery. International Journal of Gynecology and

Obstetrics.121: 56-59.

Bou-Abdallah, J. Z., Murthy, U. K., Mehta, N., Prasad, H. N., & Kaul, V. (2012). Clinical

communications: Adults: Coffee ground emesis: Not just an upper GI bleed. The Journal

of Emergency Medicine. 43 (1): 44-46.

Heyland, D. K., Cahill, N. E., Dhaliwal, R., Wang, M., Day, A. G., Alenzi, A., Aris, F., Muscedere, J.,

Drover, J. W., & McClave, S. A. (2010). Enhanced protein-energy provision via the

enteral route in critically ill patients: A single center feasibility of the PEP uP protocol.

Critical Care. 14: R78.

Hiranyakas, A., Bashankaev, B., Seo, C. J., Khaikin, M., & Wexner, S. D. (2011). Epidemiology,

pathophysiology and medical management of postoperative ileus in the elderly. Drugs

Aging. 28(2): 107-118.

Kuy, S., Sosa, J. A., Roman, S. A., Desai, R., & Rosenthal, R. A. (2011). Age matters: a study of

clinical and economic outcomes following choecystectomy in elderly Americans. The

American Journal of Surgery. 201: 789-796.

Madl, C., & Druml, W. (2003). Systemic consequences of ileus. Best Practice & Research Clinical

Gastroenterology. 17(3): 445-456.

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Rice, T. W., Mogan, S., Hays, M. A., Bernard, G. R., Jensen, G., L., & Wheeler, A. P. (2011) A

randomized trial of initial trophic versus full-energy enteral nutrition in mechanically

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