Tropical Medicine 11: Disorders of Nutrition and Hydration
The majority of the Tropical Medicine Section is devoted to tropical diseases that may be encountered in the United States primary healthcare setting. This portal and the next (Vol III—TM12 Medicine in Austere Environs) shift the focus to include clinical situations that may be encountered by medical personnel serving abroad.
Many conditions that are benign and self limiting in industrialized nations may
become life threatening in developing nations. A significant contribution to this
morbidity and mortality is dehydration and
malnutrition. Dehydration tends to
be an acute condition; malnutrition is more chronic and may be encountered in
both stateside and overseas locations.
Dehydration
Dehydration is an imbalance between fluid intake and fluid loss. Examples of increased fluid loss include GI loss (diarrhea and vomiting), skin loss (perspiration due to fever or exertion), urinary loss (diabetes, renal disease), and pulmonary loss (tachypnea from fever or exertion).
Dehydration is classified based on the amount of fluid loss:
- Mild: 0% to 5% of body weight lost
- Moderate: 5% to 10% of body weight lost
- Severe: >10% of body weight lost
Signs of dehydration include tachypnea, hypotension, oliguria and dark urine, tenting of the skin (distinguish inelastic skin due to aging from wasting due to dehydration), dry mucous membranes, sunken eyes (and sunken fontanelles in infants), and altered consciousness.
Mild dehydration can generally be treated by encouraging fluid intake. In developing countries or disaster situations, it is important to stress safety of water (ie, boiling or iodine treatment).
Moderate-to-severe dehydration (except for severely dehydrated infants or patients in shock) is best treated via oral rehydration.
Several different commercially available oral rehydration solutions (ORS) exist; in general, evidence of significant superiority of one formulation over another is lacking. These include glucose, sucrose, and rice-based ORS, each of which may include citrate, bicarbonate, or glycine. An alternative to commercially available ORS is a solution consisting of 2 tablespoons sugar or honey (PEDS: honey should be avoided in children < 1 year, if possible), ¼ teaspoon salt, and ¼ teaspoon baking soda in a liter of water.
In moderate-to-severe dehydration, ORS can be consumed at 750 cc/hour in adults (PEDS: up to 300 cc/hour in children) until signs of dehydration have resolved, then 20 cc/kg/hour maintenance. Patients with mild-to-moderate dehydration can be rehydrated at 50 to 100 cc/kg every 4 hours.
Initiate ORS for rehydration in all patients except those in shock, (PEDS) severely dehydrated infants, or those with intractable vomiting. (Note that severe dehydration is defined by actual or evolving circulatory compromise.) These patients should receive IV rehydration. PEDS: Isotonic crystalloid is the solution recommended for emergency volume resuscitation in pediatric patients. Isotonic saline (0.9% saline or normal saline) is the isotonic solution of choice by many experts in the field, although an alternative is the infusion of lactated Ringer’s solution. Emergent IV therapy must be begun with a rapid infusion of 20 cc/kg of isotonic solution. The patient is reassessed during and after each fluid bolus, and similar boluses are repeated as needed until adequate perfusion is restored and the signs of severe dehydration resolve. After the severe extracellular volume depletion has been restored with IV fluid, further fluid replacement can be continued with either oral rehydration therapy unless clearly contraindicated.
Indications for continued IV therapy include:
- Inability of the patient to take ORS due to altered level of consciousness
- Failure of the ORS to be tolerated as due to intractable vomiting.
- Severe electrolyte problems such as severe hypernatremia
Of course, in dehydrated patients, the underlying cause leading up to the dehydration should not be overlooked.
Water purification—When traveling or living in remote or rustic situations, a safe water supply may not be readily available. Water can be purified in one of several ways:
- Boiling for 3 minutes followed by cooling to room temperature (do not add ice) to kill bacteria, parasites, and viruses
- Adding 2 drops of 5% sodium hypochlorite (bleach) to a quart of water kills most bacteria within 30 minutes
- Adding 5 drops of tincture of iodine to a quart of water kills bacteria within 30 minutes
- Compact water filters in which the filters are impregnated with iodine remove parasitic pathogens and kill viral and bacterial pathogens; they provide a reasonable alternative for those who expect to be traveling under rustic circumstances. These are available commercially at camping or wilderness supply stores.
Boiling water is usually the most palatable solution to water purification if
sanitary storage is feasible. The addition of iodine or chlorine to water can impart
an unpleasant taste.1
Malnutrition
Marasmus
Marasmus is the condition of starvation. Total caloric intake is below caloric
expenditure. Untreated, it is terminal. Marasmus patients are lethargic and
apathetic, with a thin and wasted appearance. Their skin and hair may be more
normal appearing than kwashiorkor patients’ (see below). However, most
marasmus patients also have features of kwashiorkor as well.
Treatment priorities in the acute setting include addressing dehydration, hypoglycemia, and hypothermia first and foremost. The first two of these may be addressed by use of ORS with added sugar (4 tsp per 100 cc). The next priority is addressing caloric and protein needs. ORS alone are usually given only for 12 to 24 hours; protein and calories must be added to prevent worsening of the nutritional status. Protein foods (eg, porridge with a mix of cereals and grains to ensure a complete protein source) are administered in increasing amounts each day. Slow advancement of the diet, specifically the amount of food, is essential to prevent intolerance. Frequent feedings of small amounts are optimal, beginning every 2 hours for the first day or two, stretching to every 3 hours for the next 3 days, and finally to every 4 hours. The goal intake is 100 to 150 calories/kg/day. The third priority in treating malnutrition is to address comorbidities, such as parasitic infection, anemia, and tuberculosis.
Occasionally, congestive heart failure may develop during the treatment of malnutrition. Often, it is the result of overly aggressive parenteral rehydration, too quickly advanced diet, or high salt content in the diet. After identifying and correcting possible nosocomial causes, use of furosemide or digoxin may be helpful. In some cases, the CHF is due to anemia, which on occasion may require transfusion to correct.
Kwashiorkor
This condition, most common in recently weaned toddlers, represents adequate
caloric intake, but inadequate protein intake. These children will appear
apathetic, with brittle
and discolored hair, skin rashes, and edema of the face, extremities, and abdomen.
Treatment is similar to that noted above. Kwashiorkor children are generally not
significantly dehydrated, and the protein intake is key to treatment. Parental
education on proper nutrition using locally available protein sources (especially
combinations of plant
sources that yield a complete protein) is essential to
prevent recurrence.
Vitamin Deficiency Diseases
Anemia (Iron, Folate, B12)
Microcytic (Iron)
Patients with anemia suffer from fatigue, weakness, palor, diminished cognitive
performance, and increased susceptibility to infection.
History and clinical exam can uncover anemia as the cause of the patient's symptoms. Laboratory studies can establish it as microcytic. Most iron-deficient anemia cases are due to iron loss (blood loss), and it is imperative to identify the source of the loss. Usually, the loss is due to a gastrointestinal bleed. In industrialized nations, this is often from peptic ulcers or is neoplasm-related. In developing nations, hookworm infection is the most common cause. A stool exam is a vital part of the anemia work-up abroad.
Treatment consists primarily of correcting the underlying pathology, generally treating the hookworm infection. (Vol III—TM4 Gastrointestinal and Abdominal Manifestations) In the case of peptic ulcer disease, use of a proton-pump inhibitor or similar agent is indicated. This is also accompanied by iron supplementation. The dose is 3 mg/kg (PEDS: age <5 years) or 60 mg PO daily for 3 months. Iron gluconate may be more tolerable than iron sulfate, but it is more costly. Dietary sources of iron include red meats, legumes, and dark green vegetables.
Megaloblastic Anemia (Folate, B12)
These deficiencies
present with pallor, weakness, glossitis, and diarrhea. B12 deficiency also includes peripheral neuropathy, disequilibrium, and
neuropsychiatric changes.
Diagnosis consists of recognizing the anemia, and classifying it as megaloblastic. Serum levels of these nutrients may be checked and are of great value when they are available.
Treatment consists of folic acid 1 to 2 mg/day. The administration regimen for B12 is 0.2 to 1.0 mg IM (or via nasal spray) daily for 1 to 2 weeks, then weekly for a month (if neurological signs are present, this is followed by 1 mg every 2 weeks for 6 months), then monthly for life. An alternative to parental or nasal spray therapy, that appears to be just as effective in greatly compliant patients, is the use of high dose oral cobalamin (Vitamin B12). Oral doses of 1 to 2 mg/day (which is more that 200 times higher than the minimal daily requirement for normal patients) can be effective due to the presences of a lower efficiency transport system of cobalamin that does not require intrinsic factor. It is important to note that treatment of B12 deficiency with folate alone and no B12 causes the neurological deterioration to accelerate; it is a good practice to treat every case of megaloblastic anemia with both folate and B12. Folate is naturally occurring in green leafy vegetables, organ meats, and legumes; B12 is found in organ meats.
Xerophthalmia (Vitamin A)
Presentation begins as night blindness, progresses to keratinizing metaplasia of
the conjunctiva (the eponymous Bitot’s spots
are a focal manifestation of this), and ultimately to corneal ulceration and necrosis (keratomalacia). Although the
ocular manifestations are the most dramatic, deficiency of this vitamin affects
many bodily functions. Significantly, mortality to infections such as
measles dramatically decreases when vitamin A deficiency is treated.
Diagnosis is clinical; no reliable laboratory test is available.
Treatment in the case of xerophthalmia and measles requires immediate treatment with 200 000 IU of vitamin A PO on 2 successive days (PEDS: 100 000 IU in children aged < 12 months). Treatment of more mild deficiency and prevention of deficiency calls for 200 000 IU (PEDS: 100 000 IU if aged < 12 months) PO every 3 to 6 months, (PEDS) 50 000 IU PO to neonates, and 200 000 to 300 000 IU PO postpartum in nursing mothers. Dietary sources of vitamin A include liver, oil, eggs, and yellow/orange fruits and vegetables.
Rickets and Osteomalacia (Vitamin D)
Vitamin D is
synthesized during casual dermal sun exposure. As synthesis can
vary with latitude, season, and clothing, fortified foods are used to prevent
deficiency. This fortification is not always available, and deficiency
may develop.
Clinically, vitamin D deficiency may present as rickets (prior to closure of the growth plates) or osteomalacia. In rickets, hypotonia and weakness progress to severe tetany. Long bone epiphyses and costochondral junctions develop a knobby appearance described as the rickets rosary. Dental and skull deformities may also be seen. Osteomalacia presents as muscle and bone pain, weakness, and a waddling gate. In this condition, pseudofractures may be seen on x-ray.
Diagnosis is clinical, supplemented by radiology and serum vitamin D levels. In addition, serum calcium, phosphorus, parathyroid hormone (PTH), and alkaline phosphatase levels may be altered.
Treatment is oral vitamin D replacement with attention to providing adequate calcium (800 to 1000 mg/day). Vitamin D is available in several forms. Give dihydrotachysterol (DHT, D1) 60 000 IU once, then 6000 IU daily until the rickets are clinically and radiologically resolved. Give ergocalciferol (D2) 1000 to 5000 IU daily for 6 to 12 weeks (PEDS: 1000 IU/day if aged < 1 month, 3000 IU/day if aged 1 to 12 months, 5000 IU/day if aged > 12 months). The final form, cholecalciferol (D3), is typically administered as either 5000 to 10 000 IU daily for 2 to 3 months or as 600 000 IU in 1 day divided into 4 to 6 doses. In cases when follow up and multiple dosing can be a challenge due to logistics or noncompliance, stosstherapy2 may be employed. This consists of a bolus of calcitriol 150 000 to 600 000 IU given as a single dose or divided over several days (PEDS: 300 000 IU over 1 to 7 days in children aged 1 to 12 months.) Its onset of action is less than 1 day, with maximal effects seen in 1 month. Some preparations contain propylene glycol, which should be limited to <25 mg/kg of body weight due to potential toxicity.
Wernicke-Korsakov
Wernicke-Korsakov syndrome is the result of thiamine deficiency. The first
eponym refers to an encephalopathy, the second to a dementia. The syndrome is
most commonly seen in the United States as a complication of the malnutrition in
alcoholics, but may be seen in other settings as well. For treatment approaches, see the beriberi section that follows.
Beriberi (Thiamine)
Beriberi presentation is fatigue, anorexia, weakness, and calf tenderness and
numbness. Dry beriberi progresses on to overt chronic polyneuropathy and
severe muscle atrophy.
Wet beriberi involves the
myocardium and progresses to
congestive heart failure, cachexia, and death. While onset may be
insidious in
adults, in infantile beriberi, it may be fulminant with death in 1 to 2
days. Infantile beriberi is seen in breastfeeding by thiamine-deficient
(usually
subclinical) mothers when the child is 2 to 6 months old.
There are good laboratory tests to assess thiamine status; these may not be available abroad.
Treatment is parenteral thiamine at 20 mg IM twice daily for 3 days, followed by 30 mg PO daily until thiamine status is normalized. Prevention is by ensuring adequate intake of grains; processing may remove some of this, necessitating oral supplementation. Thiamine may also be found in organ meats and milk.
Scurvy (Vitamin C)
Presentation
is related
to defective connective tissue formation. Scurvy begins as
weakness and fatigue
and progresses to follicular hyperkeratosis, petechiae, bruising, and
bleeding gums. Ultimately, hemarthrosis, hemopericardium, anemia, and
shock may result. Infantile scurvy has subperiosteal hemorrhages
predominantly, manifested as bone pain.
Laboratory diagnostic tests are available, and (PEDS) in children, radiological studies can aid in diagnosis by demonstrating scorbutic bone lesions.
Treatment is oral replacement of ascorbic acid, 0.5 to 1 g/day until clinical
signs resolve and leukocyte
ascorbic acid levels return to normal. Prevention consists
of adequate dietary intake of vitamin C containing foods (eg, citrus fruits), especially when
weaning infants.
Pellegra (Niacin)
This condition progresses as the
4 Ds: dermatitis
(red or brown discoloration, affecting areas exposed to sun or pressure), diarrhea, dementia, and
death.
Diagnosis is primarily by identifying the characteristic rash on individuals at risk. Laboratory evaluation of urine N'methyl--nicotinamide or erythrocyte nicotinamide adenine dinucleotide levels may be helpful.
Treatment with nicotinamide 50 to 250 mg/day brings about rapid improvement; prevention is via a diet adequate in tryptophan, found in meats, legumes, milk, fish, and poultry.
Ariboflavinosis (Riboflavin)
Ariboflavinosis presents clinically as rash that looks similar to pellagra, except it
is more commonly found in the skin folds and non-sun-exposed regions. Other
manifestations include fatigue and weakness, angular stomatitis, and soreness of
the mouth.
Although ariboflavinosis is largely diagnosed clinically, erythrocyte glutathione reductase activity is a good indicator of riboflavin status.
Treatment is 5 to 10 mg of riboflavin daily until clinically improved. Prevention is adequate intake of dairy products and organ meats.
Goiter (Iodine)
Goiter (ie, enlargement of the thyroid gland) is the most common presentation of
iodine deficiency in adults. Clinical
hypothyroidism (ranging from fatigue and
skin and hair changes to cognitive deficits and myxedema) may accompany this
if the compensatory hypertrophy is inadequate. Perhaps the most tragic
presentation is cretinism—the severe mental
retardation, neurological
impairment, and short stature that
results from the effects of hypothyroidism on
the developing brain in early life.
Diagnosis of goiter can be made by physical exam. Urine iodine and serum thyroid-related hormones may be used to confirm the diagnosis.
Treatment is via intramuscular injection of 480 mg/mL iodized vegetable oil or consumption of iodinized salt or water (the latter two as part of the local public health measures). Prevention consists of these public health measures or the injection every 2 to 3 years.
Miscellaneous Minerals
There are several other minerals required in trace amounts. No clear deficiency
syndrome for copper, zinc, manganese,
or
molybdenum, except in the context
of
overall malnutrition (including iatrogenic in patients receiving total parenteral
nutrition [TPN]), exists. Low
fluoride is associated with an increased incidence
of dental caries. Chromium
deficiency, usually seen iatrogenically in patients
receiving TPN, is associated with hyperglycemia, metabolic syndrome, and
glaucoma. Selenium
deficiency has been implicated as a cofactor in
myxedematous cretinism, Keshan Disease (progressive cardiomyopathy in
preschoolers), and Kashin-Beck Disease (osteoarthropathy affecting
adolescents). No specific replacement regimens for any of
these trace minerals are well
established. Clear toxic syndromes are known for each of them. Exercise caution
to avoid overdose.
References
- Wanke, CA, Travelers’ Diarrhea: In UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2007.
- Cesur Y, Caksen H, Gundem A, Kirimi E, Odabas D. Comparison of low and high dose of vitamin D treatment in nutritional vitamin D deficiency rickets. J Pediatr Endocrinol Metab. 2003;16:1105-1109.