overhydration
•Hypertonic overhydration
•Hypotonic overhydration
Overhydration or edema is commonly seen in patients with congestive heart failure, low blood pressure, renal insufficiency, liver failure (ascites) and physical inactivity. The fluid retention is usually a symptom of a bigger medical problem.
Edema is usually treated with loop diuretics. Overdose of loop diuretics can cause extracellular fluid depletion and a potassium deficiency. The success of loop diuretics is measured by a significant weight loss and a decrease in edema. Laboratory tests will change rapidly as edema diminishes. Typical lab values seen in edema are summarized in Table 5. Additional information about each laboratory test is in the next section of this text.
Table 5. Screening for Overhydration
| Lab Test | Hypotonic | Isotonic | Hypertonic |
| Osmolality (S) | < normal | WNL | > normal |
| Sodium, (S) | < normal | WNL | > normal |
| Albumin (S) | < normal | WNL or slightly low | < normal |
| H/H | < normal | WNL or slightly low | < normal |
| BUN | < normal | WNL or slightly low | < normal |
Key: WNL= within normal limits
Assessment of Protein Status
Assessment of protein status is essential for baseline assessment and to predict risk for malnutrition and skin failure. A patient’s protein status is a reflection of the body’s ability to synthesize dispensable amino acids (DAA) and to absorb and utilize indispensable amino acids (IDAA). As the protein status declines the patient is at higher risk for infection, delayed wound healing and new skin breakdown. The traditional method to estimate visceral protein status is using a variety of lab test results including retinol binding protein level, prealbumin (transthyretin) and serum albumin. However all of these measures are negative acute phase proteins and are dramatically affected by inflammatory processes. Changes in these values do not appear to reflect changes in nutritional status. For more information refer to Protein, Blood, for more information on retinol binding protein, prealbumin and albumin.
Nitrogen Balance Studies
Nitrogen balance studies reflect the balance between exogenous nitrogen intake (by mouth or parenteral) and renal removal of nitrogen containing compounds (urinary, fecal, wound and other nitrogen sources). Nitrogen balance studies are often part of research studies to determine if the endogenous protein is being utilized. However, in a healthcare setting, nitrogen balance studies are not a measure of protein anabolism and catabolism because true protein turnover studies require consumption of labeled (stable isotope) protein to track protein utilization (Hoffenberg, 1966). The acutely ill patient is losing protein rapidly due to the inflammatory process, traumatic or surgical wounds. In addition, it is unclear if increasing exogenous protein will ameliorate the loss of endogenous protein. Adequate nutrition and specifically high biological value protein cannot circumvent the inflammatory metabolism, but may prevent excessive loss of muscle mass and immunosuppression (Griffiths, 1996).
Nitrogen balance studies are challenging to achieve because valid 24-hour urine collections are difficult to obtain unless the patient has a catheter. In addition, changes in renal function are common in patients with inflammatory metabolism, making standard nitrogen balance calculations inaccurate without calculation of nitrogen retention. In these patients, urea kinetics provides a more accurate estimation of nitrogen balance.
Urinary Creatinine
Creatinine is formed from creatine, a compound found almost exclusively in muscle tissue. Creatine is synthesized from the amino acids glycine and arginine with addition of a methyl group. It is a high-energy phosphate buffer, maintaining a constant supply of ATP for muscle contraction. Creatinine has no specific biologic function. It is continuously released from the muscle cells and excreted by the kidneys with little reabsorption. When a patient follows a meat-restricted diet, the size of the patient’s somatic (muscle) protein pool is directly proportional to the amount of creatinine excreted. The clinical significance is that men generally excrete larger amounts of creatinine than women do and that individuals with greater muscular development excrete larger amounts than those who are less muscular. Total body weight is not proportional to creatinine excretion. Creatinine excretion rate is related to muscle mass in healthy individuals.
The use of urinary creatinine to assess somatic protein status in a healthcare setting in which patients are consuming a mixed diet has its limitations. Creatine is a component of muscle meats which is converted to creatinine. The body can not distinguish between the two sources of creatinine. In addition, urinary creatinine can vary significantly within individuals, probably due to sweat losses. Urinary creatinine concentration as a biomarker of muscle mass is typically used only in research.
Nutritional Anemias
The prevalence of anemia increases with each decade of life over age 70 and is associated with both frailty and mobility impairment (AMDA, 2007). Macrocytic anemia in older adults is often due to insufficient dietary vitamin B12 or folic acid. Other causes of macrocytic anemia include kidney disease, hemolytic anemia, hypothyroidism, or certain medications.
With aging, there is a decrease in iron in RBC (Fischbach, 2008; Corbett, 2000). The mechanism is not known, although iron seems to be absorbed from the intestine. However, there is a decreased incorporation of iron into the RBC resulting in lower hemoglobin levels (Beers, 2005). The significance of this drop in hemoglobin is not known. In addition, MCV (MCV) increases slightly with age.
Anemia is a deficiency in the erythrocyte mass and hemoglobin contents. A low hemoglobin or hematocrit needs to be evaluated further by a complete blood cell count (CBC), including hemoglobin concentration, hematocrit, red blood cell mass, and MCV (Blackwell, 2001). Norms are assuming adequate hydration. If the patient is dehydrated, the values will be falsely high. Overhydration will result in falsely low values.
Patients with an infection or other inflammatory processes present often have low hemoglobins and hematocrits related to redistribution of iron rather than a change in nutritional status. With infection, the cytokine interleukin-1β (IL-1β) inhibits the production and release of transferrin while stimulating the synthesis of ferritin. The net result is that iron is moved from transferrin and hemoglobin to ferritin. The redistribution of iron stores is a protective mechanism since many virulent bacterium have specialized receptors for iron uptake. The survival of the bacterium within the host is dependent upon its ability to extract nutrients from the surrounding environment.
Classification of Anemias
