PEDIATRIC NURSING

NURSING CARE OF THE CHILD WITH A GASTROINTESTINAL DISORDER

FLUID, ELECTROLYTE AND ACID-BASE IMBALANCE

FLUID BALANCE
Fluid is distributed in 3 body compartments: a. Intracellular compartment- 35 to 40% of body wt. b. Interstitial compartment- 20% of body wt. c. Intravascular compartment- 5% of body wt. The INTERSTITIAL AND INTRAVASCULAR FLUID MAKES UP THE ECF (EXTRACELLULAR FLUID COMPARTMENT).

Fluid is normally obtained through oral ingestion of fluid and by the water formed in the metabolic breakdown of food. Fluid is lost through our urine and feces. Minor losses, INSENSIBLE LOSSES occur from evaporation.

DEHYDRATION
A body fluid disturbance where the total output of fluid exceeds the total amount of intake.

TYPES OF DEHYDRATION
Are categorized on the basis of osmolality and depends primarily on the serum sodium concentration.

ISOTONIC (ISOSMOTIC OR ISONATREMIC) DEHYDRATION

The primary form of DHN in children Water and salt are lost in approximately equal amounts. There is no osmotic force between the ICF and ECF so the major loss is form the ECF. The effect would be: a. DECREASE in the plasma volume and circulating blood volume b. It would affect the skin, muscles and kidneys SHOCK is the greatest threat in children with this type of DHN. Plasma sodium remains at normal limits between 130 & 150 meq/L.

HYPOTONIC (HYPOSMOTIC OR HYPONATREMIC) DEHYDRATION

Electrolyte deficit > water deficit Plasma concentration of Sodium and chloride will be low. ICF is more concentrated than the ECF, water moves from the ECF to the ICF to establish osmotic equilibrium. Shock is a common finding Can be due to excessive GI loss from vomiting, low intake of salt associated with extreme losses through therapeutic diuresis. It can also occur when there is extreme electrolyte loss in diseases (adrenocortical insufficiency, diabetic acidosis).

HYPERTONIC (HYPEROSMOTIC OR HYPERNATREMIC ) DEHYDRATION

Water loss> electrolyte loss Usually caused by a proportionately larger loss of water and a larger intake of electrolytes It is the most dangerous type of DHN Fluid shifts from the ICF to the ECF. Plasma Na concentration is > 150 meq/L. Neurologic disturbances is more apparent such as alteration in LOC, poor ability to focus attention, lethargy, increased muscle tone with hyperreflexia, hyperirritability to stimuli. May occur in a child with nausea, profuse diarrhea, renal disease associated with polyuria. RBC and HCT increases because the blood is more concentrated. Levels of electrolytes (Na, Cl,and bicarbonate) is increased.

SIGNS AND SYMPTOMS OF DEHYDRATION

ISOTONIC Thirst Skin turgor Skin consistency Skin temperature Urine output Activity mild poor dry cool decreased irritable HYPOTONIC moderate Very poor clammy cool Decreased lethargic reduced HYPERTONIC Extreme moderate moderate Warm decreased Very lethargic increased

Serum Sodium level normal

DIAGNOSTIC EVALUATION FOR DEHYDRATION

a. b. c. Degree of DHN is described as a percentage: 5% (mild DHN) 10% (moderate DHN) 15% (severe DHN) Reflecting acute loss in ml/kg. of body wt. Wt. is the most important determinant of the total percent of body wt. Other predictors include: Changing LOC Response to stimuli Prolonged capillary refill Increased HR Sunken eyes and fontanelles

a. b. c. d. e.

LEVEL OF DHN Wt. loss-infants Wt. loss- children Pulse Blood pressure Behavior Thirst Mucous membrane Tears Anterior fontanel External jugular vein

MILD 5% 3-4% Normal Normal Normal Slight Normal Present Normal Visible when supine

MODERATE 10% 6-8% Slightly increased Normal to orthostatic (>10 MMHG CHANGE) Irritable, more thirsty Moderate Dry Decreased Normal to sunken

SEVERE 15% 10% Very increased Orthostatic to shock Hyperirritable to lethargic Intense Parched Absent, sunken eyes Sunken

Not visible except with Not visible even with supraclavicular supraclavicular pressure pressure Slowed CRT (2-4 seconds) Very delayed crt (4 seconds) and tenting; skin cool, acrocyanotic or mottled Oliguria or anuria

Skin (less useful in children >2 y/o)

Capillary refill> 2 seconds

Urine specific gravity

>1.020

>1.020; oliguria

OVERHYDRATION
It occurs in children receiving IV fluid. Excessive fluid is in the extracellular compartment. When large amount of hypotonic solutions (tap water) are ingested or are given by enema, the body transfers water from the ECF into the Intracellular space to restore normal osmotic relationships. This results in INTRACELLULAR EDEMA. S/sx. Of INTRACELLULAR EDEMA Headache Nausea and vomiting Dimness Blurring of vision Cramps Muscle twitching Seizures

a. b. c. d. e. f. g.

ACID-BASE IMBALANCE
In the GI system, it occurs because of severe diarrhea or vomiting. To determine acid-base balance, a key component is pH. pH denotes whether a solution is acid or alkaline and is determined by the proportion of Hydrogen ions (H+) ions in relation to Hydroxide (OH-) ions. A solution is ACID if it contains more H ions than OH ions, it is ALKALINE if OH ions exceeds H ions. ABG (Arterial Blood Gas) is used to determine whether the body is acidotic. NORMAL VALUES FOR ABG: pH 7.35 to 7.45 Pco2- 35 to 45 mmhg HCO3- 22 to 26 meq/L.

METABOLIC ACIDOSIS
May result from diarrhea. In diarrhea, Na is lost with the stool which in turn causes the body to conserve H+ ions in an attempt to keep the total number of + and ions in the serum balanced. As a result, the number of H+ ions in the blood INCREASES proportionately over the OH-ions making the child ACIDOTIC. To correct the acidosis, the body uses 2 BUFFERING SYSTEM. 1. RESPIRATORY BUFFERING SYSTEM - Attempts to correct imbalance quickly - H+ ions combine with HCO3- ions to form carbonic acid. - This CARBONIC acid is broken down into CO2 and water which is eliminated by the lungs during expiration.

The child breathes rapidly (hyperpnea) to blow off CO2 to prevent it from combining with H2O and reforming HCO3. S/sx. 1. Headache 2. Nausea and vomiting 3. Weakness 4. Apathy 5. Disorientation 6. Tremors 7. Convulsions 8. Coma 9. Kussmaul s respiration

NURSING MANAGEMENT FOR METABOLIC ACIDOSIS

Administer sodium bicarbonate. Monitor fluid and electrolyte levels If patient has changes in sensorium, implement safety precautions. Monitor for arrhytmias

METABOLIC ALKALOSIS
With vomiting, HCL is lost INCREASE K loss in diuretic therapy When CL- ions are lost, the number of H+ ions decrease so the number of + and charges remains balanced. The number of H+ ions LOWER than the number of OH- ions in HCO3, and Ph To further reduce no. of H+ ions, lungs conserve water and CO2 by slowing respirations (hypopnea). The excessive CO2 retained by this maneuver dissolves in the blood as carbonic acid and is converted into excessive H and HCO3.

a. b. c. d. e. f. g. h.

S/sx: Nausea Diarrhea Tingling fingers Numbness Bradycardia Respiratory depression Shallow RR with periods of apnea Irregular PR, arrhythmias and muscle twitching due to Ca level.

K and

NURSING MANAGEMENT
Fluid and Electrolyte replacement Monitor I and O Assess for signs of hypokalemia Seizure precautions Avoid taking OTC antacids

CLINICAL MANIFESTATIONS OF GI DYSFUNCTION IN CHILDREN

1. Failure to thrive- wt. consistently below the 3rd percentile or BMI below the 5th percentile or a decrease from established growth pattern. 2. Spitting up or regurgitation- passive transfer of gastric contents into the esophagus or mouth 3. Vomiting- forceful ejection of gastric contents; is under CNS control and usually accompanied by nausea Projectile vomiting- vomiting accompanied by vigorous peristaltic waves and typically associated with PYLORIC STENOSIS or PYLOROSPASM. 4. Nausea- Unpleasant sensation vaguely referred to the throat or abdomen

5. Constipation- delay or difficulty with the passage of stools that is present for 2 or more weeks 6. Encopresis- involuntary overflow of incontinent stools causing soiling or incontinence secondary to fecal retention or impaction 7. Diarrhea- increase in the number of stools with an increased water content as a result of alterations of water and electrolyte transport by the GIT. 8. Hypoactive, Hyperactive, or Absent bowel sounds- evidence of intestinal motility problems that may be caused by inflammation or obstruction 9. Abdominal distention- protuberant contour of the abdomen that may be caused by delayed gastric emptying, accumulation of gas or stool, inflammation or obstruction

10. Abdominal pain- may be localized, diffuse, acute or chronic and often caused by inflammation, obstruction or hemorrhage 11. GI Bleeding- may be from upper or lower GI source and acute or chronic Hematemesis- vomiting of bright red blood or denatured blood that is due to upper GI bleeding or swallowed blood from the nose or oropharynx Melena- passage of dark colored tarry stools suggesting upper GI tract bleeding or bleeding from the right colon Hematochezia- passage of bright red blood per rectum indicating lower GI bleeding

11. jaundice- yellow discoloration of the skin and sclerae associated with liver dysfunction 12. dysphagia- difficulty swallowing due to abnormalities in the neuromuscular function of the pharynx or upper esophageal sphincter or by the disorders of the esophagus 13. Dysfunctional swallowing- impaired swallowing caused by CNS defects or structural defects of the oral cavity, pharynx, esophagus 14. Fever- common GI manifestation in children; usually associated with DHN, infection or inflammation

DISORDERS OF MOTILITY
1. DIARRHEA - It is a symptom resulting from disorders involving digestive, absorptive and secretory functions - Is caused by abnormal intestinal water and electrolyte transport - Involves the stomach and intestines (gastroenteritis), small intestine (enteritis), colon (colitis), colon and intestines (enterocolitis) - Is classified as acute or chronic

ACUTE DIARRHEA
A sudden increase in frequency and a change in consistency of stools often caused by an infectious agent in the GIT. It may be associated with URTI or UTI, antibiotic therapy or laxative use. Is usually self-limited and subsides without specific tx. If DHN does not occur.

CHRONIC DIARRHEA
An increase in stool frequency and increased water content with a duration of > 14 days. Often caused by malabsorption syndromes, inflammatory bowel disease, immune disease, food allergy, lactose intolerance, chronic nonspecific diarrhea or inadequate mgt. of acute diarrhea.

DIFFERENCE BETWEEN INFANT NORMAL STOOL AND DIARRHEAL STOOL

CHARACTERISTIC Frequency Color Effort of expulsion Ph Odor Occult blood Reducing substances INFANT NORMAL STOOL 1-3 stool Yellow Some pushing effort > 7.0 (alkaline) Odorless (-) (-) DIARRHEAL STOOL Unlimited number Green Effortless; may be explosive < 7.0 (acidic) Sweet or foul smelling (+); blood may be overt (+)

ETIOLOGY OF DIARRHEA
Pathogens are spread by fecal-oral route through contaminated water or food or from person-person where there is close contact ROTAVIRUS- is the most important cause of serious gastroenteritis among children and a significant nosocomial pathogen Is most severe in children between 3-24 mons. Of age Other agents include: a. Bacterial agents - E.coli - Salmonella groups (nontyphoidal) - Salmonella typhi b. Vibrio cholerae c. Clostridium difficile

d. Clostridium perfingens e. Clostridium botulinum f. staphylococcus

SIGNS AND SYMPTOMS OF DIARRHEA

MILD DIARRHEA
Fever 38.4 to 39.0C) Anorexia Irritable and appear unwell Consist of 2-10 loose watery bowel movt. Per day Mucous membrane of the mouth appears dry Rapid pulse Skin is warm Skin turgor not yet decreased UO is usually normal

SEVERE DIARRHEA
rectal tempt. Is often as high as (39.5 to 40.0C) PR and RR are weak and rapid Skin is pale and cool Infants appear apprehensive, listless and lethargic Obvious signs of DHN: sunken eyes, poor skin turgor Stool is liquid green perhaps mixed with mucus and blood UO is scanty and concentrated

Elevated Hct, Hgb and serum CHON levels Metabolic acidosis

THERAPEUTIC MANAGEMENT FOR DIARRHEA

1. Assess fluid and electrolyte balance. 2. Rehydration 3. Maintenance of fluid thrapy 4. Reintroduction of an adequate diet. 5. Obtain sample of stool for stool culture so definite antibiotic therapy can be prescribed. 6. If child can drink, institute ORT (ORAL REHYDRATION THERAPY).

NURSING MANAGEMENT FOR PATIENTS WITH DIARRHEA

1. Promote adequate hydration and comfort a. (+) vomiting- NPO temporarily b. Wet lips with a moisturizing jelly if it is dry c. Give pacifier to promote comfort d. (+) fever- do TSB e. Increase OFI f. Do not obtain BT in the rectal area. g. Assess perianal skin for irritation. h. Keep perianal area clean and dry. i. Change diapers frequently 2. Record I and O strictly. 3. Weigh child daily to assess for DHN.

4. Discourage intake of clear fluids, carbonated drinks and gelatin. 5. Assess V/S, skin turgor, mucous membranes, and mental status. Expose slightly reddened intact skin to air when possible to promote healing 6. Avoid use of commercial baby wipes with alcohol on excoriated skin 7. Observe buttocks and perineum for skin infection.

CONSTIPATION
NEWBORN PERIOD
Alteration in the frequency, consistency or ease of passing stool. OBSTIPATION - Having extremely long intervals between defecation ENCOPRESIS - Constipation with fecal soiling

MECONIUM STOOL - 1st stool an infant passes within 24-36 hrs. after birth. (-) after 24-36 hrs. assess for evidence of intestinal atresia, stenosis, Hirschprung s disease, hypothyroidism, meconium plugs or meconium ileus

MECONIUM PLUGS - Caused by meconium that has reduced water content and are usually evacuated after DRE (digital rectal exam) MECONIUM ILEUS - Initial manifestation of cystic fibrosis w/c is the luminal obstruction of the distal small intestine by abnormal meconium.

MGT. OF CONSTIPATION 1. In infancy, increase CHO in the formula. 2. During childhood, the diet must consist of increased fiber and fluid. HIGH FIBER FOODS a. bread, grains - Whole grain bread or rolls - Whole grain cereals - bran

Pancakes, waffles, muffins with fruit or bran - Unrefined (brown) rice b. Vegetables - Raw vegetables especially broccoli, cabbage, carrots, cauliflower, celery, lettuce, and spinach - Cooked vegetables like asparagus, brussels sprouts, corn, potatoes, squash, string beans and turnips

c. Fruits - Raw fruits especially those with skins or seeds other than ripe banana or avocado - Raisins, prunes or dried fruits

DISORDERS OF THE STOMACH AND DUODENUM

I. GASTROESOPHAGEAL REFLUX (ACHALASIA)

CAUSES OF GER
Dysfunction of the lower esophageal sphincter Delay in gastric emptying Poor clearance of esophageal acid Susceptibility of esophageal mucosa to acid injury Gastric distention Increased abdominal pressure because of coughing, CNS disease, hiatal hernia and gastrostomy placement

A neuromuscular disturbance in which the gastroesophageal (cardiac) sphincter and the lower part of the esophagus are lax and thus allow easy regurgitation of gastric contents into the esophagus. Usually starts 1 week after birth and may be associated with hiatal hernia.

Clinical manifestations and complications SYMPTOMS IN INFANTS a. Spitting up, regurgitation b. Excessive crying, irritability, arching of the back, stiffening c. Wt. loss d. Failure to thrive e. Respiratory problems (cough, wheeze, stridor, gagging, choking with feeding f. Hematemesis g. Apnea

SYMPTOMS IN CHILDREN a. Heartburn b. Abdominal pain c. Noncardiac chest pain d. Chronic cough e. Dysphagia f. Nocturnal asthma g. Recurrent pneumonia

COMPLICATIONS
a. b. c. d. e. f. Esophagitis Esophageal stricture Laryngitis Recurrent pneumonia Anemia Barrett s esophagus

DIAGNOSTIC EVALUATION
1. Upper GI Series/Barium swallow X-ray of upper GI tract To detect presence of anatomic abnormalities Nx. Interventions a. NPO post midnight b. Instruct pt. about the procedure c. Educate pt. that barium has a thick consistency and chalky taste. d. Administer laxative to help expel barium and prevent fecal impaction

NX. MGT.
e. Assess abdomen for distention f. Observe the stool. Initially it is white but returns to normal color within 72 hrs. g. Instruct ct. to inform physician if constipation and abdominal distention occur. 2. Scintigraphy - Detects radioactive substances in the esophagus after a feeding of a compound and assesses gastric emptying

1. Identify symptoms 2. Avoid caffeine, chocolate and spicy foods that may weaken the LES. 3. Wt. mgt. in children 4. Monitor Iand O

HYPERTROPHIC PYLORIC STENOSIS

PYLORIC SPHINCTER - It is the opening between the lower portion of the stomach and beginning portion of the intestine, the duodenum. - Occurs when the circumferential of the pyloric sphincter becomes thickened resulting in elongation and narrowing of the pyloric channel.
It is usually evident at 4-6 wks. Of age Exact cause is unknown There is a genetic predisposition 1stborn children and males are affected 5x more frequently than females More common in full term infants

CLINICAL MANIFESTATIONS OF HPS

a. b. c. d. Projectile vomiting w/c occur shortly after feeding Nonbilious vomitus; blood tinged Infant hungry; avid nurser, No evidence of pain or discomfort except chronic hunger Wt. loss DHN Distended upper abdomen h. Readily palpable olive shaped mass in the epigastrium just to the right of the umbilicus Visible gastric peristaltic waves that move from L-R across the epigastrium

e. f. g.

DIAGNOSTIC EVALUATION
a. UTZ Will reveal an elongated, sausage shaped mass with an elongated pyloric channel b. Upper GI radiography c. Decreased serum Na and K d. Decrease in serum CL levels e. Increase Ph and bicarbonate f. Elevated BUN

THERAPEUTIC MGT.
1. PYLOROMYOTOMY - Sxcal relief of pyloric obstruction - An incision is made in the RUQ 2. LAPARAOSCOPY - Use of a laparoscope

NX. MGT.
PRE-OPERATIVE CARE 1. Restore hydration and electrolyte balance 2. Monitor Iand O and urine specific gravity 3. (+) gastric lavage- ensure patency of the tube and measure and record the amount and type of drainage; position infant flat on bed or head slightly elevated POST-OPERATIVE CARE 1. After 4-6 hrs. start infants on a small amt. of ORS . If (-) vomiting, the amt. is increased orally or breast-feeding is begun. 2. Monitor Iand O 3. Observe for evidence of pain

HERNIA
Protrusion of a portion of an organ or organs through an abnormal opening.

TYPES OF HERNIA
1. Diaphragmatic Hernia - Protrusion of abdominal organs through an opening in the diaphragm Symptoms: a. Mild to severe respiratory distress few hrs. after birth b. Tachypnea c. Cyanosis d. Dyspnea e. Absent breath sounds in affected area f. Impaired CO
g. Possible symptoms of shock h. Severe acidosis DX: Confirmed by radiographic study, often diagnosed prenatally as early as 25th AOG MGT: 1. Correction of acidosis 2. Possible use of intubation 3. GI decompression 4. Prophylactic antibiotic administration 5. Sxcal reduction of hernia and repair of defect

2. Hiatal Hernia - Protrusion of the stomach up through the esophageal opening in the diaphragm. Sx: a. Dysphagia b. Failure to thrive c. Vomiting d. Neck contortions e. Frequent unexplained respiratory problems f. Bleeding

DX: a. By FLUOROSCOPY MGT: 1. Mgt of GER symptoms 2. Position infant in an upright position 3. Laparoscopic sx. May be done to correct the problem

3. Abdominal Hernia -Umbilical-weakness in abdominal wall around umbilicus; incomplete closure of abdominal wall that allows intestinal contents to protrude through an opening. Sx: - Noted by inspection and palpation of the abdomen - High incidence in premature and african-american infants - Usuall closes spontaneously by 12 y/o.

Mgt: a. No treatment on small defects b. Operative repair if persists to age 406 or if defect is > 1.5-2.0 cm by age 2. c. Discourage use of home remedies ( belly bands, coins)

Abdominal Omphalocele- protrusion of intraabdominal viscera into base of umbilical cord; sac is covered with peritoneum w/o skin Sx: - Obvious on inspection Mgt: - Sxcal repair of defect - Preoperative: a. Gradual reduction of abdominal contents b. Prohylactic antibiotic administration

Gastroschisis - Protrusion of intraabdominal contents through a defect in the abdominal wall lateral to umbilical ring; no peritoneal sac Sx: - Obvious on inspection Mgt: - Sxcal repair of defect - Preoperative: a. Keep sac or viscera moist with saline soaked pads b. Use overhead warming unit c. Nasogastric suction d. NPO

PEPTIC ULCER DISEASE

It is a shallow excavation formed in the mucosal wall of the stomach, pylorus or duodenum In infants, ulcers tend to be gastric; in adolescents they are usually duodenal Etiology: - Exact cause is unknown - Increased in persons with blood type O - H.Pylori- weakens gastric mucosal barrier allowing damage to the mucosa - Ulcerogenic drugs Smoking Alcoholism Stressful life events It is most likely caused by an imbalance between the CYTOTOXIC (DESTRUCTIVE) factors and CYTOPROTECTIVE (DEFENSIVE) factors in the GIT. DESTRUCTIVE FACTORS: a. Acid b. Pepsin c. ASA and NSAID- inhibits prostaglandin synthesis d. Bile acids e. Infections with H.Pylori

DEFENSIVE FACTORS: a. Mucous layer - Acts to diffuse acid form the lumen to the gastric mucosal surface b. Local bicarbonate secretion - Produced by the stomach and duodenum - Decreases acidity on epithelial cells, minimizing effects of low ph

ASSESSMENT: 1. neonate- hematemesis or melena, respiratory distress, abdominal distention vomiting if rupture may occur and if extensive cardiovascular collapse. 2. Toddler- anorexia, vomiting, bleeding after few weeks 3. Preschool or early school age- pain w/c may be mild, severe, colicky or continuous 4. School age and adolescents- pain in epigastric area before meals relieved by eating

Dx: a. FIBEROPTIC ENDOSCOPY- most reliable diagnostic test b. CBC- to detect anemia c. Stool analysis d. Liver function tests Mgt: 1. Promote healing of ulcer through compliance with medications. Medications for PUD: 1. Antacids- neutralizes gastric acid

2. H2 Receptor antagonists (Famotidine, Ranitidine)- suppresses gastric acid production 3. Proton Pump Inhibitors (omeprazole) - Inhibit Hydrogen ion pump in th parietal cells thus blocking the production of acid 4. Mucosal protective agents (sucralfate, bismuth containing compounds) Sucralfate- aluminum containing agent that forms a protective barrier over ulcerated mucosa

Bismuth containing compounds -inhibit growth of microorganisms 2. Do not use ASA or NSAIDS if an antipyretic or analgesic is needed, use ACETAMINOPHEN (TYLENOL). 3. Avoid heavily spiced foods such as pizza or sausage. 4. Avoid carbonated drinks and beverages.

HEPATIC DISORDERS

FUNCTIONS OF THE LIVER - Liver lies immediately under the diaphragm on the right side. 1. Essential for the normal metabolism of CHO, proteins and fats. 2. Maintains normal blood sugar level by exchanging glucose to glycogen and storing it until cells needs it. 3. Changes glycogen to glucose and releases it into the blood stream when needed by the body cells.

4. Aids in the catabolism of fatty acids and proteins and serves as temporary space for both fat and protein. 5. By the means of the enzyme, GLUCORONOSYLTRANSFERASE converts indirect or unconjugated bilirubin into direct or conjugated bilirubin so it can be excreted in bile and from the body. 6. Manufactures bile- necessary for the digestion of fat; fibrinogen and prothrombin, heparin. 7. Produces large amounts of body heat

8. Destroys RBCs and detoxifies harmful substances such as drugs.

LIVER FUNCTION TESTS

Serum bilirubin
 INCREASE indirect bilirubin means it is not converted into direct bilirubin hence liver function may be impaired  Normal value of total bilirubin in serum is 1.5 mg per 100 ml.  INCREASE direct bilirubin implies obstruction of the bile duct  (+) bile pigments in the stool, bile is manufactured and excreted form the liver  (-) bile pigment, stool is clay colored  (+) bilirubin in urine indicate possible liver dysfunction An enzyme produced by the liver and bone and excreted in the bile  INCREASED levels in the blood indicates bile duct obstruction  Is associated with blood coagulation. In chronic liver disease, level of prothrombin falls severely so PT time is INCREASED.

Stool and urine bilirubin

Alkaline phosphatase

Prothrombin time

Aspartate transaminase (AST; serum glutamic-oxaloacetic transaminase (SGOT)

 an enzyme in the heart and liver Is released into the bloodstream when there is damage to the organ  blood levels INCREASE by 8 hrs. after injury; level reaches a peaks in 24-36 hrs. and falls to normal in 4-6 days  Found mostly in the liver Rises for the same reasons as AST (SGOT) an enzyme in the heart and liver  is increased in INFECTIOUS MONONUCLEOSIS Albumin, is a serum CHON synthesized in the liver  Is DECREASED in acute or chronic liver disease

Alanine Transaminase (ALT; serum glutamate pyruvate transaminase (SGPT) Lactic dehydrogenase

Serum albumin

HEPATITIS
 Inflammation and infection of the liver  Caused by invasion of the Hepa A, B, C, D, E viruses, chemical or drug reaction, autoimmune hepatitis, Wilson's disease, steatohepatitis

HEPATITIS A
Causative agent: A picornavirus, hepatitis A virus Incubation period: 25 days on average Period of communicability: Highest during 2 wks. Preceding onset of symptoms Mode of transmission: fecal-oral route Immunity: natural Active artificial immunity: HAV vaccine Passive artificial immunity: Immune globulin (IG)

HEPATITIS B
Causative agent: A hepadnavirus, hepatitis B virus Incubation period: 120 days on average Period of communicability: later part of incubation period and during the acute stage Mode of transmission: principal routeparenteral; least- oral, sexual, any body fluid or perinatal transfer- transplacental blood (last trimester), at delivery or during breast-feeding Immunity: natural Active artificial immunity: HBV vaccine Passive artificial immunity: Specific hepa B immune serum globulin

HEPATITIS C, D, E, G
Hepa C is a single strand RNA virus and is primarily transmitted by blood or blood products, IV use or sexual contact Hepa D is a defective RNA virus that requires function of the HBV. Incubation period is 2-8 wks. Hepa E is eneterally transmitted and transmission may occur through fecal-oral route or from contaminated water Hepa G is a bllod-borne virus that may be transmitted by organ transplantation

Assessment
Headache Fever Anorexia Jaundice Generalized aching RUQ pain Headache Pruritus Urine becomes darker in color Sclerae becomes jaundiced Stool becomes white or gray

MGT:
Lab findings show an INCREASE AST and ALT INCREASED bilirubin levels in the urine Bile pigments in the stool are decreased. Serum bilirubin levels are increased. 1. 2. 3. 4. Strict hand washing. Dispose carefully feces, needles and syringes. Screen pregnant women for hepa B surface antigen. Infants born to (+) hepa B mothers must be given HBIG and active immunization Increased rest and maintain a good caloric intake

5.

FULMINANT HEPATIC FAILURE

Is present when acute, massive necrosis or sudden impairment of the liver function occurs leading to HEPATIC ENCEPHALOPATHY. HEPATIC ENCEPHALOPATHY- is due to the liver s inability to metabolize ammonia to form urea so it can be excreted. Ammonia is a CNS depressant and is produced in the GIT when CHON is broken down by bacteria, by the liver and in lesser amounts by gastric juices and peripheral tissue metabolism. The kidneys are another source in the presence of hypokalemia. Clinical features: 1. Confusion 2. Drowsiness 3. Disorientation Treatment: 1. Reduce CHON intake 2. Administer lactulose to prevent absorption of Ammonia in the colon 3. Administer nonabsorbable antibiotics such as neomycin to decrease production of ammonia by the intestinal bacteria.

OBSTRUCTION OF THE BILE DUCTS

Occurs in children generally from congenital atresia, stenosis or absence of the duct. It is a congenital disorder so the chief sign does not develop until 2 wks. Of age Clinical features: Jaundice INCREASE alkaline phosphatase AST is normal in the early phase and becomes abnormal when liver damage occurs. absorption of fat soluble vitamins is poor. Calcium absorption is also poor.

1. 2. 3.

4. 5.

Therapeutic mgt: 1. Appropriate blood work ad liver biopsy must be done under local anesthesia to rule out hepatitis. 2. Collect duodenal secretions by endoscopy to assess bile. 3. Radionuclide imaging 4. Mucus plug is suspected, pt. may be given MgSO4 (to relax the bile duct) or dehydrochoric acid (Decholin) IV to stimulate flow of blie. 5. (+) atresia of bile duct, sxcal correction is the tx.

CIRRHOSIS
Is the fibrotic scarring of the liver It means yellow or the typical color of hepatic tissue A cirrhotic liver is irreversibly damaged. May be caused by biliary atresia, chronic hepatitis, autoimmune, hemophilia and cystic fibrosis
Clinical features 1. Jaundice 2. Poor growth 3. Anorexia 4. Muscle weakness 5. Lethergy 6. Ascites 7. Edema 8. GI bleeding 9. Anemia 10. Abdominal pain 11. Dyspnea and cyanosis especially on exertion

12. spider angiomas and prominent blood vessels are seen on the upper torso 13. Decreased ability to detoxify substances 14. Decreased CHON synthesis 15. Decreased ability to produce prothrombin 16. Decreased ability to produce bile 17. Hypoglycemia 18. Esophageal varices 19. hypersplenism

THERAPEUTIC MGT: 1. Frequent assessment of liver status with PE and liver function tests 2. Mgt. of specific complications 3. Liver transplantation

ESOPHAGEAL VARICES
Or distended veins Form at the distal end of the esophagus near the stomach 2ndary to back pressure on the veins due to increased BP in the portal circulation. Its rupture is an E MGT: 1. Vasopressin or Nitroglycerin may be given IV to lessen hypertension 2. Injection of sclerosing agent into veins 3. Iced saline NGT lavage may be given 4. Insert a SENGSTAKEN-BLAKEMORE TUBE or a LINTON-NACHLAS catheter into the stomach to apply pressure against the bleeding vessels. Compression must be reduced for 5-10 minutes every 6-8 hrs.

STRUCTURAL DEFECTS
CLEFT LIP OR CLEFT PALATE Description: failure of soft tissue and/or bony structure to fuse during embryonic development ; may occur separately or together and involve one or both sides of the palate s midline. Etiology: caused by fetal insult; teratogenic factors which include: 1. Drugs 2. Exposre to radiation 3. Exposure to rubella virus 4. Chromosomal abnormalities Pathophysiology 1. In CLEFT LIP- maxillary prominence fails to fuse with medial nasal prominence between 7th and 8th wk. of intrauterine life. 2. In CLEFT PALATE- failure of maxillary bone plate to close during 7th to 12th weeks of intrauterine life

 ASSESSMENT: 1. LIP- unilateral or bilateral; extent varies from a slight notch in the vermillion border to a complete separation from the floor of the nose 2. PALATE- unilateral or bilateral; varying degree for the extent of palate involvement that is evident upon visual inspection

THERAPEUTIC MGT: 1. Surgery: plastic surgical correction of cleft lip is during 1st 3 mons. Of life; palate correction arte done at either 12 or 18 m0ns. Or delayed until 4 yrs. Of age 2. Meds: analgesics to control postop pain 3. Use of feeding devices: use of soft elongated lambs nipples; Brecht feeder for infant with a large cleft palate 4. Speech therapy

 1. a. b. c. d. e. f. g. h.

2. POST- OP CARE: NX. MGT: 1. Assess suture line for PRE-OP CARE: drainage, crusting and signs of Assess feeding requirements infection Assess nature of defect and its impact 2. Cleft lip repair: cleanse suture on feeding line after feeding and as Monitor respiratory status and ability ordered; use a cotton tip to suck during feeding applicator moistened with Encourage BF if appropriate saline or solution preferred by Initiate feeding w/ special devices as surgeon required 3. Position infant on back or on Feed small amounts gradually side; avoid prone position to Burp frequently every 15-30 cc prevent rubbing of surgical Demonstrate special feeding or site on mattress suctioning techniques to parents 4. Maintain lip protective device logan bow on operative site

5.

6. 7.

8.

9.

Restrain with soft elbow or jacket restraint; remove one at a time and periodically to perform ROM exercises Avoid contact with sharps, straws or forks near surgical site Feed with cup, wide bowl or soup spoon; if palate repaired avoid inserting spoon into mouth. Avoid use of oral suction or placing objects into mouth such as tongue depressor or oral thermometer Prevent sucking: no pacifiers, use of straw for oral fluid intake

INFLAMMATORY DISORDERS APPENDICITIS

Inflammation of the appendix, a blind sac connected to the end of cecum; may lead to perforation, peritonitis and sepsis if left untreated. Etiology: 1. Obstruction of the lumen of the appendix as a result of fecalith or hardened feces 2. Other causes are lymphoid hyperplasia, tumors, fibrotic stenosis, worms or low fiber diet pathophysiology: 1. Lumen obstruction causes blocking of mucous secretion, blood vessels compressed and ischemia results. 2. Bacterial invasion and necrosis subsequently occur 3. Acute inflammation rapidly progresses to perforation and peritonitis if left undiagnosed

 ASSESSMENT 1. Appendicitis a. pain, cramping initially located in periumbilical area descends to RLQ; most intemse at Mc Burney s pointlocated midway between the anterior superior iliac crest and the umbilicus b. Rebound tenderness of abdominal rigidity c. Low grade fever d. N/V e. Constipation or diarrhea f. Side lying position w/abdominal guarding; legs flexed

2. Peritonitis a. Fever increases b. Progressive abdominal distention c. increase abdominal pain d. Rigid guarding of abdomen e. Tachycardia, tachypnea f. Pallor, chills and restlessness

 DIAGNOSTIC PROCEDURES: 1. Lab studies: a. CBC: WBC count increases to 15,000-20,000 usually with polymorphonuclear pyuria b. U/A- reveals pyuria 2. Diagnostic studies: a. Abdominal X-ray- reveals presence of fecalith in appendix b. UTZ- reveals location of abscess before sx.

THERAPEUTIC MGT: 1. sx.- appendectomy 2. Medications: a. Analgesics b. Antibiotics 2. NX. MGT: a. pre-op care: 1. assess pain and check for rebound tenderness 2. Assess VS, noting for tachycardia, shallow fast respirations and fever >100F 3. Keep NPO

4. Provide comfort measures: a. Give analgesics b. Frequent mouth care c. Right side lying or low to semifowlers position to promote comfort or localize abscess when appendix ruptures d. Report any changes in type, level or location of pain e. Provide diversional activity for quiet play f. Avoid use of laxatives or enemas

 Post- op care: 1. Assess incision for signs of infection: redness, swelling, pain, character of drainage 2. Position in right side lying r low to semifowlers with legs flexed to facilitate drainage 3. Change dressing as ordered or reinforce as necessary; record amount and type of drainage 4. Administer antibiotics and analgesics as ordered 5. If open incision, observe sterile technique in wound dressing 6. Monitor BT for elevation

INTUSSUSCEPTION
Telescoping of one portion of bowel into another portion resulting in obstruction to passage of intestinal contents. Etiology: cause is unknown Children at risk are those with cystic fibrosis, celiac disease and gastroenteritis. Most common site is the ILEOCECCAL VALVE Pathophysiology: 1. Inflammation and ischemia occur in the intestinal wall as portions press against each other 2. Eventual tissue necrosis, perforation and peritonitis may occur

ASSESSMENT: 1. Paroxysmal, acute pain in abdomen 2. Vomiting 3. Currant jelly-like stools 4. Cylindrical mass above affected area DX. PROCEDURS: 1. Abdominal x-ray 2. Barium enenma

 THERAPEUTIC MGT: a. Hydrostatic reduction- by barium enema b. Sx. If reduction by barium enema is not successful or there is tissue necrosis c. Meds: 1. Antibiotics 2. analgesics

NX. MGT: 1. Assess for findings of intussusception 2. Maintain patency of NG tube 3. Administer IV fluids as ordered 4. Ensure NG tube is appropriate to age Newborns and infants- catheter size 5 to 6, 8 >6 y/o- 8 to 10 Adolescent- 12 to 16 Inform need for sx. If reduction is not successful

HIRSCHPRUNG DISEASE (CONGENITAL AGANGLIONIC MEGACOLON)

Congenital defect that result in mechanical obstruction form inadequate motility of an intestinal segment Etiology: may be accompanied by anomalies of other GI or GU anomalies Pathophysiology: 1. Absence of ganglion cells in an intestinal segment results in lack of peristalsis 2. Bowel proximal to defect dilates because of a lack of peristalsis 3. Failure of anal sphincter tyo relax; fecal matter accumulates in aganglionic segment

ASSESSMENT: 1. Neonatal period a. Failure to pass meconium w/in 48 hrs. after birth b. Bile-stained vomitus c. Abdominal distention 2. Early childhood a. Ribbon-like stools b. Constipation c. Foul smelling stools d. Visible peristalsis e. Recurrent diarrhea

DX. PROCEDURES: 1. Barium enema- reveals narrowed segment of bowel 2. Rectal biopsy- absence of aganglion cells 3. Abdominal x-ray- dilated loops of intestine 4. Rectal manometry- failure of internal sphincter to relax

THERAPEUTIC MGT: a. medications: preoperative antibiotics b. Treatments: ENEMA, NGT placement c. sx: 2 stage process 1. Temporary colostomy construction 2. Resection of aganglionic segment; anastomosis of the intact ganglion segment to the rectum is erformed during a pull through procedure 3. Colostomy closure is done 3 mons. Following pull through

 NX. MGT: 1. PRE-OP CARE: a. Assess wt, I and O, abdominal girth and fluid and electrolyte status b. Offer diet high in calories and CHON and low in residue 2. POST-OP CARE: a. Monitor hydration status including NG, colostomy and indwelling urinary catheter drainage; IV, NG and oral intake b. Maintain patency of NG tube

c. Monitor for return of bowel sounds for 48-72 hrs. d. Provide instructions regarding colostomy carte e. Provide dietary instructions including high residue or normal diet, adequate fluid intake

MALABSORPTION SYNDROMES
CELIAC DISEASE (GLUTEN INDUCED ENTEROPATHY) - Intolerance to gluten, the CHON component of BROW (barley, rye, oat, wheat) - Symptoms of disorder occur 3-6 mons. Following introduction of gluten-containing grains into diet usually before 2 yrs. Of age
ASSESSMENT: 1. Early signs a. diarrhea; failure to gain wt. following diarrheal episode b. Constipation c. Vomiting d. Abdominal pain e. Steatorrhea 2. Later signs a. Behavioral changes: irritability, apathy b. Muscle wasting with loss of subcutaneous fat c. Celiac crisis- rare event which require immediate medical attention 1. Severe DHN 2. Metabolic acidosis

 Diagnostic procedures: a. lab. Studies- stool analysisreveals steatorrhea b. Diagnostic studies 1. Jejunal biopsy- reveals atrophy of mucosal cells 2. Serum antigliadin and antireticulin antibodies (+) indicative of disorder 3. Sweat test- to rule out cystic fibrosis

Therapeutic mgt: 1. Acute care a. Assess for findings related to celiac disease b. Instruct parents on GLUTEN FREE DIET: NO BROW and BROW containing substances throughout life. c. Teach parents to adhere to diet, prevent stress and infection to prevent celiac crisis.

INFLAMMATORY BOWEL DISEASE: ULCERATIVE COLITIS AND CROHN S DISEASE

Involves the development of ulcers of the mucosa or submucosa layers of the colon and rectum. Both probably represent an alteration in immune system response or an autoimmune processes. There is an INCREASED IgAa and IgG on the intestinal mucosa. Smoking and frequent use of ASA are correlated with Crohn s disease. Crohn s disease is an inflammation of segments of the intestine and commonly involves the terminal ileum. In ulcerative colitis, the colon and the rectum are involved, with the distal colon and rectum most severely affected.

 ASSESSMENT: 1. Abdominal pain 2. Diarrhea 3. Malnutrition 4. Complications: a. Hemorrhage b. Bowel perforation c. Peritonitis d. Formation of fistulas between bowel loops

COMPARISON OF CROHN S DISEASE AND ULCERATIVE COLITIS

Comparison factor Part of bowel affected Nature of lesions Diarrhea Anorexia Weight loss Growth retardation Anal and perianal lesions Ccrohrohn s Disease Ileum Intermittent Moderate Severe Severe Marked Common Ulcerative Colitis Colon and rectum Continuous Severe and bloody Mild Mild Mild Rare Common

Association with carcinoma Rare

 Diagnosis: 1. It is established by colonoscopy and barium enema. COLONOSCOPY- shallow ulcerations along the bowel can be seen, mucosa is friable ( easily irritated). 2. BIOPSY- for definite diagnosis * After biopsy- observe BP, PR and assess for occult blood

Therapeutic mgt: 1. Provide an enteral or TPN to allow the bowel to rest and heal. 2. When food is reintroduced after the resting period, provide a HIGH CHON, CHO, VITAMIN diet 3. Assess I & O. 4. Administer anti-inflammatory durg such as prednisone, sulfasalazine, or azathioprine which is an immunosuppressive agent. 5. For ulcerative colitis, cyclosporine may be used.

 Sx: bowel resection to remove a portion of the bowel (colectomy) followed by an ileoanal pull through.

DISORDERS CAUSED BY FOOD, VITAMIN AND MINERAL DEFICIENCIES

1. KWASHIORKOR A disease caused by CHON deficiency - Occurs most frequently in children ages 1-3 yrs.old - Tends to occur after weaning ASSESSMENT: 1. Growth failure 2. Severe muscle wasting 3. Dependent edema 4. Ascites 5. Irritable and lack interest in the surroundings 6. Hair shafts develop a striped appearnce of brown, then white and so on- a zebra sign . 7. Diarrhea 8. Iron deficiency anemia 9. Hepatomegaly THERAPEUTIC MGT: 1. High CHON diet

2. NUTRITIONAL MARASMUS - Is a disease caused by a deficiency of all food groups which is basically a form of starvation - Is most common in children < 1 yr. of age ASSESSMENT: - Have many of the symptoms as with Kwashiorkor including growth failure, muscle wasting, irritability, IDA and diarrhea. TX: diet rich in all nutrients

VITAMIN DEFICIENCY DISORDERS

Vitamin Vitamin A Cause of deficiency Lack of yellow vegetables in diet Signs and symptoms Tender tongue; cracks and corners of mouth Night blindness Xeropthalmia (dry and lusterless conjunctivae) Keratomalacia (necrosis of the cornea with perforation, loss of ocular fluid, and blindness) Beriberi (tingling and numbness of extremities; heart palpitations; exhaustion)

Vitamin B1

Most common in children who eat polished rice as dietary staple

Vitamin B1

Diarrhea and vomiting Aphonia (cry w/o sounds) Anesthesia of feet Common in children who eat corn as dietary staple Peliagra (dermatitis, resembles a sunburn) Diarrhea Mental confusion (dementia) Scurvy (muscle tenderness; petechiae) Poor muscle tone, delayed tooth formation Rickets (poor bone formation) Craniotabes (softening of the skull Swelling at joints particularly of wrists and cartilage of ribs Bowed legs tetany

Niacin

Vitamin C Vitamin D

Lack of fresh fruits in the diet Lack of sunlight