Diarrhea

It constitutes 25-30% of deaths in children below 5 years of age, and on the average 3 episodes of diarrhea per year are observed in children.                                                                                                                   

Definition

Increase in fluidity, volume and frequency of stool relative to the usual habits of the individual.

N.B. greenish stool without change in consistency is not diarrhea. It is due to the presence of biliverdin from hurried intestinal motility.

Clinical types

  1- Acute diarrhea: with an acute onset and less than 14 days duration.

  2- Persistent diarrhea: it begins as acute and lasts for more than 14 days and less      

     than 28 days.

  3- Chronic diarrhea: lasts for more than 28 days

  4- Dysentery diarrhea: it is diarrhea with visible blood in stools.

N.B. excessive mucus alone is not suggestive of dysentery.  

     

Epidemiology and etiology of acute diarrhea

The age incidence is between 3 months to 5 years with a peak at 6-12 months. It is common in summer and autumn but less in winter and spring.

The causes may be infectious or non infectious.

A-Infectious diarrhea  

1- Bacterial (30%): e.g., E-coli, Shigella, Salmonella, Cambylobacter, Cholera, Staphylococcus aureus, Proteus, and Yersenia.

2- Viral (30%): e.g., rotavirus, norwalk, enterovirus and hawaii viruses.

3- Parasitic: e.g., Entamoeba -histolytica, Giardia lamblia and Cryptosporidium.

4- Fungal: e.g. Candida.

B-Non infectious diarrhea

1- Lactose intolerance.

2- Feeding problems.

  a- In breast fed infants: from overfeeding or irregular feeding.

  b- In formula fed infants: from over concentrated formula.

  c- During weaning: from food intolerance.

3- Cow's milk protein allergy.

4- Heavy metal and insecticides poisoning.

Etiology of chronic or persistent diarrhea

1-Idiopathic: in 30% of the cases, no definite cause could be found.

2- Infection

  a- Bacterial: TB. and Salmonella.

  b- Parasitic: E-histolytica and Giardia infestations.

  c- Fungal: Candida.

  d- Viral: Rotavirus in immunocompromised patients.

3- Intestinal enzyme deficiency: e.g. congenital or acquired lactase deficiency.

4- Prolonged use of antibiotics e.g. ampicillin, chloramphenicol, and tetracycline.

5- Acrodermatitis enteropathica: which is due to zinc deficiency. There is chronic diarrhea with inflammation of the skin in the extremities and around the anus and mouth.

5- Protein losing enteropathy: due to increased permeability of intestinal mucosa to plasma protein and/ or lymphatic obstruction.

6- Endocrinal disorders: e.g. thyrotoxicosis.

7- Malignancy: e.g. neuroblastoma.

8- Milk protein allergy.

Causes of bloody diarrhea

1- Infectious: invasive bacteria (Shigella, Cambylobacter or enteroinvasive E.coli),   

    bilharziasis and salmonellosis or invasive parasites (E. histolytica).               

2- Non-infectious: intussusception, protein milk allergy or bleeding tendency.

3- Inflammatory bowel disease e.g. ulcerative colitis.

Complications of acute diarrhea

1- Dehydration.

2- Metabolic and electrolyte disturbances: Metabolic acidosis, Metabolic alkalosis, Hyponatremia, Hypernatremia, Hypokalemia, Hypocalcemia and hypomagnesemia

3- Protein-energy malnutrition.

Mechanisms by which diarrhea produces malnutrition

a- Decreased food intake through:

  · Anorexia from the infection or the use of antibiotics.

  · Starvation or the use of diluted formula.

b- Decreased absorption due to:

  · Damage of intestinal epithelium leading to digestive enzyme deficiency especially lactase.

  · Rapid motility of the intestine.

c- Increased losses: Loss of nutrients in the stools and vomiting.

d- Increased nutritional requirements due to:

  · Hypercatabolic state from infection and fever.  

  · The needs for repair of mucosal epithelium.

  · The needs to restore plasma proteins.

Mechanisms by which malnutrition produces diarrhea:

a- Gastro-intestinal changes: disturbed gastrointestinal digestive and absorptive functions,  with carbohydrate and fat intolerance e.g decreased synthesis of enzymes (lactase and lipase).

b- Decreased systemic and local gut  immunity.

4- Convulsions: may occur due to:

  a- Hypo/ hypernatremic dehydration.                   b- Tetany (low Ca or Mg,alkalosis).                     

  c- Brain edema: due to hyponatraemic dehydration or with rapid IV infusion or over

                            hydration.

  d- Hypoglycemia.

   e- Cerebral thrombosis.                                         f- Febrile convulsions.

5- Abdominal distension: this is a common complication and may be due to:

a-      Paralytic ileus from hypokalemia, toxemia of infection or use of antimotility     

drugs.

  b- Intussusception: the child presents with distention and colicky abdominal pain usually preceding passage of red currant jelly stools. Palpable mass may be detected by abdominal or rectal examination. Intussusception may proceed to perforation and peritonitis.

c-Fermentation and gas production.                         

 6- Heart failure: this may occur as a result of rapid IV infusion, over hydration, toxic myocarditis and septic shock.

7- Disseminated intravascular coagulopathy (DIC): this is not a common complication which may occur as a result of disseminated thrombosis of small vessels with consumption of the coagulation factors leading to liability to bleeding, ecchymosis and purpuric eruptions. Ischemic manifestations as superficial gangrene of the skin and soft tissues may occur.   

8- Acute renal failure: may result from marked hypovolemia.

9- Septicemia: this occurs more commonly with E-coli and Salmonella infections which may spread to other systems, leading to pneumonia, arthritis, osteomyelitis, peritonitis, or   meningitis.

Dehydration

It results from loss or deprivation of water and ions from the body.

Dehydration can lead to hypovolemia, cardiovascular collapse and death, if not treated promptly.

Degree of dehydration:

 The patient may present with one of the following presentations:

  · No signs of dehydration (weight loss<5%). 

  · Signs of some dehydration (weight loss 5-10%).

  · Signs of severe dehydration (weight loss >10%).

Assessment of degree of dehydration

Item	No dehydration	Some dehydration	Severe dehydration
General condition Eyes Tears Mouth and tongue Thirst Skin pinch Treatment plan	Well, alert Normal Present Moist Drinks normal Goes back quickly Plan A.	Restless, irritable* Sunken Absent Dry Drinks eagerly * Goes back slowly* Plan B.	Lethargy, unconscious* Very sunken, dry cornea Absent Very dry Poor or unable to drink* Goes back very slowly* Plan C.

N.B. Signs that are most valuable in assessing some or severe dehydration, termed key signs, are marked with asterisks (*). Two or more signs in one column including at least one key sign means that the patient falls in that category of dehydration.

Other signs that may be of help in assessing dehydration:

  1- Rapid pulse and low blood pressure. 

  2- Anterior fontanel may be depressed.

  3- Cold clammy, mottled skin.

  4- Oliguria or anuria.

Assessment of dehydration in severe malnutrition: it is difficult because:

a- The skin turgor appears poor from loss of subcutaneous fat in severe malnutrition even without dehydration. On the other hand, skin turgor may appear normal in children with   edema  (kwashiorkor) even with dehydration.

b- Sunken eyes are unreliable sign of dehydration in marasmus.

c- The apathy of children with kwashiorkor and the irritable child with marasmus make the interpretation of mental status difficult.

d- Absence of tears is difficult to assess in children with severe malnutrition because they do not readily cry.

Signs for detection of some dehydration in severe malnutrition:

1- Dry tongue and mouth.                       2- Thirst (drinks eagerly).

Signs for detection of severe dehydration in severe malnutrition:

1-      Very dry mouth and tongue.       

2-       2- Cool and moist extremities (in non edematous cases).

      3- Rapid thready pulse.                       4- Oliguria or anuria.

Prevention of acute diarrhea 

  1- Promotion of breast-feeding.

  2- Improving the weaning practice.

  3- Proper use of water for hygiene and drinking.

  4- The use of sanitary latrines.

  5- Safe disposal of stools of young infants.

  6- Washing hands after defecation and before preparation of foods.

  7- Measles vaccination decreases diarrheal episodes by 25% in children below 5 years age.

  8- Improvement of nutritional status and continued feeding during diarrhea.

Treatment of acute diarrhea

The main goals for treatment: fluid therapy, feeding, zinc supplementation and additional therapies including antibiotics and probiotics.

I-Fluid therapy

There are 3 plans for fluid therapy (A, B,&C)

.

Plans of fluid therapy

Plan A	Plan B	Plan C
For cases with no signs of dehydration. ORS or home made fluid. At home.	For cases with some dehydration. ORS At hospital.	For cases with severe dehydration. IV fluid therapy or nasogastric rehydration. At hospital.

1-Plan A:( 3F)→Fluid, Food and Follow up  

 Amount of fluid needed for plan A

Age	Amount	Amount of ORS for each loose stool
< 2 years 2- 10 years > 10 years	500 ml/day 1000 ml/day 2000ml/ day	50 - 100 ml. 100- 200 ml. As much as wanted

Advantages of ORS  

  1- It is effective in 95% of cases.

  2- It is suitable for all types of diarrhea and all types of dehydration.

  3- It can be used for all ages including neonates.

  4- It can be used even in the presence of vomiting.

  5- It is cheap and easily prepared.

ORS is usually given as 1-2 teaspoons every one minute modified by infant desire.

2- Home made fluids: these are fluids containing some salt with carbohydrate or protein such   as soup, rice water  and cereals. They should be:

  · Feasible and acceptable.

  · Not sweetened-such as soft drinks, so as not to cause osmotic diarrhea.

  · Easily prepared.

N.B. home made sugar salt solution (SSS) is unsafe because of improperly calculated ratio.

The mother should be instructed to: 

· Give the child more fluids (ORS or home made) to prevent dehydration.

· Give the child plenty of food (breast, usual formula, solid food, cereals, fruits) to prevent malnutrition.

· Return to health unit if the child does not improve in 3 days or when develops any of the following:

a- Many watery stools.                                             b- Eating or drinking poorly.                                           

c- Repeated vomiting.                                              d- Fever.                                              

e- Marked thirst.                                                       f- Blood in stool.                    

2-Plan B: includes replacement of deficit and assessment of progress of the patient.

Replacement of the deficit in the first 4 hours

The amount of ORS in the first 4 hours can be calculated as: patient weight in kg x75 = … ml.

For infants under 6 months who are not breast fed, 100-200 ml of clean water is added. Breast-feeding should be encouraged, but no other food is offered during this period.

Assessment of progress of the patient after 4 hours

· If there are no signs of dehydration, shift to plan A.

· If signs indicating some dehydration are still present, repeat plan B, but start to offer food, milk and juice as described in plan A.

· If signs indicating severe dehydration have appeared, shift to plan C.

· If puffy eyelids (overhydration) occur, treatment with ORS should be stopped although breast-feeding and the provision of plain water should continue.

· If vomiting occurs, wait 10 minutes and then give ORS slowly every 3 minutes by spoon.

3-Plan C: intravenous or nasogastric hydration. Intravenous rehydration needs close observation.

Indications for IV rehydration

  1- Shock or coma.                 2- Failure of oral or nasogastric rehydration.   

  3- Severe dehydration.          4- Persistent vomiting (more than 4 times/hour).

  5- Anuria.                              6- Gastric dilatation.

  7- Convulsions.                     8- severe abdominal distension.

The amount of IV fluids

Amount of fluid needed for plan C

Age	First give 30 ml/kg	Then give 70 ml/kg
Under 12 months	In the first hour	In the next 5 hours
Older	In the first half hour	In the next 2.5 hours

· Small amounts of ORS may also be given by mouth (5 ml/kg/hour) as soon as the patient is able to drink (after 2-3 hours) and tolerating the oral intake in order to provide additional potassium and base.

Reassessment of the patient every 2 hours to choose the appropriate plan (A,B or C) to    continue the treatment.

Types of intravenous infusion solutions:

 Polyvalent or Ringer’s lactate or Normal saline 0.9% (9 g Nacl/L) o rHalf normal saline (4.5 g Nacl/L)

N.B. Blood or plasma transfusion is given in a dose of 10-20 ml /kg in cases with DIC, fresh bleeding and anemia (Hb less than 8 gm/dL).

Complications of IV therapy.

  1- Electrolyte disturbances.              2- Rapid infusion may lead to heart failure.

  3- Brain  edema.                                4- Infection.

Indications for nasogastric rehydration

1-      Failure of ORS by cup and spoon method.

2-      Repeated vomiting.

3-      Severe anorexia or inability to swallow.            

4-      When child refuses the taste of  ORS

5-      When the child or the mother is tired

6-      During transfer to IV rehydration unit.

7-      In severe dehydration when IV is not available.                                                                                                                        

                                                                                                                    

 The amount of fluid required: 20 ml/kg/hour for 6 hr. (total 120 ml/kg).

The rate of drip = weight (kg) x 5 drop/minute.

N.B.: it is important to ensure that the tube is passed to the stomach, not to the trachea.

Reassessment of patient: the child should be reassessed every two hours:

· If repeated vomiting or abdominal distension occurs, the fluid should be given more slowly.

· If there is no improvement after 3 hours, IV rehydration should be started.

· After 6 hours, reassessment of the patient should be done and appropriate plan of treatment is chosen.

II-Feeding during acute diarrhea

Early feeding together with ORS and avoidance of fasting are the main goals of nutritional management during diarrhea. Feeding during diarrhea doesn't increase the severity or duration of diarrhea but hastens recovery.

Advantages of continued feeding during diarrhea            

1- Contact of food to the mucosa will enhance and stimulate the digestive enzymes.

2- Easily digestible foods enhance water and salt absorption and about 60% of nutrients are absorbed.

3- Feeding helps the regain of intestinal mucosal repair and function.

4- It preserves body weight for sustained growth and increases resistance to infection.

Types of feeding

Breast-feeding: should be continued. It reduces the stool output and shortens the duration of diarrhea.

Formula feeding: feeding should be continued with the usual milk formula and in full concentration to maintain normal growth. If diarrhea persists or increases which indicates lactose intolerance, low lactose milk or yogurt is given for l-2 weeks. This low lactose milk has the following advantages:

  1- It decreases the number of stools and the duration of diarrhea.

  2- It helps recovery of the mucosa and restores its functions.       

Solid and semisolid foods: they should be small, frequent, easily digestible and high caloric such as starches, rice, potato, vegetable soup, yogurt and chicken.

· The frequency of meals should be at least 6 times/day and one more extra meal than usual is given for 2 weeks after stoppage of diarrhea.

· Introduction of new foods should be avoided. They may lead to food allergy and diarrhea.    

N.B: Vitamin A 200,000 U should be given and repeated after 15 days to help re-epithelization of   the intestinal mucosa.

N.B: Zinc sulphate is given for 10-14 days in a dose of 10mg/kg/d for infants < 6 month and 20 mg/kg/d for infants > 6 month.

Drug therapy in acute diarrhea

Antimicrobial therapy

· There is usually no need for antibiotics in diarrhea. The antibiotics are not effective and in most cases, are harmful.

· Acute diarrhea is almost always a self-limited disease.

· In 30% of cases, diarrhea is caused by viral infection.

· Antibiotics may prolong the course of diarrhea.

· It may lead to development of antibiotic resistant organisms.

· It may cause malabsorption (e.g. neomycin).

· It may produce the side effects of the drug used.

· It represents an economic load.

N.B. fever is not an indication for antimicrobial treatment. It may be due to dehydration.

Indications for antimicrobial treatment in specific cases

1- The immunocompromized patients (newborn, premature, malnourished children, and those with malignant diseases or using corticosteroids or immunosuppressive drugs).

2- Parenteral diarrhea with systemic illness such as otitis media, pneumonia, or meningitis.

3-Specific enteric infection

A-    Treatment of dysentery:

·         TTT of bacillary dysentery

a-      Shigellosis: 5 days treatment of parenteral ampicillin (100 mg/kg/day in 4 divided doses) or         

oral trimethoprim (10mg/kg/day) in combination with sulfamethoxazole (50  mg/kg/day) in two divided doses.

b-      Salmonellosis: treatment by ampicillin (200 mg/kg/day) or trimethoprim +      

sulfamethoxazole should be continued till 3 successive negative stool cultures.

·         TTT of amebic dysentery (Amebiasis):

Metronidazole 35-50 mg/kg/d for 7-10 days orally.

B- Giardiasis: Metronidazole 15 mg/kg/d t.i.d for 5 days orally.

C- Cholera: trimethoprim with sulfamethoxazole in two divided doses. Erythromycin (40mg/24hour ) may be used.

Antipyretics

Control of fever is best done by hydration, cold compresses or a water bath.

Salicylates may cause hemorrhagic tendency and in viral cases may cause Reye's syndrome. Acetaminophen may cause agranulocytosis and bone marrow depression.  

Anticonvulsants: for cases with convulsions.

Antidiarrheal drugs, antimotility drugs and antiemetics should not be given.

Antidiarrheal drugs: e.g. cholestyramine is used only in intractable diarrhea and cholera.  

Antiemetics: the best way to stop vomiting is to give ORS at a slower rate, if not effective give ORS by nasogastric tube drip, if not effective give IV fluids. Metoclopramide may be used. It accelerates gastric emptying and may cause extrapyramidal symptoms.

Dysentery

It is diarrhea with visible blood in stools.

Commonest causative organisms is shigella, Other causes include Salmonella, Enteroinvasive

  E. coli and Entamoeba histolytica.

Stools contain blood,mucus and pus cells.

There are usually fever, cramping abdominal pains and tenesmus.

Complications

1-      Intestinal perforation.

2-     Rectal prolapsed.

3-     Septicemia.

4-     Malnutrition

Treatment

1-     Fluids and feeding.

2-     Drug therapy:

·         TTT of bacillary dysentery

c-      Shigellosis: 5 days treatment of parenteral ampicillin (100 mg/kg/day in 4 divided doses) or        

oral trimethoprim (10mg/kg/day) in combination with sulfamethoxazole (50  mg/kg/day) in two divided doses.

d-     Salmonellosis: treatment by ampicillin (200 mg/kg/day) or trimethoprim +     

sulfamethoxazole should be continued till 3 successive negative stool cultures.

·         TTT of amebic dysentery (Amebiasis):

Metronidazole 35-50 mg/kg/d for 7-10 days orally.

Protein-energy malnutrition (PEM)

Definition: Inappropriate intake of one or more of the nutrient sessential for normal growth and development.

Types:

1-     Underweight ( mild form).

2-     Marasmus or kwashiorkor or Marasmus  kwashiorkor (severe forms)

Causes of PEM 

1- Dietary deficiency: poverty and ignorance of mothers are the most important factors.

2- Age of the child: rapidly growing young age groups are more susceptible to severe malnutrition.

3- High prevalence of infection; especially chronic infections e.g. TB., empyema, otitis media, urinary tract infection and whooping cough. Chronic or recurrent attacks of diarrhea contribute to deterioration of nutritional state that leads to reduction of host resistance, and worsening the outcome of infection, establishing a vicious diarrhea-malnutrition cycle. 

Impaired immunity

                                                                                            

                          Malnutrition             Intestinal enzyme deficiency          Diarrhea

                                                     

                                                            Hypercatabolism                           

                                                                      

    Malabsorption

4- The prevalence of parasitic infestations: ascariasis and ankylostomiasis are commonly associated with malnutrition.

5- Congenital anomalies: such as cleft palate, palatal paralysis, gastroesophageal reflux, congenital pyloric stenosis and congenital heart diseases.

6- Inborn errors of metabolism: such as galactosemia.

7- Food allergy: is an infrequent cause of malnutrition

1-Kwashiorkor

It results mainly from lack of protein in diet with adequate supply of calories.

Age incidence: ranges from 6 months-3 years.

General appearance: a child with kwashiorkor may have a fat appearance with a doll like facies  where the diet provides an adequate energy source and there is preservation of subcutaneous fat with the gradual development of edema that masks the  wasting of the underlying tissues.

Growth failure, Muscle wasting, Pitting edema, Mental changes, apathy is a constant, early and pathognomonic sign of kwashiorkor. Apathy means decreased emotional reactivity. Most children are disinterested in their environment and have an expression of misery and prefer darkness. In some hospitals, the return of smiles signals the time of discharge. Skin changes: the skin changes consist of erythema, hyperpigmentation, desquamation, depigmentation and ulceration. The pigmented areas become confluent with fissures in between. The epidermis peels off in large scales, this gives rise to flaky (cracky) paint dermatosis. Underneath these flacks the skin is atrophic and depigmented. Flaky paint dermatosis is a pathognomonic sign of kwashiorkor. The distribution of the dermatosis is typically on the buttocks, perineum and upper thighs (the area of soiling, wet diapers, continuous pressure or irritation). The lesion may be found anywhere on the body especially extensor surfaces of the body. Hair changes: hypochromotrichia means reduced hair pigmentation; black hair becomes brown or reddish yellow and sometimes even gray. Flag sign (segmental hypochromotrichia) means appearance of alternating bands of depigmented and normal black hair. The dyspigmented area represents periods of malnutrition. Flag sign is pathognomonic for kwashiorkor.

Gastrointestinal disturbances

1-Anorexia                                      2-Diarrhea.

1-      Abdominal distension.              4- Hepatomegaly: liver is enlarged and soft due to fatty infiltration

 Anemia: due to lack of iron, folic acid, vitamin B₆ and vitamin B₁₂. Bone marrow depression secondary to protein deficiency, infection and parasitic infestation may occur.

Signs of vitamin deficiency: cracking of the lips (cheilosis) and angular stomatitis are common due to vitamin B complex deficiency. Vitamin A absorption and probably transport are impaired. Vitamin A deficiency leads to severe ocular lesions.

Cardiovascular system: patients suffering PEM have cold, pale or cyanotic extremities due to circulatory insufficiency.

Associated infection: pneumonia, infective diarrhea and urinary tract infection are common, due to decreased immunity.                                    Features of kwashiorkor

Constant features of kwashiorkor Present in every case of Kwashiorkor	Pathognomonic signs When present, they are diagnostic	Common signs They are present in most cases
1- Apathy or misery. 2- Edema. 3- Anorexia. 4- Growth failure    - Decreased body weight.    - Muscle wasting. 5- Fatty infiltration of liver. 6- Hypoproteinemia.	1- Apathy. 2- Cracky paint dermatosis 3- Flag sign.	1- Signs of vitamin deficiency. 2- Anemia. 3- Skin changes. 4- Hair changes. 5- Infections and diarrhea

Marasmus

  It is a chronic state of general under-nutrition with progressive loss of weight, gross wasting of muscles and subcutaneous tissue.

  With severe restriction of food intake, first the infant stops growing and begins to utilize his own subcutaneous fat then his muscles leading to the gross appearance of skin over bone. The main pathological changes are the marked loss of stored fat and muscle wasting.

Clinical manifestations

Marasmus may occur at any age commonly from birth to 3 years. It is more frequent in infants than in older children due to rapid rate of growth.

• A child with fully developed picture of marasmus is extremely emaciated, weighing less than 60% of standard weight.

• The infant is very hungry, cries much, sucks his fingers and sleeps little.

• The child is usually alert and looks like a little old man.

• There is loss of subcutaneous fat that leads to a thin wrinkled skin, and skin infection is common. There  

   is loss of skin elasticity.

• There is marked muscle wasting and the bony prominences are very marked.

•The hair is usually not altered, but may be scanty and dry. 

• The liver and spleen are usually small in size.

• Constipation is common but diarrhea of infective nature or starvation diarrhea with frequent small, soft, dark green stools containing mucus may occur.

• The temperature is usually subnormal with cold extremities and pulse may be slow. 

Clinical differences between marasmus and kwashiorkor

Item	Marasmus	Kwashiorkor
History and examination - Age - Anorexia - Body weight deficit - Edema - Muscle wasting - Subcutaneous fat - Mental changes - Cracky paint dermatosis - Flag sign of hairs - Vitamin deficiency - Liver size	Common from 0-3 years Uncommon, hungry +++ Absent +++ Lost Irritability Absent Absent Uncommon Not enlarged	6 mo - 3 yrs Marked + Present + Preserved Apathy May be present May be present Common Enlarged

Marasmic kwashiorkor

    It is a combined form of severe malnutrition, with clinical signs of both marasmus and kwashiorkor. Marasmic kwashiorkor usually starts as marasmus with loss of weight more than 40% of standard weight then children are suddenly put on a starchy diet very low in protein, and signs of kwashiorkor develop such as apathy, anorexia, edema, skin changes and hair changes.

Complications of PEM

1- Dehydration, shock and acid base disturbances as a result of attacks of diarrhea. 

2- Electrolyte disturbances: hypocalcemia, hypomagnesemia, hypokalemia and hyponatremia.

3- Increased susceptibility to infections: such as respiratory, gastrointestinal, urinary tract infection, otitis media and chronic infections as TB. Decreased immunity leads to intercurrent infections. Septicemia is a serious complication that is fatal if associated with shock, hypothermia and hypoglycemia. Measles is also a fatal disease in the malnourished infants.

4- Heart failure: it is related to several factors:

   a- Low hemoglobin level may result in anemic heart failure.

   b- Excessive intake of salt in diet.

   c- Weakened myocardium by nutritional deficiency.

   d- Toxic myocarditis secondary to infection.

  The impaired cardiac function combined with an expanded blood volume will lead to heart failure with sudden collapse and peripheral circulatory failure.

5- Hypothermia: related to reduced SC fat, and to deficient energy intake. Unexplained and prolonged hypothermia may be fatal if associated with hypoglycemia and or septicemia.

6- Hypoglycemia due to starvation, defective glucose metabolism and low glycogen stores in the liver.

7- Hemorrhagic tendency: is grave and a bad prognostic sign. It is related to several factors: 

a- Fragile blood vessels.

b- Deficiency of coagulation factors and platelets. 

c- Disseminated intravascular coagulation (DIC): it is due to wide spread intravascular deposition of fibrin which leads to tissue ischemia and necrosis and consumption  coagulopathy with bleeding tendency.

8- Other non fatal complications:

a- Severe PEM in early infancy and childhood may have a permanent retardation in intellectual development. Attention span, memory, abstract thinking are more prone to be affected by nutritional deficiencies.

b- Some permanent short stature may occur (nutritional dwarfism).

c- Blindness may occur due to vitamin A deficiency.

Management of PEM

The patient is evaluated as regards the severity of PEM, presence of infection or parasitic infestation, associated nutritional deficits such as vitamin deficiencies or anemia and associated fluid and electrolyte disturbances.

I- Emergency treatment 

1- Severe malnourished children must be admitted to hospital for emergency treatment of dehydration, acidosis, and electrolyte imbalance. Shock if present is managed by blood or plasma transfusion or IV ringer solution. Anti- shock measures e.g. hydrocortisone may be used.

Total parenteral nutrition can be used when there is contraindication to oral feeding as in cases of persistent vomiting inspite of nasogastric feeding or failure or intolerance to oral feeding.

2- Treatment of concurrent infection by proper antibiotics. Combination of penicillin and aminoglycoside is effective in most cases, till results of culture (stools, blood) and sensitivity are obtained.

3- Mebendazole is effective for helminthic infestation and metronidazole for amebiasis and giardiasis.

4- Treatment of hypoglycemia by giving extra food and extra glucose IV or by mouth. Oral prednisone 0.5 mg/kg/ every 6 hours is indicated especially if blood sugar is less than 40 mg/dL with disturbed conscious level.

5- Treatment of hypothermia by warming the baby using mother’s body, heavy clothes and radiant external heat.

6- Fresh blood transfusion: is given in cases with anemia, shock or bleeding tendency in a dose of 15 ml/kg very slowly. Blood transfusion corrects anemia, hypoproteinemia, hypoimmuno- globulinemia, platelets and coagulation factors deficiency.

II- Nutritional therapy

Mild malnutrition: children should receive adequate calories and proteins in a diet of locally available inexpensive and culturally acceptable foods.

Moderate malnutrition: children are treated at home and should be kept under surveillance so as to detect early deterioration in their nutritional status, 150 kcal/kg/day should be given.

Severe malnutrition

Marasmus

· Caloric requirement is 200 kcal/kg/day. In the first-degree marasmus, calculate the amount of caloric requirement according to the expected weight.  In the second and third degree marasmus calculate the amount of caloric requirement midway between actual and expected weight then gradually increase the amount according to the gain of weight and tolerance of the baby.

About 10% of total calories should be from animal proteins of high biological value. Part of dietary protein may be of vegetable origin, mixing legumes e.g. beans with seeds (e.g. maize and wheat) to increase their biological value as they contain different essential amino acids. Higher intake of protein is not necessary, because excess protein is utilized for energy.

• Feeds are given every two hours.

• Breast-feeding is continued after correction of any difficulties. Artificially fed infants are given humanized milk.

• Lactose free or low lactose milk is given in secondary transient lactose intolerance, it is suspected if the pH of the stool is below 5 on two separate occasions, while the child is receiving milk diet.

• For weaned infants, give a well balanced diet and supply a high amount of calories. Diet should be rich in protein with a good amount of carbohydrates and vitamins. The amount of fat in diet depends upon tolerance of the patient.

Kwashiorkor

• Caloric supply in kwashiorkor is 120- 140 kcal/kg/day. Caloric requirement is calculated midway between that for the expected weight and that for the actual weight at presentation, gradually increasing the amount of food according to the tolerance and desire of the baby till the expected weight is reached.

• The fundamental line of treatment is the correction of protein deficiency through a diet supplying high biological value proteins, 4-6 gm/kg/day but not more than 6 gm. The diet should contain sufficient calories to save protein for growth and other essential nutrients as vitamins and minerals.

• Nasogastric tube feeding is indicated in cases with severe anorexia, failure of oral feeding, frequent vomiting and severe stomatitis. Tube feeding is used early in management until oral feeding can be tolerated either by spoon or dropper.

• The best source of animal protein is the breast milk. If breast milk is not available or scanty, humanized milk is given. In patients with lactose intolerance, low lactose or lactose free milk or yogurt is supplied. The small amount of lactose in the milk stimulates the columnar epithelium of the intestine to re-synthesize lactase enzyme.

• For weaned infants, food needs to be rich in protein easily digestible, low cost and available. Cheese especially cottage cheese, eggs, yogurt, mixed legumes (e.g. beans, peas, lentils, chick peas) and minced meat may be given.

III- Adjuvant therapy

    Replenishment of specific nutrients

• Potassium chloride 4-6 mEq/kg/day should be given orally once urine output is established.

• Magnesium is administered in a dose of 1-3 mEq/kg/day.

• Sodium intake should be less than 2 mEq/kg/day.

• Zinc deficiency is suspected if there is chronic diarrhea, zinc acetate is given in a dose of 2mg/kg/day.

• Copper deficiency: is common in all diets based on cow’s milk. Copper can be given as acetate or chloride in a dose of 0.2 mg/kg/day.

• Iron: although iron deficiency is common, it is advisable to give iron after recovery from acute state. Severe anemia needs transfusion of fresh blood.  

• Vitamin A and B complex supplementation in double the daily requirements is recommended. In severe PEM vitamin A may be given in a dose of 200.000 IU.

• Vitamin D supplements should be instituted in the treatment once the bowel condition allows because these children are liable to develop rickets on recovery (due to rapid growth).

• Folic acid in a dose of 1 mg/day is required.

• Treatment of skin lesions by gentian violet paint 2% and local antibiotic cream. If monilial skin infection is present, nystatin cream can be used.

Signs of recovery

  1- Improvement of appetite with decrease of the edema.

  2- Increasing alertness and interest in the surroundings.

  3- Gradual gain in weight.

Prevention of PEM

1- Encouraging prolonged breast-feeding up to 2 years.

2- Use of locally available protein sources as lentils, beans and low cost milk diet as cottage cheese and yogurt.

3- The best early indication that a child is at risk is poor growth. Supervision of a child’s progress and recording his growth at a child health clinic are important tools in the early detection and treatment of malnutrition. This will allow advice and treatment to be given well before the severe affection occurs.    

4- The clinician will also help in prevention of PEM by health education, immunization programes and family planning.

 

Rickets

Definition

  • Rickets means failure of mineralization of growing bone.

 Causes:

1-      Deficiency of vitamin D in diet.

2-      Inadequate exposure to sunlight.

3-      Defective absorption of vitamin D.

4-      Renal or hepatic diseases.

Vitamin D deficient rickets

Metabolism of vitamin D:there are two forms of vitamin D:

1- Vitamin D₂ is present in animal source diet such as fish liver oil and egg yolk.

2- Vitamin D₃ is found in some diet and in the skin as provitamin (7 dehydrocholesterol) that is activated by ultraviolet rays of sunlight to cholecalciferol.

Both forms of vitamin D undergo 25 hydroxylation in the liver to 25-hydroxycholecalciferol. Further hydroxylation takes place in the kidney to 1,25 dihydroxycholecalciferol. This end product is considered a hormone and it is the active form of vitamin D. 

            Clinical manifestations of rickets

Age incidence: 3 months - 3 years.

A- Early clinical signs 

1- Craniotabes: it is due to thinning and softening of the outer table of the skull bones and it is detected by pressing firmly over the occiput or posterior parietal bone eliciting ping-pong ball sensation. It is rarely present after 8 months of age.

2- Flaring of ends of the long bones.

a- Broad ends of radius and ulna.

b- Marfan sign: flaring of the lower tibial metaphyses forms a prominence above the normal prominence of medial malleolus with a relative groove in between.

c - Rosary beads: they are due to enlargement of costo-chondral junctions. They are palpable.  

3- Increased sweating around the head may be present.

B- Clinical signs of advanced rickets 

1- Head

• Softness of the skull may cause asymmetry of the head with flattening of sites of continuous pressure.

• The head may be larger than normal.

• There is bossing of the parietal and frontal bones due to excessive osteoid tissue. The head has a box like appearance (caput quadratum).

• Delayed closure of anterior fontanel.

• Delayed eruption of teeth with defective enamel and tendency to develop caries.

2- Thorax

• Rosary beads: they are both palpable and visible.

• Pigeon chest:  the sternum with its adjacent cartilage appears to be projecting forwards. 

• Vertical grooves (longitudinal grooves): these sulci are seen posterior to rosary beads due to yielding of the chest wall at the weakest points i.e. the costochondral junctions under the   effect of atmospheric pressure.

• Harrison sulcus:a horizontal groove at the lower border of the chest along the costal insertion of the diaphragm. The sulcus is the result of pulling of the diaphragm on soft ribs at the site of its insertion.

3- Abdomen

• Displacement of liver and spleen downward due to thoracic deformity.

• Potbelly abdomen and constipation may occur due to hypotonia of abdominal and intestinal   muscles.

4- Spinal column: dorsal kyphosis appears during sitting and disappears when the child is pulled-up by his arms (postural kyphosis). Scoliosis and lumbar lordosis may also occur.

5- Pelvis: contracted inlet and outlet may be present. Pelvic deformities may be responsible for difficult labor in females and may necessitate cesarean section.

6- Extremities

• Enlargement of ends of bones: This may be visible.

• Bow legs (Genu varum) and knock knees (genu valgum).

• Fractures (complete or greenstick).

7- Muscles: muscle weakness and hypotonia are common causes of delayed motor activities as delayed sitting, standing and walking.

8-      Rachitic dwarfism: deformities of spine, pelvis and legs result in short stature.

9-      Ligaments: relaxation of ligaments helps in the production of abnormal range of joint movement and deformities.

Diagnosis

A- By clinical manifestations

B- Biochemical changes

1- Increased phosphaturia.

2- Low serum phosphorus level (normal range: 4.5-6.5 mg/dL).

3- High alkaline phosphatase level (normally up to 450 U/L).

4- Serum calcium level is usually normal. Hypocalcemia may occur in advanced untreated cases.

C- Radiological changes .

Assessment of healing of rickets

If vitamin D is given in adequate dose, healing will occur within 2-4 weeks and can be assessed by:   

1- Clinical manifestations

• Disappearance of hypotonia: improvement of motor activities, (the child is able to sit, stand or walk), disappearance of potbelly abdomen, kyphosis and constipation.

• Disappearance of craniotabes.

• The child may start teeth eruption.

2- Biochemical manifestations: the earliest signs of recovery are decreased level of phosphorus in urine and increased serum phosphorus level.  Alkaline phosphatase then drops.

3- Radiological manifestations

Complications

1- Capacity of the chest to expand is limited by chest deformities. This increases the susceptibility to respiratory infections and atelectasis.

2- Anemia may be due to iron deficiency.

3- There are bouts of diarrhea alternating with constipation.

   4-Tetany occurs when total serum calcium level decreases below 7 mg/dL or when ionized calcium is    

        below 3 mg/dL. It is a state of hyperexcitability of the central and peripheral nervous system.

Clinical manifestations of manifest tetany

a-Carpopedal spasm: abduction of hands, flexion of the wrist, flexion of the metacarpophalangeal joints, extension of interphalangeal joints and adduction of the thumb. Feet are extended, with the sole cupped and toes flexed.

b- Laryngismus stridulous: laryngospasm may cause suffocation, due to laryngeal obstruction. 

c- Convulsions: they are usually generalized and brief. There are no abnormal neurologic manifestations between the attacks.

5- In advanced cases, permanent bone deformities may occur.

Prevention

Rickets can be prevented by exposure to ultraviolet rays or by oral administration of vitamin D (daily requirements), as medicinal vit. D or by eating diet rich in vitamin D as egg yolk and fish.

Treatment

Previous administration of vitamin D should be inquired about in the history to avoid

hypervitaminosis D. When   rickets is complicated by tetany, tetany should be treated at first.

• Oral administration of vitamin D in a dose of 1500-5000 IU per day in 3 divided doses. This will produce healing within 4 weeks.

• Shock therapy: IM injection of 600.000 IU in single dose. If healing does not occur within 2 weeks, the dose may be repeated once.

·         After complete healing, the dose of vitamin D should be reduced to 400 IU/day.

·         Treatment of hypocalcemic tetany;

IV injection of calcium gluconate 10% solution. Tissue necrosis may occur if solution is given IM or extravasates. The dose is 2ml / kg (18 mg/kg elemental calcium). Calcium solution should be given IV very slowly with monitoring the heartbeats to avoid bradycardia or cardiac arrest. There is a dramatic response immediately after calcium injection. The dose may be repeated every 8 hours until serum calcium level reaches normal values.

I.V therapy should be followed by oral medication. Calcium gluconate is given in a dose of 50 mg/kg/day of elemental calcium for one week.