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U P - P H I L I P P I N E G E N E R A L H O S P I TA L

DEPARTMENT O F EM ERG ENCY M E D I CI NE

A Case Study of

I D I OPAT HI C T HR O M B O CY TO P EN I C P U RP U RA

GRO UP IV Perez, Erich Lou S. Pl acido, Geraline D. R a p a con, John Jeremiah B.


APCN Batch 31

N ovember 22, 2011

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TA B L E O F C O N T E N T S
CONTENT
I. Clinical History

PAGE
3

II.Functional Health Patterns

III.Course in the Hospital

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IV.Diagnostics

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V.Therapeutics

22

VI.Anatomy & Physiology

27

VII.Idiopathic Thrombocytopenic Purpura (Overview)

33

VIII.Pathophysiology

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IX.Discharge Plan

40

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CLINICAL HISTORY

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CLINICAL HISTORY

D E MO G R APHI C DATA Name: Sean Address: Libra St. Greenville, Bagbaguin, Caloocan City Sex: Male Birthdate: April 13, 2010 Age: 1 year and 6 months Birthplace: Valenzuela City Nationality: Filipino Religion: Roman Catholic Attending Physician: Dr. Maao / Dr. Capul Provisional Diagnosis: Idiopathic Thrombocytopenic Purpura

Mothers Name: Mary Grace Fathers Name: Richard Siblings: 1 Brother (4 years old)

G E N E R A L DATA Our patient is Sean, 1 year old and 6 months male patient residing at Valenzuela City. He was admitted last October 25, 2011, 5:18PM at UP-Philippine General Hospital Pediatric Emergency Room. Informant: Mother of Sean Reliability: Good reliability Chief Complaint: Subjective Data: As verbalized by patients mother: Dinala namin siya dito dahil sa mga pasa pasa niya sa ulo, hita, puwet, tiyan at braso. Di namin alam bat bigla siyang nagkaroon ng mga pasa. Di naman siya nababangga.

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Objective Data: Hematoma on forehead, buccal cavity, abdominal area, upper and lower extremities and right ank area.

HISTORY OF PRESENT ILLNESS On October 10, 2011, the mother noticed a hematoma at patients right ank area, violet blue in color and about the size of a 25 cent coin. The following day, October 11, 2011, new hematomas were noted at patients right and left temporal area and left lower quadrant of abdomen, all violet blue in color, and almost the size of a 25 cent coin each. Pinpoint red petechiae marks were also noted at clients forehead. When the mother checked patients mouth, she also noticed a reddish pink mark on the hard palate area, about the size of a 1 peso coin. On October 12, 2011, the mother decided to bring her child to Valenzuela Medical Center OPD wherein she was given requests for laboratory work-ups. The following day, Oct. 13, 2011, blood was extracted for the laboratory work-ups (CBC with platelet count, and Urinalysis, and Blood Chemistry). Results of the laboratory were released on Oct.14, 2011, wherein clients most signicant reading was his platelet count of 78. The physician advised the mother to have a repeat test of her sons platelet count for verication. No denitive diagnosis was given by the physician and the patient was only prescribed Vitamin C syrup. The same day, Oct. 14, patients mother decided to go to Bewell Clinic Laboratory wherein her sons repeat platelet count was made. Result was released the same day and patients platelet count was 229. The mother did not bring her son back to Valenzuela Medical Center OPD. For one week, patients mother opted to observe her son for appearance of hematoma. Vitamin C syrup (Ceelin) was given once a day. New hematomas were formed on clients both lower extremities, cheeks, and right ank area. This prompted her to bring her son back to Bewell Clinic Laboratory for CBC with platelet count. Results were released the same day and patients platelet count was 202. No consultation was made. Patient was observed for 4 days. Hematoma remained and persisted on said body areas.

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On Oct. 25, 2011, patient was brought to CTK Medical and Diagnostic Laboratory wherein CBC with platelet count was done. Platelet count was 55 and patients mother was advised by the physician to have her son admitted at UP-PGH the same day hence admission.

REVIEW OF SYSTEMS (+) hematoma on right and left temporal area, hard palate, abdominal area, upper and lower extremities, right ank area (+) cough and colds since Oct. 24, 2011 (-) fever (- ) overt bleeding (-) cardiorespiratory distress (-) discharges

PAST MEDICAL HISTORY December 2010: Patient was admitted at Valenzuela Medical Center for acute gastroenteritis (Amoebiasis). Prior to admission, patient vomited excessive amounts of water; (-) blood. Patient stayed at the hospital for one day only. No aggressive treatment was given and was eventually discharged the next day. Past illnesses: cough and colds which usually last for 1 week. Previous Surgery: None Allergy/Others: None

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FAMILY MEDICAL HISTORY Mother Side: (+) Hypertension, (+) Rheumatoid Arthritis Father Side: (+) Hypertension (+) Heart Disease Patient has one sibling (4 year old brother) who occasionally experiences coughs and colds. Previous hospitalization was also last December 2010 due to Acute Gastroenteritis (Amoebiasis). Hospitalization was only one day and he was discharged the following day.

BIRTH HISTORY Patient is the second child of her parents. Her mother gave birth to her through Normal Spontaneous Delivery at Valenzuela Medical Center.

IMMUNIZATION HISTORY (+) BCG at birth (+) DPT x 3 Doses: No adverse reactions such as convulsions (+) OPV x 3 Doses (+) Hepa B Vaccine x 3 doses (+) Measles Vaccine x 1 dose

*Complete Immunization

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NUTRITIONAL HISTORY 0-6 Months: Patient was exclusively breastfed since birth up to 6 months of age. 6 Months Age: Cerelac was gradually added to patients food along with fruits such as bananas. Breastfeeding was continued. 1 Year-Old - Present: Bottlefeeding of Enfagrow Milk was given alternately with breastmilk; rice and porridge were also added to patients meal along with fruits.

GROWTH AND DEVELOPMENTAL MILESTONES HISTORY Current Weight: 9 kilogram (Ideal Wt: 9-13kg) Current Height: 88 centimeters (0.88 meter) (Ideal Ht: 80-90cm.) BMI: 11.62 (Ideal BMI for 12mos-24mos.: 11-20) *Patients weight is within the expected weight of an 18 month old child. His height is also within the expected length of an 18 month old child. BMI of patient is within the ideal range.

Growth & Developmental Milestones : Informant: Mother of Sean 4 months: started to lie on his stomach 6 monhts: started to sit up with support 8 months: started to crawl 9 months: rst word Ma was uttered by patient 1 year old: rst walk with assistance 18 months (Present): walks without assistance; can utter 2-3 words; has 12 teeth (6 teeth above and 6 teeth below)

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F U N C T I O NA L H E A LT H PAT T E R N S

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GORDONS FUNCTIONAL H E A LT H PAT T E R N S


*Informant: Mother of Sean HEALTH PERCEPTION AND MANAGEMENT Patient has good appetite as evidenced by his per demand breastfeeding and bottlefeeding along with supplemental foods such as fruits, Cerelac, and porridge. Even with the appearance of hematomas, patients appetite did not change.

NUTRITIONAL & METABOLIC PATTERN Patient has a steady weight and height gain since birth according to mother. His current weight (9 kg) and height (88cm) are within the expected ranges. He only has occasional problems with feeding when he experiences cough and colds. However, this does not gravely affect the clients nutritional status. He currently has 12 teeth (6 teeth above and 6 teeth below). Her mother brushes her teeth every night but doesnt use toothpaste.

ELIMINATION Patient moves his bowels everyday with yellow fecaloid output. He is not yet toilet trained. He voids light yellow urine. He still wears diapers and points it out to her mother once he feels that it is already soaked.

ACTIVITY Patient plays with his car toys and usually plays with his big brother. He also likes playing with children of his same age. When with other children of his age, he exhibits parallel play wherein they play the same toys but doesnt really interact. This is consistent with his age. He also likes scribbling at papers and is also curious with laptops and computers. He has no problems with mobility.
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SLEEP & REST Patient sleeps well and is most of the time rested. His usual sleeping time is from 11PM-9AM, 1PM-3PM, and 6PM-8PM with occasional interruptions. During hospitalization, patient had some problems with sleep due to medical and nursing procedures and his possible unfamiliarity with the environment in the emergency room.

COGNITIVE-PERCEPTUAL Client able to understand and follow symbolic gestures made by his primary caregivers and people around him. Patient can follow simple commands such as getting things pointed out by his parents. He is also able to retain informations. Patients ve senses are intact. *The client is under the Pre-operational Phase of Piagets Cognitive Theory. The child develops the ability to express self with language, understands the meaning of symbolic gestures and begins to classify objects.

SELF-PERCEPTION / SELF-CONCEPT Objective Data: The client is often shy when strangers come near him. However, when nurses approach him, he often cries and clings to his mother. He also has good eye contact with his parents and to us when we were playing with him. Separation anxiety wasnt evident.

ROLE & RELATIONSHIP The patient is more clingy and dependent to his mother because she is the primary caregiver of the child at the house. He is also close to his father especially when his father comes from work. Patient plays with his brother everyday.

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SEXUALITY We cannot completely ascertain this aspect as the client is just 18 months.

COPING & STRESS TOLERANCE When patient is sick, he usually is irritable, cannot focus and cries a lot. He also has problems with sleep pattern due to frequent sleep problems such as having insomnia and frequent awakenings during sleep.

VALUE & BELIEF PATTERN Patient is brought to church by his parents everyday and he usually touches Christ images inside the church. It is uncertain however if he has a vivid or clear idea of God. According to Fowlers Spiritual Theory, he is in the Intuitive-Projective Phase wherein children just imitates acts of older people such as the sign of cross and gestures such as praying.

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COURSE IN THE H O S P I TA L

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C O U R S E I N T H E H O S P I TA L
MEDICAL MANAGEMENT October 25, 2011 10PM -Admitted under PER -VS q2 -I & O q1 -Diagnostics were ordered (CBC with platelet, Blood Chemistry, Blood Typing, Urinalysis) -DAT with SAP -IVF: Heplock -Refer to Hema-Onco service October 26, 2011 Hematology-Oncology 11:30AM -Facilitate BT of 2 units Platelet Concentrate as fast drip Q6 x 3 doses -May give Tranexamic Acid PM Rounds -post BT CBC after 6 units PC (3rd dose) -Start Tranexamic acid 80 mg/pptab TID -DAT with SAP except dark colored foods -For BT of 2 more doses of PC as ordered -VS q 2h October 27, 2011 Hematology-Oncology -for post BT CBC -continue Tranexamic Acid -Start Prednisone 10 mg/5ml 4ml BID -VS Q2 4PM -Hold Prednisone -For possible IV IG -For Ward 9 Transfer 10pm-6am -Noted S/P 2 unis PC -checked IV line with PNSS infusing well -hooked 2 units Platelet Concentrate A positive -(-) BT reactions 6am-2pm -VS as follows: RR: 50, HR: 123, BP: 90/60mmHg, Temp: 37.1C -noted (+) RIV of 6 units platelet concentrate 2-10pm -admitted at PER Bed 9 -admitting VS as follows: RR: 37, HR: 126, BP:90/60mmHg, Temp: 37.0C -Heplock inserted at right metacarpal vein -advised on prescribed diet -(-) fever -(-) cardiorespiratory distress -hematoma noted at forehead, upper and lower extremities & abdominal area NURSING MANAGEMENT

2pm-10pm -pale looking -hooked to PNSS 500cc x KVO -hooked 2 units Platelet Concentrate as fast drip A positive -(-) BT reactions

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MEDICAL MANAGEMENT

NURSING MANAGEMENT 6am-2pm -(+) hematoma and rashes all over body -hooked to 2 units Platelet Concentrate -VS as follows: PR=137 cpm, RR=33 bpm, Temp= 36.2 degrees Celsius -(-) BT reactions 2pm-10pm -noted S/P 6 units Platelet Concentrate -IV line shifted to heplock -monitored accordingly

October 28, 2011 Hema-Onco -for possible another BT of platelet concentrate -for Bone Marrow Aspiration on OPD basis -still for IV IG -MGH for now -OPD follow up on Nov.4, 2011 at Cancer Institute -for repeat CBC on follow up -Home Medication: Tranexamic Acid 80mg pptab TID 10pm-6am -with verbal order by Dr. Advincula to transfuse 2 units platelet concentrate -hooked to 2 units Platelet Concentrate -(-) BT reactions 6am-2pm -still pale; hematomas noted all over body -maintained heplock -S/P 8 units Platelet Concentrate -monitored accordingly 3pm -discharged as ordered -instructed on home medication and OPD follow up

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DIAGNOSTICS

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DIAGNOSTICS
HEMATOLOGY
BLOOD TYPE:

APOSITIVE
RESULTS 10/13/11 Valenzuela Medical Center 10/14/11 Bewell Clinical Laboratory 10/20/11 10/25/11 10/26/11 PGH 10/27/11 PGH

REFERENCE VALUES

Bewell CTK Medical Clinical & Diagnostic Laboratory Laboratory

RBC 4 6 x 1012/l

4.74 x 1012/l

4.28 x 1012/l

4.07 x 1012/l

3.8 x 1012/l

4.27 x 1012/l

4.13 x 1012/l

Hemoglobin 120 g/l M: 149-170 g/l F: 120-150 g/l Hematocrit 0.346 / l M: 0.42-0.51 /l F: 0.37-0.47 /l Platelet 150450 x109 /l 78 x 109 / l 229 x 109 / l 202 x 109 / l 55 x 109 / l 4 x 109 / l 252 x 109 / l 0.40 / l 0.38 / l 0.35 / l 0.32 / l 0.36 / l 136 g/l 129 g/l 116 g/l 105 g/l 119 g/l

MCV 80 -100 fL MCH 27.0 31 pg MCHC 320360 g/L

73.0 fL

N/A

N/A

N/A

74.2 fL

74.6 fL

25.3 pg

N/A

N/A

N/A

24.5 pg

25.1 pg

347

N/A

N/A

N/A

330 g/l

338 g/l

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RESULTS
REFERENCE VALUES

10/13/11 Valenzuela Medical Center

10/14/11 Bewell Clinical Laboratory

10/20/11 Bewell Clinical Laboratory

10/25/11 CTK Medical & Diagnostic Laboratory

10/26/11 PGH

10/27/11 PGH

White Blood Cell 510 x 109/l Neutrophil

11.0 x 109 / l

9.39 x 109 / l

5.8 x 109 / l

6.03 x 109 / l

17.30 x 109 / l

14.20 x 109 / l

0.63 0.45 0.65 Lymphocyte 0.20 0.50 Monocyte 0.02 0.09 Eosinophils 0.01 0.04 0.01 0.06

0.57

0.60

0.35

0.45

0.52

0.30

0.40

0.40

0.61

0.43

0.44

0.02

N/A

0.01

0.08

0.07

0.01

N/A

0.03

0.03

0.02

Note: CBC Result Analysis on next page PT/PTT


REFERENCE VALUES 10/13/2011 Valuenzuela Medical Center 12.6 secs. 0.87 25.5 secs. 10/26/2011 PGH 12 secs 0.84 30.6 secs.

Prothrombin Time 11-16 secs. INR 0.8-1.2 Partial Thromboplastin Time 24-36 secs.
*

Within normal range.


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CBC RESULT ANALYSIS


BLOOD COMPONENT INTERPRETATION/ANALYSIS

Hemoglobin

Clients low hemoglobin concentration may indicate the presence of an anemia or a recent hemorrhage.

Hematocrit

Low hematocrit suggests anemia, hemodilution, or massive blood loss. This is consistent with clients hemoglobin level.

Platelet

Patient had dangerously low platelet levels during admission. This is due to his present condition (ITP) which caused her platelet count to drop. Platelet levels only improved and were within reference range after transfusion of 6 units of platelet concentrate.

Mean Corpuscular Volume

MCV is a measure of the average red blood cell volume. Clients decreased MCV suggests that he might be suffering from microcytic anemia wherein his RBCs are smaller than the normal size of an RBC

Mean Corpuscular Hemoglobin

MCH is the average mass of hemoglobin per red blood cell in a sample of blood. Clients low level may indicate that he is suffering from hypochromic anemia wherein RBCs are paler than normal.

WBC

During hospitalization, clients WBC count was higher than normal. This may indicate the presence of an active infection. However, there were no medications ordered by doctors for the high WBC count.

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BLOOD CHEMISTRY
RESULT 10/26/11 PGH 77.64 11.80 0.31 0.00 0.00 1138 10.76 0.00 2.43 143 3.70 105

SERUM Glucose BUN Creatinine Uric Acid Alkaline Phosphatase LDH Calcium Phosphorus Magnesium Sodium Potassium Chloride

NORMAL VALUES 70 123 mg/dl 5 22 mg/dl 0.31 0.80 mg/dl 4.8 8.7 mg/dl 32 91 IU/L 140 304 IU/L 9 10.9 mg/dl 2.5 4.6 mg/dl 1.8 2.4 mg/dl 131 145 mmol/L 3.9 6.8 mmol/L 99.0 118.0 mmol/L

ANALYSIS
LDH - Lactate Dehyrogenase is often used as a marker of tissue breakdown as LDH is

abundant in RBC and can function as a marker for hemolysis. A blood sample that has been handled incorrectly can show false-positively high levels of LDH due to erythrocyte damage. It is possible that the clients blood sample was handled incorrectly hence the possible false high result. Potassium: A potassium reading of 3.7mmol/L is still considered within normal range according to some references.
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URINALYSIS
RESULTS 10/13/11 10/26/11 MICROSCOPIC Valenzuela Medical PGH Center Color Transparency Glucose Albumin Specic Gravity pH WBC RBC Amorphous Urate Epithelial Cells Bacteria Mucus Thread Yellow Slightly Cloudy Negative Negative 1.015 6.0 0-3 0-3 0 0 0 Some Yellow Slightly Cloudy Negative 10mg/dl (Trace) 1.028 5.5 2 2 0 0 0 Some

REFERENCE VALUES Straw/Amber Clear <50mg/dl (Trace) <10mg/dl (Trace) 1.005 1.030 4.6 8 0 5/hpf 0 5/hpf Rare Rare Rare Rare

*Urine Analysis results are all normal. There is no signicant nding related to clients case.

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THERAPEUTICS

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THERAPEUTICS
TRANEXAMIC ACID
Dose: 80 mg/pptab i pptab TID Date Ordered: October 26, 2011 Indication: This medication is used short-term in people with a certain type of bleeding disorder (e.g. Hemophilia) to prevent and reduce bleeding from having a tooth pulled (extraction). It is also used in people with other high-risk bleeding conditions to control bleeding at such times as after surgery or an injury, during heavy nosebleeds, or during heavy menstrual bleeding. Tranexamic acid works by helping the blood clot normally to prevent and stop prolonged bleeding. It belongs to a class of drugs known as anti-brinolytics wherein it acts by blocking the binding sites of plasminogen, thereby inhibiting the conversion of plasminogen into plasmin by tissue plasminogen activator. The end result is a decreased lysis of brin clots Effect on our patient: Our client did not experience any overt bleeding episodes. The clients bruising and petechiae did not also worsen. Nursing Considerations:

1. Unusual change in bleeding pattern should be immediately reported to the physician. 2. Tranexamic Acid should be used with extreme caution in CHILDREN younger than 18
years old; safety and effectiveness in these children have not been conrmed.

3. The medication can be taken with or without meals. 4. Swallow Tranexamic Acid whole with plenty of liquids. Do not break, crush, or chew
before swallowing.

5. If you miss a dose of Tranexamic Acid, take it when you remember, then take your next
dose at least 6 hours later. Do not take 2 doses at once.

6. Inform the client that he/she should inform the physician immediately if the following
severe side effects occur: Severe allergic reactions such as rash, hives, itching, dyspnea, tightness in the chest, swelling of the mouth, face, lips or tongue Calf pain, swelling or tenderness

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Chest pain Confusion Coughing up blood Decreased urination Severe or persistent headache Severe or persistent body malaise Shortness of breath Slurred speech Vision changes

PREDNISONE
Dose: 10mg/5ml 4ml BID Date Ordered: October 27, 2011 (Morning) Date Discontinued: October 27, 2011 (Afternoon: 4PM) Indication: Prednisone is a synthetic corticosteroid drug that is particularly effective as an immunosuppressant drug. It is used to treat certain inammatory diseases and (at higher doses) some types of cancer, but has signicant adverse effects. Because it suppresses the immune system, it leaves patients more susceptible to infections. It is usually taken orally but can be delivered by intramuscular injection or intravenous injection. It has mainly a glucocorticoid effect. Prednisone is a prodrug that is converted by the liver into prednisolone, which is the active drug and also a steroid. Effect on our patient: It might have helped suppress the immune system of our client. There were also no adverse effects noted during the patients stay in the ER. Nursing Considerations:
1.

Take drug as prescribed and do not alter dosing regimen or stop medication without consulting physician. Prednisone may slow growth and development in children. Your child's doctor will watch his or her growth carefully.

2.

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3.

In taking the concentrated solution, use the specially marked dropper that comes with the medication to measure your dose. You may mix the concentrated solution with juice, other avored liquids, or soft foods such as applesauce. Be aware that a slight weight gain with improved appetite is expected, but after dosage is stabilized, a sudden slow but steady weight increase [2 kg (5 lb) per week] should be reported to physician. Report symptoms of GI distress to physician and do not self-medicate to nd relief. Do not use aspirin or other OTC drugs unless they are prescribed specically by the physician. Report slow healing, any vague feeling of being sick, or return of pre-treatment symptoms. Be fastidious about personal hygiene; give special attention to foot care, and be particularly cautious about bruising or abrading the skin.

4.

5. 6.

7.

8.

INTRAVENOUS IMMUNOGLOBULIN
Date Ordered: October 27, 2011 *Not given due to unavailability of funds Indication: IVIG is a blood product administered intravenously. It contains the pooled IgG (immunoglobulin (antibody) G) extracted from the plasma of over one thousand blood donors. IVIG's effects last between 2 weeks and 3 months. It is mainly used as treatment in three major categories:

Immune deciencies such as X-linked agammaglobulinemia, hypogammaglobulinemia (primary immune deciencies), and acquired compromised immunity conditions (secondary immune deciencies) featuring low antibody levels. Autoimmune diseases e.g. Immune thrombocytopenia ITP and Inammatory diseases e.g. Kawasaki disease. Acute infections.

Effect to the body: The immune system recognizes and attacks foreign substances, called "antigens". Antigens are molecules on the surface of viruses, fungi, or bacteria. Some non-living substances such as toxins, chemicals, and drugs can be antigens, too. For each new antigen
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encountered, the immune system forms a defense that is specic to that antigen, allowing the body to destroy it. Immunoglobulins are an important part of that defense. Each immunoglobulin attaches to its specic, matching antigen and makes it easier for phagocytes (a type of white blood cell which engulfs and digests antigens) to destroy the antigen. Binding of the immunoglobulin to an antigen also activates a set of proteins called the "complement" system, which ruptures bacteria and viruses. When the immune system is too immature (as in the case of a young infant) or does not otherwise have the ability to form its own antibodies, "passive immunity" can protect against infection. Passive immunity involves antibodies that are produced in someone's body other than your own. Infants have passive immunity because they are born with antibodies that are transferred through the placenta and in breast milk from the mother. IVIG confers similar passive immunity through antibodies present in pooled donor plasma, harvested from carefully screened donors through plasmapheresis. Paradoxically, immunoglobulins can also down-regulate an immune response, which is why IVIG is used to treat some autoimmune diseases. For immune decient patients who have decreased or abolished antibody production capabilities, IVIG is administered to maintain adequate antibody levels to prevent infections and confers a passive immunity. Treatment is given every 34 weeks. In the case of patients with autoimmune disease, IVIG is administered at a high dose (generally 1-2grams IVIG per kg body weight) to attempt to decrease the severity of the autoimmune diseases.

Nursing Considerations:
1.

IVIG cannot be mixed with other drugs or IV infusion uids, therefore it must be given through a separate infusion line. The bottle or vial must be either rotated or swirled in order to dissolve the particles. Shaking, which results in foaming, should be avoided because it may impede the dissolution process. Vital signs should be taken at a minimum every 15 minutes for the rst 30 minutes, every 30 minutes for the next hour, then hourly until the infusion is complete. Should patients report any signs or symptoms consistent with an infusion reaction (e.g., fever, chills, rigors, ushing, sweating, hives, shortness of breath), rst slow the infusion considerably, as many reactions are related to too-rapid infusion. If a serious reaction occurs (compromised airway, drop in blood pressure, change in level of consciousness), stop the infusion immediately and maintain IV access; call for assistance and administer pre-ordered emergency medications per protocol (in a nonhospital setting).

2.

3.

4.

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A NATO M Y & P H YS I O L O G Y

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P L AT E L E T S
Platelets or thrombocytes are small, irregularly shaped clear cell fragments which are derived from fragmentation of precursor megakaryocytes. The average lifespan of a platelet is normally just 5 to 10 days. Platelets are a natural source of growth factors. They circulate in the blood of mammals and are involved in hemostasis, leading to the formation of blood clots.

If the number of platelets is too low, excessive bleeding can occur. However, if the number of platelets is too high, blood clots can form (thrombosis), which may obstruct blood vessels and result in such events as a stroke, myocardial infarction, pulmonary embolism or the blockage of blood vessels to other parts of the body, such as the extremities of the arms or legs. An abnormality or disease of the platelets is called a thrombocytopathy, which could be either a low number of platelets (thrombocytopenia) a decrease in function of platelets (thrombasthenia) increase in the number of platelets (thrombocytosis).

There are disorders that reduce the number of platelets, such as heparin-induced thrombocytopenia (HIT) or thrombotic thrombocytopenic purpura (TTP) that typically cause thromboses, or clots, instead of bleeding.

Platelets release a multitude of growth factors including Platelet-derived growth factor (PDGF), a potent chemotactic agent, and TGF beta, which stimulates the deposition of extracellular matrix. Both of these growth factors have been shown to play a signicant role in the repair and regeneration of connective tissues.

Other healing-associated growth factors produced by platelets include basic broblast growth factor, insulin-like growth factor 1, platelet-derived epidermal growth factor, and vascular endothelial growth factor. Local application of these factors in increased concentrations through Platelet-rich plasma (PRP) has been used as an adjunct to wound healing for several decades.

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H E M ATO P O E I S I S

Hematopoiesis is the formation of blood cellular components. All cellular blood components are derived from hematopoietic stem cells. In a healthy adult person, approximately 10111012 new blood cells are produced daily in order to maintain steady state levels in the peripheral circulation. Hematopoietic stem cells (HSCs) reside in the medulla of the bone (bone marrow) and have the unique ability to give rise to all of the different mature blood cell types. HSCs are self renewing: when they proliferate, at least some of their daughter cells remain as HSCs, so the pool of stem cells does not become depleted. The other daughters of HSCs (myeloid and lymphoid progenitor cells), however can each commit to any of the alternative differentiation pathways that lead to the production of one or more specic types of blood cells, but cannot self-renew. This is one of the vital processes in the body.

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PLATELET KEY POINTS:

Platelets are produced in blood cell formation (thrombopoiesis) in bone marrow, by budding off from megakaryocytes. The physiological range for platelets is (150400)109 per liter. Around 1011 platelets are produced each day by an average healthy adult. The lifespan of circulating platelets is 5 to 10 days. Megakaryocyte and platelet production is regulated by thrombopoietin, a hormone usually produced by the liver and kidneys. Each megakaryocyte produces between 5,000 and 10,000 platelets. Old platelets are destroyed by phagocytosis in the spleen and by Kupffer cells in the liver. Reserve platelets are stored in the spleen, and are released when needed by sympatheticallyinduced splenic contraction.

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H E M O S TA S I S
P l a t e l e t P l u g Fo r m a t i o n

The function of platelets is the maintenance of hemostasis. This is achieved primarily by the formation of thrombi, when damage to the endothelium of blood vessels occurs.

When there is a damage in the endothelium of blood vessels, platelet plug formation occurs in three phases: 1. Platelet Adhesion - The rst phase begins when platelets detect damage to a blood vessel and begin to adhere to the exposed surfaces. 2. Platelet Release Reaction - Once stuck to a site of damage, the platelets begin to change. Firstly they create extensions so that they can contact each other, and then they release their contents. There are two types of chemical packages (granules) held within

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the cytoplasm of platelets: alpha granules that contain clotting factors, growth factors, and broblasts; and dense granules that contain ADP, ATP, Calcium ions, and Serotonin. Other components are also present within the platelet that aids its work. Nearby platelets are stimulated into action by the release of ADP and Thromboxane A2 (a prostaglandin found within platelets). Thromboxane and Serotonin act to cause vasoconstriction. 3. Platelet Aggregation - The ADP acts to make the nearby platelets sticky and adhere to the other recruited platelets, and when the collection is large enough it creates a platelet plug stopping the loss of blood through holes in small vessels.

Once the platelet plug is formed, a chain of events is initiated to form a clot. The reactions that occur are catalyzed by enzymes called clotting factors.

After a platelet plug forms, the coagulation phase begins, which involves a cascade of enzyme activations that lead to the conversion of prothrombin to thrombin. Calcium is required for this reaction to occur. Thrombin itself acts as an enzyme and causes brinogen one of the two major plasma proteins to form long brin threads. Fibrin threads entwine the platelet plug forming a mesh-like framework for a clot. The framework traps red blood cells that ow toward it, forming a clot. Because red blood cells are tangled in the meshwork, clots appear to be red. As the red blood cells trapped on the outside dry out, the color turns a brownish red, and a scab forms.

The blood clot is only a temporary solution to stop bleeding; vessel repair is therefore needed. The aggregated platelets help this process by secreting chemicals that promote the invasion of broblasts from surrounding connective tissue into the wounded area to completely heal the wound or form a scar. The obstructing clot is slowly dissolved by the brinolytic enzyme, plasmin, and the platelets are cleared by phagocytosis.

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I D I O PAT H I C THROMBOCYTOPENIC PURPURA


-Overview-

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I D I O PAT H I C T H R O M B O C Y T O P E N I C P U R P U R A
Idiopathic thrombocytopenic purpura (ITP) is an acquired hemorrhagic disorder characterized by:

(1) thrombocytopenia - excessive destruction of platelets (2) purpura - a discoloration caused by petechiae beneath the skin (3) normal bone marrow with normal or increased number of immature platelets (megakaryocytes) and eosinophils

Although the cause is unknown, it is believed to be an autoimmune response to disease-related antigens. It is the most frequently occurring thrombocytopenia of childhood. The greatest frequency of occurrence is between 0 and 10 years of age. The disease occurs in one of two forms: an acute, self limiting course or a chronic condition (greater than 6 months duration). The acute form is most often seen after upper respiratory infections; after the childhood diseases measles, rubella, mumps, and chickenpox, or after infection with parvovirus B19.

DIAGNOSTIC EVALUATION The diagnosis is suspected on the basis of clinical manifestations. In ITP, the platelet count is reduced to below 20,000 mm3 ; therefore, tests that depend on platelet function such as the tourniquet test, bleeding time, and clot retraction are abnormal. Although there is no denitive test on which to establish a diagnosis of ITP, several are usually performed to rule out other disorders in which thrombocytopenia is a manifestation, such as systemic lupus erythematosus, lymphoma or leukemia.
CLINICAL MANIFESTATIONS OF ITP Easy Bruising ! Petechiae ! Ecchymoses ! Most often over bony prominences Bleeding from mucous membranes ! Epistaxis ! Bleeding Gums ! Internal hemorrhage evidenced by: hematuria, hematemesis, ! ! ! ! melena, hemarthrosis, menorrhagia Hematomas over lower extremities

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THERAPEUTIC MANAGEMENT Management of ITP is primarily supportive, because the course of the disease is selflimited in the majority of cases. Activity is restricted at the onset while the platelet count is low and while active bleeding or progression of lesions is occurring. Treatment for acute presentation is symptomatic and has included prednisone, intravenous immunoglobulin (IVIG), and anti-D antibody. These are not curative therapies. Some experts suggest that no therapy is necessary for the asymptomatic patient, with no difference in the recovery of platelet counts over time. Anti-D antibody is a relatively new therapy for ITP. Infusion of anti-D antibody causes a transient hemolytic anemia in the patient. Along with the clearance of antibody-coated RBCs, there is prolonged survival of platelets resulting from the blockade of the Fc receptors of the reticuloendothelial cells. The platelet count does not increase until 48 hours after an infusion of anti-D antibody; therefore, it is not appropriate therapy for patients who are actively bleeding. The benets of choosing anti-D antibody therapy over prednisone or IVIG is that antiD antibody can be given in one dose over 5-10minutes and is signicantly less expensive than IVIG. Historically, patients who are treated with prednisone must rst undergo a bone marrow examination to rule out leukemia. Therefore the use of anti-D antibody alleviates the need for a bone marrow examination. Patients must meet certain criteria before the administration of anti-D antibody. Premedication with acetaminophen (Tylenol) 5-10minutes before infusion is recommended.
CRITERIA FOR ANTI-D ANTIBODY THERAPY Children between age 1 year and 19 years Normal white blood cell count and hemoglobin for age: platelets <30,000/ul No active mucosal bleeding No prior history of reaction to plasma products No patient known to be immunoglobulin A decient No concurrent infection No patient with Evans Syndrome (characterized by the combination of ITP and ! ! ! ! ! autoimmune hemolytic anemia) No patient with suspected lupus erythematosus or other collagen/vascular disorder

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Splenectomy is reserved for those patients in whom ITP has persisted for 1 year or longer. It is the only treatment associated with long term remission for 60% to 90% of children. Splenectomy removes the risk of hemorrhage but increases the risk of septicemia. Before considering splenectomy, it is generally recommended to wait until the child is older than 5 years of age because of the increased risk of bacterial infection. Pneumococcal and meningococcal vaccines are recommended before splenectomy. The child also receives penicillin prophylaxis after splenectomy. The length of prophylactic therapy is controversial, but in general, a minimum of 3 years is recommended.

PROGNOSIS The majority of children have a self-limited course without major complications. Some children will develop chronic ITP and require ongoing therapy. A splenectomy may modify the disease process, and the child will be asymptomatic.

NURSING CONSIDERATIONS Nursing care is largely supportive and should include teaching regarding possible side effects of therapy and limitation in activities while the childs platelet count is 50,000 to 100,000 mm3.Children with ITP should not participate in any contact sports, bike riding, skateboarding, in-line skating, gymnastics, climbing, or running. Parents are encouraged to to engage their children in quiet activities and to prevent any injury to the childs head. The harmful effects of using aspirin and NSAIDs to control pain are critical for these children; therefore, salicylate substitutes (e.g. Acetaminophen) are always used. As in any condition with an uncertain outcome, the family needs emotional support.

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PAT H O P H Y S I O L O G Y

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PAT H O P H Y S I O L O G Y
!
MODIFIABLE*FACTORS:* >Environmental!Factors! !!!!!!0*Viral*Infection* !!!!!!1!Bacterial!Infection! >Lifestyle:!Activity! >Medications:!Sulfanomide!drugs! !!!Ex.!sulfonylureas,!thiazide!diuretics,! loop!diuretics,!COX2!inhibitors,! Acetazolamide! NON0MODIFIABLE*FACTORS:* >Age*0010*years*old* >Sex!(female)! >Hereditary!Factor!

Triggers!clients!immune! system!

Activation!of!Immune!system! response!

!! Molecular!mimicry!

IgG!antibodies!are!generated! against!viral!infection!

! Opsonization:! (Renders!the!virus)! !

Platelets!misleadingly! opsonized!by!IgG! antibodies!

Phagocytosis!of!platelets! occur!

! Thrombopoietin!is! released!by!the!kidney!or! liver!

Excessive!destruction!of! platelets!

THROMBOCYTOPEN IA! Pt.=*4*x*109*/* l*

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Increased!risk!of!bleeding! !

Bone!marrow!produces! blood!cell!components!! Platelets!are!produced! Increased!platelet!and! immature!platelets! (megakaryocytes)! production!

Blood!vessels!weakened! easily! ! TRIGGER:! Trauma! ! Damage!in!blood!vessels! !

Inc.! eosinophil! count!


Splenic!Sequestration! Splenomegaly! Dec.!platelet!count!

Decreased!platelet!plug! formation!at!damaged!site! !

Prolonged!bleeding!time! !

BLEEDING!IN!GUMS!AND! MOUTH! ! PETECHIAE! ! PURPURA! !

Bleeding!in!urine!and! stool! !

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DISCHARGE PLAN

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DISCHARGE PLAN

HOME MEDICATION: Tranexamic Acid 80mg/pptab i pptab TID

OPD FOLLOW-UP: 1. Cancer Institute - November 4, 2011, 10AM 2 Pediatric Emergency Room - October 31, 2011, 10AM ; for repeat CBC with platelet count PLANS: 1. Bone Marrow Aspiration 2. IVIG Transfusion

HEALTH TEACHINGS Come back on the specied follow-up visit.

MEDICINES:

Keep a current list of your child's medicines: Include the amounts, and when, how, and why they are taken. Bring the list and the medicines in their containers to followup visits. Carry your child's medicine list with you in case of an emergency. Throw away old medicine lists. Give vitamins, herbs, or food supplements only as directed. Give your child's medicine as directed: Call your child's primary healthcare provider if you think the medicine is not working as expected. Tell him if your child is allergic to any medicine. Ask before you change or stop giving your child his medicines. Do not give your child any medicine that has aspirin or ibuprofen-like medicines in it. Ask caregivers before giving your child any over-the-counter medicine.

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DOs & DONTs:

Do encourage him to eat more fruits, and drink fruit juices and lots of water, to avoid constipation. Constipation can cause bleeding in your child's bowel movement. Ask your child's caregiver for information on ways to prevent and treat constipation. Do give your child a soft-bristled toothbrush to use to help prevent bleeding gums. Teach him to brush his teeth slowly and gently. Use lip balms to prevent your child's lip from drying and cracking. Do apply lotion on your child's dry skin to prevent itching and scratching. Scratching may lead to bruising and bleeding. Do not allow your child to join in rough play or contact sports. This may cause skin bruising and head injuries, which may lead to bleeding. Do not give your child any medicines without asking his caregiver rst. Do not give him aspirin, ibuprofen, or antihistamines as these medicines may cause bleeding.

FOR SUPPORT & MORE INFORMATION Having thrombocytopenic purpura may be a life-changing disease for you, your child, and your family. Accepting that your child has thrombocytopenic purpura may be hard. You and those close to you may feel angry, sad, or frightened. These feelings are normal. Talk to your caregivers, family, or friends about your feelings.

CONTACT A CAREGIVER IF:


Your child has a fever. Your child is bleeding from his gums, mouth, or nose. Your child has abdominal (belly) pain. Your child's bowel movement has blood in it or is dark-colored. Your child has a sudden, severe headache.

SEEK CARE IMMEDIATELY IF:


Your child just had a head injury. Your child had a seizure (convulsion).
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Your child is drowsy, cannot be awaken, or does not respond to you. Your child does not know where he is, or does not know people that he did know. Your child has problems seeing (blurry or double vision), talking, or hearing. Your child has repeated or forceful vomiting (throwing up). Your baby has a bulging soft spot (fontanel) on his head. Your child has sudden weakness, numbness, or problems with his balance and movement.

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