A 71-year-old Caucasian man was brought to the emergency department (ED) for left-sided weakness and confusion. According to his wife, he was found on the floor in his bathroom at home with a paralyzed left arm and leg and slurred speech. This was 6 hours before he came to the ED. The patient has a history of non–insulin-dependent diabetes, hypertension, and hyperlipidemia. On arrival to the ED, he is confused and is noted to have left hemiparesis and left facial droop with aphasia. The vital signs reveal a blood pressure of 119/60 mm Hg, pulse of 119 beats per minute (bpm), respiratory rate of (RR) 33 breaths/min, and arterial oxygen saturation (Sao2) of 85%. He is intubated and ventilated after appropriate sedation and chemical paralysis. A noncontrast computed tomography (CT) scan of the head is performed, which shows a dense right middle cerebral artery sign and no evidence of acute intracranial hemorrhage. The electrocardiogram reveals atrial fibrillation. The radiograph of the chest reveals appropriate endotracheal tube position and a right lower lobe infiltrate.
On his arrival in the neurologic intensive care unit (NeuroICU), his vital signs show a temperature of 36.4°C, pulse of 132 bpm (sinus), respirations (ventilated) at 14 breaths/minute, blood pressure of 113/47 mm Hg, and oxygen saturation of 100%. On physical examination, he appears acutely ill and cachectic. The carotid pulses are equal, and there are no bruits. A pulmonary examination demonstrates right lower lobe crackles. The heart sounds are normal. The limbs are well perfused, and the abdomen reveals diminished bowel sounds with a soft and nondistended abdomen. A musculoskeletal examination shows moderate diffuse muscle wasting. The neurologic examinations were not informative because of deep sedation. The results of laboratory tests are shown in Table 57-1.
According to his wife, he retired a year ago from his previous occupation as a taxicab driver for 40 years. He had been smoking 1 pack of cigarettes per day on average for 35 years and drank alcohol occasionally. For the last 5 months, his appetite has decreased, and he has been eating small portions at 2 to 3 meals per day. He has lost 15 lb (6.8 kg) during the past 5 months, and his most recently measured weight is 115 lb (52 kg). His height is 5 feet and 8 inches (172 cm).
| Laboratory Test | Value | Normal Range |
|---|---|---|
| Sodium | 149 mEq/L | 136-145 mEq/L |
| Potassium | 5.0 mEq/L | 3.6-4.9 mEq/L |
| Cl | 114 mEq/L | 101-111 mEq/L |
| CO2 | 20 mEq/L | 23-31 mEq/L |
| Blood urea nitrogen | 31 mg/dL | 23-31 mg/dL |
| Creatinine | 1.3 mg/dL | 0.6-1.0 mg/dL |
| Glucose | 233 mg/dL | 80-120 mg/dL |
| Albumin | 2.5 g/dL | 4.0-5.5 g/dL |
| C-Reactive protein | 25 mg/L | < 5 mg/L |
| White blood cell count | 15 k/μL | 4.5-11.0 k/μL |
| Hematocrit | 35% | 41-53% |
| Platelets | 552 k/μL | 150-350 k/μL |
What is your nutritional assessment of this patient? How would you calculate his metabolic requirements?
The severity of his ischemic stroke and pneumonia that resulted in low serum albumin concentration put him at risk for prolonged admission and potentially poor outcome. He has had significant weight loss (12% over 5 months). Subsequent to his weight loss, the patient’s body mass index (BMI) is 17.6 (kg/m2). Based on his clinical status of having had significant weight loss and being currently underweight, he is considered to be at nutritional risk (Table 57-2).
| Severity of Illness | Severity of neurological injury History of trauma Sepsis Seizure Systemic organ function |
| Weight History | Body mass index, Recent weight changes, Ideal body weight Significant weight loss1,* 5% over 1 month, 7.5% over 3 months, 10% over 6 months Malnutrition1,* > 5% of weight loss based on usual body weight < 90% of Ideal body weight |
| Physical Examination | Neurological functionality Fat and muscle mass Gastrointestinal function Volume status Body composition |
Laboratory Data Interpretation | Urinary urea protein for nitrogen balance Serum transport protein** Albumin, Prealbumin, Transferrin Systemic inflammatory makers** C-reactive protein, Interleukin-6, Tumor necrosis factor Acid base balance, electrolyte, liver function, cholesterol |
The Academy of Nutrition and Dietetics and the American Society for Parenteral and Enteral Nutrition (ASPEN) have proposed etiologic-based definitions of malnutrition based on the degree of inflammation. These definitions classify malnutrition into three categories: (1) starvation-related malnutrition, (2) chronic disease–related malnutrition, and (3) acute disease–related malnutrition.2 Based on the degree of inflammation and critical illness, his malnutrition can be classified as acute disease–related malnutrition (Table 57-3).
| Malnutrition type | Degree of Inflammation | Patient Conditions |
|---|---|---|
| Acute disease–related malnutrition | Severe | Sepsis, Trauma, Acute head injury |
| Chronic disease–related malnutrition | Mild to moderate | Cancer, Rheumatoid arthritis, Organ failure |
| Starvation–related malnutrition | None | Simple starvation, Anorexia nervosa, Low calorie diet |
Critical illness is typically associated with a catabolic stress state and a systemic inflammatory response, which increases intravascular permeability and suppresses the production of transport proteins such as albumin and transthyretin (prealbumin).3 A patient who was previously well nourished may develop severe hypoalbuminemia due to critical illness within hours to days. Therefore, traditional nutrition assessment markers (serum albumin, prealbumin, transferrin) are not validated in critically ill patients because these protein markers vary depending on vascular permeability, catabolic rate, and hepatic protein synthesis4 and not on nourishment.5
Indirect calorimetry may be used to determine this patient’s energy requirement (Table 57-4). It is difficult to estimate his caloric requirements accurately because of his acute respiratory failure, neurologic injury, and malnutrition. When indirect calorimetry is not an option, energy requirements may be calculated through either simplistic formulas (20-30 kcal/kg/d) or published predictive equations, many of which have been published in the literature (eg, Harris-Benedict, Scholfield, Owen, Mifflin-St. Jeor, Swinamer, and Ireton-Jones).6 The calculation of energy requirements using kilocalories per kilogram is, however, more often used and widely accepted by clinicians than the published predictive equations because of convenience and practicality. Consultation with a nutrition clinician is strongly recommended.
| Indication | Example |
|---|---|
Unable to estimate caloric requirements accurately7,* | ARDS, sepsis, malnutrition, neurological injury, multisystem organ failure, use of paralytic or barbiturate |
Inadequate clinical response in the patient with the use of predictive equations** | Poor wound healing, failure to wean from mechanical ventilator |
The presence of clinical signs suggesting either underfeeding or overfeeding** | Underfeeding—Decreased respiratory muscle strength, poor wound healing, immunosuppression Overfeeding—Hyperglycemia, hepatic steatosis, electrolyte imbalance |
When would you initiate feeding? Which method of feeding, enteral feeding or parenteral feeding, is more suitable to this patient?
You should initiate nutrition support therapy in the form of enteral nutrition as soon as possible, preferably within the first 48 hours after injury. Early feeding of patients who have had a cerebral vascular accident (CVA) has been proven to shorten the hospital length of stay.8
A large multicenter, randomized, controlled clinical trial showed a reduction in mortality risk when tube feedings were initiated within the first 7 days following a CVA (P = .09).9 Early enteral feeding in patients with severe brain injury has resulted in decreasing infectious complications and an inflammatory response after injury. Neurologic recovery may also be accelerated in patients who are given an adequate amount of calories within the first 48 hours after injury.10
Whether the method of delivery, parenteral or enteral, has any effect on mortality in critically ill patients has been called into question in one recent study.11 However, enteral feeding may have benefits beyond providing nourishment. These include maintenance of gut integrity, preservation of a systemic immune response (especially, mucosal immunity), and attenuation of the severity of an inflammatory response. Enteral feeding is the preferred method over parenteral feeding, except in the presence of prolonged and severe gut dysfunction or where the risk of obtaining enteral access exceeds the risk of malnourishment for an extended period. A comparison of enteral and parenteral nutrition has not been done in neurologically injured patients; however, in general, enteral feeding is the preferred method of feeding over parenteral nutrition for critically ill patients who require nutrition support therapy.12-14
Enteral feeding of the hemodynamically compromised patient may increase the risk of ischemic bowel. Therefore, if patients require significant hemodynamic support, including high-dose catecholamine agents and large-volume fluid or blood product resuscitation, to maintain cellular perfusion, enteral nutrition should be withheld until the patient is resuscitated or stabilized.15
The patient developed diarrhea 24 hours after continuous enteral tube feeding is initiated. What would you do differently with regard to his feeding method?
The enteral tube feeding should be continued. In critically ill patients, the pathophysiology of diarrhea is usually attributable to multiple simultaneous factors particularly medications, infections, and underlying disease. Enteral feeding, while likely to increase stool volume in those with diarrhea, is rarely the underlying cause and changing feeds rarely improves the diarrhea.16 Before making a change in the feeding formula, an analysis should be performed to determine whether the diarrhea was caused by an excessive intake of hyperosmolar medications, such as liquid medications delivered in sorbitol; use of broad-spectrum antibiotics; Clostridium difficile pseudomembranous colitis; or another infectious etiology. Stool (measured osmolality: 2 × [stool Na + stool K]) can be calculated to make a differential diagnosis between osmotic diarrhea (high osmotic gap > 160 mOsmol/kg: pancreatic insufficiency, lactulose, use of laxative) and secretory diarrhea (low osmotic gap < 50 mOsmol/kg: toxin-mediated causes).17 Fecal leukocyte count, pH level, fat, and cultures can be used to make the diagnosis.
If you are using a calorically dense formula, it may cause or exacerbate diarrhea because of its osmotic density. Therefore, it would be reasonable to consider changing the feeding formula to one that is isotonic. Most products designed for use in tubes that are 1 kcal/mL are isotonic.
In hemodynamically stable patients with diarrhea, you may utilize soluble fiber–containing or small peptide feeding formulations. Although expert opinions support the use of the small peptide enteral formulations, large prospective trials are not available to justify a strong recommendation for these products, which may cost 15 times that of a standard feed product.4 Fiber should be avoided in hemodynamically unstable patients and those with hypoperistaltic states because of the risk of bezoar formation (Figure 57-1).
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