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Presentators Day, Date Supervisor
: Halimatusakdiah, Daniel Rajkumar : Tuesday, August 27th,2013 : dr.Supriatmo, SpA (K) CHAPTER 1 INTRODUCTION
Tuberculosis (TB) is contagious and airborne. It is a disease of poverty affecting mostly young adults in their most productive years. The vast majority of TB deaths are in the developing world- 1.7 million people died from TB (including 380 000 women) in 2009, including 380 000 people with HIV, equal to 4700 deaths a day. The TB death rate has fallen by 35% since 1990, and the number of deaths is also declining TB is among the three greatest causes of death among women aged 15-44. There were 9.4 million new TB cases (including 3.3 million women) in 2009, including 1.1 million cases among people with HIV . The estimated global incidence rate fell to 137 cases per 100 000 population in 2009, after peaking in 2004 at 142 cases per 100 000. The rate is still falling but too slowly. Globally, the percentage of people successfully treated reached the highest level at 86% in 2008. Since 1995, 41 million people have been successfully treated and up to 6 million lives saved through DOTS and the Stop TB Strategy. 5.8 million TB cases were notified through DOTS programmes in 2009. Of the 22 TB high burden countries, 13 countries are on track to meet the 2015 Millennium Development Goal target and 12 countries are on track to reach the 2015 Stop TB Partnership targets. 1.6 million TB patients knew their HIV status in 2009 compared to 1.4 million in 2008 with the highest HIV testing rates of TB patients in Europe (86%) Africa (53%) and the Americas (41%). In 55 countries, including 16 in Africa, at least 75% of TB patients knew their HIV status. 37% of HIV-positive TB patients were enrolled on antiretrovirals and 75% started on cotrimoxazole preventive treatment in 2009. Multidrug-resistant TB (MDR-TB) is a form of TB that is difficult and expensive to treat and fails to respond to standard first-line drug. There were an
estimated 440 000 new MDR-TB cases in 2008, and 150 000 deaths from MDRTB. It was estimated that in 2009, 3.3% of all new TB cases had MDR-TB. In 2010, the largest WHO MDR-TB survey reported the highest rates ever of MDRTB, with peaks of up to 28% of new TB cases in some settings of the former Soviet Union. - Many countries have developed plans to address MDR-TB, but the response globally is still insufficient. Extensively drug-resistant TB (XDRTB) occurs when resistance to second-line drugs develops on top of MDR-TB. XDR-TB cases have been confirmed in 58 countries. The World Health Organization (WHO) defines malnutrition as "the cellular imbalance between the supply of nutrients and energy and the body's demand for them to ensure growth, maintenance, and specific functions." The term protein-energy malnutrition (PEM) applies to a group of related disorders that include marasmus, kwashiorkor, and intermediate states of marasmuskwashiorkor. The term marasmus is derived from the Greek word marasmos, which means withering or wasting. Marasmus involves inadequate intake of protein and calories and is characterized by emaciation. The term kwashiorkor is taken from the Ga language of Ghana and means "the sickness of the weaning." Williams first used the term in 1933, and it refers to an inadequate protein intake with reasonable caloric (energy) intake. Edema is characteristic of kwashiorkor but is absent in marasmus. Studies suggest that marasmus represents an adaptive response to starvation, whereas kwashiorkor represents a maladaptive response to starvation. Children may present with a mixed picture of marasmus and kwashiorkor, and children may present with milder forms of malnutrition. For this reason, Jelliffe suggested the term protein-calorie (energy) malnutrition to include both entities. Although protein-energy malnutrition affects virtually every organ system, this article primarily focuses on its cutaneous manifestations. Patients with protein-energy malnutrition may also have deficiencies of vitamins, essential fatty acids, and trace elements, all of which may contribute to their dermatosis
CHAPTER 2 LITERATURE REVIEW 2.1. TUBERCULOSIS 2.1.1 Definition TB is an airborne disease caused by the bacterium Mycobacterium tuberculosis (M. tuberculosis) . M. tuberculosis and seven very closely related mycobacterial species (M. bovis, M. africanum, M. microti, M. caprae, M. pinnipedii, M. canetti and M. mungi) together comprise what is known as the M. tuberculosis complex. Most, but not all, of these species have been found to cause disease in humans. 2.1.2. Etiology TB is caused by M tuberculosis, a slow-growing obligate aerobe and a facultative intracellular parasite. The organism grows in parallel groups called cords (as seen in the image below). It retains many stains after decoloration with acid-alcohol, which is the basis of the acid-fast stains used for pathologic identification. Acid-fast bacillus smear showing characteristic cording in Mycobacterium tuberculosis. Mycobacteria, such as M tuberculosis, are aerobic, non–spore-forming, nonmotile, facultative, curved intracellular rods measuring 0.2-0.5 μm by 2-4 μm. Their cell walls contain mycolic, acid-rich, long-chain glycolipids and phospholipoglycans (mycocides) that protect mycobacteria from cell lysosomal attack and also retain red basic fuchsin dye after acid rinsing (acid-fast stain). Transmission Humans are the only known reservoir for M tuberculosis. The organism is spread primarily as an airborne aerosol from an individual who is in the infectious stage of TB (although transdermal and GI transmission have been reported). In immunocompetent individuals, exposure to M tuberculosis usually results in a latent/dormant infection. Only about 5% of these individuals later show evidence of clinical disease. Alterations in the host immune system that lead to decreased immune effectiveness can allow M tuberculosis organisms to reactivate, with tubercular disease resulting from a combination of direct effects from the replicating infectious organism and from subsequent inappropriate host immune responses to tubercular antigens. Molecular typing of M tuberculosis isolates in the United States by restriction fragment-length polymorphism analysis suggests more than one third
older persons. about 5 to 10% of infected persons who do not receive treatment for latent TB infection will develop TB disease at some time in their lives. Overall. Although mycobacteria are spread by blood throughout the body during initial infection.3. liver. 2. generalized disease. when their immune system becomes weak for another reason. Verhagen et al demonstrated that large clusters of TB are associated with an increased number of tuberculin skin test–positive contacts. The remainder results from reactivation of latent infection. which ingest the bacterium. Generally.4 of new patient occurrences of TB result from person-to-person transmission. and brain. Infants. the risk of developing TB disease is much higher than for persons with normal immune systems. spleen. even after adjusting for other risk factors for transmission. Extrapulmonary spread Because of the ability of M tuberculosis to survive and proliferate within mononuclear phagocytes. primary extrapulmonary disease is rare except in immunocompromised hosts. or otherwise immunosuppressed hosts are unable to control mycobacterial growth and develop disseminated (primary miliary) TB. Other people may get sick years later.1. Risk Factor Some people develop TB disease soon after becoming infected (within weeks) before their immune system can fight the TB bacteria. For persons whose immune systems are weak. persons at high risk for developing TB disease fall into two categories: Persons who have been recently infected with TB bacteria Persons with medical conditions that weaken the immune system Persons who have been Recently Infected with TB Bacteria This includes: Close contacts of a person with infectious TB disease . This suggests that some TB strains may be more transmissible than other strains and that isoniazid resistance is associated with lower transmissibility. usually via hematogenous routes. bones. M tuberculosis is able to invade local lymph nodes and spread to extrapulmonary sites. Patients who become immunocompromised months to years after primary infection also can develop late. especially those with HIV infection. kidneys. The number of positive contacts was significantly lower for index cases with isoniazid-resistant TB compared with index cases with fully-susceptible TB. such as the bone marrow.
are part of the innate immune system and provide an . correctional facilities. too. homeless shelters.1.5 Persons who have immigrated from areas of the world with high rates of TB Children less than 5 years of age who have a positive TB test Groups with high rates of TB transmission. the next line of host defense. such as homeless persons. nursing homes. and residential homes for those with HIV Persons with Medical Conditions that Weaken the Immune System Babies and young children often have weak immune systems. Bacteria in droplets that bypass the mucociliary system and reach the alveoli are quickly surrounded and engulfed by alveolar macrophages.and the cilia on the surface of thecells constantly beat the mucus and its entrapped particles upward for removal. Pathophysiology Once inhaled.the most abundant immune effector cells present in alveolar spaces. and persons with HIV infection Persons who work or reside with people who are at high risk for TB in facilities or institutions such as hospitals. the infectious droplets settle throughout the airways. Other people can have weak immune systems. injection drug users.4. These macrophages. especially people with any of these conditions: HIV infection (the virus that causes AIDS) Substance abuse Silicosis Diabetes mellitus Severe kidney disease Low body weight Organ transplants Head and neck cancer Medical treatments such as corticosteroids or organ transplant Specialized treatment for rheumatoid arthritis or Crohn’s disease 2. The majority of the bacilli are trapped in the upper parts of the air ways where the mucus-secreting goblet cells exist. The mucus produced catches foreign substances. This system provides the body with an initial physical defense that prevents infection in most persons exposed to tuberculosis.
and is characterized by low oxygen levels. Regardless of whether the infection becomes controlled or progresses.11 The mycobacterial lipoarabinomannan is a key ligand for a macrophage receptor. and limited nutrients. This condition restricts further growth and establishes latency. low pH. however.6 opportunity for the body to destroy the invading mycobacteria and prevent infection.the microorganisms continue to grow until they reach sufficient numbers to fully elicit the cell-mediated immune response.The outcome is essentially determined by the quality ofthe host defenses and the balancethat occurs between host defenses and the invading mycobacteria. initial development involves production of proteolytic enzymes and cytokines by macrophages in an attempt to degrade the bacteria. successfully controlling the infection sothat the bacilli are contained in the dormant. The complement system also plays a role in the phagocytosis of the bacteria. or progression to active disease. which can be detected by a skin test. which creates a microenvironment that limits replication and the spread of the mycobacteria. For persons with intact cellmediated immunity. such as protein regulation. These nodulartype lesions form from an accumulation of activated T lymphocytes and macrophages. The complement protein C3 binds to the cell wall and enhances recognition of the mycobacteria by macrophages. the mycobacteria continueto multiply slowly. By 2 or 3 weeks. After being ingested by macrophages. to enhance survival. Lesions in persons with less effective immunesystems . This environment destroys macro phages and produces early solid necrosis at the center of the lesion. the cells that constitute cell-mediated immunity. Several mechanisms and macrophage receptors are involved in uptake of the mycobacteria. healed lesions. M tuberculosis organisms can change their phenotypic expression. called primary progressive tuberculosis. the bacilli are able to adapt to survive. the necrotic environment resembles soft cheese. In fact.often referred to caseous necrosis. Lesions in persons with an adequate immune system generally undergo fibrosis and calcification. followed by latent tuberculosis. Released cytokines attract T lymphocytes to the site. even in the air spaces of a host with no previous exposure to M tuberculosis. Opsonization by C3 is rapid.11Macrophages are readily available phagocytic cells that combat many pathogens without requiring previous exposure to the pathogens.This initial immune process continues for 2 to 12 weeks.The subsequent phagocytosis by macrophages initiates a cascade of events that results in either successful control of theinfection.with bacterialcell division occurring every 25 to 32 hours.Macrophages then present myco -bacterial antigens on their surface to the T cells. the next defensive step is formation of granulomas around the M tuberculosis organisms.
granuloma formation is initiated yet ultimately is unsuccessful in containing the bacilli.1.leaving an air-filled cavity at theoriginal site. An individual who is suspected of having TB disease requires a complete medical evaluation. symptoms. In patients infected with M tuberculosis. and risk factors • Human immunodeficiency virus (HIV) screening • Physical examination • Tuberculin skin test (TST) or interferon gamma release assay (IGRA) • Chest radiography • Bacteriologic examination Medical History The clinician should interview patients to document their medical histories.5. medical history. and physical examination. previous treatment for TB. Bacilli can also drain into the lymphatic system and collect in the tracheobronchial lymph nodes of theaffected lung. such as the patient’s age. where the organisms can form new caseous granuloma 2. Diagnostic Tests For Detecting Active Tuberculosis Consideration of tuberculosis (TB) disease as a possible diagnosis is the first step that must be taken before further evaluation. The semiliquid necrotic material can then drain into a bronchus or nearby blood vessel. and coexisting diseases. The diagnosis of TB disease is often overlooked because of the failure to consider it among possible diagnoses. If discharge into a vessel occurs. While a definitive diagnosis may involve the addition of laboratory and radiographic findings. a high degree of suspicion can be based on epidemiology. A written record of a patient’s medical history should include the following: . droplets can be coughed up from the bronchus andinfect other persons. including the following: • Medical history. and management can occur. For less immunocompetent persons. and the fibrous wall loses structural integrity. diagnosis. it is also important to consider factors that may affect the typical presentation of TB.7 progress to primary progressive tuberculosis. The necrotic tissue undergoes liquefaction. occurrence of extrapulmonary tuberculosis is likely. including exposure. nutritional status. In considering TB disease.
most patients with TB disease have one or more symptoms that led them to seek medical care... such as ruling out a cancer diagnosis (e. Pulmonary General: Pulmonary and Extrapulmonary •Coughing •Chills • Coughing up sputum •Fever or blood •Night sweats •Pain in the chest when •Loss of appetite •Weight loss •Weakness or easy fatigability •Malaise (a feeling of Extrapulmonary • The symptoms depend on part of body affected by tuberculosis (TB) disease • TB of the spine may cause pain in the back. . Clinicians should also consider demographic factors that may increase a patient’s risk for exposure to TB disease and drug-resistant TB. ethnic or racial group. Occasionally. Be aware that most persons become infected with Mycobacterium tuberculosis without knowing they were exposed. occupation.g. When symptoms are present.g. or refugee camp). through a chest radiograph given to patients before surgery). homeless shelter. Symptoms of TB Disease: Ask patients about their symptoms. going to the emergency department for pneumonia) • Previous antibiotic therapy Exposure to infectious TB: Ask patients if they have spent time with someone with infectious TB. age. TB is discovered during a medical examination for an unrelated condition.Although TB disease does not always produce symptoms. they usually have developed gradually and been present for weeks or even months. It is important to note that patients often refer to latent TB infection (LTBI) as TB disease. such as country of origin.8 • Exposure to infectious TB • Symptoms of TB disease • Previous TB infection or disease • Risk factors • Recent medical encounters (e. and residence in congregate settings (such as a jail. Question patients about whether they know of any contact in the recent or distant past with persons diagnosed with pulmonary or laryngeal TB. however.
For persons previously skin tested. • Pleural • Laryngea Previous Latent TB Infection or TB Disease: Ask patients whether they have ever been diagnosed with or treated for TB infection or disease. Ask how many pills were taken per day (to determine what treatment regimen was used and whether they received injections). Risk Factors for Developing TB Disease: Determine whether patients have any conditions or behaviors that are risk factors for developing TB disease Human Immunodeficiency Virus Screening .9 general • TB of the kidney may cause blood in the urine. and it may be resistant to one or more of the drugs used. they are at high risk for TB disease if certain immunosuppressive conditions exist or if immunosuppressive therapies are being taken. • Lymphatic TB may cause swollen and tender lymph nodes. If the regimen prescribed was inadequate or if the patient did not follow the recommended treatment. • Patients who have had TB disease before should be asked when they had the disease and how the disease was treated. If they were infected within the past two years. • Meningeal TB may cause headaches or psychiatric symptoms. • Patients known to have a positive skin test reaction or positive Interferon Gamma Release Assay (IGRA) probably have TB infection. often at the base of the neck. an increase in induration of 10 mm within a two-year period is classified as a conversion to positive or positive Interferon Gamma Release Assay (IGRA). TB may recur.
tuberculosis infection. The IGRAs currently approved by the Food and Drug Administration (FDA) and available on the market are QuantiFERON®-TB Gold in tube(QFT™). QuantiFERON®-TB test (QFT). but is not limited to IGRAs.34 Other cytokine-based immunoassays are under development and may also become useful in the diagnosis of M. but it can provide valuable information about the patient’s overall condition. • Persons at high risk for HIV infection should be screened for HIV at least annually Physical Examination A physical examination is an essential part of the evaluation of any patient. IGRA usually can be used in place of the TST. However. such as human immunodeficiency virus (HIV) infection. are required to confirm TB disease. tuberculosis. which may affect how TB is manifested.10 Voluntary counseling and testing for human immunodeficiency virus (HIV) is recommended for all patients with TB. such as chest radiography and bacteriologic examination. Note that for patients with a previous documented positive TST reaction. Tuberculin Skin Test and Interferon Gamma Release Assays (IGRA) Use the Mantoux tuberculin skin test (TST) or an interferon gamma release assay (IGRA) to test for M. an IGRA can be done if there is suspicion that the TST result was a false positive. The Centers for Disease Control and Prevention (CDC) recommends the following: • HIV screening for patients in all health-care settings after the patient is notified that testing will be performed unless the patient declines (opt-out screening). Blood assay for Mycobacterium tuberculosis (BAMT) is a general term referring to recently developed in vitro diagnostic tests that assess for the presence of infection with M. which can be used in all circumstances in which the TST is used. • Routine HIV testing for persons suspected of having TB disease and contacts to TB patients. other factors. and the presence of extrapulmonary TB. in .TB test. HIV counseling and testing has also been recommended for contacts of persons with TB. QuantiFERON®-TB Gold test (QFT-G) and the TSPOT®. a TST is not necessary. Future FDA-licensed products. It cannot be used to confirm or rule out TB. tuberculosis infection. Additional tests. This term includes.
are that results can be obtained after a single patient visit. lordotic) or additional studies (e. of TB. are required to confirm TB disease. However. chest radiograph. In addition. when indicated. A negative TST does not rule out TB disease—as many as 20% of patients with TB disease have a negative TST reaction. the blood must be incubated with the test antigens less than 12 hours after collection..11 combination with Centers for Disease Control and Prevention (CDC)-issued recommendations. computed tomography [CT] scans) may be necessary. and.g. additional tests. the IGRA test has practical limitations that include the need to draw blood and to ensure its receipt in a qualified laboratory in time for testing. Certain abnormalities on chest radiographs are suggestive. In pulmonary TB. may provide additional diagnostic alternatives. lesions may appear anywhere in the lungs and may differ in size. Persons with a positive TST result. lateral. the IGRA test appears to be less affected by past bacille of Calmette-Guérin (BCG) vaccination than the TST and may eliminate the unnecessary treatment of patients with BCG-related false-positive results. For IGRA tests. In some instances. other views (e. Children younger than 5 years of age should receive posterior-anterior and lateral radiographs. should be evaluated for TB disease before LTBI is diagnosed. such as chest radiography and bacteriologic examination. a chest radiograph should be examined for abnormalities consistent with TB disease.. A negative TST result should not be used alone to exclude M. However. The advantages of IGRA. other tests or studies Chest Radiography A posterior-anterior radiograph of the chest is the standard view used for the detection and description of chest abnormalities in adults. compared with the TST. bacteriologic studies. (Note: When newer IGRA tests are available. but are not diagnostic.g. and that. radiographic abnormalities are often seen in the apical and posterior segments of the upper lobe or in the superior segments of the lower lobe. serology for human immunodeficiency virus (HIV). . this time frame may differ.) For both the TST and IGRA. while the lymphocytes are viable. the variability associated with skin test reading can be eliminated. because it is a blood test performed in a qualified laboratory. tuberculosis infection in persons with symptoms or signs suggestive of TB disease. At a minimum. Medical evaluation of such persons should include a history and physical examination. regardless of signs and symptoms.
including nucleic acid amplification (NAA). If a diagnosis of pulmonary TB cannot be established from sputum smear. bronchoscopy. Depending on the anatomical site. • If positive. For example. other procedures may be necessary. pulmonary TB may present atypically on the chest radiograph. gives a semiquantitative Laboratory Turnaround Times • Within 24 hours from receipt of specimen in the laboratory . In fact.12 shape. It usually is the first bacteriologic evidence of the presence of mycobacteria in a clinical specimen. In HIV-infected persons. especially in HIV-infected and other immunosuppressed persons. and presence or absence of cavitation. such as: • Urine • Cerebrospinal fluid • Pleural fluid • Pus or other aspirated fluid • Biopsy specimens • Blood Extrapulmonary TB Bacteriologic Tests Used In Diagnosing Tuberculosis Disease Test Acid-Fast Bacilli (AFB) Smear Description • Provides the physician with a preliminary confirmation of the diagnosis. or it may cause mediastinal or hilar lymphadenopathy with or without accompanying opacities and/or cavities. and gastric aspiration in children. In HIVinfected persons. almost any abnormality on a chest radiograph may indicate TB. the radiograph of an HIV-infected person with TB disease may even appear entirely normal. TB may cause opacities without cavities in any lung zone. other clinical specimens are necessary. Bacteriologic Examination Specimens For Diagnosing Tuberculosis Disease Suspected Diagnosis Pulmonary or laryngeal tuberculosis (TB) Specimen Needed Sputum (phlegm from deep in the lungs) samples for smear and culture examination. density.
WAPHL performs confirmation for the First line drugs (up to 14 days MTBC identification) and Second line drug (28 days from the receipt of the specimen [reference cultures] or MTBC identification).6. TB Disease Treatment Regimens Anti-tuberculosis drugs . 2. Drug Resistance Screening by Sequencing (DRSS) • DRSS results are available within 3-4 business days from the receipt of specimen at the WA PHL laboratory. • A test done on sputum specimens for the direct and rapid identification of the Mycobacterium tuberculosis complex. • DRSS is a presumptive test and needs to be confirmed by traditional susceptibility testing.1. • Allows for the amplification of specific target sequences of nucleic acids that will be detected by a nucleic acid probe. fluroquinolones (FQ) and the injectables amakacin (AMK).13 Nucleic Acid Amplification (NAA) Assay Culture estimate of the number of bacilli being excreted (which is of vital clinical and epidemiologic importance in assessing the patient’s infectiousness). • Second-line drugs: within 4 weeks from date of request. • Does not replace the need for routine AFB smear and culture • Usually necessary for species identification of all clinical specimens suspected of containing mycobacteria. Also the DRSS examines the genetic loci that are associated with resistance to the most effective second-line drugs. • For both first-line and second-line drugs: Is repeated on interim isolates when a patient remains culture-positive after 3 months of treatment Allows rapid confirmation of MDR TB through the identification of genetic mutations associated with RIF and INH resistance – MDR case. • Within 2-3 working days from receipt of specimen in the laboratory Drug Susceptibility Testing • Mycobacterial growth detection: within 14 days from specimen collection • Identification of mycobacteria: within 21 days from specimen Collection • First-line drugs: within 30 daysfrom specimen collection. kanamycin (KAN) and capreomycin (CAP) will be examined. • Is required for drug susceptibility testing and genotyping • For first-line drugs: Is performed on initial isolates of all patients to identify an effective antituberculosis regimen.
such as those of the American Thoracic Society. Fewer drugs are generally used in the continuation phase because the risk of acquiring drug resistance is low. severe forms of EPTB. new smear-negative pulmonary TB with extensive parenchymal involvement. as it has been associated with severe reactions (Stevens-Johnson Syndrome) in adults and children with TB who are coinfected with the human immunodeﬁciency virus (HIV). Thiacetazone is no longer recommended as part of a ﬁrstline regimen to treat TB. particularly for isoniazid (INH) (some guidelines. The purpose of the intensive phase is to rapidly eliminate the majority of organisms and to prevent the emergence of drug resistance. recommend a dose of INH of 10–15 mg/kg). The intensive phase uses more drugs. Table 1 Doses of ﬁrst-line anti-tuberculosis drugs in adults and children Recommended dose in mg/kg body weight (range) Essential drug Daily Isoniazid (H) Rifampicin (R) Pyrazinamide (Z) Ethambutol (E) Streptomycin (S)† Treatment regimens 5 (4–6) max. New cases fall under Category I (newsmear-positive pulmonary TB. The need for better data on anti-tuberculosis drug pharmacokinetics in children is highlighted by the variations in national recommendations for drug doses in children. 600 mg daily 35 (30–40) 30 (25–35) 15 (12–18) The recommended treatment regimens for each TB diagnostic category are generally the same for childrenas for adults. Either phase can be give daily or three times weekly. 300 mg daily 10 (8–12) max. Table 1 shows the essential anti-tuberculosis drugs and their recommended doses. The purpose of the continuation phase is to eradicate the dormant organisms.14 Anti-tuberculosis treatment is divided into two phases: an intensive (initial) phase and a continuation phase. as most of the organisms have already been eliminated. 600 mg daily 25 (20–30) 20 (15–25)* 15 (12–18) Three times weekly 10 (8–12) 10 (8–12) max. severe concomitant .
extensive pulmonary involvement. Previously treated cases fall under diagnostic Category II (previously treated smear-positive pulmonary TB) or IV (chronic and multidrug resistant [MDR] TB). 3) following a letter (drug abbreviation) is the number of doses per week of that drug. There is a standard code for TB treatment regimens.15 HIV disease) or Category III (new smear-negative pulmonary TB—other than in Category I.which uses an abbreviation for each anti-tuberculosis drug. If there is no subscript number following a letter.. with H and R given three times weekly (number in subscript after the letters).g. orsevere forms of EPTB (e. Table 2 Recommended treatment regimens for each diagnostic category TB diagnostic category TB cases Regimen (daily or 3 times weekly)* Intensive phase Continuation phase smear-positive 2HRZE 4HR or 6HE New pulmonary TB New smear-negative pulmonary TB with extensive parenchymal involvement Severe forms of EPTB (other than TB meningitis—see below) . A subscript number (e. The continuation phase is 4H3R3. Children with TBmeningitis and miliary TB deserve special consideration(see below). RMP) and pyrazinamide (Z. Example: 2HRZ/4H3R3 The initial phase is 2HRZ.g. The duration of the continuation phase is 4 months. A regimen consists of two phases. The duration of the initial phase is 2 months. The number in front of each phase represents the duration of that phase in months. and therefore fall under diagnostic Category III. An alternative drug (or drugs) appears as a letter (or letters) in parentheses. Table 2 shows the recommended treatment regimens for each treatment category. Those children with smear-positivepulmonary TB. Most children with TB have uncomplicated(smear-negative) pulmonary/intrathoracic TB or nonsevere forms of EPTB. Drug treatment is daily (no subT script numbers after the letters) with INH (H). rifampicin (R. treatment with that drug is daily. based on the best available evidence.. PZA). abdominal or bone/jointTB) fall under diagnostic Category I. less severe forms of EPTB).
tuberculous meningitis (TBM). corticosteroids have been shown to improve survival and reduce morbidity. whether or not the child is smear-positive at diagnosis. Preferably someone other than the child’s parent or immediate family should observe or administer treatment. e. The drug most frequently used is prednisone. Conditions that merit hospitalisation include: 1) TB meningitis and miliary TB. 2) any child with . and TB pericarditis. the complications of airway obstruction by TB lymph glands.16 Severe concomitant HIV disease TB meningitis Previously treated smearpositive pulmonary TB: —relapse —treatment after interruption —treatment failure New smear-negative pulmonary TB (other than in category I) Less severe forms of EPTB Chronic and MDR-TB 2RHZS 4RH 2HRZES/1HRZE 5HRE 2HRZ† 4HR or 6HE Specially designed standardised or individualised regimens (see treatment guidelines for MDR-TB3) Adjunctive treatment with corticosteroids Corticosteroids may be used for the management of some complicated forms of TB. Children with severe forms of TB should be hospitalised for intensive management where possible. preferably for the ﬁrst 2 months. Fixed-dose combinations (FDCs) should be used whenever possible to improve simplicity and adherence. The support of the child’s parents and immediate family is vital to ensure a satisfactory outcome of treatment. and are thus recommended in all cases of TBM. Patient treatment cards are recommended for documenting treatment adherence. TREATMENT ADMINISTRATION AND ADHERENCE Children. The dose should then be slowly reduced (tapered off) over 1–2 weeks before stopping. All children should receive treatment free of charge. In advanced TBM cases.. in a dosage of 2 mg/kg/day (maximum dosage 60 mg/day) for 4 weeks.g. their parents and other family members and other care givers should be educated about TB and the importance of completing treatment.
respiratory distress, 3) spinal TBand 4) severe adverse events, such as clinical signs of hepatotoxicity (e.g., jaundice). If it is not possible toensure good adherence and treatment outcome as an out-patient, some children may require hospitalisation for social or logistical reasons. FOLLOW-UP Ideally, each child should be assessed by the National Tuberculosis Programme (NTP) (or those designated by the NTP to provide treatment) at least at the following intervals: 2 weeks after treatment initiation, at the end of the intensive phase, and every 2 months until treatment completion. The assessment should include, at a minimum, a symptom assessment, an assessment of adherence, enquiry about any adverse events, and weight measurement. Medication dosages should be adjusted to account for any weight gain. Adherence should be assessed by reviewing the treatment card. A follow-up sputum smear for microscopy at 2 months should be obtained for any child who was smearpositive at diagnosis. Follow-up chest radiographs are not routinely required in children, particularly as many children willhave a slow radiological response to treatment. A child who is not responding to TB treatment should be referred for further assessment and management. These children may have drug-resistant TB, an unusual complication of pulmonary TB, other causes of lung disease, or problems with treatment adherence. The NTP is responsible for organising treatment in line with the Stop TB Strategy, and ensuring the recording and reporting of cases and their outcomes. Good communication is necessary between the NTP and clinicians treating children with TB. Adverse events notedby clinicians should be reported to the NTP. Immune reconstitution Sometimes referred to as a paradoxical reaction, thistemporary exacerbation of symptoms, signs or radiographic manifestations sometimes occurs after beginning anti-tuberculosis treatment. This can simulate worsening disease, with fever, and increased size of lymph nodes or tuberculomas. Immune reconstitution can be brought about by improved nutritional statusor by the antituberculosis treatment itself. Clinical deterioration due to immune reconstitution can occur after initiation of antiretroviral therapy (ART) in HIVinfected children with TB, and is known as the immune reconstitution inﬂammatory syndrome (IRIS). Antituberculosis treatment should be continued, although in some cases the addition of corticosteroids might be useful. If in doubt, refer the child to the next level of care.
Adverse events Adverse events caused by anti-tuberculosis drugs are much less common in children than in adults. The most important adverse event is the development of hepatotoxicity, which can be caused by INH, RMP, or PZA. Serum liver enzyme levels should not be monitored routinely, as asymptomatic mild elevation of serum liver enzymes (less than 5 times normal values) is not an indication to stop treatment. However, the occurrence of liver tenderness, hepatomegaly or jaundice should lead to investigation of serum liver enzyme levels and the immediate stopping of all potentially hepatotoxic drugs. Patients should be screened for other causes of hepatitis,and no attempt should be made to reintroduce these drugs until liver functions have normalised. An expert should be involved in the further management of such cases. If treatment for TB needs to be continued for severe forms of TB, non-hepatotoxic anti-tuberculosis drugs should be introduced (e.g., ethambutol [E, EMB], an aminoglycoside and a ﬂuoroquinolone). INH may cause symptomatic pyridoxine deﬁciency, particularly in severely malnourished children and HIVinfected children on highly active antiretroviral ther- apy (HAART). Supplemental pyridoxine (5–10 mg/day) is recommended in 1) malnourished children, 2)HIV-infected children, 3) breastfeeding infants, and 4) pregnant adolescents.
2.1.7. Prevention of TB Disease The key method of preventing tuberculosis (TB) is prompt identification and treatment of patients with TB. Other strategies include patient education, treatment of latent infection, and vaccination. The World Health Organization (WHO) launched the Stop TB strategy in 2006 (modelled after the directly observed theraphy [DOT] strategy) and the core components include pursuing high-quality DOT expansion and enhancement; addressing TB and human immunodeficiency (HIV) infection, multidrug-resistant (MDR) TB, and other challenges; contributing to health system strengthening; engaging all care providers; empowering people with TB; and enabling and promoting research. Patient education Thoroughly educate patients regarding compliance to therapy, adverse effects of medications, and follow-up care. Treatment of latent TB infection
Recommendations for preventive therapy are based on a comparative analysis of the risk of administration of isoniazid (INH) versus the risk of acquiring the disease. Adults with a positive tuberculin skin test (TST) result and no clinical or radiographic manifestations who are receiving INH therapy have been demonstrated to have 54-88% protection against the development of the disease, whereas children have been shown to have 100% protection. The risk of acquisition of TB is particularly high in very young children (< 5 y) and in the adolescent population. Thus, patients in these age groups with a positive TST result and no other manifestations should receive INH therapy. Active TB should be carefully excluded before the initiation of preventive therapy. For recent contacts of patients with contagious TB (ie, in the past 3 mo), INH therapy is indicated even if the TST result is negative. This is especially true for contacts who are infected with HIV or for household contacts younger than 5 years. Household contacts of any age should be considered for INH therapy if they are from a high-prevalence area, even if the TST result is negative. The recommendations from the American Academy of Pediatrics (AAP) are to administer 9 months of therapy. The drug of choice is INH. A treatment period of 12 months is recommended for patients with HIV infection. For the management of contacts of INH-resistant cases, rifampin is recommended for 6 months in children. In case of a high probability of infection with MDR TB, observation is recommended, because none of the other drugs have been evaluated for preventive therapy. Several drugs have been used in these circumstances, including pyrazinamide, fluoroquinolones, and ethambutol, depending on the susceptibility patterns.
Vaccination The bacille Calmette-Guérin (BCG) vaccine is available for the prevention of disseminated TB. BCG is a live vaccine prepared from attenuated strains of M bovis. The major role of BCG vaccination is the prevention of serious and lifethreatening disease such as disseminated TB and TB meningitis in children. The BCG vaccine does not prevent infection with M tuberculosis.
However. is exposed to persons with untreated or ineffectively treated contagious pulmonary TB. may necessitate administration of anti-TB therapy. in areas of the world where the risk of TB is high. a TST is mandatory before vaccination. including steroid use and HIV infection. except for pyrazinamide. 2 meta-analyses of the various trials concluded that the vaccine is efficacious against miliary and meningeal TB. Adverse reactions due to the vaccine include subcutaneous abscess formation and the development of lymphadenopathy. In the United States. its efficacy continues to be debated. The WHO’s Expanded Program on Immunization recommends the administration of BCG at birth. administration of BCG does not require a previous TST. The vaccine is used in more than 100 countries. the WHO recommends using the BCG vaccine in children who have asymptomatic HIV infection. such as osteitis of the epiphyses of the long bones and disseminated TB. However. Thereafter. Contraindications to the administration of the vaccine include immunosuppressed conditions such as primary or secondary immunodeficiency.20 Although the BCG vaccine has been in use since 1921 and approximately 3 billion doses have been administered. Several trials have been performed to assess the efficacy of the vaccine. and cannot be removed from the exposure Child has negative HIV and TST results. including the following: Child has negative HIV and TST results. and results vary. . is exposed to persons with contagious MDR (resistant to INH and rifampin) pulmonary TB. BCG vaccination is currently recommended only in certain situations. Rare complications. Controversy surrounds the efficacy of BCG vaccination against pulmonary TB. and cannot be removed from the exposure or treated with anti-TB medication From birth to age 2 months.
described in detail the condition she termed "kwashiorkor" (using the local Ga word meaning "the disease of the displaced child").6 percent in 1975 to 34. This stress on kwashiorkor and on protein led to a relative neglect of nutritional marasmus and adequate food and energy intakes for children. it was not until the 1930s that Cicely Williams. It was often described as the most important form of malnutrition.6 percent in 1995. at the other end of the spectrum. the Near East and Africa. Latin America. A child who manifests growth failure may be shorter in length or height or lighter in weight than expected for a child of his or her age. the number of malnourished children has in fact risen. kwashiorkor (characterized by the presence of oedema) and nutritional marasmus (characterized by severe wasting) have high case fatality rates. In fact the number of underweight children worldwide has risen from 195 million in 1975 to an estimated 200 million at the end of 1994. especially energy. At one end of the spectrum. However. It often results from consuming too little food. mild PEM manifests itself mainly as poor physical growth in children. In the 1950s kwashiorkor began to get a great deal of attention. It is unknown why a given child may develop one syndrome as opposed to the other. The current view is that most PEM is the result of inadequate intake or poor utilization of food and energy. not a deficiency of one nutrient and not usually simply a lack of dietary protein. but World Health Organization (WHO) estimates suggest that the prevalence of PEM in children under five years of age in developing countries has fallen progressively. working in Ghana. MALNUTRITION Protein-energy malnutrition (PEM) in young children is currently the most important nutritional problem in most countries in Asia. and it was believed to be caused mainly by protein deficiency. and is frequently aggravated by infections. or may be thinner than expected for height. It has also been increasingly realized that infections contribute importantly to PEM. The term PEM is used to describe a broad array of clinical conditions ranging from the mild to the serious. and it is now seen that these two serious clinical forms of PEM constitute only the small tip of the . Energy deficiency is the major cause. which means that more than onethird of the world's under-five population is still malnourished. Failure to grow adequately is the first and most important manifestation of PEM. from 42.21 2. It has been known for centuries that grossly inadequate food intake during famine and food shortages leads to weight loss and wasting and eventually to death from starvation. The solution seemed to be to make more protein-rich foods available to children at risk.2. However. No accurate figures exist on the world prevalence of PEM. Nutritional marasmus is now recognized to be often more prevalent than kwashiorkor. in some regions this fall in percentage has not been as rapid as the rise in population. thus in some regions. such as Africa and South Asia.
may play a part. Causes and epidemiology PEM. In most populations studied in poor countries. particularly in the young child. 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.22 iceberg. Although termed PEM. The aetiology. however. often caused by insufficient food intake. breastfeeding and weaning. is a macronutrient deficiency. Inadequate care. 2.2. including maternal and family practices such as those related to frequency of feeding. · inappropriate use of infant formula in place of breastfeeding for very young infants in poor families. unlike the other important nutritional deficiency diseases. the agent (the diet) and the environment. Factors that adversely influence any of these requisites can be causes of malnutrition. therefore. The cause of PEM (and of some other deficiency diseases prevalent in developing countries) should not. the point prevalence rate for kwashiorkor and nutritional marasmus combined is 1 to 5 percent. and there should be no conditions that prevent body cells from utilizing the nutrients or that result in abnormal losses of nutrients. are related to the host. can be complex. whereas 30 to 70 percent of children up to five years of age manifest what is now termed mild or moderate PEM. for example infrequent feeding. the metabolism of the person must be reasonably normal. health (including protection from infections and appropriate treatment of illness) and care. . particularly PEM.1. be viewed simply in terms of inadequate intake of nutrients. Energy deficiency is more important and more common than protein deficiency. there must be proper digestion and absorption of the nutrients in the food. not a micronutrient deficiency. The underlying causes could also be categorized as those related to the child's food security. Certain factors that contribute to PEM. diagnosed mainly on the basis of anthropometric measurements. · inappropriate weaning practices. the individual must have an appetite to consume the food. It is very often associated with infections and with micronutrient deficiencies. the correct balance of foods and nutrients must be fed at the right intervals. For satisfactory nutrition. foods and the nutrients they contain must be available to the family in adequate quantity. it is now generally accepted to stem in most cases from energy deficiency.
civil disturbances. Prematurity or low birth weight may predispose the child to the development of nutritional marasmus. natural disasters. and problems related to intrafamily food distribution. reduce food intake. In a child who consumes much less food than required for his or her energy needs. for example. various metabolic changes take place which contribute to the development of oedema. The view that kwashiorkor is the result of protein deficiency and nutritional marasmus the result of energy deficiency is an oversimplification. · inadequate availability of food for the family because of poverty. etc. Gluconeogenesis in the liver is enhanced. low in protein and fat content and not fed frequently enough to children. Therefore promotion of infant formula and insufficient support of breastfeeding by the medical profession and health services may be factors in the aetiology of marasmus. energy is mobilized from both body fat and muscle. · infections (viral. More sodium and more water are retained. inequity or lack of sufficient arable land. as the causes of both conditions are complex. An underlying cause of PEM is any influence that prevents mothers from breastfeeding their newborn infants when they live in households where proper bottle-feeding may be difficult or hazardous. Both endogenous and exogenous causes are likely to influence whether a child develops nutritional marasmus. and much of the water collects outside the cardiovascular system in the tissues. which results in pitting oedema. · inadequate or inappropriate child care because of. The actual role of infection has not been .23 · staple diets that are often of low energy density (not infrequently bulky and unappetizing). especially when protein intake is very low relative to carbohydrate intake (with the situation perhaps aggravated by nitrogen losses from infections). and there is loss of subcutaneous fat and wasting of muscles. bacterial and parasitic) which may cause anorexia. separation from the mother or lack of or insufficient breastmilk may be causes in poor societies where breastfeeding is often the only feasible way for mothers to feed their babies adequately. wars. It has been suggested that under these circumstances. Prolonged exclusive breastfeeding without the introduction of other foods after six months of age may also contribute to growth faltering. PEM and eventually nutritional marasmus. time constraints for the mother or lack of knowledge regarding the importance of exclusive breastfeeding. kwashiorkor or the intermediate form known as marasmic kwashiorkor. · famine resulting from droughts. hinder nutrient absorption and utilization or result in nutrient losses. Failure of breastfeeding because of death of the mother.
Irrespective of which theory of aetiology may be proved correct. it would merely explain a mechanism for the pathogenesis of kwashiorkor. is likely to occur only in children who have inadequate food intake and are subjected to infection.24 adequately explained. there is little indication that any one micronutrient deficiency is the main cause of PEM or is by itself responsible for the oedema of kwashiorkor. nutritional anaemia and/or zinc deficiency. for example. In both nutritional marasmus and kwashiorkor (and also in moderate PEM). Most researchers agree that potassium deficiency and sodium retention are important in the pathogenesis of oedema. improving the quantity of food consumed. it has been hypothesized that most of the clinical features of kwashiorkor could be caused by an excess free radical stress. which is very low in protein. nor is there adequate convincing research to uphold the view of individual dysadaptation as the cause of severe PEM. vitamin A deficiency. Some evidence supports the classical argument that oedematous malnutrition is a sign of inadequate protein intake. In severe PEM there is usually biochemical evidence. which derives from amino acids in muscle tissue. of micronutrient deficiencies. which is not surprising in a child or adult who consumes a grossly inadequate diet. It would not change the fact that improving diet and reducing infection lead to significant reduction in both kwashiorkor and nutritional marasmus. Epidemiological evidence also shows higher rates of kwashiorkor in Uganda. however. taking steps to ensure that diets are nutritionally well balanced and controlling infection all help to prevent PEM. that kwashiorkor. where the staple diet is plantain. but certain infections cause major increases in urinary nitrogen. Recently two new theories have been advanced to explain the cause of kwashiorkor. than in neighbouring areas where the staple food is a cereal. clinical examinations or biochemical tests often give clear evidence of. even if produced by free radicals. The first is that kwashiorkor is due to aflatoxin poisoning. Neither the aflatoxin nor the free radical theory has been proved experimentally. and often clinical evidence. There is not yet broad agreement on the actual cause of the oedema that is the hallmark of kwashiorkor. However. no studies have been able to give conclusive proof of either similarities or differences in dietary consumption between children who develop kwashiorkor with oedema and those who show clinical signs of nutritional marasmus without any oedema. fatty liver and a kwashiorkorlike condition can be induced in pigs and baboons on a protein-deficient diet. relatively untested theory also suggests. For example. The second is that free radicals are important in the pathogenesis of kwashiorkor. . Thus even if this theory were to be proved correct. Surprisingly. oedema. This new.
kwashiorkor. the prevalence of highly visible. except in famine areas. Manifestations and clinical picture Mild and moderate PEM The condition of PEM is often likened to an iceberg.2. marasmic kwashiorkor and nutritional marasmus) is usually between about 1 and 5 percent.2. kwashiorkor and nutritional marasmus. In contrast. It suggests that protein deficiency plays a greater part in kwashiorkor and energy deficiency in nutritional marasmus. they are shorter and/or thinner than would be expected for their age. . In these areas often only 15 to 50 percent of young children between six months and 60 months of age do not have evidence of PEM.constitute the top. nutritional marasmus and marasmic kwashiorkor . especially using measurements of weight and height and sometimes other measurements such as arm circumference or skinfold thickness. moderate and mild malnutrition in many countries of sub-Saharan Africa and South Asia add up to 30 to 70 percent. and the overriding feature of nutritional marasmus is severe underweight. but that energy deficiency is more important. The two severe forms of malnutrition. The severe forms of PEM . and they may have deficits in psychological development and perhaps other signs not easy to detect. rather. As shown by the iceberg diagram (Figure 5). moderate and mild PEM depends on how these terms are defined. The diagram illustrates that both energy deficiency and protein deficiency play a part. Children who have both oedema and severe underweight are diagnosed as having marasmic kwashiorkor. The percentage of children classified as having severe. exposed part of the iceberg: they are relatively easy for a doctor or health worker to diagnose simply from their clinical manifestations. On the other hand. have very different appearances and clinical features as described below. described below. serious PEM (kwashiorkor. of which 20 percent is visible above the water and about 80 percent submerged. Mild and moderate PEM are diagnosed mainly on the basis of anthropometry.25 2. children with moderate or mild malnutrition often do not have clear clinical manifestations of malnutrition. It is generally agreed that the hallmark of kwashiorkor is pitting oedema.
PEM iceberg The so-called Wellcome classification of severe forms of PEM has been widely used for over 20 years (see Table 19). Subsequently these categories came to be known as follows: · wasting: acute current.26 FIGURE 5. In the early 1970s a number of nutrition workers began to suggest that judging the degree of malnutrition only on the basis of weight for age had many disadvantages. In the 1950s and 1960s the degree of malnutrition was almost always based on the child's percentage of standard weight for age. A method was suggested that distinguished three categories of mild to moderate PEM based on weight and height measurements of children. where weight for age and weight for height are low but height for age is normal. It has the advantage of simplicity because it is based on only two measures. . but not many children would be reclassified. The category "undernourished" includes children who have moderate or moderately severe PEM but no oedema and whose weight is above 60 percent of the standard. Today a cut-off point using standard deviations (SD) is considered more appropriate than percentage of standard. namely the percentage of standard weight for age and the presence or absence of oedema. short-duration malnutrition. In Latin America and elsewhere the Gomez classification was very widely used (Table 20).
TABLE 19 Wellcome classification of severe forms of protein-energy malnutrition Percentage of standard weight for Oedema present age 60-80 Kwashiorkor <60 Marasmic kwashiorkor Oedema absent Undernourishment Nutritional marasmus TABLE 20 The Gomez classification of malnutrition based on weight-for-age standards Classification Normal Grade I (mild malnutrition) Grade IIIa (severe malnutrition) a Percentage of standard weight for age >90 75-89. In country reports published based on weight for age alone. "underweight" is commonly used to denote weight below 2 SD of the NCHS standards in children up to five years of age. stunting is more prevalent than wasting worldwide. Prevalence above that . In a normal distribution it is expected that 2 to 3 percent of children will fall below the -2 SD cut-off point. it is now generally recommended that malnutrition be judged on the basis of SD below the growth standards of the United States National Center for Health Statistics (NCHS) as published by WHO. This became known as the Bengoa modification. The assessment of nutritional status. It also has advantages for nutritional surveys and surveillance. This classification makes a distinction between current and past influences on nutritional status. Bengoa of WHO suggested that all children with oedema be placed in Grade 111. where weight for age and height for age are low but weight for height is normal. · wasting and stunting: acute and chronic or current long-duration malnutrition.9 J. In general. and it gives the clinician some clue as to the history of the malnutrition in the patient. height for age and weight for height are all low. where weight for age.9 <<60 Grade II (moderate malnutrition) 60-74.27 · stunting: past chronic malnutrition. It helps the examiner assess the likelihood that supplementary feeding will markedly improve the nutritional status of the child.
Policy-makers and health workers need to decide which growth standards to use as a yardstick for judging malnutrition and for surveys. which will in turn reduce severe PEM. 2. measles. Kwashiorkor Kwashiorkor is one of the serious forms of PEM. These . but it may occur at any age. The international growth standards have been found to be applicable for developing countries.2. including the malnutritioninfection complex. and it may not be provided very frequently. had poorer physical fitness and had lower scores on psychological development tests than children from the same villages who grew better as young children. and that the poorer growth seen among the underprivileged results from social factors. The reduction and eventual prevention of mild or moderate malnutrition will automatically reduce severe malnutrition. then the children can be further divided into those who are wasted. stunted. Recent investigations in Guatemala indicated that teenagers who had manifested poor growth when examined in early childhood were smaller in stature. it may be very bulky. or even precipitated by. The functional significance of mild or moderate PEM is still not fully known. Studies from several countries show that the risk of mortality increases rather steadily with worsening nutritional status as indicated by anthropometric measures. resources are often better spent on controlling mild and moderate PEM. Often the food provided to the child is mainly carbohydrate. The attempt to control the extent and severity of PEM using many different strategies and actions is at the heart of nutritional programmes and policies in most developing countries. although it may be tempting (particularly for doctors and other health workers) to put major emphasis on the control of nutritional marasmus and kwashiorkor. rather than from ethnic or geographic differences. such as the Harvard and Denver growth standards) have gained increasing acceptance.3. In recent years the WHO/NCHS growth standards (which do not differ very much from previously used standards. If measurements are also taken of length or height.28 level suggests that there is a nutritional problem in the population assessed. respiratory infections. Thus. as evidence shows that the growth of privileged children in developing countries does not differ importantly from these standards. or wasted and stunted. whooping cough. It is seen most frequently in children one to three years of age. Kwashiorkor is often associated with. These results suggest long-term consequences of PEM in early childhood. infectious diseases. monitoring and surveillance. did less well at school. It is found in children who have a diet that is usually insufficient in energy and protein and often in other nutrients. intestinal parasites and other infections are common underlying causes of PEM and may precipitate children into either kwashiorkor or nutritional marasmus. Diarrhoea.
Later. a typical dermatosis. All cases of kwashiorkor have oedema to some degree. the symptoms reported and the clinical signs observed (Figure 6). Other signs include mental changes. diarrhoea and often evidence of other micronutrient deficiencies. Poor growth. in kwashiorkor this condition is always present to some degree. Laboratory tests are not essential but do throw more light on each case.29 infections often result in loss of appetite. It usually starts with a slight swelling of the feet and often spreads up the legs. lighter in weight than normal (usually 60 to 80 percent of standard or below 2 SD). If the child's precise age is known. abnormal hair. . anaemia. If oedema is present the pit formed takes a few seconds to return to the level of the surrounding skin. The accumulation of fluid in the tissues causes swelling. the hands and face may also swell. Infections. poor growth. which is important as a cause of serious PEM. Growth failure always occurs. wasting of muscles and fatty infiltration of the liver. Oedema. These signs may be obscured by oedema or ignorance of the child's age. To diagnose the presence of oedema the medical attendant presses with a finger or thumb above the ankle. especially those resulting in fever. Clinical signs of kwashiorkor Kwashiorkor is relatively easy to diagnose based on the child's history. except in cases of gross oedema. lead to an increased loss of nitrogen from the body which can only be replaced by protein in the diet. the child will be found to be shorter than normal and.
30 FIGURE 6. Characteristics of kwashiorkor .
plucked hair exhibits root changes and a narrower diameter than normal hair. On examination under a microscope. The hair of a normal Asian. blistered paint has given rise to the term "flaky-paint dermatosis". The child prefers to remain in one position and is nearly always miserable and unsmiling. In Latin America bands of discoloured hair are reported as a sign of kwashiorkor. Hair changes. . Underneath the flaking skin are atrophic depigmented areas which may resemble a healing burn. In kwashiorkor. Dermatosis develops in some but not all cases of kwashiorkor. The tensile strength of the hair is also reduced. This condition is always found in post-mortem examination of kwashiorkor cases. The similarity of these patches to old sun-baked. Fatty infiltration of the liver. The child's arms and legs are thin because of muscle wasting. It tends to occur first in areas of friction or of pressure such as the groin. Appetite is nearly always poor. the hair becomes silkier and thinner. Wasting of muscles is also typical but may not be evident because of oedema. Skin changes. behind the knees and at the elbow. It may cause palpable enlargement of the liver (hepatomegaly). African or Latin American child is usually dark black and coarse in texture and has a healthy sheen that reflects light. African hair loses its tight curl. Sometimes small tufts can be easily and almost painlessly plucked out.31 Wasting. The child is usually apathetic about his or her surroundings and irritable when moved or disturbed. These reddish-brown stripes have been termed the "flag sign" or "signa bandera". is dull and lifeless and may change in colour to brown or reddish brown. Mental changes are common but not invariably noticed. At the same time it lacks lustre. Darkly pigmented patches appear. Mental changes. which may peel off or desquamate.
hookworm. Moonface. It may occur at any age. malaria. Anaemia may be complicated by iron deficiency. Xerosis or xerophthalmia resulting from vitamin A deficiency may be seen. diarrhoea. Stools are frequently loose and contain undigested particles of food. and therefore also of energy. ometimes they have an offensive smell or are watery or tinged with blood.2. whooping cough. These include measles. and the amount gives an indication of the degree of energy deficiency. The cheeks may appear to be swollen with either fatty tissue or fluid. Mouth and lip changes characteristic of vitamin B deficiency are common. In marasmus the main deficiency is one of food in general. malaria and other parasitic diseases. is now much more prevalent than kwashiorkor. but in contrast to kwashiorkor it is more common during the first year of life. and the possible underlying causes are numerous. giving the characteristic appearance known as "moonface". For whatever reason. Deficiencies of zinc and other micronutrients may occur. Most cases have some degree of anaemia because of lack of the protein required to synthesize blood cells. Chronic infections such as tuberculosis may also lead to marasmus.4. Signs of other deficiencies. the child does not get adequate supplies of breastmilk or of any alternative food.32 Anaemia. the other severe form of PEM. 2. Nutritional marasmus In most countries marasmus. mental deficiency and digestive upsets such as malabsorption or vomiting. etc. Clinical features of nutritional marasmus . A very common cause is early cessation of breastfeeding. Other common causes of marasmus are premature birth. Perhaps the most important precipitating causes of marasmus are infectious and parasitic diseases of childhood. most commonly up to about three and a half years. Nutritional marasmus is in fact a form of starvation. Diarrhoea. In kwashiorkor some subcutaneous fat is usually palpable.
and once seen is never forgotten. Similarly. In severe cases the loss of flesh is obvious: the ribs are prominent. Poor growth In all cases the child fails to grow properly. Diarrhoea. The following are the main signs of marasmus. but this is not a constant feature of the disease. Alertness. the child may be ravenous. the weight will be found to be extremely low by normal standards (below 60 percent or -3 SD of the standard). An advanced case of the disease is unmistakable. The muscles are always extremely wasted. When the skin is taken between forefinger and thumb. There is little if any subcutaneous fat left. may commonly have been a precipitating factor. like any starving being. Diarrhoea of an infective nature. . If the age is known. Some children are anorexic. the child may be less miserable and less irritable. the usual layer of adipose tissue is found to be absent. The child often has a good appetite. Appetite. the face has a characteristic simian (monkeylike) appearance. Wasting. and the limbs are very emaciated. as mentioned above.33 The important features of kwashiorkor and nutritional marasmus are compared in Table 21. may be protuberant. Stools may be loose. Anaemia. Instead the deep sunken eyes have a rather wide-awake appearance. The child appears to be skin and bones. In fact. The skin hangs in wrinkles. Anorexia. the belly. Children with marasmus are quite often not disinterested like those with kwashiorkor. especially around the buttocks and thighs. in contrast to the rest of the body. Sometimes they make sucking noises. Children with marasmus often violently suck their hands or clothing or anything else available.
Serum albumin drops to low or very low levels usually only in clinically evident kwashiorkor. There may be pressure sores. they may also have any of the features of kwashiorkor described above. Dehydration. but these are usually over bony prominences. hair changes. the globulin fraction in the serum is normal or even raised. Laboratory tests Laboratory tests have a limited usefulness for the diagnosis or evaluation of PEM. There is more frequently a change of texture than of colour. there is no oedema and no flaky-paint dermatosis in marasmus. Many of these children have diarrhoea. In kwashiorkor there is a reduction in total serum proteins. dehydration is a frequent accompaniment of the disease.2. which is always present. because of infections. it results from severe diarrhoea (and sometimes vomiting). In nutritional marasmus the reduction is usually much less marked. Serum albumin levels are not useful in predicting imminent kwashiorkor development in moderate PEM cases. Often.34 Anaemia is usually present. and especially in the albumin fraction. There may be skin changes including flaky-paint dermatosis. lack of subcutaneous fat and poor growth. In contrast to kwashiorkor. Some biochemical estimations are used. mental changes and hepatomegaly. It is often true that . and in addition to oedema. In the Wellcome classification (see above) this diagnosis is given for a child with severe malnutrition who is found to have both oedema and a weight for age below 60 percent of that expected for his or her age. and give different results for children with kwashiorkor and nutritional marasmus than for normal children or those with moderate PEM. Hair changes. not in areas of friction. similar to those in kwashiorkor can occur. Although not a feature of the disease itself.5. Skin sores. Children with marasmic kwashiorkor have all the features of nutritional marasmus including severe wasting. 2. Marasmic kwashiorkor Children with features of both nutritional marasmus and kwashiorkor are diagnosed as having marasmic kwashiorkor.
the lower the serum albumin.9 _ 2. However. which is low in kwashiorkor but not much influenced by nutritional marasmus. Levels of two other serum proteins. There is general agreement that serum albumin concentrations below 3 g/dl are low and that those below 2. serum transferrin levels are also influenced by iron status. pre-albumin and serum transferrin. also tend to be reduced in kwashiorkor and to a lesser degree in nutritional marasmus.8 g/dl should be considered deficient and indicate a high risk. . TABLE 22 Levels of serum albumin concentrations in malnourished children Concentration Interpretation (g/dl) _ 3. and unlike the other biochemical tests mentioned below. · ratio of serum essential amino acids to non-essential amino acids.5-2. Serum albumin determinations are relatively easy and cheap to perform.5 Normal Subnormal Low Pathological Source: Alleyne et al. other diseases. may also influence RBP levels. such as liver disease.35 the more severe the kwashiorkor.. vitamin A and zinc deficiencies and hyperthyroidism. It has also been suggested that serum albumin levels below 2. Other biochemical tests that have been used or recommended for diagnosing or evaluating PEM have limited usefulness. 1977. However. These include tests for: · fasting serum insulin levels.5 g/dl are seriously deficient (see Table 22).4 2. they can be done in modest laboratories in many developing countries. are also of use and not too difficult to determine. Levels of both are reduced in kwashiorkor and may be useful in judging its severity. Levels of retinol binding protein (RBP). but serum albumin levels are not useful in evaluating less severe PEM. which is the carrier protein for retinol.5 3-3. which reduces their usefulness as an indicator of kwashiorkor. which are elevated in kwashiorkor and low in marasmus.
however. In young children kwashiorkor is often also present. In most developing countries kwashiorkor is a much more common cause of oedema than nephrosis. Oedema is also a feature of nephrosis. Pellagra is rare in young children. There may frequently be diarrhoea and weight loss. but no oedema or hair changes. 2. The skin lesions are sometimes similar to those of kwashiorkor. for example). the diagnosis is established. but only rarely in kwashiorkor. Differential diagnosis Nephrosis. the urine contains much albumin as well as casts and cells. In all cases the stools should be examined. In nephrosis. Pellagra. In this disease oedema is not a feature.36 · hydroxyproline and creatinine levels in urine. Oedema may result from this cause alone. and most cannot be performed in ordinary hospital laboratories. which if low may indicate current growth deficits and nutritional marasmus. marked Less common Present (sometimes mild) Absent . which may therefore be confused with kwashiorkor. Severe hookworm anaemia. In pure hookworm anaemia there are no skin changes other than pallor. there is usually only a trace of albumin. but in pellagra they tend to be on areas exposed to sunlight(not the groin. These tests are not specific. Ascites is frequently seen in nephrosis.2. In kwashiorkor. If flakypaint dermatosis or other signs of kwashiorkor are present.6. TABLE 2 Comparison of the features of kwashiorkor and marasmus Feature Growth failure Wasting Oedema Hair changes Kwashiorkor Present Present Common Marasmus Present Present. Chronic dysentery.
The child should receive 150 ml of this mixture per kilogram of body weight per day. Often hospital treatment is not possible. given in six feeds at approximately four-hour intervals. Diet. Attention to providing all micronutrients is important. Each feed is made by adding five teaspoonfuls of DSM powder to 125 ml of water.2. There is a risk if non-vitaminized DSM is used. monkey-like Absent Dermatosis. Treatment is often based on dried skimmed milk (DSM) powder. In that case the best possible medical treatment available at a health centre. urine and blood tests (for haemoglobin and malaria parasites) should be performed.which is possible if the child does not have sufficient appetite and is unable to cooperate or if the child is seriously ill the same mixture is best given through an intragastric tube. divided into six feeds = 125 ml per feed. The tube should be made of polyethylene. a 5-kg child should receive 5 x 150 ml per day = 750 ml per day.7. The child should be weighed and measured. If the child is still being breastfed. be admitted to hospital with the mother. less severe Absent Drawn in. dispensary or other medical facility is necessary. Stool. The milk mixture should be fed to the child with a feeding cup or a spoon. flaky-paint Common Fatty infiltration of liver Present 2.37 Mental changes Appetite Anaemia Subcutaneous fat Face Very common Poor Severe (sometimes) Reduced but present May be oedematous Uncommon Does not occur Good Present. if possible. including careful examination for any infection and a special search for respiratory infection such as pneumonia or tuberculosis. If cupor spoon-feeding is difficult . it should be about 50 cm long and should have an internal .1 DSM may most simply be reconstituted in hospital by adding one teaspoonful of DSM powder to 25 ml of boiled water and mixing thoroughly. nutritional marasmus or marasmic kwashiorkor should. For example. The child should be given a thorough clinical examination. Treatment of severe pem Hospitalization All children with severe kwashiorkor. breastfeeding should continue.
the money is well spent. in a serious case a packet might be added to 1. DSM and sugar. The milk mixture is then given in feeds at four-hour intervals. cottonseed). For severely malnourished children. with water added to make 20 parts. unusually dilute ORS often provides some therapeutic advantage.g. Rehydration. as is described for the treatment of diarrhoea (see Chapter 37). as for a transfusion.38 diameter of 1 mm. To make a feeding. feeding cup or intragastric tube). There are better mixtures than plain DSM. a 5kg child should receive 750 ml per day in six 125-ml feeds. Untreated hypothermia is a common cause of death in malnourished children. As with the plain DSM mixture. whisking will ensure an even mixture. one part casein. termed hypothermia. The seriously malnourished child has difficulty maintaining his or her temperature and may easily develop a lower than normal body temperature. Even in tropical areas temperatures at night often drop markedly in hospital wards and elsewhere. 1 g protein and 12 mg potassium. Children with kwashiorkor or nutritional marasmus who have severe diarrhoea or diarrhoea with vomiting may be dehydrated. Alternatively. 150 ml of liquid SCOM mixture should be given per kilogram of body weight per day. A stock of the dry SCOM mixture can be stored for up to one month in a sealed tin. Treatment of hypothermia. better still. A good and easily remembered formula for the sugar/casein/oil/milk (SCOM) mixture is: one part sugar. The vegetable oil increases the energy content and energy density of the mixture and appears to be tolerated better than the fat of full cream milk. At home the child may have been kept . Intravenous feeding is not necessary unless the vomiting is severe or the child refuses to take fluids orally. It is passed through one nostril into the stomach. Thus if standard ORS packets are used which are normally added to 1 litre of boiled water. Before and after each feed. 5 ml of warm. Casein increases the cost of the mixture. A 30-ml portion of made-up liquid feed provides about 28 kcal. The tube can safely be left in position for five days.5 litres of water. one part oil and one part DSM. the desired quantity of the mixture is placed in a measuring jug. Rehydration should be achieved using standard oral rehydration solution (ORS). The protruding end should be secured to the cheek either with sticky tape or zinc oxide plaster. and water is added to the correct level. casein (pure milk protein). Stirring or. sesame. the mixture can be administered intermittently using a large syringe and a needle that fits the tube. previously boiled water should be injected through the lumen of the tube to prevent blockage. but as it often serves to reduce the length of the hospital stay. The milk mixture is best given as a continuous drip. each made by adding five teaspoonfuls of SCOM mixture to 125 ml of boiled water. They can all be administered in exactly the same way (by spoon. Most of these mixtures contain a vegetable oil (e.
with consequent loss in weight. then half a tablet weekly. half a tablet (125 mg) of chloroquine daily for three days. then an appropriate anthelmintic drug such as albendazole should be given after the general condition of the child has improved. No two children have identical needs. and there must be an effort to ensure that the room is adequately warm. Gentamycin and chloramphenicol are alternative options but are less often used. chloroquine should be given by injection. Infections are so common in severely malnourished children that antibiotics are often routinely recommended. If a stool examination reveals the presence of hookworm. roundworm or other intestinal parasites. Benzyl-penicillin by intramuscular injection. can also be given. In severe cases and when vomiting is present. 250 mg in tablet form four times a day by mouth.39 warm sleeping in bed with the mother. Although it is useful to establish standard procedures for treating kwashiorkor and nutritional marasmus in any hospital or other health unit. and skin lesions should begin to clear. each case should nevertheless be treated on its own merits. e. is often used. or amoxycillin. 125 mg three times a day by mouth. In areas where malaria is present an antimalarial is desirable. a child with serious kwashiorkor would usually begin to lose oedema during the first three to seven days. the diarrhoea should ease or cease. If the child's temperature is below 36°C. and the staff may keep the windows open. 1 million units per day in divided doses for five days. efforts must be made to warm the child. During this period. He or she must be kept in warm clothes and must be kept covered with warm bedding. Sometimes hot-water bottles in the bed are used. If the disease is found to be present. Ampicillin. In the hospital ward the child may sleep alone. or the windows of the house may have been kept closed. Severely malnourished children not infrequently have tuberculosis and should be examined for it. Recovery On the above regime. Medication. specific treatment is needed. the child should become more cheerful and alert. If anaemia is very severe it should be treated by blood transfusion. which should be followed by ferrous sulphate mixture or tablets given three times daily. The child's temperature should be checked frequently.g. .
e. If suitable vitamin-containing foods are not available. However. Protein-rich foods of animal origin are often relatively expensive. the child would now receive maize gruel with DSM added. the oedema has disappeared and the appetite has returned. after having been well chopped. If the staple food is plantain or cassava. crushed groundnuts can be added twice a day. and weight gain may be quite rapid. This is not feasible in every case in a large hospital. A bottle and teat should not be used. these can be used instead of maize. then a vitamin mixture should be given. It is much better if such cases can visit separately from other patients (i. usually during the second week in hospital. After discharge. In both conditions. or. If anaemia is still present. A few teaspoonfuls of ripe papaya. a mixed diet should gradually be introduced. groundnuts. a raw egg can be broken into some simmering gruel. on a particular afternoon or at a child welfare or growth . Thus in a maize-eating area. If eggs are available and custom allows their consumption. for example. it is desirable to stop tube-feeding if this method has been used. The above maize-based diet is just an example. or if a moderate case of kwashiorkor has been treated at home and not in the hospital. and half a tablet (125 mg) of chloroquine should be given weekly. For an older child. the child should now start a course of iron by mouth. the mother can watch as it is prepared. but the diet should at least be based on locally available foods. She must be told what the child is being fed and why. The same SCOM or plain DSM mixture can be continued with a cup and spoon or feeding bowl. peas. the child should be followed if possible in the outpatient department or a clinic. meat.g. the length of time needed in hospital or for full recovery may be longer than for children with kwashiorkor. aimed at providing the energy. as recovery continues. At one or two meals per day. then protein-rich supplements are important. Alternatively. minerals and vitamins needed by the child. Protein-rich foods (e. an egg can be boiled or scrambled for the child. roasted groundnuts can be eaten. the patient gains weight. Children with severe nutritional marasmus may consume very high amounts of energy. beans. protein. orange or other fruit can be given. Her cooperation with and follow-up of this regime is much more likely if the hospital diet of the child is based mainly on products that are used at home and that are likely to be available to the family. They are not essential. legumes and vegetables serves just as well. fish or meat that the mother eats can be fed to the child. because the DSM and SCOM mixtures are not rich in vitamins.40 When the diarrhoea has stopped. If the diet of the area is based on rice or wheat. if preferred by custom. a small portion of the green vegetable and the beans. mango. If the disease is not to recur. While feeding of milk is continued. sour milk or eggs) can be given. it is important that the mother or guardian participate in the feeding at this stage. a good mixture of cereals.
In some societies sick children are taken to hospital very late in the disease. then some female relative should spend a few days in the hospital before the child is discharged. Case fatality rates depend on many factors including the seriousness of the child's illness at the time of admission and the adequacy of the treatment given. Instruction and nutrition education are vital for the person who will be responsible for the child. Prognosis deaths in children hospitalized for kwashiorkor or nutritional marasmus occur in the first three days after admission. If the child has been brought by the father.2. At each visit the child should be weighed. and the medical attendant should have time to explain matters to the mother and to see that she understands what is expected of her. The cause and the severity of the disease determine the prognosis. In this situation fatality rates are high. It is useless just to hand over a bag of milk powder or other supplement. or she may have insufficient or no breastmilk. The prospects of a child with mild marasmus and no other infection are better. The mother should be shown a teaspoon and told how many teaspoonfuls to give per day based on the child's weight. If he or she is fed only at family mealtimes and the family eats only twice a day. Satisfactory weight gain is a good measure of progress. Many supplements. but in most cases it is best that this supplement be given as part of the diet. If facilities exist and it is feasible. 2.8. Response to treatment is likely to be slower with marasmus than with kwashiorkor. It is often difficult to know what to do when the child is cured. A child with severe marasmus and lungs grossly damaged by tuberculous infection obviously has poor prospects. The best procedure is usually to provide a thin gruel made . are best provided by adding them to the child's usual food (such as cereal gruel) rather than by making a separate preparation. especially if the child is under one year of age.41 monitoring clinic) to avoid the tumult of most out patient sessions. It is best provided ready mixed in sealed polyethylene bags. She should be instructed in feeding with a spoon or cup and told not to feed the child from a bottle unless he or she is under three months of age. The mother should be asked how many times a day she feeds the child. the SCOM mixture can be used for outpatient treatment. There may be no mother or she may be ill. Out-patient treatment should be based on the provision of a suitable dietary supplement. then the mother should be told to feed the child two extra times. or simply to weigh the child but not provide simple guidance. Weight is plotted on a chart to provide a picture for the health worker and the mother. when they are almost moribund. especially DSM. A relaxed atmosphere is desirable.
Supplies of a suitable supplement to last for slightly longer than the interval between visits should be given at each visit. Thus a 10-kg child should receive about 1200 kcal and 30 g of protein daily. It is essential that the diet provide adequate energy and protein. The mother or guardian should be advised to attend the hospital or clinic at weekly intervals if the family lives near enough (within about 10 km) or at monthly intervals if the distance is greater. It should be noted that a marasmic child during the early part of recovery may be capable of consuming and utilizing 150 to 200 kcal and 4 to 5 g of protein per kilogram of body weight per day. . Usually 120 kcal and 3 g of protein per kilogram of body weight per day are sufficient for long-term treatment. Instruction regarding other items in the diet must be given if the child is over six months old.42 from the local staple food plus two teaspoonfuls of DSM (or some other proteinrich supplement) and two teaspoonfuls of oil per kilogram of body weight per day.
History of blood transfusion was not found. History of previous illness: Patient was referral from Rumah Sakit Bandung and diagnosed as anemia History of previous medications: IVFD Ringer Lactate. Sign of other spontaneous bleeding wasn’t found. Diarrhea(-). 1 years of soft rice. Dyspnoe (-).Patient admitted of having a significant weight loss in the last two months. Patient also complains of abdomen distention since two months ago. Nausea (+). Ranitidine Injection. Immunization : complete History of Feeding: 0-6 months of breastfeeding. History of bleeding was not found. Patient also complaint loss of appetite since 2 months ago. Paracetamol Physical Examination Body weight : 12kg Height BW/Age: BH/Age: : 108 cm . Ceftriaxone Injection. Patient also complains of fever for about seven days. Vomitting (-). Patient just eating 3-4 tablespoon per meal. 21th 2013 Main Complaint : Pallor History : Pallor happen since one months ago. sputum (). Patient also complains of cough for about three days. Fever was remittent and relieved by consumption of anti-pyretic drugs. 6 months-1 years old of breast feeding & soft rice.43 CHAPTER III CASE REPORT Name Age Sex Date of Admission : DA : 10 years : Male : July.
1 oC. Abdomen: distention (+). HR: 92 bpm. Pulse: 92 bpm. Ear : Normal appereance .warm acral. TD: 90/60mmhg. Crackles (-/-). Body temperature: 37. Pain(-) 5. reguler. CRT< subcutaneous fat left. blunt edge. isochoric pupil. pitting oedem(-). Beggy pants(+). reguler. Respiratory Rate: 30 bpm. 2. adequate pressure and 3”. regular.44 BW/BH: Presens status Sens. . Decreased soepel. Epigastrial retraction (-). Nose: Normal appereance. Head : Eye : Light reflexes(+/+). flat surface. Hepar: palpable 4cm BAC. murmur (+) systolic grade III-IV RR: 30 bpm. muscle hypotrophy.Mouth : Sianosis (-). Extremities : Pulse 90 bpm. Thorax : Symmetrical fusiformis. Localized status 1. little volume. Compos Mentis. interposed rib clearly visible 4. conjunctiva palpebra inferior ane (+/+). symmetrical. Neck : Lymph node enlargement (-) 3. icteric (-/-) . Peristaltic (+) normal.
30 16.75-4.0.30 12.91 unit detik value 1.97 Normal value % % % % % 103/µL 103/µL 103/µL 103/µL 103/µL 59.19 4.08 0.4 .30 0.07 2.85 4.1 0.45 Laboratory Result: July.10 .01 37 – 80 20 – 40 2–8 1–6 0–1 2.0.60 0.7. 21th 2013 Homeostasis Function Protombin APTT Trombin 0.3 1.10 0.1 g% 106/ mm3 103/ mm3 % 10 / mm fL Pg g% % 3 3 1.03 0.77 5.90 27.2 .5.8 .0-14.5 36 – 42 150-450 75-87 25-31 33-35 11.6 0.80 129 62.00 0.30 0 .7 .4 4.21th 2013 Darah Lengkap (CBC) Hemoglobin (HGB) Eritrosit (RBC) Leukosit (WBC) Hematokrit Trombosit (PLT) MCV MCH MCHC RDW Hitung Jenis Neutrofil Limfosit Monosit Eosinofil Basofil Neutrofil Absolut Limfosit Absolut Monosit Absolut Eosinofil Absolut Basofil Absolut Laboratory Result: July.0.200 3.5.10 40.13.6 – 14.10 34.00 0.
5 96-106 Mg/dl Mg/dl 18.46 METABOLISME KARBOHIDRAT Glukosa ad random GINJAL Ureum Kreatinin ELEKTROLIT Natrium (Na) Kalium (K) Klorida (Cl) mEq/L mEq/L mEq/L 129 4.60 0.90 Mg/dl 250.26 <50 0.0 109 135-155 3.50 <200 Differential Diagnosis Thalassemia+ Marasmus type malnutrition Working Diagnosis Thalassemia + Marasmus type malnutrition Treatment O2 1-2 l/I nasal canule IVFD D5% NacL 0. 1x1 mg Inj.45% Folic acid 1x5mg .50-0.Ampicilin 250mg/6 hr/IV Multivitamin without Fe 1Xcth I Vitamin A 200.6-5.000 IU Diet F75 110cc/2 hr/oral Transfusion Consult to Respirology department Consult to nutritionand metabolic disease department .
little subcutaneous fat left. pitting oedem(-). reguler.warm acral. regular.5mg . symmetrical.Mouth : Sianosis (-).25th 2013 S: Pallor O: Sens: CM. Beggy pants(+).000 IU Diet F75 110cc/2 hr/oral Inj.47 FOLLOW UP July. 22 . Decreased soepel. flat surface. Epigastrial retraction (-). Thorax Symmetrical fusiformis. Nose: Normal appereance. HR: 92 bpm. CRT< 3”. blunt edge. adequate pressure and volume. pale conjunctiva palpebra inferior (+/+). isochoric pupil. Pain(-) Extremities Pulse 90 bpm. interposed rib clearly visible Abdomen distention (+). murmur (+) systolic grade III-IV RR: 30 bpm. 1x1 mg Inj. Crackles (-/-).Ampicilin 250mg/6 hr/IV Multivitamin without Fe 1Xcth I Vitamin A 200. A: Thalassemia + Marasmus Type Malnutrition+ Moderate – Severe Pericardial effusion P: - O2 1-2 l/I nasal canule IVFD D5% NacL 0. Hepar: palpable 4cm BAC. muscle hypotrophy. Temp: 36. Peristaltic (+) normal. TD: 90/60mmhg. Ear : Normal appereance .45% Folic acid 1x5mg .furosemid 15mg/12h Spironolacton 2x12. icteric (-/-) . reguler.8 oC Head Eye : Light reflexes(+/+).
2 <300 <38 <41 Echocardiography Result (25th July 2013) : Moderate-Severe Pericardial Effusion .Consult Nutrition and Metabolic disease .74 37 20 11 <1 0-0.20 0.Echocardiography . 22th 2013 Homeostasis Function Ferritin (Fe/iron) TIBC unit Hasil menyusul mg/dl µg/dl 173 165 51-157 112-346 value Normal value Hepar Total bilirubin Direct bilirubin ALP AST/SGOT ALT/SGPT mg/dl mg/dl mg/dl U/L U/L 1.Transfusion Laboratory Result: July.48 - Premed Furosemid 1mg before transfusion Plan : .
45% Folic acid 1x1mg Inj. Peristaltic (+) normal. isochoric pupil. Hepar: palpable 4cm BAC. TD: 90/60mmhg. reguler. 26-29th 2013 S: Dyspnoe (+). Temp: 36. flat surface. Epigastrial retraction (-).8 oC. Head Eye : Light reflexes(+/+). CRT< 3”. blunt edge. Ear : Normal appereance . regular.49 July. murmur (-)RR: 30 bpm. icteric (-/-) . pitting oedem(-).Mouth : Sianosis (-). Pain(-). Pallor(+) O: Sens: CM. soepel. Beggy pants(+). adequate pressure and volume.5mg Premed Furosemid 1mg before transfusion Plan: Transfusion . reguler. interposed rib clearly visible Abdomen distention (+). HR: 92 bpm. pale conjunctiva palpebra inferior (+/+). Crackles (-/-). little subcutaneous fat left. Nose: Normal appereance. Thorax Symmetrical fusiformis.Ampicilin 250mg/6 hr/IV Multivitamin without Fe 1Xcth I Diet F75 110cc/2 hr/oral Inj. muscle hypotrophy.warm acral.furosemid 15mg/12h Spironolacton 2x12. Extremities Pulse 90 bpm. A: Thalassemia + Marasmus Type Malnutrition+ Moderate – Severe Pericardial effusion P: O2 1-2 l/I nasal canule IVFD D5% NacL 0. symmetrical.
flat surface. symmetrical. Pallor(+) O: Sens: CM.warm acral. pitting oedem(-). Temp: 36.furosemid 15mg/12h Spironolacton 2x12. murmur (-)RR: 30 bpm. HR: 92 bpm. reguler.8 oC. blunt edge. little subcutaneous fat left. Crackles (-/-). Peristaltic (+) normal. Head Eye : Light reflexes(+/+).Mouth : Sianosis (-). soepel. muscle hypotrophy. CRT< 3”. Thorax Symmetrical fusiformis. regular. A: Thalassemia + Marasmus Type Malnutrition+ Moderate – Severe Pericardial effusion P: O2 1-2 l/I nasal canule IVFD D5% NacL 0. Epigastrial retraction (-). reguler. Pain(-). Extremities Pulse 90 bpm. interposed rib clearly visible Abdomen distention (+). adequate pressure and volume.5mg Premed Furosemid 1mg before transfusion Plan: Transfusion . TD: 90/60mmhg. icteric (-/-) . isochoric pupil. 30-31th 2013 S: Dyspnoe (+). Nose: Normal appereance. Ear : Normal appereance .45% Folic acid 1x1mg Inj. Beggy pants(+). pale conjunctiva palpebra inferior (+/+). Hepar: palpable 4cm BAC.50 July.Ampicilin 250mg/6 hr/IV Multivitamin without Fe 1Xcth I Diet F75 110cc/2 hr/oral Inj.
40 25.4 4.30 0 .00 37 – 80 20 – 40 2–8 1–6 0–1 2.6 <50 0.4 .31th 2013 Darah Lengkap (CBC) Hemoglobin (HGB) Eritrosit (RBC) Leukosit (WBC) Hematokrit Trombosit (PLT) MCV MCH MCHC RDW Hitung Jenis Neutrofil Limfosit Monosit Eosinofil Basofil Neutrofil Absolut Limfosit Absolut Monosit Absolut Eosinofil Absolut Basofil Absolut GINJAL Ureum Kreatinin Uric Acid Mg/dl Mg/dl Mg/dl 27.5 36 – 42 150-450 75-87 25-31 33-35 11.3 1.06 0.40 0.60 37 72.30 1.7.50 24.51 Laboratory Result: July.90 <7.70 0.43 4.10 34.40 2.80 2.5.0 % % % % % 103/µL 103/µL 103/µL 103/µL 103/µL 71.70 21.0-14.0.1 g% 106/ mm3 103/ mm3 % 10 / mm fL Pg g% % 3 3 9.10 .1 0.09 1.75-4.2 .85 4.5.8 .35 3.6 0.6 – 14.10 0.50-0.000 188.8.131.52 12.0.07 0.7 .32 17.
warm acral. icteric (-/-) . interposed rib clearly visible Abdomen distention (+).52 Hepar Total bilirubin Direct bilirubin ALP AST/SGOT ALT/SGPT mg/dl mg/dl mg/dl U/L U/L 1. symmetrical. Hepar: palpable 4cm BAC. Peristaltic (+) normal. isochoric pupil. Extremities Pulse 90 bpm.46 61 86 33 <1 0-0.Mouth : Sianosis (-). muscle hypotrophy. CRT< 3”. regular. A: Thalassemia + Marasmus Type Malnutrition+ Moderate – Severe Pericardial effusion P: O2 1-2 l/I nasal canule IVFD D5% NacL 0.45% Folic acid 1x1mg Inj. Pallor(+) O: Sens: CM. flat surface. Ear : Normal appereance . Temp: 37 oC.88 1.furosemid 15mg/12h Spironolacton 2x12. blunt edge. pale conjunctiva palpebra inferior (+/+). TD: 90/60mmhg. little subcutaneous fat left.Ampicilin 250mg/6 hr/IV Multivitamin without Fe 1Xcth I Diet F75 110cc/2 hr/oral Inj.2 <300 <38 <41 August 1-3th 2013 S: Dyspnoe (+). Pain(-). Thorax Symmetrical fusiformis. adequate pressure and volume. pitting oedem(-). soepel. Beggy pants(+). Head Eye : Light reflexes(+/+). reguler. reguler. Crackles (-/-). Epigastrial retraction (-).5mg Premed Furosemid 1mg before transfusion Plan: Transfusion . HR: 92 bpm. Nose: Normal appereance. murmur (-)RR: 30 bpm.
00 21.0-14.800 1.7. 2013 Darah Lengkap (CBC) Hemoglobin (HGB) Eritrosit (RBC) Leukosit (WBC) Hematokrit Trombosit (PLT) MCV MCH MCHC RDW Hitung Jenis Neutrofil Limfosit Monosit Eosinofil Basofil Neutrofil Absolut Limfosit Absolut Monosit Absolut Eosinofil Absolut Basofil Absolut % % % % % 103/µL 103/µL 103/µL 103/µL 103/µL 52.00 20 74.00 41.03 0.6 – 14.25 1.70 4.85 4.00 2.3 1.0.8 .53 Laboratory Result: August 2.10 0.7 .5.4 .1 0.4 184.108.40.206 36 – 42 150-450 75-87 25-31 33-35 11.60 26.6 0.2 .13.00 0.30 0 .02 37 – 80 20 – 40 2–8 1–6 0–1 2.68 2.1 g% 106/ mm3 103/ mm3 % 103/ mm3 fL Pg g% % 7.40 20.10 35.30 0.10 12.20 1.0.75-4.10 .
reflex physiology(+) Normal. muscle hypotrophy. Crackles (-/-). Temp: 38. reguler.Mouth : Sianosis (-).Encephalitis. HR: 160 bpm. little subcutaneous fat left.225% Folic acid 1x1mg Inj. Extremities Pulse 90 bpm.Ampicilin 500mg/6 hr/IV Inj Ceftriaxone 500mg/12hr IV Multivitamin without Fe 1Xcth I Diet F75 110cc/2 hr/oral Inj. Meningoencephalitis) P: O2 1-2 l/I nasal canule IVFD D5% NacL 0. Hepar: palpable 4cm BAC.warm acral. Dyspnoe(-) O: Sens:GCS 10( E4M4V2). interposed rib clearly visible Abdomen distention (+). isochoric pupil. symmetrical. Epigastrial retraction (+). murmur (-)RR: 20 bpm.(4/8/2013) Acidosis Correction 42meQ(1/2 dose myelon in 200cc D5% finish in 1 hour/240gtt/mikro (5/8/2013) Plan: Transfusion Check AGDA post correction I . pitting oedem(-). Pain(-).54 August 4-6th 2013 S: Seizure(+). reguler. blunt edge. adequate pressure and volume. regular. pale conjunctiva palpebra inferior (-/-). icteric (-/-) . soepel. Nose: Normal appereance. TD: 90/60mmhg.furosemid 15mg/12h Spironolacton 2x12. Beggy pants(+). Peristaltic (+) normal.2 oC. reflex pathology(-) A:Thalassemia + Marasmus Type Malnutrition+ Moderate – Severe Pericardial effusion+Central Nervous System Infection (dd: Meningitis. Ear : Normal appereance . CRT< 3”. flat surface.5mg Premed Furosemid 1mg before transfusion Potassium Correction :KCL 5meQ +20cc D5% finish in 2 hours. Neck: Thorax Symmetrical fusiformis. Head Eye : Light reflexes(+/+).
4 220.127.116.11 7.20 73 80. 2013 Darah Lengkap (CBC) Hemoglobin (HGB) Eritrosit (RBC) Leukosit (WBC) Hematokrit Trombosit (PLT) MCV MCH MCHC RDW Hitung Jenis Neutrofil Limfosit Monosit Eosinofil Basofil Neutrofil Absolut Limfosit Absolut Monosit Absolut Eosinofil Absolut Basofil Absolut % % % % % 103/µL 103/µL 103/µL 103/µL 103/µL 75.1 g% 106/ mm3 103/ mm3 % 103/ mm3 fL Pg g% % 11.900 6.3 1.30 12.10 .2 .03 33.75-4.5 36 – 42 150-450 75-87 25-31 33-35 11.8 .4 .70 16.40 4.55 Laboratory Result: August 4.13.30 21.48 0.0.84 1.7 .13 9.0-14.0.00 0.0.85 4.5.08 37 – 80 20 – 40 2–8 1–6 0–1 2.63 0.1 0.6 – 14.00 0.60 34.00 0.6 0.30 0 .40 27.
6 98.56 Laboratory Result: August.90 Mg/dl 362.3 21.8 106 135-155 3.174 60.50-0.9 23.8 164.34 <50 0.7 -6.45 38-42 85-42 22-26 19-25 (-2)-(+2) 95-100 .5 96-106 Mg/dl Mg/dl 15.00 <200 mmHg mmHg mmol/L mmol/L Mmol/L % 7.6-5.6 7.35-7.00 0.4 2013 AGDA Ph pCO2 pO2 Bikarbonat (HCO3) Total CO2 Kelebihan Basa (BE) Saturasi METABOLISME KARBOHIDRAT Glukosa ad random GINJAL Ureum Kreatinin ELEKTROLIT Natrium (Na) Kalium (K) Klorida (Cl) mEq/L mEq/L mEq/L 135 2.
13.10 34.0-14.80 3.4 164 135-155 3.6-5.5 96-106 Mg/dl 94.2 93.85 4.30 12.6 7.27 24 83.45 38-42 85-42 22-26 19-25 (-2)-(+2) 95-100 Laboratory Result: August 6.26 28.1 <200 mmHg mmHg mmol/L mmol/L Mmol/L % 7.35-7.5 11.62 4.57 Laboratory Result: August.5 36 – 42 150-450 75-87 25-31 33-35 . 2013 Darah Lengkap (CBC) Hemoglobin (HGB) Eritrosit (RBC) Leukosit (WBC) Hematokrit Trombosit (PLT) MCV MCH MCHC g% 106/ mm3 103/ mm3 % 103/ mm3 fL Pg g% 9.5 2013 AGDA Ph pCO2 pO2 Bikarbonat (HCO3) Total CO2 Kelebihan Basa (BE) Saturasi METABOLISME KARBOHIDRAT Glukosa ad random ELEKTROLIT Natrium (Na) Kalium (K) Klorida (Cl) mEq/L mEq/L mEq/L 145 3.75-4.0 11.7 14.00 27.4 4.60 147 79.5.
01 Laboratory Result: August.0.2 .30 0 .5 99.1 0.5.10 0.6 32.35-7.543 37.3 1.70 0.03 0.1 % % % % % 10 /µL 103/µL 103/µL 103/µL 103/µL 3 51.6 2013 AGDA Ph pCO2 pO2 Bikarbonat (HCO3) Total CO2 Kelebihan Basa (BE) Saturasi mmHg mmHg mmol/L mmol/L Mmol/L % 7.7 7.10 .58 RDW Hitung Jenis Neutrofil Limfosit Monosit Eosinofil Basofil Neutrofil Absolut Limfosit Absolut Monosit Absolut Eosinofil Absolut Basofil Absolut % 20.3 31.7 .43 0.200 2.60 11.60 10.61 0.18 1.7.20 37.0.6 – 14.4 .8 8.45 38-42 85-42 22-26 19-25 (-2)-(+2) 95-100 .6 0.0.5 179.8 37 – 80 20 – 40 2–8 1–6 0–1 2.
pdf . APRIL 2009 http://www. No.cdc.6-5.aacn.gov/tb/education/corecurr/pdf/chapter2.pdf Critical care nurse Vol 29.5 96-106 Mg/dl 138 <200 REFERENCE http://www.4 96 135-155 3.59 METABOLISME KARBOHIDRAT Glukosa ad random ELEKTROLIT Natrium (Na) Kalium (K) Klorida (Cl) mEq/L mEq/L mEq/L 132 2.org/wd/cetests/media/c0923. 2.
medscape.doh.wa.gov/tb/topic/basics/risk.com/Tuberculosis_International http://www.60 http://emedicine.org/wg/dots_expansion/assets/documents/IJTLD_OS_Childhoo dTB_Chapter2.pdf http://www.pdf .oxfordimmunotec.stoptb.gov/Portals/1/Documents/Pubs/343-071-WATBManualDiagnosisofTBDisease.cdc.htm http://www.com/article/230802http://www.