Gestational Diabetes Mellitus

-DM is a hereditary endocrine disorder due to inadequate or lack of insulin production that results in impaired glucose absorption & metabolism. - all women appear to develop an insulin resistance as pregnancy progresses ( insulin does not seem normally effective during pregnancy) a phenomenon that is probably caused by the presence of the hormone Human Placental Lactogen (HPL)

SSx: 1. Hyperglycemia pancreas does not produce enough insulin , thus glucose is unable to enter the cells & accumulates in the bloodstream resulting in hyperglycemia

2. Glycosuria when blood glucose levels goes beyond the renal threshold for sugar, glucose spills on the urine.
3. Polyuria glucose attracts water so that when it is excreted in the kidney, it brings along with it large amounts of water resulting in the woman excreting large amounts of urine, a condition called, POLYURIA. 4. Polydipsia the excretion of large amounts of fluid from the body leads to dehydration. Excessive thirst or polydipsia is an important symptom of dehydration.

Effects of Diabetes:

Mother:
1. Increased tendency to pre-eclampsia & eclampsia, UTI, & candidiasis 2. Increased risk for postpartum hemorrhage d/t overdistention of the uterus. 3. Maternal mortality 4. Preterm delivery

Infant:
1. Macrosomia 2. Hydramnios 3. Prematurity 4. Hypoglycemia ( lowered serum glucose levels)

5. Predisposition to diabetes mellitus later in life as the disease is hereditary

Complications:
1. Macrosomia Infants of women with poorly controlled diabetes tend to be large ( more than 10 lbs) because glucose can cross the placental barrier, it acts acts as a growth stimulant. The increased glucose adds subcutaneous fat deposits. All the nutrients that the fetus receives comes directly from the mothers blood. 2. Birth Injury may occur due to the babys large size and difficulty being born.( may cause CPD which may necessitate being born by CS)

3. HYPOGLYCEMIA refers to low blood sugar in the baby immediately after delivery. This problem occurs if the mothers blood sugar levels have been consistently high, causing the fetus to have a high level of insulin in its circulation. After delivery, the baby continues to have a high insulin level, but no longer has the high level of sugar from its mother, resulting in the newborns blood sugar level becoming very low. The babys blood sugar level is checked after birth, and if the level is too low, it may be necessary to give the baby glucose intravenously

4. Respiratory distress (difficulty breathing) too much insulin or too much glucose in a babys system may delay lung maturation and cause respiratory difficulties in babies. This is more likely if they are born before 37 weeks of pregnancy.

Prenatal Management:
1.

Diagnosis; Suspect DM in a woman

a. b.

With family history of DM

With history of unexplained repeated abortions and stillbirth

With glycosuria

c. d. e.

Who are obese

Who have history of giving birth to large infants, over 10 lbs. and infants with congenital anomaly

2. Screening tests
a.

Universal screening- 50 gram oral glucose tolerance test ( OGTT) between 24-28 weeks gestation irregardless of the time of the day and meals taken for all pregnant women. If the plasma value is more than 140 mg/dl after one hour, 100 gram three hour oral glucose tolerance test is performed to confirm if the woman is having hypergycemia.

3.

Diet
a.

Caloric intake should be enough to meet needs of pregnancy, fetus and mother (1,800 to 2,400 cal/day) but not too much to promote excessive weigh gain. 20% of caloric intake should come from protein foods, 50% from carbohydrates, 30% from fats. Weight gain should be about 24 lbs. Too much weight gain can lead to large infants and cephalopevic disproportion.

b.

d.

The goal is to maintain a fasting blood sugar level of 80 mg/dl and postprandial blood sugar level of 110mg/dl

4.

Exercise
A liberal cardiovascular-conditioning exercise and diet therapy is the management for Gestational Diabetes Mellitus

Exercise lowers blood glucose levels and decreases the need for insulin.
The exercise regimen should be individualized, performed regularly and under supervision. Advise woman to eat complex carbohydrates before exercising to prevent hypoglycemia.

Remember that hypoglycemia could occur in persons undergoing insulin therapy during peak action hour of insulin:

Short acting or regular insulin after 2-3 hours of injection Intermediate or Lente insulin after 6-8 hours of injection Long-acting or ultralente after 16 18 hours of injection The sign of hypoglycemia are: dizziness, diaphoresis, weakness, blurring of vision Give a hypoglycemic person a glass of orange juice.

5.

Insulin therapy
Insulin requirements increase during pregnancy
Oral hypoglycemics such as Tolbutamide and Diamicron are contraindicated during pregnancy because they are teratogenic for they can cross the placenta and may cause fetal and new born hypoglycemia. Combined fast acting and intermediate insulin made up of human derivative/humulin. Humulin is the insulin of choice during pregnancy because it is the least allergenic 2/3 in the morning, 1/3 at dinner administered subcutaneously hour before meals.

Insulin requirement is decreased on the first trimester due to nausea & vomiting and highest during the third trimester.

Delivery:
1.

Delivery is effected when the fetus is mature enough after 38 weeks gestation, but not too large so as to cause cephalopelvic disproportion. Thus, early hospitalization and labor induction is performed to deliver the baby before it becomes too large to pass the birth canal If cervix is not yet ripe, baby is macrosomic and fetal distress occurs, CS is performed Regular insulin is given on the day of delivery not long acting insulin because insulin requirement drop immediately after delivery. The woman may not require insulin during the first 24 hours postpartum and her insulin requirements usually fluctuates during the next few days.

2. 3.

4. Contraception:
a.

IUD and combined oral contraceptives are contraindicated *Progesterone interferes with insulin activity therefore increases blood glucose levels. *Estrogen increases lipid & cholesterol levels & risk for increased blood coagulation

a.

Norplant (subcutaneous progestin implant system) or Depo -provera may be good choices & safely used by diabetic women

HYPERTENSIVE DISORDERS IN PREGNANCY:

GESTATIONAL HYPERTENSION: - HYPERTENSION THAT DEVELOPS DURING PREGNANCY OR DURING THE FIRST 24 HOURS AFTER DELIVERY WHICH IS NOT ACCOMPANIED BY EDEMA, PROTEINURIA & CONVULSIONS & DISAPPEARS WITHIN 10 DAYS AFTER DELIVERY.

CHRONIC HYPERTENSION:
- THE PRESENCE OF HYPERTENSION BEFORE PREGNANCY OR HYPERTENSION THAT DEVELOP BEFORE 20 WEEKS GESTATION IN THE ABSENCE OF H-MOLE & PERSIST BEYOND THE POSTPARTUM PERIOD. PREGNANCY INDUCED HYPERTENSION (TOXEMIA): - HYPERTENSION THAT DEVELOPS AFTER THE 20TH WEEK OF GESTATION TO A PREVIOUSLY NORMOTENSIVE WOMAN.

RISK FACTORS:
1. SAID TO BE A DISEASE OF PRIMIPARAS HIGHER INCIDENCE IN PRIMIPARAS BELOW 17 & ABOVE 35 YEARS. 2. LOW SOCIO ECONOMIC STATUS ( LOW PROTEIN INTAKE )
3. HISTORY OF CHRONIC HYPERTENSION ON THE MOTHER, H-MOLE, DIABETES MELLITUS,MULTIPLE PREGNANCY, POLYHYDRAMNIOS, RENAL DISEASE, HEART DISEASE 4. HEREDITARY hx of preeclampsia in mothers or sisters 5. Previous hx of preeclampsia

CAUSES: 1. THE EXACT CAUSE IS UNKNOWN = The primary cause of these & other s/Sx is damage to the endothelium ( cells that line the blood vessels), resulting in vasospasm throughout the body

2. PROTEIN & CALCIUM DEFICIENCY THEORY

3. UTERINE ISCHEMIA 4. GENETIC PREDISPOITION

TRIAD SX:
I HYPERTENSION 2. EDEMA ( INCREASE IN WEIGHT)

3. PROTEINURIA
= 2nd leading cause of maternal death = chief causes of maternal death due to PIH: - cerebral hemorrhage - cardiac failure with pulmonary edema

- renal, hepatic or resp. failure

- obstetric hemorrhage assoc. with abruptio

placenta

Warning Signs:

Rapid weight gain, 4-5 lbs in a single week Sudden swelling Swelling of face & hands

Swelling of ankles or feet that does not go away after 12 hours rest
A rise in BP Protein in the urine

Severe headaches
Blurry vision Seeing spots in the eyes

Severe pain over the stomach, under the ribs

Decrease in the amount of urine

S & SX BLOOD PRESSURE

MILD PREECLAMPSIA

SEVERE PREECLAMPSIA

140/90; Systolic elevation 160/110 of 30 mm/Hg Diastolic elevation of 15 mm/Hg +1 to +2 300 mg/ L24 hour urine collection Digital edema ( +1 +2) Dependent edema 3 lb/week Not less than 500 ml/24 hours Occasional headache Normal to +1 +2 Absent +3 to +4 in clean catch urine or 5 g/24 hour urine collection Pitting edema (+3 +4) Generalized edema More rapid weight gain Less than 500 ml/24 hours; oliguria Severe headache Hyperreflexia,+3 +4 Photophobia, blurring spots before the eyes

Proteinuria

Edema

Weight Gain Urinary Output Headache Reflexes Visual Disturbances

Epigastric Pain (liver involvement)

Absent

Right upper quadrant pain (aura to convulsion)

.
With

hpn, the cardiac system can be overwhelmed bec the heart is forced to pump against rising peripheral resistance. This reduces the blood supply to organs, most markedly the kidney, pancreas, liver, brain and placenta. Poor placental perfusion may reduce the fetal nutrient & O2 supply. Ischemia in the pancreas may result in epigastric pain & an elevated amylase-creatinine ratio. Spasm of the arteries in the retina leads to vision changes . If retinal hemorrhage occur, blindness could occur.

EDEMA: (+1) PHYSIOLOGIC TYPE IN PREGNANCY, THERE IS SLIGHT EDEMA IN THE LOWER EXTREMITIES ( DUE TO PRESSURE & POSTURE) (+2) MARKED EDEMA OF LOWER EXREMITIES (PATHOLOGIC) (+3) EDEMA FOUND ON THE FACE & FINGERS. (+4) GENERALIZED EDEMA ( ANASARCA)

Non pitting edema if there is swelling or puffiness at some points in the body and a palpating finger is depressed but the swelling cannot be indented with finger pressure Pitting edema if the tissue can be indented slightly,1+ pitting edema; moderate indentation 2+; deep indentation is 3+ & indentation is so deep it remains after removal of the finger is 4+ pitting edema

SEIZURE PRECAUTIONS: 1. SIDE RAILS UP 2.PAD THE SIDE RAILS

3. PUT BED AT LOWEST POSITION.

4. ROOM SHOULD BE DIM, QUIET,& AWAY FROM AREAS OF ACTIVITY. ( AVOID BRIGHT LIGHTS SUCH AS FLASHLIGHTS) 5. RESTRICT VISITORS TO ALLOW PATIENT TO REST. 6. HAVE EMERGENCY EQUIPMENT AVAILBLE: - SUCTION APPARATUS, O2

MEDICATIONS: 1.HYDRALAZINE ( APRESOLINE ) - ANTIHYPERTENSIVE ( PERIPHERAL VASODILATOR) USED TO DECREASE Hpn

Dosage 5-10 mg/IV - administer slowly to avoid sudden fall in BP

- Maintain diastolic pressure at 90 mm/Hg to ensure adequate placental filling

2. MAGNESIUM SULFATE ( MgSO4) - DRUG OF CHOICE TO TREAT & PREVENT CONVULSIONS, also a muscle relaxant - Classified as CATHARTIC reduces edema by causing a shift in fluid from extracellular spaces into the intestine - Loading dose is 4-6g. Maintenance dose is 1-2g/h IV - Therapeutic dose 4-7 g - Infuse loading dose slowly over 15-30 min. - Always administer as a piggyback infusion - Serum Mg level should remain below 7.5 mEq/L

ACTIONS OF MgSO4: = decreases neuromuscular irritability and blocks the release of acetylcholine at the neuromuscular junction; depresses vasomotor center; depresses central nervous system (CNS) irritability
CHECK THE FOLLOWING FIRST BEFORE ADMINISTERING MgSO4: 1. DEEP TENDON REFLEX PRESENT - +2 ( NORMAL) 2. RR SHOULD BE AT LEAST 12 BPM

3. URINE OUTPUT SHOULD BE AT LEAST 30 ML/HR

4. Woman should be able to answer questions asked of her

** IF MgSO4 TOXICITY DEVELOPS AS SHOWN BY RR DEPRESSION TO LESS THAN 12 BPM & DISAPPEARANCE OF THE DTR, GIVE THE ANTIDOTE CALCIUM GLUCONATE & NOTIFY PHYSICIAN.
- 1g/IV ( 10 ml of a 10% sol) - have prepared at bedside when administering MgSO4 ** IF MgSO4 IS GIVEN POSTPARTUM, MONITOR FOR UTERINE ATONY AS IT CAN CAUSE UTERINE RELAXATION.

Repeat doses should not be given & physician should be notified if any of the following signs of Mg toxicity exist:

Patellar knee jerk absent ( test brachial reflexes if epidural anesthesia is present) Respirations less than 12/min Urine output less than 30 ml/hr Signs of fetal distress Elevated serum Mg levels ( more than 8 mg/dl)

SX of MgSO4 overdose:

Disappearance of the DTR Decreased urine output Depressed respirations Reduced consciousness

Patellar Reflex score:

0 no response, hypoactive, abnormal

1+ - somewhat diminished response but not abnormal

2+ Average response
3+ Brisker than average but not abnormal 4+ Hyperactive, very brisk, abnormal

Ankle clonus a continued motion of the foot ( should be minimal )

Dorsiflex the womans foot 3x in succession. As you take your hand away, observe the foot. If no further motion is present, no ankle clonus is present If the foot continues to move involuntarily, clonus is present: Mild ( 2 movements) Moderate ( 2-5 movements)

Severe ( over 6 movements)

Diazepam ( Valium)

Halt seizures 5-10 mg/IV

Administer slowly
Dose may be repeated every 5-10 mins ( up to 30 mg/hr) Observe for respiratory depression or hypotension in mother & respiratory depression & hypotonia in infant at birth.

PHARMACOLOGICAL MANAGEMENT OF PREGNANCY-INDUCED HYPERTENSION Medications Side Effects Nursing Considerations Magnesium sulfate Flushing, sweating CNS depressant, anticonvulsant Symptoms of toxicity: Monitor BP, P, R, FHR at least every 15 sudden drop in BP, min; MgSO4 levels and DTR prior to respirations <12/min, administration, mental status urinary output <25-30 frequently; have resuscitation ml/hr, equipment and calcium gluconate/ decreased/absent DTRs, chloride (antidote) in room toxic serum levels Hydralazine Tachycardia, palpitations Vasodilator (Apresoline) Headache Maintain diastolic BP Nausea and vomiting 90-100 mm Hg for adequate Orthostatic hypotension uteroplacental flow; monitor FHT and neonatal status Diazepam Risk of neonatal Sedative, anticonvulsant (Valium) depression if given Monitor FHT and neonatal status within 24 h of delivery Methyldopa May masks symptoms of Used for chronic HTN (Aldomet) preeclampsia; Monitor maternal, fetal, and neonatal risk of maternal vital signs orthostatic Monitor maternal mental status hypotension and decreased pulse and BP in neonate for 2-3 d Hemolytic anemia Propranolol Decreased heart rate, Take apical rate before giving MLNG CELESTE, RN, MD (Inderal) depression, Monitor BP, EKG hypoglycemia

39

MANAGEMENT:

A. AMBULATORY MX
1. HOME MANAGEMENT IS ALLOWED ONLY IF: a. BP IS 140/90 OR BELOW b. THERE IS NO PROTEINURIA c. THERE IS NO FETAL GROWTH RETARDATION d. THE PATIENT IS NOT A YOUNG PRIMIPARA. 2. BED REST THE WOMAN SHOULD BE IN BED REST FOR MOST PART OF THE DAY & FREE FROM PHYSICAL & EMOTIONAL STRESS.

3. THE WOMAN SHOULD CONSULT THE CLINIC AS OFTEN AS NECESSARY. 4. DIET SHOULD BE HIGH IN PROTEIN & CARBOHYDRATES WITH MODERATE SODIUM RESTRICTION. 5. HOSPITALIZATION IS NECESSARY IF CONDITION WORSENS.

6. PROVIDE DETAILED INSTRUCTIONS ABOUT WARNING SIGNS:

a. EPIGASTRIC PAIN AURA TO CONVULSION b. VISUAL DISTURBANCES c. SEVERE CONTINUOUS HEADACHE

d. NAUSEA & VOMITING

B. HOSPITAL MANAGEMENT: 1. BP GOES ABOVE 140/90 mm Hg 2. BED REST IS ONE OF THE MOST IMPORTANT PRINCIPLES OF CARE. a. REST IN LEFT LATERAL POSITION TO PROMOTE BLOOD SUPPLY TO THE PLACENTA & THE FETUS.

SIGNS & SYMPTOMS OF ECLAMPSIA: 1. ALL THE SIGNS & SYMPTOMS OF PREECLAMPSIA 2. CONVULSION FOLLOWED BY COMA IS THE MAIN DIFFERENCE OF ECLAMPSIA & PREECLAMPSIA 3. OLIGURIA

RESPONSIBILITIES DURING A CONVULSION

1. ALWAYS MONITOR PATIENT FOR IMPENDING SIGNS OF CONVULSION: EPIGASTRIC PAIN, SEVERE HEADACHE, NAUSEA & VOMITING. 2 THE MAIN RESPONSIBILITIES OF A NURSE DURING A CONVULSION ARE: MAINTENANCE OF PATENT AIRWAY & PROTECTION OF PATIENT FROM INJURY. 3. TURN PATIENT TO HER SIDE TO ALLOW DRAINAGE OF SALIVA & PREVENT ASPIRATION. 4. NEVER LEAVE AN ECLAMPTIC PATIENT ALONE

5. DO NOT RESTRICT MOVEMENT DURING A CONVULSION AS THIS COULD RESULT IN FRACTURES. 6. WATCH FOR SIGNS OF ABRUPTIO PLACENTA: VAGINAL BLEEDING, ABDOMINAL PAIN, DECREASED FETAL ACTIVITY. 7. TAKE VITAL SIGNS & FHT AFTER A CONVULSION. 8. DO NOT GIVE ANYTHING BY MOUTH UNLESS THE WOMAN IS FULLY AWAKE AFTER A CONVULSION

** THE ONLY KNOWN CURE OF PIH IS DELIVERY OF THE BABY.

** AS SOON AS THE BABY IS STABLE, THE BABY IS DELIVERED. ** THE PREFERRED METHOD OF DELIVERY IS VAGINAL .

** IF LABOR INDUCTION IS UNSUCCESSFUL & FETAL DISTRESS IS SO SEVERE THAT THE FETUS NEED TO BE DELIVERED, CESARIAN SECTION IS PERFORMED.

POSTPARTUM CARE:
1. THE DANGER OF CONVULSION EXISTS UNTIL 24 HOURS AFTER DELIVERY. MgSO4 THERAPY IS CONTINUED UNTIL THE IMMEDIATE 24 HOUR POSTPARTUM. 2. ERGOT PRODUCTS ARE CONTRAINDICATED BECAUSE THEY ARE HYPERTENSIVES. 3. TWO YEARS SHOULD ELAPSE BEFORE ANOTHER PREGNANCY IS ATTEMPTED TO DECREASE THE LIKELIHOOD THAT PIH WILL RECUR ON THE SUBSEQUENT PREGNANCY.

NURSE ALERT!!! The risk of preeclampsia is increased for multigravida women if they have a new partner (father of the baby different than the previous children) due to new genetic makeup of the fetus.

9. POSTPARTUM PSYCHOLOGICAL ADAPTATION:RUBIN

1. TAKING- IN PHASE = 1 3 DAYS POSTPARTUM WHEN MOTHER RELIES ON OTHERS TO CARE FOR HER & HER NEWBORN.PREOCCUPIED WITH SELF & OWN NEEDS ( FOOD & SLEEP), CLIENT MAY VERBALIZE HER FEELINGS REGARDING RECENT DELIVERY. HESITANT ABOUT MAKING DECISIONS.

2. TAKING HOLD PHASE = 4 7 DAYS POSTPARTUM WHEN MOTHER BEGINS TO INITIATE ACTIONS & DECISIONS; FLACTUATION OF HORMONES ( ROLLER COASTER) DEPENDENCY /INDEPENDENCY; READY FOR MOTHERING ROLE; POSTPARTUM BLUES (AN OVERWHELMING FEELING OF SADNESS THAT CANNOT BE ACCOUNTED FOR) MAY BE OBSERVED. COULD BE DUE TO HORMONAL CHANGES, FATIGUE OR FEELINGS OF INADEQUACY IN TAKING CARE OF A NEW BABY.

= BEST TIME TO TEACH MOTHER AND INFANT CARE

MX:
- EXPLAIN THAT IT IS NORMAL & THAT CRYING COULD BE THERAPEUTIC. BUT IF POSTPARTUM BLUES EXTEND BEYOND TWO WEEKS, IT COULD LEAD TO POSTPARTUM DEPRESSION & POSTPARTUM PSYCHOSIS ;THEREFORE CONSTANT MONITORING SHOULD BE DONE TO THE MOTHER. IMPLICATION: PROVIDE PSYCHOLOGICAL SUPPORT .

3. LETTING GO PHASE = 10 DAYS

- WOMAN ATTAINS COMPLETE INDEPENDENCE; ASSUMING NEW ROLES AND RESPONSIBILITIES

may Experience grief for relinquished roles; adjustment to accommodate for infant in family

AFTERPAINS / AFTERBIRTH PAINS = STRONG UTERINE CONTRACTIONS FELT MORE PARTICULARLY BY MULTIS,THOSE WHO DELIVERED LARGE BABIES, & THOSE WHO BREASTFEED BECAUSE OF OXYTOCIN PRODUCTION. IT WILL BE RELIEVED IN 3 -4 DAYS.
may be relieved by lying on abdomen with small pillow, heat, ambulation, mild analgesic (if breast feeding, 1 h before nursing)

Complications of the Post partum period

Complications of the Postpartum Period

1. Postpartum Hemorrhage is the leading cause of maternal mortality.

Blood loss of more than 500 ml is considered hemorrhage. The most dangerous time at which hemorrhage is likely to occur is during the first hour postpartum

Types of postpartum hemorrhage

Early postpartum hemorrhage occurs during the first 24 hrs after delivery

Causes:

. Uterine atony
Laceration of the birth canal Inversion of the uterus

Late postpartum hemorrhage occurs from 24 hrs after birth until 4 weeks postpartum

Uterine Atony

Most common cause of EARLY postpartum hemorrhage. When the uterus fails to contract, open blood vessels in the placental site continue to bleed resulting in hemorrhage.

Causes of Uterine Atony:

Overdistention of the uterus hydramnios, multiple pregnancy Complication of labor precipitate, prolonged labor High parity & advanced maternal age Presence of fibroid tumors Overmassage of the uterus Retained placental fragments

Management

First action taken when uterus is relaxed & boggy is to MASSAGE IT GENTLY.

Keep bladder empty since a full bladder interferes with effective uterine contractions
Monitor vital signs & amount of blood loss during the early postpartal period

Administer oxytocin if uterus is not contracted

BT & IVF to replace blood loss If retained placental fragments is the cause, curettage is performed If bleeding cannot be controlled by the above measures, HYSTERECTOMY is performed as the last resort.

Retained Placental Fragments

Uterus will not be able to contract effectively if placental fragments are retained resulting in uterine atony & hemorrhage. Most common cause of LATE postpartum hemorrhage.

Causes of retained placenta

Partial separation of a normal placenta Manual removal of the placenta Entrapment of placenta in the uterus Abnormal adherent placenta acreta, increta, percreta

Management

D & C to remove adherent placenta Hysterectomy for severe cases

Aganglionic megacolon

HIRSCHPRUNGS DISEASE

Absence of innervation to a bowel segment usually rectosigmoid colon

No peristaltic activity in affected area

Familial
males S/sx:constipation, ribbonlike stools or no meconium, abdominal distention, vomiting Dx: Ba enema, biopsy Mx:colostomy, surgery
Re x K arl S. Te o x o n, RN MD

Re x K arl S. Te o x o n, RN MD

Re x K arl S. Te o x o n, RN MD

PRE OP CARE
1. Daily enemas w/ 0.9% NaCl *Tap/hypotonic water will cause cardiac congestion or cerebral edema 2. Minimal residue diet w/ vitamin supplementation 3. Position semi fowlers to relieve dyspnea from distended abdomen 4. pacifier

Re x K arl S. Te o x o n, RN MD

POST OP CARE
1. 2.

Observe for abdominal distention Small frequent feedings after NGT removal

3.
4.

Colostomy care
Assist parents to cope with childrens feeding problems

Re x K arl S. Te o x o n, RN MD

INTUSSUSCEPTION

2-6 mos
Invagination of intestine < 1 yo idiopathic > 1 yo Lead point

S/sx:intense abdl pain, vomiting, blood in stool currant jelly, abdominal distention (sausage shaped mass)
NECROSIS: fever, tachycardia, rigid abdomen Dx:sonogram coiled spring Mx:Ba enema (reduction by hydrostatic pressure), surgery
Re x K arl S. Te o x o n, RN MD

Re x K arl S. Te o x o n, RN MD

NURSING CARE
1.

Provide comfort measures - pacifier for infants

NPO Adequate hydration via IV therapy Promote parent-infant bonding

2. 3. 4.

Re x K arl S. Te o x o n, RN MD

PYLORIC STENOSIS

Hypertophy/hyperplasia of pyloric sphincter

Males S/sx:nonbillous vomiting, s/sx of of dehydration and wt loss, abdominal distention, olive sized mass RUQ, visible peristalsis

Dx:xray- string sign, USG, endoscopy

Mx: surgery
Re x K arl S. Te o x o n, RN MD

Re x K arl S. Te o x o n, RN MD

Ndx:

Risk for deficient fluid volume r/t inability to retain food

Risk for infection at site of surgical incision r/t danger of contamination from feces d/t proximity of incision to diaper area

Re x K arl S. Te o x o n, RN MD

Nursing care

Hydration Pacifier may give thickened feedings on upright position then NPO just before surgery

Monitor I and O, weight, and vomiting

Postop 1. dropper feeding 4-6 hrs after surgery 45 min- 1 hr duration; oral rehydration soln then half strength breastmilk/formula at 24 hr interval 2. Side lying position 3. Monitor weight and return of peristalsis

4. Wound care
5. Pacifier for oral needs

Re x K arl S. Te o x o n, RN MD

HYDROCEPHALUS

Impaired circulation and absorption of CSF Obstructive/Noncommunicating w/n ventricular system Nonobstructive/Communicating obliteration of SA cisterns or malfunction of arachnoid villi

2 TYPES:
1. 2.

S/sx: head enlargement, ant fontanel wide and bulging, scalp veins dilated, broad forehead, sclera shows above iris, brisk tendon reflexes, spasticity, irritability, lethargy, poor appetite, cracked pot sound on percussion
Re x K arl S. Te o x o n, RN MD

Re x K arl S. Te o x o n, RN MD

Ndx: Risk for ineffective cerebral tissue perfusion related to increased intracranial pressure - monitor vs, head circumference, I and O - O2 - position flat or head 30 deg - do not lie on operative site

Re x K arl S. Te o x o n, RN MD

Risk for imbalanced nutrition, less than body requirements, related to increased intracranial pressure - NPO until bowel sounds return - position head w/o flexion

- observe for constipation

- note how child sucks - IV fluids

- obtain daily weight

Re x K arl S. Te o x o n, RN MD

Re x K arl S. Te o x o n, RN MD

-end-

D R. TINIO

82

CROUP (LTB)

inflammation of the larynx, trachea, and major bronchi one of the most frightening diseases of early childhood for both parents and children <5 yrs old; peak 1-2 yrs old

Re x K arl S. Te o x o n, RN MD

ETIOLOGIC AGENT

Influenza virus Parainfluenza virus most common RSV adenovirus

Re x K arl S. Te o x o n, RN MD

SIGN AND SYMPTOMS

1. low grade fever 2. barking cough at night 3. Hoarseness 4. inspiratory stridor 5. Retractions

6. Restlessness and iritability

Re x K arl S. Te o x o n, RN MD

LABORATORY

CBC
neck x - ray

Re x K arl S. Te o x o n, RN MD

MANAGEMENT

Assess airway Keep E equipment (E cart) Administer O2 and inc atmospheric humidity

Administer meds as ordered (corticosteroids, epinephrine,bronchodilator)

intravenous hydration

Nursing dx: Ineffective airway clearance related to edema

Re x K arl S. Te o x o n, RN MD

Re x K arl S. Te o x o n, RN MD

Re x K arl S. Te o x o n, RN MD

D R. TINIO

90

PHARYNGITIS

it is an inflammation of mucous membrane of the throat and involves the nasopharynx, uvula and soft palate peak incidence - 4 to 7 y either bacteria or viral result of a chronic allergy

Re x K arl S. Te o x o n, RN MD

VIRAL PHARYNGITIS
causative agent is virus

Re x K arl S. Te o x o n, RN MD

SIGN AND SYMPTOMS

1. Sore throat 2. fever 3. general malaise 4. enlarged lympnodes 5. erythema on the back of the pharynx

Re x K arl S. Te o x o n, RN MD

TREATMENT
1. antipyretic
2. gargle with warm water- school age 3. provide liquid foods - (+) difficulty of swallowing Nursing diagnosis: risk for fluid volume deficit

Re x K arl S. Te o x o n, RN MD

STREPTOCOCCAL PHARYNGITIS

cause by group A beta-hemolytic strep can lead to cardiac and kidney damage more severe than viral infection Spread by infected nose or throat mucus through coughing or sneezing

Re x K arl S. Te o x o n, RN MD

Re x K arl S. Te o x o n, RN MD

SIGN AND SYMPTOMS

1. marked erythema of the back of throat and palatine tonsils
2. tonsils are enlarged and white exudates in the tonsillar crypts

3. high grade fever

4. difficulty swallowing 5. Headache Dx: throat swab and culture

Re x K arl S. Te o x o n, RN MD

TREATMENT
1. antibiotics- 10 days course of pen G or clindamycin 2. high fluid intakes

3. relief of pain
4. antipyretics

Re x K arl S. Te o x o n, RN MD

COMPLICATION
1. Rheumatic fever
2. Glomerulonephritis

Re x K arl S. Te o x o n, RN MD

ACUTE LYMPHOCYTIC LEUKEMIA

Uncontrolled proliferation of WBC Lymphoblast Most frequent CA in children 2-16 yo

Males

Re x K arl S. Te o x o n, RN MD

S/sx: pallor, low grade fever, lethargy, petechiae, bleeding, vomiting, anorexia, bone pain, painless lymphadenopathy Dx:WBC variable w/ blasts, low platelet and hematocrit, anemia BMA > 25% blast cells

Re x K arl S. Te o x o n, RN MD

Re x K arl S. Te o x o n, RN MD

Mx: chemotherapy

Cx: CNS s/sx, renal failure

NDx: Risk for infection r/t decreased immune function Activity intolerance r/t reduced oxygen carrying capacity of blood

Re x K arl S. Te o x o n, RN MD

NURSING CARE

Prevent infection

monitor bleeding and transfusion reactions

Provide comfort and pain alleviation Health teaching Emotional and psychological support

Re x K arl S. Te o x o n, RN MD

MANAGEMENT OF CLIENTS WITH

DEGENERATIVE NEUROLOGICAL DISORDER
By: DRA. TINIO

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The ability to concentrate and to use your time well is everything. if you want to succeed in life--or almost anywhere else for that matter. By: Lee Iacocca

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NEURONS

Basic functional unit of the nervous system Primary component of nervous system Composed of a cell body ( gray matter), dendrite and an axon

dendrites usually receive signals while axons usually transmit them

NEURON

Information is transmitted in the CNS in the form of nerve impulses through succession of neuron..one after the other Nerve signal are transmitted from one neuron to the next

Through interneuronal junctions called SYNAPSES

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NEURON
Through interneuronal junctions called SYNAPSES

All synpases utilized for signal transmission in the CNS Called CHEMICAL SYNAPSES

First neuron secretes a chemical substance called NEUROTRANSMITTER @ synapse

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NEUROTRANSMITTER
First neuron secretes a chemical substance called NEUROTRANSMITTER @ synapse

Act on the receptor proteins in the membrane of the next Neuron ( to excite or inhibit)

Example of neurotransmitters: chemical agent involved in the transmission of impulse across synapse Acetylcholine NE, histamine, GABA, glutamate
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THEY ALWAYS SIGNALS IN ONE DIRECTION

NEUROTRANSMITTER FROM NEURON SECRETES TRANSMITTER

CALLED PRE-SYNAPTIC NEURON

TO THE NEURON ON WHICH THE TRANSMITTER ACT CALLED POSTSYNAPTIC NEURON

ALLOW SIGNAL TO BE DIRECTED TOWARD SPECIFIC GOAL

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MYELIN SHEATH

A WRAPPING OF MYELIN WHITISH FATTY MATERIAL THAT PROTECTS AND INSULATE NERVE FIBERS AND ENHANCES THE SPEED OF IMPULSE CONDUCTION.

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MYELIN SHEATH

BOTH AXON & DENDRITES MAY OR MAY NOT HAVE A MYELIN SHEATH ( MYELINATED/ UNMYELINATED) MOST AXONS LEAVING THE CNS ARE HEAVILY MYELINATED BY SCHWANN CELLS

Myelin sheath is essential in normal conduction of nerve impulses

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Degenerative disordersNON- demyelinating

Alzheimers disease Parkinsons disease Multiple sclerosis

Demyelinating

Guillain-Barre syndrome

 Motor

dysfunction- cranial nerve

Bells palsy Trigeminal neuralgia

Motor

dysfunction- peripheral

Myasthenia gravis

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ALZHEIMERS disease (non-demyelenating)

A progressive, irreversible, degenerative neurologic disorder that affects the brain resulting in cognitive impairments Not exclusive in the elderly 1 10% occurs in middle age

7 th decade of life

DEMENTIA

TERMINOLOGIES:

DEMENTIA- refer to loss of memory, reasoning, judgment and language to such extent it interferes with everyday life. COGNITION- is the act or process of thinking, perceiving and learning.

Decision making judgment, memory, thinking, reasoning, calculation, personality, and verbal communication.

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Dementia

Types

ALZHEIMERS Disease
Multi-infarct dementia

Parkinsons disease
Lewy body disease Alcoholic dementia

Toxic or traumatic injury

Genetic or metabolic diseases
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ALZHEIMERS Disease

Most common form of dementia among 65 yrs and older Prevalence: 2x every 5 years after the age of 65 .

Nearly half of all people older than 85 have AD.

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ALZHEIMERS Disease

Etiology:

The CAUSE of AD has NOT BEEN FOUND Increase age Genetic factors Clinical situation

RISK FACTOR:

Inflammation

Stroke
Oxidative damage from free radicals

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ALZHEIMERS Disease

Dr. ALOIS ALZHEIMER- first described pre-senile dementia 1907.

Changes Noted: Beta- amyloid plaque, neurofibrillary tangle.

PLAQUE insoluble deposit of protein and cellular material Outside and around neurons; develops in HIPPOCAMPUS. Degenerating nerve terminals both dendritics & axonal contain Amyloid protein
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PATHOPHYSIOLOGY
Healthy neuron has internal support structure Called MICROTUBULES

Serve as tract to guide nutrients to end of the axon And back. This is stable because of PROTEIN CALLED TAU

Tau changed chemically & become TANGLED

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PATHOPHYSIOLOGY
Once tangled degenerates & So do the cell support

Destruction Memory failure Personality changes Unable to do ADL

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PATHOPHYSIOLOGY

Thickening of Leptomeninges Shrunken gyri Enlarged ventricle Hippocampal shrinkage Generalized atrophy

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Neurotransmitter changes Acetylcholine

decreases
because of decline in cholinergic neurons in basal nucleus due to loss of choline acetyltransferase within neocortex and hippocampus
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Clinical Manifestation

AD characterized by a RELENTLESS impairment in decision making . Insidious and progress for decade

First affected part : HIPPOCAMPUS

Affected regions begin to shrink and in time lead to memory loss 10-20 years perhaps

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Clinical Manifestation

I- Mild Alzheimers disease

Cerebral cortex begin to shrink

Cognitive losses become apparent

Memory disturbance noticeable by family & co-worker

Poor judgment and problem solving skills Careless in work habits & household chores Confused about where they are

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Clinical Manifestation

I- Mild Alzheimers disease

They begin to get lost easily Routine activities & daily task get longer to be accomplished Do well in familiar surrounding Lack of ability to adapt new challenges

Irritable, suspicious, indifferent, agitation, apathy.

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Clinical Manifestation

II- Moderate Alzheimers disease

Language disturbance Impaired word-finding and circumlocution

Spontaneous speech becomes increasingly empty & paraphasia ( wrong context)

Palilalia or echolalia Apraxia Hyperorality

Depression, irritability may worsen

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Clinical Manifestation

II- Moderate Alzheimers disease

Delusion and psychosis appear Person fears personal harm, theft of property or infidelity of the spouse May see bug crawling on the bed or throughout the house Wandering at night is common if admitted to a long term facility, nursing action includes placing the pt in a room close to the nurses station Occasional incontinence may occur
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Clinical Manifestation

III- Severe Alzheimers disease

Final Stage : plaques and tangles are widespread throughout the brain Client cannot recognize family or friends Do not communicate in any way Voluntary movement is minimal Limb become rigid with flexor posturing Urinary and fecal incontinence Aspiration & aspiration pneumonia is frequent
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Diagnostic Finding

No definitive test for AD Made by exclusion of known cause of dementia

Diagnosis is confirmed with:

1. presence of dementia involved 2 or more cognition. 2.insidious onset & steady progression 3.loss of normal alertness

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DIAGNOSTIC TEST

Health history = Neurologic examination EEG Other tests to rule out Vit B deficiencies and hypothyroidism

Autopsy is the most definitive

Diagnostic Finding

CT- scan- identify ventricular dilatation sulcal enlargement, Cerebral atrophy MRI

Single positron emission CT ( SPECT)

Positron emission tomography (PET) Lab studies:

CBC, ESR, Electrolytes, BUN, Crea, thyroid, liver function test HIV testing

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MANAGEMENT

NO CURE HAS BEEN FOUND FOR AD Maintain mental function and slowing the process of deterioration

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Drug therapy
Drug therapy

1. drugs to treat behavioral symptomsantipsychotics

2. anxiolytics
3. Tacrine HCL(cognex) first meds used, 1993 4. Donepezil (Aricept) 2 nd meds, 1997 5. Rivastigmine (Exelon) - 2000

OMEGA-3 FATTY ACIDS FROM FISH 60% less risk of developing Alzheimers compared with those who rarely eat or never eat fish.
-Morris -Archive

M., et al ( 2003)

of Neurology,60,940-946

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Major Goal of Intervention

HELP

client achieve an optimal level of functioning in light of chronic neurologic deficit

-MS, By Joyce Black , 8TH edition-

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INTERVENTION

FAMILY:

Usual area of declines How to provide care and support to client How to manage stress & cope with the progressive nature of the disorder.

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Nursing Interventions
1.

Support cognitive function

Memory deficit occur all stages Reorient the client ( calendar, clock)

2.

Provide emotional support

Long term memory retained -Allow client to reminisce Repetition is useful for ensuring maximal retention of information. Listening behavior

3. Establish an effective communication system with the patient and family

The nurse should be prepared to adapt to the communication level of the client. If client speak only single words or short phrases

Speak slowly and simply with a firm volume and low pitch. Tone of voice should always be calm and reassuring and project control of the situation

BE PREPARED TO APPLY NEW TECHNIQUES FOR COMMUNICATING WITH THE CLIENT

Maintain a calm and consistent approach

Attempt to analyze behavior for meaning

4. protect the patient from injury

Provide a safe and structured environment

Requests a family member to accompany client if he wanders around

Keep bed in low position Provide adequate lightning Dangerous object should be kept out reach Assign consistent caregivers

= nightlights are helpful

5. Encourage exercise to maintain mobility 6. Promoting independence in self-care activities - simplify daily activities by organizing them into short, achievable steps so that the patient experience a sense of accomplishment

PARKINSONS DISEASE

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PARKINSONs Disease (non-demyelenating)

A

PROGRESSIVE DISORDER with degeneration of the nerve cells in the basal ganglia resulting in generalized decline in muscular function; disorder of extrapyramidal system Results loss of neurotransmitter dopamine ( control movt )

CAUSATIVE FACTORS: unknown

Potential factors: genetics, atherosclerosis, free radical stress, viral infection, head trauma and environmental factors

Parkinsonian symptoms occur in the

5 th decade of life

Pathophysiology
Degenerative changes are found in an area of the brain called SUBSTANTIA NIGRA which produce dopamine ( normal and smooth movement)

Once cell loss in the substantia nigra reaches 80% manifestation appear
CAUSE of Nigral cell degeneration is NOT KNOWN

severe shortage of dopamine in relation with Ach in the basal ganglia

--Joyce Black; 8th edition-

Clinical Manifestation

Manifestation do not appear until about 60% of the normal amount of dopamine is lost 6 cardinal features Tremor at rest on one side ( 70 %) Rigidity( cog wheel) increased tone and stiffness in the muscle at rest. Bradykinesia- slow movement, fine movt become clummsy
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1. 2. 3.

Clinical Manifestation

4. flexed posture of the neck , trunk and limbs 5. loss of postural reflexes

6. freezing movement

1.Periodically lie prone without a neck pillow

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Clinical Manifestation
EARLY DISEASE

Bradykinesia slowing in the ability to perform ADL

General feeling of stiffness, mild diffuse muscular pain.

Tremor common- pill rolling movement of the thumb against the finger.

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Clinical Manifestation
Bradykinesia- difficult voluntary movement to execute.

Severe AKINESIA ( total lack of movt )

frozen on one spot Affect gait

slight stiffness of 1 leg while walking ipsilateral arms flexed at the elbow and abducted at the shoulder
Drag one foot Shuffling gait with short step develops

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Advanced PD:

Stands with head, shoulder and spine flexed forward Giving appearance of stooped shoulder FACE : appear stiff, mask-like without expression Speech low volume, monotonous tone (+) dysarthria- words are poorly articulated Saliva flow involuntarily Micrographia- small cramped handwriting
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PD

Does not affect intellectual ability 15-20% developed

dementia AD
Fatigue- common Immobility Slow gastric motility
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GOAL OF MANAGEMENT OF PD

manifestation with lowest possible dose of medication in order to avoid side effect

Control

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Every client respond differently from the medication or dosage level Process of experimentation, persistence and patience

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Medical Management
1. Levodopa ( L-dopa) increase level of dopamine in the brain, relieves tremors, rigidity and bradykinesia.
-

Administer with food or snack to decrease G.I irritation Avoid multiple Vitamins prep containing B6

Inform client urine and sweat may be darkened

2 . Cardiodopa-levodopa prevent breakdown of dopamine in the periphery and cause fewer side effect

3. Amantadine- used in mild cases in combination with L-dopa 4. Anticholinergic drugs ( benztropine- cogentine) inhibit action of acetycholine ( SE: inability to uinate)

5. Antihistamine- dec. tremor & anxiety

6. Bromocriptine stimulate release of dopamine in substantia nigra

PHARMACOLOGIC:
Eldepryl

(MAOI) inhibits dopamine breakdown

Tricyclic

antidepressanttreat depression

NURSING INTERVENTIONS
-Health assessment

-Medication instruction and monitoring

-Client & family education
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Advise client to maintain fluid intake 2L/day Increase dietary intake Stool softener and mild laxative

Regular time for bowel movements should be established hours after the morning or evening meal

NURSING INTERVENTIONS
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Teach the client various techniques to enhance voluntary physical movt .

-

Bradykinesia Rock back and forth to start movement.

Encourage daily range of motion exercises to avoid rigidity and contractures.

Remind the client to maintain good posture and avoid flexion of the neck and shoulder.

Regular daytime rest should be encouraged

-

Bed laying flat for 30 mins-1 hrs

NURSING INTERVENTIONS
-

Self care activities are performed more slowly by the client.

-

Extra time should be allowed for completion of task.

Praise for the perseverance

Recommend rests periods during meals to avoid aspiration.

ADL or exercise should be performed when drugs are working well to avoid injury to the client and caregiver

NURSING INTERVENTIONS
-

Teach the client about home safety

-

Loose carpeting should be removed Grab bars should be placed in the bathroom Elevated toilet should be installed Severe tremor should avoid carrying hot liquids Walking aids provided add stability

Multiple sclerosis (MS)

demyelinating

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Multiple Sclerosis(MS)
Is

a chronic demyelinating disease that affects the myelin sheath of neuron of CNS of myelin deteriorates at irregular intervals along the nerve axon- causing slowing of nerve conduction.
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Patches

MS
Onset

usually 20-40 y 2x

Women

Whites

affected more
in colder climates

Prevalent

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MS

CAUSE: UNKNOWN THEORIES: Immunogenetic-viral disease Triggering Factor

Viral infection ( EBV)

Multiple genes involved HLA-6

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MS

Precipitating factor:

Infection Physical injury Emotional stress Pregnancy- 3 months postpartum

fatigue

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Pathophysiology
Precipitating factor/ Triggering factor

Autoimmune & infectious agent implicated

Recognized self antigen expressed in the CNS

Activated T cell & macrophages enter the brain from Peripheral circulation

Initiate the inflammation through production of inflammatory Cytokines and reactive oxygen species.

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Pathophysiology
Activated T-Lymphocytes and macrophages

Demyelinization and destruction of oligodendrocytes

Whiter matter CNS Optic nerves, cerebrum Cervical spinal cord

Plaque form along the myelin sheath causing destruction And scarring
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CLINICAL MANIFESTATION
1.

FOUR CLINICAL PATTERN RELAPSING-REMITTING -episode of acute worsening with recovery and a stable course between relapse

2. -

SECONDARY PROGRESSIVE Gradual neurologic deterioration with or without superimposed acute relapse

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CLINICAL MANIFESTATION
3.PRIMARY PROGRESSIVE Gradual, nearly continuous neurologic deterioration from the onset of manifestation 4.PROGRESSIVE RELAPSING Gradual neurologic deterioration from the onset of manifestations but with subsequent superimposed relapses

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CLINICAL MANIFESTATION

Weakness or tingling sensation ( paresthesias) Vision loss from optic neuritis Incoordination- cerebellar involvement Bowel and bladder dysfunction- spinal cord involvement

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CLINICAL MANIFESTATIONS
1.

Primary symptomsa. fatigue- throughout the course

b. depression as reaction to diagnosis

c. weakness, numbness, difficulty in coordination, loss of balance

d. pain occurs in 66% due to demyelination of pain fibers

2. Visual disturbances lesion in the optic nerve a. blurring of vision b. Diplopia initial sign c. patchy blindness (scotoma) d. total blindness CHARCOTS TRIAD Scanning speech

Intentional tremors
Nystagmus

3. Spasticity (muscle hypertonicity) of the extremities and loss of abdominal reflexes 4. Ataxia

5. Emotional lability and euphoria

6. bladder, bowel and sexual dysfunction

DIAGNOSTIC TESTS

NO DEFINITIVE DIAGNOSTIC TEST Detailed history, clinical findings 1.

MRI- primary diagnostic study

2. CSF Immunoglobulin G 3. Evoked potentials of the optic pathway and auditory system- assess slowed nerve conduction

NURSING INTERVENTIONS
1. Promote physical mobility

Exercise Schedule activity and rest periods Warm packs over the spastic area Swimming and cycling are very useful

2. Protect client from injury by providing safety measures

Wide stance walking

Use of walking aids

Wheelchair

3. Enhance bladder and bowel control

Set a voiding schedule Intermittent bladder catheterization Adequate fluids, dietary fibers and bowel training program

4 . Manage speech and swallowing difficulties

Careful feeding, proper positioning, suction machine availability

Speech therapist

5. Improve Sensory and Cognitive function

Vision- use eye patch for diplopia Obtain large printed reading materials Offer emotional support Involve the family in the care

6. Strengthen coping mechanism

Alleviate the stress Referral to the appropriate agencies

7. improve self-care abilities

Modify activities according to physical strength

Provide assistive devices

8. promote sexual functioning

Refer to sexual counselor

MOST IMPORTANT THERAPEUTIC AIM IS PREVENT OR POSTPONE LONGTERM DISABILITY

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TREAT ACUTE REPLASE

USE OF IV/ORAL CORTICOSTERIOD Azathioprine/ ( Imuran) cyclophosphamide ( Cytoxan) severe form more

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Treat Exacerbation

Interferon- 1b (Betaseron) used for ambulatory client with relapsing-remitting

Antiviral and immunoregulatory SQ every other day Provide delayed disability

Interferon- 1a (Avonex)- for relapsing form

Glatiramer (Copaxone)- use for relapsingremitting MS. Mimic myelin basic CHON; prevent damage

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Immunosuppresants to stabilize disease process Corticosteroids to reduce edema and inflammatory porcess BACLOFEN for muscle spasms NSAIDS for pain

Antidepressants

Guillian- Barre Syndrome (Demyelinating)

An auto-immune attack of the peripheral nerve myelin Acute, rapid segmental demyelination of peripheral nerves and some cranial nerves producing ascending weakness

POTENTIALLY FATAL!

CAUSE: post-infectious polyneuritis of unknown origin commonly follows viral infection (66%) Assoc. with Gastrointestinal infection (Campylobacter Jejuni) and respiratory infection

PATHOPHYSIOLOGY

Cell-mediated immune attack to the myelin sheath of the peripheral nerves

Infectious agent may elicit antibody production that can also destroy the myelin sheath of the PERIPHERAL NERVES!!

Because this syndrome causes inflammation and degenerative changes in the posterior and anterior nerve roots, MOTOR and SENSORY losses occur

SIMULTANEOUSLY!

CLINICAL MANIFESTATIONS: occurs 2 weeks before symptoms begins

1. Ascending weakness and paralysis: Leg

affected first (1 month)

3. paresthesia

2. diminished reflexes of the lower extremities

4. potential respiratory failure

Duration of symptoms are variable:complete functional recovery may take up to 2 yrs.

5. blindness 6. bulbar muscle weakness 7. autonomic dysfunction

LABORATORY EXAMINATION
1.

CSF protein level is INCREASED but the WBC remains normal in the CSF

2.

EMG and nerve conduction velocity studies

NURSING INTERVENTIONS
1.

Maintain respiratory function Chest physiotherapy and incentive spirometry Mechanical ventilator

2. Enhance physical mobility

Support paralyzed extremities Provide passive range of motion exercise Prevent DVT and pulmonary embolism Padding over bony prominences

3. Provide adequate nutrition

IVF Parenteral nutrition Assess frequently return of gag reflex

4. Improve communication

Use other means of communication

5. Decrease fear and anxiety

Provide Referrals Answer questions Provide diversional activities

6. Monitor and manage complications

DVT, Urinary retention, pulmonary embolism, respiratory failure

MEDICAL MANAGEMENT

ICU admission Mechanical Ventilation TPN and IVF

PLASMAPHERESIS
IV IMMUNOGLOBULIN