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1.To understand the etiology and the

pathogenesis of HDN ?

Etiology - Caused by blood type incompatibility between mother and

fetus.

Pathogenesis :-

1. Hemolysis of ABO blood type incompatibility can occurred at first

fetus.

2. Hemolysis of Rh blood type incompatibility occurred at second orlater fetus.

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3. Diagnosis and the treatment of HDN ?

Diagnosis :-

1Hemolysis of ABO blood type

incompatibility:

The antibody release test result is positive

usually.

2

Hemolysis of Rh blood typeincompatibility

The direct Coombs test is positive usually.

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Treatments:

Premature treatments :-

Premature delivery:

If labor is induced, fetal lung maturity must be determined

using the lecithin/sphingomyelon (L/S) ratio (thin layer

chromatography) to avoid respiratory distress syndrome Plasmapheresis :

For the pregnant mother unsuitable the premature delivery.

Intrauterine blood transfusion:

If fetal hydrops or fetal Hb

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Neonatal treatments: -

Phototherapy

Exchange Transfusions

Pharmacological agents

Other treatments : -

Prevention of hypoglycemia,hypothermia.

To correct hypoxia,anemia,edema and heart failure.

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4. Definition :-

Billirubin encephalopathy

Neurologic syndrome resulting from the deposition of

unconjugated bilirubin in nucleus basalis.

Main cause due to hemolytic disease.

Caused by any other disease with unconjugated

hyperbilirubinemia.

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5. Clinical manifestations and diagnosis of

Bilirubin Encephalopathy ?

Warning stage: lasts about 12-24hrs.

Spasm stage: lasts about 12-48hrs.

Convalescent stage: lasts about 2weeks.

Sequelae stage

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Warning stage of BE

Lethargy

Low response

Sucking weakness

Weak sucking and moro reflexing

Vomiting

Reduced muscle tone

Severe jaundice

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Spasm stage

Convulsion

Opisthotonos and fever

Increased muscle tone

Apnea

Stiffly extending his of her arms inward rotation with fists

clenched or even opisthotonos

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Convalescent stage

Nursing and reaction improvement

Reduction of seizure frequency

Opisthotonos gradually disappeared

Muscle tone gradually recovered

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Sequelae stage:BE of tetralogy

Athetosis

Limitation of eyes movement

Hearing impairment

Enamel dysplasia

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6. Therapy of BE ?

Phototherapy

Plasma or albumin

Exchange transfusion

Enzyme inducer: phenobarbital

Original diseases treatment

The other symptomatic treatment

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7. How do we avoid the bilirubin

encephalopathy for HDN infants?

Declining jaundice quickly is necessary 4 HDN

infants 2 avoid BE .

Phototherapy

Exchange transfusions

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8. whats the characteristics of physiologic

jaundice

The characteristics of physiologic jaundice : -1Jaundice appears at 2~3 days.

2Full-term neonates jaundice declines to adult levels

within 14d. Prematures jaundice usually delays to 3~4 wkof age.

3Bilirubin level of blood serum < 222~257 mol/L

4Conjugated bilirubin level of blood < 34 mol/L

5Bilirubin level of blood serum increases every day

< 85mol/L.

6General condition of the baby is well.

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9. Whats the characteristics of pathologic

jaundice?

The characteristics of pathologic jaundice :-

1Appear too early

2Degree too severe3Duration too long

4Progress too rapid

5Again appeared after it subsided

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10. Treatment of neonatal jaundice ?

Phototherapy

Light source : spectral outputs 420 500 nm

Exchange transfusions : -

Remove antibody

Remove bilirubin

Correct anemia

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11. Differences between physiologic jaundice

and pathologic jaundice ?

Refer to slide 16- 17.

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12. Indications & Complications of

Phototherapy ?

Phototherapy : Lipid unconjugated bilirubin water- soluble isomeride- Light source: Spectral outputs 420 to 500nm

Side effects of phototherapy :

a. Diarrheab. Fever

c. Skin rash

d. Bronze baby syndrome

(Conjugated bilirubin > 4mg/dl)

e. Riboflavin reduction

f. Dehydration and Hypocalcemia

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13. Diagnosis test of HDN ?

Sensitized erythrocytes and blood group

antibodies determination:

Coombs test : Red blood cells sensitized.

Antibody releasing test : Sensitivity test to detect

sensitized erythrocytes.

Blood type antibody test in the infant serum.

Blood type antibody test in the maternal serum.

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14. Pathophysiology of Rh ?

Pathophysiology :-

Seizures etc.

Red blood cell breakdown

Hyperbilirubinemia

Jaundice

Kernicterus

Anemia

1. Liver

2. Spleen

3. Heart, other organs

4. Hydrops

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15. Indications of Exchange Transfusions ?

Indication of transfusions:

one of the follows

a. 20mg/dl (340 mol/L)b. > 4mg/dl,Hgb

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16. Causes of neonatal hypoxic ischemic

encephalopathy ?Causes

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17. Pathology & Pathophysiological changes

of neonatal HIE ?

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Pathophysiology

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18. Clinical features of neonatal HIE ?

Muscle tone and deep tendon reflexes

Behavioral abnormalities

Neonatal reflexes Apnea and seizures

Stupor and ventilatory support

Ocular motion and pupils

Heart rate and blood pressure

Outcome

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19. Differential diagnosis of neonatal HIE ?

Methylmalonic Acidemia

Propionic Acidemia

Urea cycle defects Zellweger syndrome

Mitochondrial disorders

Neuromuscular disorders Brain tumors

Developmental defects

Infections

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20. Treatment of neonatal HIE ?

Medical Care : -

Initial resuscitation and stabilization

Supportive care: mechanical ventilation

Perfusion and blood pressure management

Fluid and electrolytes management

Hyperthermia management

Treatment of seizures

Surgical Care

Consultations

Diet

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21. Prognosis of neonatal HIE ?

Lack of spontaneous respiratory effort

The presence of seizures

Abnormal neurological findings

Abnormal EEG background

Feeding difficulties

Poor head growth

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22. Diagnosis criteria of bacterial

meningitis ?

Confirmation of the diagnosis: isolation from the CSF of a specific

bacteria pathogen by microscopy or a positive culture or rapid

antigen-detection test of CSF

Gram-stained smear of CSF: identify the causative organism in

70-90% of cases

CSF culture: positive in about 80% of cases. Definitive

diagnosis, determination of antibiotic sensitivity.

PCR: amplifies bacteria DNA(H influenzae, N meningitidis)

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23.Symptom of purulent meningitis ?

Fever

Headache

Vomiting

Increased ICP

Meningeal Irritation

Anorexia

Malaise

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25. Treatment of Meningitis

Antibiotic : Penicilln,Ampicillin,ceftriaxoneCorticosteroid : Dexamethasone

Mannitol

General and supportive measure

Maintenance fluid and thermal energy supplement.

Fluid administration: 60-80ml/kg.d

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26.Complication of epilepsy ?

1.Mental retardation

2.Loss of hearing

3.Impairment of visual area

4.Motor and sensory deficits

27 T b l M i i i

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27. Tuberculous Meningitis

(Manifestation)

Increased Intracranial Pressure

Cranial Nerve Injury

Meninges Irritation Signs

Cerebral-Parenchyma Damage

Spinal Cord Damage

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Pneumonia (Manifestation)

Tachypnea, Dyspnea,

Retractions,

Grunting,

Nasal flaring,

Cyanosis and the presence of rales or rhonchi on physical examination.

Lethargy,

Poor feeding,

Fever, temperature instability,

Apnea,

Tachycardia,

Poor perfusion,

Metabolic acidosis

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Tuberculosis Symptoms

Perpetual Cough

Fever

Weight loss

Night sweats

Loss of appetite

Fatigue

Pain while breathing

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Diagnosis of TB

Tuberculin skin test

Chest X-ray

Physical examination

Serological (blood) test

AFD test (collect sputum to smear and culture

it)

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TREATMENT FOR ACTIVE TB

A combination of the following four antibiotics are the mostcommonly used, however are not risk free:

rifampicin R

It may cause fever, rashes, liver damage, and in some rare cases has

led to death.

isoniazid H It may cause rash and abnormal liver function tests.

ethambutol E

It may cause Red-green color blindness and loss of vision

pyrazinamide Z

It may cause joint pains, nausea, vomiting, skin rash,, malaise, and

fever

When taking antibiotics, overdose and underdose is a problem

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Treatment for TB meningitis

Antituberculosis drugs

Corticosteroids

Decrease intracranial pressure

Ventriculoperitoneal shunting

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Questions

What is diagnostic criteria of nephrotic syndrome?

How to distinguish the differences between simple type and

nephritic type?

What are causes of the nephrotic syndrome ?

What is histology of primary nephrotic syndrome?

What are major complications of nephrotic syndrome?

How to treat nephrotic syndrome?

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Diagnostic Criteria

1. Nephrotic range proteinuria proteinuria(>50mg/kg/day)

Urine protein 3+ or 4+ by dipstick testing

2. Hypoalbuminaemia

serum albumin less than 25g/l

3. Oedema

The onset is insidious , with swelling around the eye and facial

puffiness .Over the next few days ,it gradually increases to involve

the extremities and abdomen

4. Hyperlipidemia

Serum cholesterol more than 5.7mmol/l

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Difference

1. Nephrotic syndrome is a disease of the kidney whilenephritic syndrome is a disease of the glomeruli. Nephriticsyndrome is also called glomerulonephritis.

2. Nephrotic syndrome manifests the classic symptoms, suchas: edema, proteinuria, hypoalbuminemia, andhyperlipidemia. Nephritic syndrome manifests the sameexcept there is an accompanying blood in the urine.

3. Diagnosis for nephrotic syndrome is a 24-hoururine/protein measurement and lipid profile while anephritic syndrome involves an ASOT, urine tests, andblood tests.

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Main causes of nephrotic syndrome (NS) in children

Primary nephrotic syndrome

Secondary nephrotic syndrome (Multisystem diseases )

Henoch-schonlein purpura Systemic lupus erythematosus Hepatitis B

Congenital nephrotic syndrome

Idiopathic CNS of Finnish type Diffuse mesangial sclerosis

Secondary Congenital syphilis

Toxoplasmosis Cytomegalovirus

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Histopathologic classification

Minimal change diseases (MCD)

Pure minimal change diseases

MCD with mesangial proliferation (MesPGN)

Focal segmental glomerulosclerosis(FSGS)

Membranoproliferative glomerulonephritis(MPGN)

Membraneous nephropathy(MN)

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Major Complications of Nephrotic Syndrome

Infection

Hypovolaemia

Thrombosis

Hyperlipidaemia

Acute renal failure

Side-effects of drugs

Corticosteroids

Alkylating agents

Cyclosporin A

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Management

Cyclophosphamide (CTX) CTX2-3mg/kg/day po for 8-12weeks ,or iv pulse CTX 0.5/m2

Cyclosporine (CsA)

Dosage of 5-6mg/kg/day to maintain the whole blood trough level

at 80 to 120ng/ml

Tacrolimus (FK506)

0.1mg/kg/day in BD doses

Trough level maintain at 5-10mcg/l

Mycophnolate mofetil (MMF)

Dosage 250-1200mg/m2/day in 2 doses

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Supportive Therapy

To minimize infection(vaccination and prophylactic antibioticcs )

To minimize risk of thrombosis

( hydration; and avoiding prolonged immobilisation)

To maintain nutrition ( high biological value protein intake ) To treat edema and hypertension

To treat hypercholesterolaemia (low cholesterol diet and lipidlowering agents)

To reduce proteinuria (ACEI or angiotensin 2 receptor blockers)

To avoid the use of nephrotoxic drugs

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General Symptoms Acute

Glomerulonephritis

Fatigue

Abdominal pain: more than half

Low-grade fever

Loss of appetite Nausea

Vomiting

Headache

Hematuria

Proteinuria

Edema Hypertension

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Lab Investigation A.G.

Urinalysis

Blood test

Blood Chemistry

Serological testing

Complement level (C3,C4)

Renal Ultrasound

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Treatment AG

Restriction

Salt

Fluid intake

Control of hypertension

Diuretics (Furosemide)

Anti hypertensives

Dialysis

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1.Inadequate storage: Premature

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Anemia three types:

Anemia of inadequate production

Hemolytic anemia

Blood loss

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1.blood filmhypochromic and microcytic2.bone marrow samplingThe bone marrow is hypercellular, with erythroid

hyperplasia,The normoblasts.may have scanty, fragmented cytoplasm with

poor hemoglobinization.

3.iron metabolism:

Iron study ID IDE IDA*serum ferritin(SF) (