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Neonatal Hyperbilirubinemia or Neonatal Jaundice is one of the most common problems encountered in term newborns. Although up to 60 percent of term newborns have clinical jaundice in the first week of life. Jaundice is considered pathologic if it presents within the first 24 hours after birth. ABO incompatibility is a reaction of the immune system that occurs if two different and not compatible blood types are mixed together. ABO incompatibility disease afflicts newborns whose mothers are blood type O , and who have a baby with type A, B, or AB. Ordinarily, the antibodies (IgG) against the foreign blood types A and B that circulate in mother's bloodstream remain there, because they are of a type that is too large to pass easily across the placenta into the fetal circulation. Some fetal red cells always leak into mother's circulation across the placental. These fetal red cells stimulate the formation of a smaller type of anti-A or anti-B antibody which can pass into the baby's circulation and there cause the destruction of fetal red cells. The increased rate of destruction of red cells causes a subsequent increase in waste product production. This excess waste product, bilirubin, can overwhelm the normal waste elimination processes and lead to jaundice, the presence of excess bilirubin. On the other hand, sepsis in a newborn is an infection that spreads throughout the babys body. Sepsis occurs in less than 1 percent of newborns (1 out of every 100), but accounts for up to 30 percent of deaths in the first few weeks of life. Infection is 5-10 times more common in premature newborns and in babies weighing less than 5 pounds than in normal-weight, full-term newborns. Complications experienced during birth, such as premature or prolonged rupture of the membranes or infection in the mother, put the newborn at increased risk of infection.

BACKGROUND OF THE STUDY Baby Girl PEDIA is a full term baby from San Roman, Victoria, Northern Samar and delivered via NSD by her mother last October 28, 2011 and was delivered at home and has been admitted at (NICU) last November 1, 2011 because of jaundice and fever, she has been diagnosed by Seizures secondary to hyperbilirubinemia; sepsis neonaturum ; ABO incompatibility. She has undergone intermittent phototherapy at her first day in Neonatal Intensive Care Unit then she was under intensive phototherapy when we last handled and visited her. Her mother blood type was O and her father blood type was A while baby Girl PEDIA blood type was A.

RATIONALE FOR CHOOSING THE CASE This case has been chosen by the group under following reasons:

To better understand Hyperbilirubinemia with ABO incompatibility its nature and appropriate interventions that may contribute to patients recovery. To benefit the student nurses in enhancing their skills in giving care for such patient diagnose with Hyperbilirubinemia with ABO incompatibility. To defy our capabilities in presenting such challenging case. Be able to construct a pathophysiology. Challenge our skills in connecting relevant details of the disease to actual care of client.

SIGNIFICANCE OF THE STUDY To the patient This study hopes to be most beneficial to the patient as the core purpose of this, is to aid in prompt and successful client recovery. To the students & to the Clinical Instructor This study presents various observations and encounters upon handling the client and sustaining for her recovery. Hence, we hope to be of help to our fellow students by sharing first hand experiences about the condition.

SCOPE AND LIMITATION OF THE STUDY This study covers and focuses on the following: A brief discussion of Hyperbilirubinemia with ABO incompatibility, its causes, manifestations and proper treatment. A pathophysiology presented via schematic diagram format of Hyperbilirubinemia with ABO incompatibility. A drug study of medications prescribed to patient. Nursing Care Plans which would present nursing analysis, diagnosis, plan and appropriate interventions that would aid in patients recovery. Discharge plan which presents follow up care and treatment after confinement.


Eclectic Model 1. Bio-demographic Data a. Name b. Age c. Sex d. Diagnosis : Baby Girl PEDIA : : : 4 days old Female Seizures secondary to hyperbiliribinemia

Sepsis Neonaturum ABO Incompatibility e. Address : San Roman, Victoria, Northern Samar : : November 1, 2011 11:35 AM R. C. Ebdane, M.D.

f. Date of Admission g. Time of Admission

h. Attending Physician :

2. Source of Information a. Primary Sources: Mother Father Nurses on Duty

b. Secondary Sources: Patients records and chart

3. Chief Complaint: Onset of fever and jaundice

4. History of the Present Illness: According to her mother, her baby was delivered via normal spontaneous vaginal delivery at home with the help of a manaram or untrained midwife or untrained hilot. At the 1st day of life, mother noticed that her baby has a yellow color. On the 3rd day of life, her baby becomes more yellowish all over her body, has a poor sucking reflex and with high fever.

5. Current Health Status: According to her mother, Baby Girl PEDIA was responsive to the treatment, as she noticed in everyday life; her childs color improves from yellowish to less yellow in color. Phototherapy has a great help and also the antibiotics. a. Body Movement: Baby Girl PEDIA is poorly active and flexes her upper and lower extremities oftentimes. b. Manner of Dressing Baby Girl PEDIA is properly and neatly dressed by her mother. c. Affect and Mood Shes crying at oftentimes.

6. Activities of Daily Living a. Nutrition Baby Girl PEDIA is being breastfed with aspiration precaution through the help of syringes. Baby Girl PEDIA was inside the incubator and was monitored at time to time. b. Elimination She only defecated once or twice daily with soft in consistency and is black in color. c. Hygiene, Grooming and Body Odor She has no foul odor because she usually cleaned every morning and dressed neatly by her mother.

d. Rest and Sleep Baby Girl PEDIA sleeps most of the time. 7. Past Biophysical Health a. Allergies Baby Girl PEDIA has no history of any allergies noted so far. b. Immunization She only received Vitamin K upon admission at the hospital. She has not received Hepatitis B vaccine so far. Shes not yet also undergone newborn screening. c. Foreign Travel No foreign travel so far. d. Family Health History Upon the interview, shes the 3rd child in the family. They are both delivered at home. On the 3rd child only they have a problem like this as stated by her mother. They dont have any familial diseases in their family.

8. Socio Cultural Pattern a. Cultural Pattern Her family believes in herbolarios and superstitions like putting wet silk on the babys forehead when hiccups occur. And they also prefer home deliveries because of financial constraints. b. Economic Pattern Baby Girl PEDIAs father works as a farmer in the coconut farm of their neighbors while her mother is only a housewife. They only received enough income to meet the needs of their family in everyday living. c. Environment They lived in a well-adjusted community in the farm at San Roman, Victoria, Northern Samar.

9. Spiritual

a. Religious Belief and Practice Baby Girl PEDIAs family is a Roman Catholic and goes to church every Sunday. They believed in hilots or herbularios. Physical Assessment General Observation a. General Appearance and behavior Weak in appearance With yellowish discoloration of the skin Skin warm to touch

b. Vital Signs Temperature CR RR = 38.8 C

= 146 bpm = 46 cpm

c. Height and Weight Height (Length) Weight = 48 cm

= 2.7 kg

Complete Physical Examination (Head to Foot/ Cephalo caudal Approach) PHYSICAL ASSESSMENT Baby Girl PEDIA anthropometric measurements are: Length= 48 cm; Head Circumference= 32 cm; Chest Circumference= 34 cm; abdomen circumference= 30 cm; weight= 2.7 kg. She is mostly asleep for long hours and awakes oftentimes during changing of diapers. She is responsive to pain manifested by a slow and weak cry. With ongoing IVF of DW 100 cc + 10 cc D +100 mEq calcium gluconate per soluset regulated at 10gtts/minute; infusing well at her right metatarsal vein of the forearm. No edema noted. Skin is yellowish in color, warm, and dry with poor skin

General Appearance


turgor. No pallor and edema. Hair Has a short, thin, black hair mix well distributed. No presence of flakes, lice or lesions noted. Nails are short and clean. Are pale in color and slightly curved with smooth and uncut edges. No clubbing of fingers noted. Head is normocephalic, no palpable nodules or masses noted. lesions are not noted. Fontanels are open and palapable. Face is soft and caress. (+) Facial grimace when in pain noted. Nicteric sclerae with pupils round and black in color which constricts from 4mm-2mm. Has brisk reaction to light. No cataract noted. Slightly pale conjunctiva noted. Top of pinna is aligned with the outer corners of both eyes; size is normal and equal; similar in color to face; (-) discharges and swelling. Cerumen not noted. Soft and flexible pinna upon palpation. With presence of cilia. Has no discharges nor sinusitis. Nasal cannula attached to both nostrils at 0.5 LPM. Lips are dry with cracking and slightly pale oral mucosa was noted. With no inflammation of tonsils. Distention of jugular vein noted. Breast are firm. No mass palpated. Both arms are weak. Can perform passive movements only. Respiratory rate of 46 breaths/min; shallow breaths in uniform rhythm. Weak cry noted. No cough noted. With supplemental O2 @ 0.5 LPM. No abnormal breath sounds noted. Cardiac pulse taken and recorded at 146 beats per minutes. Bowel movement of twice or thrice a day with blackcolored, soft in consistency and presence of foul smell.


Head Face




Mouth Neck Breast Upper Extremities

Chest Respiratory System

Cardiovascular System Gastrointestinal System

Genito-urinary System

Passes yellow colored urine in minimal amounts.

Musculoskeletal System

Body weaknesses are noted. Hand and foot movements usually are noted.

Laboratory and Diagnostic Examination November 1, 2011 Test Neonatal Bilirubin Result 428.8 UMOL/L Normal Values Up to UMOL/L Indication 17Above normal Significance Due to ABO incompatibility, increase destruction of RBC resulting in increase unconjugated bilirubin Due to ABO incompatibility, increase destruction of RBC resulting in increase unconjugated bilirubin

Unconjugat 278.8 UMOL/L ed bilirubin

Up to UMOL/L

5.1Above normal

Conjugated 149.9 UMOL/L Bilirubin


Test WBC

Result 14.7

Normal Values Indication 5-10 x 10 /L


Above Normal Increase related to compensatory of immune system in response to infection Normal

Hemoglobi n


120-160 grams/L

Hematocrit Neutrophils

0.42 0.77

0.37-0.45 vol % 0.57-0.65

Normal Above Normal Increase

indicate bacterial, parasitic infections may viral,

Lymphocyt es


0.25-0.35 vol %

Below Normal A low normal to

low absolute lymphocyte concentration is associated with increased rates of infection after surgery or trauma.

Alkaline Phosphate SGOT

250.9 u/L 97.11 u/L

Normal Values
180-1,200 u/L Up to 31 u/L

Normal Above Normal


An increase is

an indicator of liver inflammation , can be elevated also in diseases affecting other organs, such as myocardial infarction, acute pancreatitis, acute hemolytic anemia, severe burns, acute renal disease, musculoskelet al diseases, and trauma. SGPT 62.41 u/L Up to 31 u/L Above Normal A test sensitive indicators of liver damage or injury from different types of diseases when it is a higher-than normal values.

Test (Blood Typing) Mother Father Baby Girl PEDIA

Blood type O A A

Rh + + -

November 13, 2011

Repeat Complete Blood Count

Test WBC

Result 9.0

Normal Values 5-10 x 10 /L

Indication Normal


Hemoglobi n




usually indicates the person has anemia. Dangerously low hemoglobin levels put a person at risk of a heart attack, congestive heart failure, or stroke. hematocrit 0.37-0.45 vol Below Normal Decreased indicates iron deficiency % anemianor other deficiencies. Other conditions that can result in a low hematocrit include mineral or vitamin deficiencies, liver cirrhosis, recent bleeding, and malignancies.

120-160 grams/L

Below Normal A low hemoglobin value

Neutrophil s Lymphocyt es


0.57-0.65 vol %



0.25-0.35 vol Above Normal Increase related to the compensatory of immune %

system in infection. response


November 16, 2011 transfusion

Repeat Complete Blood Count 6 hours after Blood

Test Hemoglobi n

Result 174

Normal Values Indication


120-160 grams/L Above Normal A



0.37-0.45 vol %

high hemoglobin value indicates the body may be making too many red blood cells. elevated Above Normal An hematocrit may also be caused by an absolute increase in blood cells, called polycythemia. This may be secondary to a decreased amount of oxygen, called hypoxia, or the result of a proliferation of blood forming cells in the bone marrow (polycythemia vera).

Initial impression and Medical Diagnosis Seizures 20 Hyperbilirubinemia ; Sepsis Neonaturum; ABO Incompatibility Course in the Ward Day 1 November 1, 2011 The shift started at 7am, the chart was checked to gather information about the patient and if there are new doctors order for the patient. Vital signs were taken at 10am. We recorded 36.80C for the temperature and 39cpm for respiration and lastly for the cardiac rate which results to 148bpm. With ongoing IVF of DW 100 cc + 10 cc D +100 mEq calcium gluconate per soluset regulated at 10gtts/minute; infusing well at her right metatarsal vein of the forearm. Physical

assessment was done to the patient. We also reminded the patients mother to feed the baby with milk formula with strict aspiration precaution. She has also undergone intermittent phototherapy. Temperature was taken again at 2pm with body temperature of 38.10C. Because of fever, nursing managements were done such as: TSB, intermittent droplight, wrap extremities with blanket and loose clothing and note for any shaking, chills or profuse sweating and given paracetamol via intravenously. Then, at 2:30pm, the temperature was decreased to 370C. The cardiac rate was maintained at 148bpm and 36cpm for the respiration. At 3pm, we endorsed her to the staff nurses. Day 2 November 2, 2011 The shift started at 7 am, the chart was checked again for any new doctors order. The new order was to place the patient under intensive phototherapy and may have direct breastfeeding. Vital signs were taken at 10 am that showed 37.20C for the temperature, 34cpm for respiration and lastly for the cardiac rate of 140bpm. . With ongoing IVF of DW 100 cc + 10 cc D +100 mEq calcium gluconate per soluset regulated at 10gtts/minute; infusing well at her right metatarsal vein of the forearm.Physical assessment was done again to the patient. Since she was at risk for infection, we monitored her visitors as indicated, practiced standard precaution aseptic technique, observed her for any shaking, chills or profuse diaphoresis and inspected her oral cavity for white plaques. Vital signs were taken again at around 2 pm with the body temperature of 37.30C, 33cpm for respiration and 140bpm for cardiac rate. At 3pm, we referred her accordingly to the staff nurses. Day 3 November 3, 2011 The shift started at 7 am, the chart was checked for progress of the condition of the patient and for new doctors order which indicated direct breastfeeding with aspiration precaution and continue intensive phototherapy. Vital signs were taken at 10 am, temperature was 370C, 40cpm for respiration and lastly, cardiac rate of 139bpm.The ongoing IVF was re-inserted at the right metatarsal vein at the right feet with a fluid of DW 100 cc + 10 cc D +100 mEq calcium gluconate per soluset regulated at 10gtts/minute. We also assessed her for any abnormalities or progress. We inspected her eyes for conjunctivitis, drainage and corneal abrasions due to irritation from eye patches. We also rendered interventions such as covering her eyes with eye patches while under phototherapy lights, removing her from phototherapy during feeding and providing minimal coverage only in the diaper area. We also repositioned the patient every 2 hours. Vital signs were taken again at around 2pm with the body temperature of 36.30C, 35cpm for the respiration and 126bpm for cardiac rate. At 3pm, we refer her accordingly to the staff nurses.


LIVER FUNCTIONS: Metabolism of carbohydrates, protein and fats Production of bile salts Bilirubin metabolism Detoxification of endogenous and exogenous substances eg. Ammonia, steroid and vitamins ADEK Blood reservoir Excretion of adrenal cortex hormone

Phagocytosis by kupffer cells

GALL BLADDER FUNCTIONS: Stores and concentrates the (greenish liquid composed of watr, cholesterol, bile salts, electrolyte and phospholipids) produce by the liver Important in fat emulsification and intestinal absorption of fatty acids, cholesterol and other lipids Bile also acids in excretion of conjugated bilirubin (an end product of hemoglobin degradation) from the liver to prevent jaundice

NORMAL ANATOMY OF BILIRUBIN PRODUCTION AND ELIMINATION Bilirubin is the potentially toxic catabolic product of heme metabolism. Fortunately, there are elaborate physiologic mechanisms for its detoxification and disposition. Understanding these mechanisms is necessary for interpretation of the clinical significance of high serum bilirubin concentrations. Furthermore, because bilirubin shares its metabolic pathway with various other sparingly water soluble substances that are excreted in bile, understanding bilirubin metabolism also provides insight into the mechanisms of transport, detoxification, and elimination of many other organic anions. An overview of the major aspects of bilirubin formation and disposition will be reviewed here. The settings in which bilirubin disposition is impaired will also be discussed briefly. Clinical aspects of serum bilirubin determination, the evaluation of patients with hyperbilirubinemia, and the classification of causes of jaundice are presented separately. FORMATION OF BILIRUBIN Bilirubin is formed by breakdown of heme present in hemoglobin, myoglobin, cytochromes, catalase, peroxidase and tryptophan pyrrolase. Eighty percent of the daily bilirubin production (250 to 400 mg in adults) is derived from hemoglobin [1]; the remaining 20 percent being contributed by other hemoproteins and a rapidly turning-over small pool of free heme. Enhanced bilirubin formation is found in all conditions associated with increased red cell turnover such as intramedullary or intravascular hemolysis (eg, hemolytic, dyserythropoietic, and megaloblastic anemias).

Heme consists of a ring of four pyrroles joined by carbon bridges and a central iron atom (ferroprotoporphyrin IX). Bilirubin is generated by sequential catalytic degradation of heme mediated by two groups of enzymes:

Heme oxygenase Biliverdin reductase



Neonatal physiologic jaundice results from simultaneous occurrence of the following 2 phenomena:

Bilirubin production is elevated because of increased breakdown of fetal erythrocytes. This is the result of the shortened lifespan of fetal erythrocytes and the higher erythrocyte mass in neonates. Hepatic excretory capacity is low both because of low concentrations of the binding protein ligandin in the hepatocytes and because of low activity of glucuronyl transferase, the enzyme responsible for binding bilirubin to glucuronic acid, thus making bilirubin water soluble (conjugation).

Bilirubin is produced in the reticuloendothelial system as the end product of heme catabolism and is formed through oxidation-reduction reactions. Approximately 75% of bilirubin is derived from hemoglobin, but degradation of myoglobin, cytochromes, and catalase also contributes. In the first oxidation step, biliverdin is formed from heme through the action of heme oxygenase, the rate-limiting step in the process, releasing iron and carbon monoxide. The iron is conserved for reuse, whereas carbon monoxide is excreted through the lungs and can be measured in the patient's breath to quantify bilirubin production. Next, water-soluble biliverdin is reduced to bilirubin, which, because of the intramolecular hydrogen bonds, is almost insoluble in water in its most common isomeric form (bilirubin IX Z,Z). Because of its hydrophobic nature, unconjugated bilirubin is transported in the plasma tightly bound to albumin. Binding to other proteins and erythrocytes also occurs, but the physiologic role is probably limited. Binding of bilirubin to albumin increases postnatally with age and is reduced in infants who are ill. The presence of endogenous and exogenous binding competitors, such as certain drugs, also decreases the binding affinity of albumin for bilirubin. A minute fraction of unconjugated bilirubin in serum is not bound to albumin. This free bilirubin is able to cross lipid-containing membranes, including the blood-brain barrier, leading to neurotoxicity. In fetal life, free bilirubin crosses the placenta, apparently by passive diffusion, and excretion of bilirubin from the fetus occurs primarily through the maternal organism. When it reaches the liver, bilirubin is transported into liver cells, where it binds to ligandin. Uptake of bilirubin into hepatocytes increases with increasing ligandin concentrations. Ligandin concentrations are low at birth but rapidly increase over the first few weeks of life. Ligandin concentrations may be increased by the administration of pharmacologic agents such as phenobarbital. Bilirubin is bound to glucuronic acid (conjugated) in the hepatocyte endoplasmic reticulum in a reaction catalyzed by uridine diphosphoglucuronyltransferase (UDPGT). Monoconjugates are formed first and predominate in the newborn. Diconjugates appear to be formed at the cell membrane and may require the presence of the UDPGT tetramer.

Bilirubin conjugation is biologically critical because it transforms a water-insoluble bilirubin molecule into a water-soluble molecule. Water-solubility allows conjugated bilirubin to be excreted into bile. UDPGT activity is low at birth but increases to adult values by age 4-8 weeks. In addition, certain drugs (phenobarbital, dexamethasone, clofibrate) can be administered to increase UDPGT activity. Infants who have Gilbert syndrome or who are compound heterozygotes for the Gilbert promoter and structural mutations of the UDPGT1A1 coding region are at an increased risk of significant hyperbilirubinemia. Interactions between the Gilbert genotype and hemolytic anemias such as glucose-6-phosphatase dehydrogenase (G-6-PD) deficiency, hereditary spherocytosis, or ABO hemolytic disease also appear to increase the risk of severe neonatal jaundice. Further, the observation of jaundice in some infants with hypertrophic pyloric stenosis may also be related to a Gilbert-type variant. Genetic polymorphism for the organic anion transporter protein OATP-2 correlates with a 3-fold increased risk for developing marked neonatal jaundice. Combination of the OATP-2 gene polymorphism with a variant UDPGT1A1 gene further increases this risk to 22-fold. Studies also suggest that polymorphisms in the gene for glutathione-S-transferase (ligandin) may contribute to higher levels of total serum bilirubin. Thus, some interindividual variations in the course and severity of neonatal jaundice may be explained genetically. As the impact of these genetic variants is more fully understood, development of a genetic test panel for risk of severe and/or prolonged neonatal jaundice may become feasible. Once excreted into bile and transferred to the intestines, bilirubin is eventually reduced to colorless tetrapyrroles by microbes in the colon. However, some deconjugation occurs in the proximal small intestine through the action of Bglucuronidases located in the brush border. This unconjugated bilirubin can be reabsorbed into the circulation, increasing the total plasma bilirubin pool. This cycle of uptake, conjugation, excretion, deconjugation, and reabsorption is termed 'enterohepatic circulation'. The process may be extensive in the neonate, partly because nutrient intake is limited in the first days of life, prolonging the intestinal transit time. In mother-infant dyads who are experiencing difficulties with the establishment of breast feeding, inadequate fluid and nutrient intake often leads to significant postnatal weight loss in the infant. Such infants have an increased risk of developing jaundice through increased enterohepatic circulation, as described above. This phenomenon is often referred to as breastfeeding jaundice and is different from the breast milk jaundice described below. Certain factors present in the breast milk of some mothers may also contribute to increased enterohepatic circulation of bilirubin (breast milk jaundice). glucuronidase may play a role by uncoupling bilirubin from its binding to glucuronic acid, thus making it available for reabsorption. Data suggest that the risk of breast milk jaundice is significantly increased in infants who have genetic polymorphisms in the coding sequences of the UDPGT1A1 or OATP2 genes. Although the mechanism that causes this phenomenon is not yet agreed on, evidence suggests

that supplementation with certain breast milk substitutes may reduce the degree of breast milk jaundice (see Other therapies). Neonatal jaundice, although a normal transitional phenomenon in most infants, can occasionally become more pronounced. Blood group incompatibilities (eg, Rh, ABO) may increase bilirubin production through increased hemolysis. Historically, Rh isoimmunization was an important cause of severe jaundice, often resulting in the development of kernicterus. Although this condition has become relatively rare in industrialized countries following the use of Rh prophylaxis in Rh-negative women, Rh isoimmunization remains common in developing countries. Nonimmune hemolytic disorders (spherocytosis, G-6-PD deficiency) may also cause increased jaundice, and increased hemolysis appears to have been present in some of the infants reported to have developed kernicterus in the United States in the past 10-15 years. The possible interaction between such conditions and genetic variants of the Gilbert and UDPGT1A1 genes, as well as genetic variants of several other proteins and enzymes involved in bilirubin metabolism, is discussed above. These discoveries also highlight the challenges involved in the common use of the terms physiologic jaundice and pathologic jaundice. Although physiologic jaundice is a helpful concept from a didactic perspective, applying it to an actual neonate with jaundice is more difficult. Consider the following metaphor: Think of total serum bilirubin in neonatal jaundice as a mountain covered by a glacier. If a measurement of the height of the mountain is taken when standing on the summit, the amount of rock and the amount of ice that comprise this measurement is unclear. The same is true for many total serum bilirubin values obtained in neonatal jaundice. An underpinning of physiologic processes and pathological process (eg, Rhesus incompatibility) may clearly contribute to the measurement. However, how much of the measured total value comes from each of these components is unclear. Also, because genetic variants in bilirubin metabolism are only exceptionally pursued in the diagnostic work-up of infants with jaundice, their possible contribution to the measured total serum bilirubin is usually unknown.

Drug Study

Nursing Responsibiliti es Generic Amino Bactericidal: Neonatal Contraindicate -confusion Assess patient name: glycosides Inhibits sepsis when d with -depression for allergic Amikac protein other glycosides -lethargy reaction: rash, in synthesis in antibodies renal or urticaria, sulfate susceptible cannot be hepatic nysthagmus pruritus and strains of used (often disease, pre- -headache hypotension DOSAG gramused in existing -fever -Obtain E: 45 negative combination hearing loss, -tremor specimen for mg bacteria and with myasthenia, -muscle culture and IVTT the penicillin gravis twitching sensitivity OD functional type drug.) parkinsonism, -seizures before initiating integrity of infant -muscular therapy. First bacterial cell botulism, weakness dose may be membrane lactation. -nausea given before appears to -vomiting receiving be -anorexia results. disrupted, -diarrhea -Monitor intake causing cell -weight loss and output and death. -increased daily weight to salivation assess hydration status and renal function. -Assess patient

Drug name

Classificati Mechanism Indication Contraindica on of action tion

Adverse effects

for sign of super infection (fever, upper respiratory infection.)

Drug Classificati Mechanism Indicatio Contraindicati name on of action n on Generic name:

Nursing Responsibiliti es AntiBactericidal Treatment Contraindicated Hypersensitivit Assess for infectives action of awith allergies to y: rash, fever, infection (Vital

Adverse effects

Ampicill in DOSAGE : 200 mg IVTT every 12

against variety ofpenicillins, wheezing, and sensitive infections cephalosporins anaphylaxis. organisms; including or other inhibits those ofallergens synthesis of the bacterial cell urinary, wall easing respiratory cell death. , biliary and intestinal tracts.

signs, urine, stool and WBC) at the beginning and throughout the therapy. -Obtain a history before initiating therapy to determine previous use reaction to penicillin or cephalosporins. -Obtain specimens for culture and sensitivity before therapy. First dose may be given before receiving results. -Observe patient for signs and symptoms of anaphylaxia (rash, pruritus, wheezing). Discontinue the drug and notify the physician or other health care. -Assess skin for ampiciilin rash a non allergic dull red. -Report pain/ discomfort at

site unusual bleeding/ bruishing, mouth sores, difficultyof breathing.

Classificat Mechanis Indicatio Contraindicat Adverse ion m of n ion effects action Antiepileptic; Acts mainly*Muscle Generic Contraindicate *Drowsiness Anxiolytic at the name: relaxant: d with*Dizziness Diazepam limbic Adjunct hypersensitivit Skeletal system andfor reliefy to*GI upset muscle relaxant DOSAGE: reticular of reflexbenzodiazepine *bradychardia (centrally formation; skeletal 0.6 cc prn s; psychoses, acting) for mat act in muscle acute narrowseizures spinal cord spasm dueangle to produce to localglaucoma, skeletal pathology shock, coma, muscle or acute alcoholic relaxation; secondary intoxication. potentiatesto trauma; Use cautiously the effects spasticity with elderly or of GABA, caused by debilitated an upper patients; inhibitory motoneur impaired liver neurotrans on or renal mitter. disorders function; and in *Parenter patients with al: history of Treatmen substance t ofabuse. tetanus

Drug name

Nursing Responsibilitie s 1. Monitor heart rate before giving drug. 2. Closely monitor cardiac rate.

Classificati Mechanis Indicatio Contraindicat Adverse Nursing on m of n ion effects Responsibilitie action s Paracetamol is-Nausea, allergic-do not exceed Analgesics The main Generic -for fever (Non-Opioid) mechanism contraindicated inreactions, skinrecommended name: -for painhypersensitivity, rashes, acutedose Paracetam Antipyretics proposed is analgesic relief the renal tubular-avoid using ol nephropathy, inhibition of necrosis. multiple renal and hepatic cyclooxyge DOSAGE: preparations impairment. nase (COX), -Fatal: Very rare, 0.3 ml and recent blood dyscrasiascontaining every 4 acetamenophen. findings (e.g. hours RTC suggest thrombocytopeni -discontinue that it is a, leucopenia,drug if highly neutropenia, hypersensitivity selective agranulocytosis); occurs. for COX-2. liver damage. -report rush, While it has abnormal analgesic bruising or and bleeding, antipyretic yellowish of skin properties and eyes, comparable changes in to those of voiding patterns. aspirin or
other NSAIDs, its peripheral antiinflammator y activity is usually limited by several factors, one of which is high level of peroxides present in inflammator y lesions.

Drug name

Drug name Generic name: Ascorbic Acid

Classificati Mechanis Indicatio Contraindicat on m of n ion action

Adverse effects

Nursing Responsibilitie s

Fat-Soluble An Vitamin CContraindicated Transient mild-Diabetics, Vitamins exogenous is in those personssoreness maypatients prone to source of recommen who have shownoccur at the siterecurrent renal Ascorbic Acid ascorbic acid ded for thehypersensitivity of intramuscularcalculi, those (vitamin c) is prevention to anyor subcutaneousundergoing stool required for and component ofinjection. Too-occult blood tests, collagen DOSAGE: treatment this preparation. rapid intravenousand those on formation 0.6 ml OD of scurvy. administration ofsodium-restricted and tissue p.o. Its the solution maydiets or repair. It is parenteral cause temporaryanticoagulant reversibly oxidized to administrat faintness ortherapy should not dehydroasco ion is dizziness. take excessive rbic acid in desirable doses of vitamin C the body. for patients over an extended These two with an period of time. forms of the acute -Caution should be vitamin are deficiency exercised when believed to or Ascorbic Acid be important for those whose (vitamin c) in oxidationabsorption Injection is reduction reactions. of orally administered to a The vitamin ingested nursing woman. is involved in ascorbic tyrosine acid metabolism, (vitamin c) conversion of is uncertain folic acid to
folinic acid, carbohydrate metabolism, synthesis of lipids and proteins, iron metabolism, resistance to infections, and cellular respiration.

IV. Nursing Care Plan

Assessme nt Physiologic al Excess: Fever Subjective: Ma-init siya oraora, hataas gud eya kalintura as verbalized by the mother.

Diagnosis Planning

Intervention Rationale


Alteration in After 8 hours To lower body After 8 hours thermoregul of temperature to of nursing ation: nursing normal range. interventions, Hyperthermi interventions, (1)Monitor (1) to evaluate the a the patient patients degree of patient was related to will temperature hyperthermia able to direct effect maintain core (2)Monitor (2) Room temp or maintain of temperature environmental no. of blanket core circulating within normal temp. limit bed should be altered to temperature endotoxin range (370C ). linens as maintain nearwithin normal on the indicated normal body temp. range from hypothalam (3)Perform (3)May help reduce 38.10C to us altering TSB, avoid use fever, alcohol may 370C. temperature of alcohol cause chills, actually Objective: regulation (4)Apply towel elevating temp., Temp as to provide alcohol is very 0 38.1 C evidenced cooling effect drying to skin Warm to by increase (5) Maintain (4)used to reduce touch. in body bed rest, assist fever. Heat loss by Weak & temp. with care conduction pale in higher than activity 5.) maximizes appearance normal effectiveness of persistent range tissue perfusion and crying energy/oxygen With (6) Promote conservation slightly dry surface cooling lips by means of (6)heat loss by flushed undressing evaporation skin; yellowish pigmentatio n noted

Assessme Diagnosis Planning nt Physiologic Ineffective infant al Deficit

Intervention Rationale


After series of To fed the infant enough nursing feeding interventions, breast milk for her daily pattern the patient Subjective: calories. related to will be able to talagsa la limited take enough (1) provide the consumption mother sya na of breast milk breast milk to parafernalias mimi, tas as evidenced fed her daily to access calories. parang by the breastfeeding. mother is maluya na (2) breastfed unable to sya para the infant per provide magmimi adequate demand as breast milk to (3) practice verbalized her baby aspiration continuously. by the precaution; emphasized mother. proper positioning Objective: poor sucking reflex body weakness noted has a poor , swallow and weak cry (4) emphasized hygiene

After series of nursing interventions, the patient (1)Parafernalias was able to such as sterile cup take enough and syriniges and also breast pump if breast milk to nescesary. fed her daily (2) fed the infant as calories. per demand not to disturb her during rest periods. (3) to avoid the infant from further injury

(5) monitor hydration (5) to assess status and watch for any abruptly and complications manage further management

(4) to prevent infection and further complications

mother was unable to provide adequate breast milk to her infant

Assessme Diagnosis Planning nt Health Threat Subjective: ug tingale ma-raot ea mata sa photothera py as verbalized by the mother. Objective: patient is in intensive photo therapy With single photo

Intervention Rationale

Evaluation After series of nursing Interventions Neonate was free from injury. As evidenced by infants eyes are free from corneal irritation and skin breakdown.

After series of To reduce and Risk for corneal nursing prevent irritation interventions, corneal and skin the patients irritation. breakdown risk of related to (1)Protects retina acquiring (1) Maintained from prolonged corneal used of and monitored damage due to high phototherap irritation/skin babys eye intensity light. breakdown y patches while will be under reduced. phototherapy. (2) Provides visual stimulation and (2) Remove facilitates baby attachment from under behaviors. phototherapy and remove eye patches during feeding. (3) to reduce (3) Inspect complications and eyes every monitor the effectiveness of the after management phototherapy

therapy Frequent removal of the eye patches Skin appearing light to bright yellow. Sclera appearing yellow. With diaper on

for conjunctivitis, drainage and corneal abrasions due to irritation from eye patches. (4) Provide minimal coverage of the body except for genitals.

(4) Provides maximal exposure and shielded the sensitive parts such as the eyes and genitals.

(5) to promote equal distribution of phototherapy (5) Reposition exposure. baby every 2hours.

V. DISCHARGE PLAN Medications: Encouraged SO to comply with medications to prevent further complications.

Environment: Encouraged SO to keep environment clean to avoid infection. Encouraged SO to keep environment quiet to make the patient comfortable.

Treatment: Emphasized SO the importance of regular follow-up check-ups and as instructed by physician. Advised SO to seek medical advice if any unusuality arises.

Health Teachings: Advised SO to expose the patient to sunlight around 6:00am-8:00am.


Emphasized to SO the importance of proper handwashing. Encouraged SO for proper hygiene of the patient.

Encouraged the mother for breast feeding.

Spirituality: Encouraged SO and Family members to go to church every Sunday. Encouraged SO to continue to seek Gods guidance and enlightenment. Emphasized SO the importance of prayers in healing. Encouraged SO to continue to have a positive outlook in life.

EVALUATION The nursing procedure was rendered to the patient accordingly. Application of these procedures was done independently by our group the knowledge, skills and attitudes of providing care for the patient.

SUMMARY Our case study is all about Hyperbilirubinemia with ABO incompatibility. Hyperbilirubinemia also known as neonatal jaundice is a yellow discoloration of the skin of a baby due to high unconjugated bilirubin because of breakdown of RBC and immaturity of the liver, while ABO incompatibility occurs when mother blood was O, and her baby blood type was A, B, or AB. Our patient Baby Girl PEDIA was diagnosed from Seizure secondary to Hyperbilirubinemia; ABO incompatibility and sepsis neonatorum because she experienced fever and her skin became yellowish in color after 24 hours after delivery which is a physiologic sign of jaundice, so she was admitted to (NICU). The doctor ordered complete blood count and bilirubin test. The laboratory result confirms her diagnosis Hyperbilirubinemia because of high neonatal bilirubin and high unconjugated bilirubin, also theres high WBC and lymphocytes in her CBC thats why she experienced fever. Our patient was also diagnosed from ABO incompatibility because her father was blood type A and her mother was blood type O while baby girl PEDIA was blood type A. During our we rendered quality nursing care for our patient to aid quick and successful patient recovery.

CONCLUSION Therefore, we conclude that ABO Incompatibility afflicts newborns whose mothers are blood type O can lead to destruction of RBCs. The increased rate of destruction of RBCs causes a subsequent increase in bilirubin that can overwhelm the normal waste product elimination processes and lead to jaundice. This type of condition of our patient requires phototherapy as its treatment. As nurses, we maintained the core temperature of our patient within normal range since she had a hyperthermia, practiced aseptic technique since she was at risk for infection and protected her from any injury. We seen her at intervals and attended her needs. At the end of our shifts, we met our goals in providing her safety and comfort. Weve also rendered some health teachings to her family and provided them support. At the last day in the ward, still, she has jaundice but has normal vital signs.

RECOMMENDATION To the students: Study their lessons first before going to the area. Bring complete parafernalias. Always follow the hospital rules. Be responsible enough as a nurse. Give quality nursing care to the patient.

To the patient: Encourage SO of the patient for regular check up. Emphasize SO for the proper hygiene of the patient. Encourage mother for breast feeding and instruct its importance. Instruct SO to take regular medication of the patient prescribed by the physician.