CHAPTER 2

LITERATURE REVIEW
2.1 Marasmus
Definition
Marasmus is one of the 3 forms of serious protein-energy malnutrition (PEM). The other 2
forms are kwashiorkor (KW) and marasmic KW. These forms of serious PEM represent a
group of pathologic conditions associated with a nutritional and energy deficit occurring
mainly in young children from developing countries at the time of weaning. Marasmus is a
condition primarily caused by a deficiency in calories and energy, whereas kwashiorkor
indicates an associated protein deficiency, resulting in an edematous appearance. Marasmic
kwashiorkor indicates that, in practice, separating these entities conclusively is difficult; this
term indicates a condition that has features of both.
Etiology
PEM, unlike the other important nutritional deficiency diseases, is a macronutrient
deficiency, not a micronutrient deficiency. Although termed PEM, it is now generally
accepted to stem in most cases from energy deficiency, often caused by insufficient food
intake. Energy deficiency is more important and more common than protein deficiency. It is
very often associated with infections and with micronutrient deficiencies. Inadequate care, for
example infrequent feeding, may play a part.
The cause of PEM (and of some other deficiency diseases prevalent in developing countries)
should not, however, be viewed simply in terms of inadequate intake of nutrients. For
satisfactory nutrition, foods and the nutrients they contain must be available to the family in
adequate quantity; the correct balance of foods and nutrients must be fed at the right
intervals; the individual must have an appetite to consume the food; there must be proper
digestion and absorption of the nutrients in the food; the metabolism of the person must be
reasonably normal; and there should be no conditions that prevent body cells from utilizing
the nutrients or that result in abnormal losses of nutrients. Factors that adversely influence
any of these requisites can be causes of malnutrition, particularly PEM. The aetiology,
therefore, can be complex. Certain factors that contribute to PEM, particularly in the young
child, are related to the host, the agent (the diet) and the environment. The underlying causes
could also be categorized as those related to the child's food security, health (including
protection from infections and appropriate treatment of illness) and care, including maternal
and family practices such as those related to frequency of feeding, breastfeeding and
weaning.
Some examples of factors involved in the aetiology of PEM are:
the young child's high needs for both energy and protein per kilogram relative to
those of older family members;
inappropriate weaning practices;
inappropriate use of infant formula in place of breastfeeding for very young infants
in poor families;
staple diets that are often of low energy density (not infrequently bulky and
unappetizing), low in protein and fat content and not fed frequently enough to
children;
inadequate or inappropriate child care because of, for example, time constraints for
the mother or lack of knowledge regarding the importance of exclusive breastfeeding;
inadequate availability of food for the family because of poverty, inequity or lack of
sufficient arable land, and problems related to intrafamily food distribution;
infections (viral, bacterial and parasitic) which may cause anorexia, reduce food
intake, hinder nutrient absorption and utilization or result in nutrient losses;
famine resulting from droughts, natural disasters, wars, civil disturbances, etc.
Epidemiology
Nearly 30% of humans currently experience one or more of the multiple forms of
malnutrition. Close to 50 million children younger than 5 years have PEM, and half of the
children who die younger than 5 years are undernourished. Approximately 80% of these
malnourished children live in Asia, 15% in Africa, and 5% in Latin America.
Marasmus is more frequent in children younger than 5 years because this period is
characterized by increased energy needs and increased susceptibility to viral and bacterial
infections. Weaning, which occurs during this period, is often complicated by factors such as
geography (eg, drought, poor soil productivity), economy (eg, illiteracy, unemployment),
hygiene (eg, access to quality water), public health (eg, number of nurses is more than
number of physicians), and culture and dietetics (eg, intrafamily distribution of high-nutrition
foods).
Pathogenesis
Diagnostics
The condition of PEM is often likened to an iceberg, of which 20 percent is visible above the
water and about 80 percent submerged. The severe forms of PEM - kwashiorkor, nutritional
marasmus and marasmic kwashiorkor - constitute the top, exposed part of the iceberg: they
are relatively easy for a doctor or health worker to diagnose simply from their clinical
manifestations, described below. On the other hand, children with moderate or mild
malnutrition often do not have clear clinical manifestations of malnutrition; rather, they are
shorter and/or thinner than would be expected for their age, and they may have deficits in
psychological development and perhaps other signs not easy to detect. Mild and moderate
PEM are diagnosed mainly on the basis of anthropometry, especially using measurements of
weight and height and sometimes other measurements such as arm circumference or skinfold
thickness.
The most perceptible and frequent clinical feature in marasmus is the loss of muscle mass and
subcutaneous fat mass. Some muscle groups, such as buttocks and upper limb muscles, are
more frequently affected than others. Facial muscles are usually spared longer. Facial fat
mass is the last to be lost, resulting, in severe cases, in the characteristic elderly appearance of
children with marasmus. Anorexia is frequent and interferes with renutrition. An irritable
and whining child who cannot be comforted or separated from the mother demonstrates
behaviours often observed with marasmus. Apathy is a sign of serious forms of marasmus:
children are increasingly motionless and seem to "let themselves die." In contrast, during
rehabilitation, even the slightest smile is a positive sign of recovery. Children's behaviour is
probably one of the best clinical signs of the severity and evolution of marasmus.
Several clinical signs must be assessed in order to detect complications, with special attention
to infectious complications (see checklist below). The physical examination must be very
thorough because even small abnormalities can be clinically significant. Clinical signs of
serious complication can be very subtle in children with marasmus. A body temperature of
37.5C can correspond to a fever of 39-40C in a child without marasmus, and a small cough
can be the only sign of a serious pneumonia. After history and physical examination,
diagnosing the type and severity of the malnutrition, as well as diagnosing associated
infections and complications affecting organs or systems, such as the GI, neurological, or
cardiovascular system, are critical. This set of diagnoses results in optimal planning of the
complementary evaluation and therapeutic strategy.
Checklist of points for conducting the physical examination

o Body temperature (measured with a thermometer) - Allowing measurement of low
temperatures to detect hypothermia as well as fever
o Anemia - Pale mucosa
o Edema
o Dehydration - Thirst, shrunken eyes
o Hypovolemic shock - Weak radial pulse, cold extremities, decreased consciousness
o Tachypnea - Pneumonia, heart failure
o Abdominal manifestations - Distension, decreased or metallic bowel sounds, large or
small liver, blood or mucus in the stools
o Ocular manifestations - Corneal lesions associated with vitamin A deficiency
o Dermal manifestations - Evidence of infection, purpura
o Ear, nose, and throat (ENT) findings - Otitis, rhinitis

Generally, for diagnosis and treatment of marasmus, no further evaluation is necessary other than
the clinical evaluation. Most laboratory results are within the reference range despite significant
changes in body composition and physiology. Furthermore, in regions where malnutrition is
frequent, health structures are poorly equipped, and laboratory evaluations are either impossible
to obtain or unreliable.
If they are available, some laboratory results can be useful to monitor treatment or to diagnose
specific complications.
Laboratory tests adapted from the WHO include the following:

Blood glucose: Hypoglycemia is present if the level is lower than 3 mmol/L.
Examination of blood smears by microscopy or direct detection test: Presence of
parasites is indicative of infection. Direct test is suitable but expensive.
Hemoglobin: A level lower than 40 g/L is indicative of severe anemia.
Urine examination and culture, Multistix: More than 10 leukocytes per high-power field
is indicative of infection. Nitrites and leukocytes are tested on Multistix also.
Stool examination by microscopy: Parasites and blood are indicative of dysentery.
Albumin: Although not useful for diagnosis, it is a guide to prognosis; if albumin is
lower than 35 g/L, protein synthesis is massively impaired.
HIV test: HIV test should not be routinely performed; if completed, it should be
accompanied by counseling of the child's parents and the result should be confidential.
Electrolytes: Measuring electrolytes is rarely helpful and it may lead to inappropriate
therapy. Hyponatremia is a significant finding.

Radiological examinations are rarely used for the same reasons as the laboratory examinations.
Thoracic radiography can show a pulmonary infection despite lack of clinical signs, a primary
tuberculosis lesion, cardiomegaly, or signs of rachitism.

Skin test results for tuberculosis are often negative in children who are undernourished with
tuberculosis or those previously vaccinated with Bacille Calmette-Gurin (BCG) vaccine.

Management

Management of moderate marasmus can be performed on an outpatient basis, but severe
marasmus or marasmus complicated by a life-threatening condition generally requires inpatient
treatment. In these cases, management is divided into an initial intensive phase followed by a
consolidation phase (rehabilitation), preparing for outpatient follow-up management. The WHO
has developed guidelines to help improve the quality of hospital care for malnourished children
and has prioritized the widespread implementation of these guidelines.

The guidelines highlight 10 steps for routine management of children with malnutrition, as
follows:

Prevent and treat the following:
o Hypoglycemia
o Hypothermia
o Dehydration
o Electrolyte imbalance
o Infection
o Micronutrient deficiencies

Provide special feeds for the following:
o Initial stabilization
o Catch-up growth
o Provide loving care and stimulation
o Prepare for follow-up after discharge

Because most patients with moderate cases of marasmus can be treated as outpatients, the
optimal environment is a pediatric nutrition rehabilitation center. Nutritional rehabilitation
should include appropriate foods for an intake up to 100-150 kcal/kg/d. Other therapeutic and
preventive actions should include rehydration using the WHO solution (see below) in case of
associated diarrhea, micronutrient supplementation (eg, iron, vitamin A), context-appropriate
screening, and review of immunization status. This management should also incorporate
nutritional and sociocultural education adapted to the local conditions. Family-based
management is preferred with the child's mother as the key player.



Prognosis

Except for complications mentioned above, prognosis of even severe marasmus is good if
treatment and follow-up care are correctly applied.

2.2 Bronchopneumonia

Definition

Bronchopneumonia or bronchial pneumonia is the acute inflammation of the walls of the
bronchioles. It is a type of pneumonia characterized by multiple foci of isolated, acute
consolidation, affecting one or more pulmonary lobules.

Etiology

A specific aetiological agent cannot be identified in 40% to 60% of cases. Viral pneumonia
cannot be distinguished from bacterial pneumonia based on a combination of clinical findings.
The majority of lower respiratory tract infections that present for medical attention in young
children are viral in origin such as respiratory syncytial virus, influenza, adenovirus and
parainfluenza virus. One helpful indicator in predicting aetiological agents is the age group as
shown in the table below.

Table 2: Pathogens causing pneumonia

AGE BACTERIAL PATHOGENS
Newborns Group B streptococcus, Escherichia coli, Klebsiella species, Enterobacteriaceae
1-3 months Chlamydia trachomatis
Preschool Streptococcus pneumoniae, Haemophilus influenzae type b, Staphylococcal
aureus
Less common: group A streptococcus, Moraxella catarrhalis, Pseudomonas
aeruginosa
School Mycoplasma pneumoniae, Chlamydia pneumoniae

Epidemiology

Pneumonia and other lower respiratory tract infections are the leading cause of death worldwide.
The WHO Child Health Epidemiology Reference Group estimated the median global incidence
of clinical pneumonia to be 0.28 episodes per child-year. This equates to an annual incidence of
150.7 million new cases, of which 11-20 million (7-13%) are severe enough to require hospital
admission. Ninety-five percent of all episodes of clinical pneumonia in young children
worldwide occur in developing countries.

Pathogenesis

Pneumonia is characterized by inflammation of the alveoli and terminal airspaces in response to
invasion by an infectious agent introduced into the lungs through hematogenous spread or
inhalation. The inflammatory cascade triggers the leakage of plasma and the loss of surfactant,
resulting in air loss and consolidation.

The activated inflammatory response often results in targeted migration of phagocytes, with the
release of toxic substances from granules and other microbicidal packages and the initiation of
poorly regulated cascades (eg, complement, coagulation, cytokines). These cascades may directly
injure host tissues and adversely alter endothelial and epithelial integrity, vasomotor tone,
intravascular hemostasis, and the activation state of fixed and migratory phagocytes at the
inflammatory focus. The role of apoptosis (noninflammatory programmed cell death) in
pneumonia is poorly understood.

Pulmonary injuries are caused directly and/or indirectly by invading microorganisms or foreign
material and by poorly targeted or inappropriate responses by the host defense system that may
damage healthy host tissues as badly or worse than the invading agent. Direct injury by the
invading agent usually results from synthesis and secretion of microbial enzymes, proteins, toxic
lipids, and toxins that disrupt host cell membranes, metabolic machinery, and the extracellular
matrix that usually inhibits microbial migration.

Indirect injury is mediated by structural or secreted molecules, such as endotoxin, leukocidin, and
toxic shock syndrome toxin-1 (TSST-1), which may alter local vasomotor tone and integrity,
change the characteristics of the tissue perfusate, and generally interfere with the delivery of
oxygen and nutrients and removal of waste products from local tissues.

On a macroscopic level, the invading agents and the host defenses both tend to increase airway
smooth muscle tone and resistance, mucus secretion, and the presence of inflammatory cells and
debris in these secretions. These materials may further increase airway resistance and obstruct the
airways, partially or totally, causing airtrapping, atelectasis, and ventilatory dead space. In
addition, disruption of endothelial and alveolar epithelial integrity may allow surfactant to be
inactivated by proteinaceous exudate, a process that may be exacerbated further by the direct
effects of meconium or pathogenic microorganisms.

Bronchopneumonia, a patchy consolidation involving one or more lobes, usually involves the
dependent lung zones, a pattern attributable to aspiration of oropharyngeal contents. The
neutrophilic exudate is centered in bronchi and bronchioles, with centrifugal spread to the
adjacent alveoli.

Diagnostics

Children with bacterial pneumonia cannot be reliably distinguished from those with
viral disease on the basis of any single parameter; clinical, laboratory or chest
radiograph findings.

1. Chest radiograph
Chest radiograph is indicated when clinical criteria suggests pneumonia. It will not
identify the aetiological agent. However the chest radiograph is not always necessary if
facilities are not available or the pneumonia is mild.

2. Complete white blood cell and differential count
This test may be helpful as an increased white blood count with predominance of
polymorphonuclear cells may suggest bacterial cause. However, leucopenia can either
suggest a viral cause or severe overwhelming infection.

3. Blood culture
Blood culture remains the non-invasive gold standard for determining the precise
aetiology of pneumonia. However the sensitivity of this test is very low. Positive blood
cultures are found only in 10% to 30% of patients with pneumonia. Even in 44% of
patients with radiographic findings consistent with pneumonia, only 2.7% were positive
for pathogenic bacteria. Blood culture should be performed in severe pneumonia or
when there is poor response to the first line antibiotics.

4. Culture from respiratory secretions
It should be noted that bacteria isolates from throat swabs and upper respiratory tract
secretions are not representative of pathogens present in the lower respiratory tract. Samples
from the nasopharynx and throat have no predictive values. This investigation
should not be routinely done.

5. Other tests
Bronchoalveolar lavage is usually necessary for the diagnosis of Pneumocystis carini
infections primarily in immunosuppressed children. It is only to be done when facilities and
expertise are available. If there is significant pleural effusion diagnostic, pleural tap will be
helpful.Mycoplasma pneumoniae, Chlamydia, Legio nella and Moxarella catarrhalis are
difficult organisms to culture, and thus serological studies should be performed in
children with suspected atypical pneumonia. An acute phase serum titre of more than 1:160
or paired samples taken 2-4 weeks apart showing four fold rise is a good indicator of
Mycoplasma pneumoniae infection. This test should be considered for children
aged five years or older with pneumonia.

Management

Treatment decisions in children with pneumonia are dictated based on the likely etiology of
the infectious organism and the age and clinical status of the patient. Antibiotic
administration must be targeted to the likely organism, bearing in mind the age of the patient,
the history of exposure, the possibility of resistance (which may vary, depending on local
resistance patterns), and other pertinent history

After initiating therapy, the most important tasks are resolving the symptoms and clearing the
infiltrate. With successful therapy, symptoms resolve much sooner that the infiltrate. In a
study of adults with pneumococcal pneumonia, the infiltrate did not completely resolve in all
patients until 8 weeks after therapy (although it was sooner in most patients). If therapy fails
to elicit a response, the whole treatment approach must be reconsidered..

Prognosis

Overall, the prognosis is good. Most cases of viral pneumonia resolve without treatment;
common bacterial pathogens and atypical organisms respond to antimicrobial therapy (see
Treatment and Management). Long-term alteration of pulmonary function is rare, even in
children with pneumonia that has been complicated by empyema or lung abscess.
Patients placed on a protocol-driven pneumonia clinical pathway are more likely to have
favorable outcomes. The prognosis for varicella pneumonia is somewhat more guarded.
Staphylococcal pneumonia, although rare, can be very serious despite treatment.