1. به نام خداوند بخشنده و مهربان

2. تشخیص آسفیکسی

3. PERINATAL ASPHYXIA
The term asphyxia, from the Greek word for suffocation,
is used to describe the interrupted supply of oxygen
through the placenta and umbilical cord to the fetus. This
will lead to a combined hypoxemia and hypercapnia.
In case of total interruption of oxygen, within minutes
anaerobic glycolysis will occur and a lactic acidosis, and
thereby metabolic acidosis, will be produced. This can
be measured by blood gas analysis. In addition, a (fetal)
bradycardia will develop, which will add ischemia to the
process, and augment cerebral hypoxia and hypercapnia.

4. Prolonged Hypoxia
Asphyxia
Ischemia
Lactic Acid Production

5. DIAGNOSIS A. Perinatal assessment of risk B. Low Apgar scores
C. Umbilical cord or first blood gas
D. Clinical presentation and differential diagnosis

6. APGAR SCORE A: appearance(skin color) P: pulse(heart rate)
G: grimace(reactive ability)
A: activity(muscular tension)
R: respiration

7. APGAR score Score 0 1 2 Heart rate none <100 > 100
Respiration none irregular regular
Muscle tone limp reduced normal
Response to none grimaced cough
stimulation
Color of trunk white blue pink

8. SYSTEMIC ADAPTATION TO HYPOXIC-ISCHEMIC INSULT
Severe fetal hypoxic-ischemic injury affects the entire organism .
Hypoxic-ischemic injury may occur at any time during pregnancy, the birth process, or the neonatal period. The pattern of brain damage is reflected by the gestational age of the fetus at the time that the injury occurs.

9. Asphyxia may be suspected when there is:
1. Prolonged (1 hour) antenatal acidosis
2. Fetal HR 60 beats/minute
3. Apgar score 3 at 10 minutes
4. Need for positive pressure ventilation for 1 minute or first cry delayed
5 minutes
5. Seizures within 12 to 24 hours of birth
6. Burst suppression or suppressed background pattern on EEG or amplitude integrated EEG (aEEG)

10. A clinical evaluation and laboratory and instrumental examinations are required in order to assess and manage the asphyxiated newborn.

11. MULTIORGAN DYSFUNCTION
A. kidney
B. Cardiac
C. Gastrointestinal effects
D. Hematologic effects
E. Liver dysfunction
F. Pulmonary effects
G. Brain

12. Effects of Asphyxia Central nervous system :
- infarction, intracranial hemorrhage,cerebral edema, seizure,
hypoxic-ischemic encephalopathy
Cardiovascular :
- bradycardia, ventricular hypertrophy, arrhythmia, hypotension,
myocardial ischemia
Respiratory system :
- apnea, respiratory distress syndrome, cyanosis

13. Effects of Asphyxia KUB : -acute tubular necrosis, bladder paralysis
Gastrointestinal tract :
- Necrotizing enterocolitis , stress ulcer
Hematology :
- Disseminated intravascular coagulation
Metabolic :
- hypoglycemia, hyperglycemia, hypocalcemia, hyponatremia
Integument :
- subcutaneous fat necrosis

14. NEUROLOGIC SIGNS. A. Encephalopathy
B. Brain stem and cranial nerve abnormalities
C. Motor abnormalities
D. Seizures
E. Increased intracranial pressure (ICP)

17. LABORATORY EVALUATION OF ASPHYXIA

18. A. Cardiac evaluation
1. Cardiac troponin I (cTNI) and cardiac troponin T (cTnT)
2. An elevation of serum creatine kinase myocardial bound (CK-MB) fraction of 5% to 10% may indicate myocardial injury.

19. B. Neurologic markers of brain injury
1. Serum CK-BB may be increased in asphyxiated newborns within 12 hours of the insult, but has not been correlated with long-term neurodevelopmental outcome. CK-BB is also expressed in placenta, lungs, gastrointestinal tract, and kidneys. Other serum markers such as protein S-100, neuron specific enolase (NSE) , and urine markers have been measured in newborns with asphyxia and HIE. 2. In practice, serum and urine markers of brain injury are not routinely used to evaluate for the presence of brain injury or to predict outcome.

20. 3. Both NRBC count and NRBC count per 100 white blood cells (NRBC/100WBCs) have been
found to be higher in those patients that exhibited a convulsion in the first 12 hours after
birth, and in those patients that subsequently developed HIE stage III.
4. Glial fibrillary acid protein (GFAP) and ubiquitin carboxyl-terminal hydrolase L1
(UCH-L1), normally expressed either in neurons and in astrocytes, are easily measurable
markers of neuronal apoptosis as they are released into blood circulation after a blood-
brain barrier damage caused by hypoxia.

21. C. Renal evaluation
1. Blood urea nitrogen (BUN) and serum creatinine (Cr) may be elevated in perinatal asphyxia. Typically, elevation is noted 2 to 4 days after the insult.
2. Fractional excretion (FE Na) of Na or renal failure index may help confirm renal insult.
3. Urine levels of -2-microglobulin have been used as an indicator of proximal tubular dysfunction, although not routinely.
4. Renal sonographic abnormalities correlate with the occurrence of oliguria.
5. Cystatin C is another marker of renal damage.

22. D. Hepatic and Gastrointestinal Systems
[LDH] is a good predictor of HIE during the first 12 h after birth. This result is of clinical interest offering a potential inexpensive and safe prognostic marker in newborn infants with perinatal asphyxia.
Elevated liver enzymes occur in 80% to 85% of asphyxiated
full-term newborn infants during the first week of life.

23. E. Hematologic System
Coagulation impairment is relatively common after a
severe asphyxial insult.
Coagulation impairment should be anticipated and
screening for hematologic abnormalities undertaken in
all severely asphyxiated newborn infants.

24. BRAIN IMAGING A. Cranial sonography B. Computed tomography (CT)
C. Magnetic resonance imaging (MRI)
-1. Diffusion-weighted imaging (DWI)
-2. Proton magnetic resonance spectroscopy (MRS)
-3. MR angiography or venography
D. Doppler ultrasonography

25. U/S Blurring of borders = snow storm pattern. Slit like ventricles.
Echodensities in regions of basal ganglia.
Signifying cerebral edema and hypoxic injury..
Cranial sonography can be used to detect severe cerebral edema.
Findings include:
a. increased echogenicity in basal ganglia
b. sulci and fissures are obscured, blurring of other anatomical landmarks
b. decreased arterial pulsations
c. compression of the ventricles.
Put pic of Clark ECHO dense RBG.
After a few days, areas of echodensity that correspond to regions of necrosis may be present.

26. Doppler HUS RI below 0.65 increases likelihood of asphyxia.
RI value below (measured in the anterior cerebral artery) correlates with a poor neurodevelopment prognosis, especially if measured in the first 24 to 72 h after HIE.
As RI are > 0.65, cerebral edema is usually apparent.
Sometimes early on from an ischemic insult, there can be reduced RI < 0.45 (first 24 – 48 hours).

27. Resistive index (RI)
RI is obtained by measuring systolic and diastolic blood flow velocities by Doppler US (usually in the anterior cerebral artery)
and calculating the RI as given by the formula:
RI = (systolic - diastolic)
systolic
RI value significantly decreased in asphyxiated term neonates compared with healthy subjects.

28. CT Scan
Blurring of the borders between WM and GM, and a localized echolucent area = infarction of the right basal ganglia.
The American Academy of Neurology (AAN) practice parameter suggests that a head CT be performed in cases of neonatal encephalopathy to rule out hemorrhagic lesions.
After a few days, areas of echodensity that correspond to regions of necrosis may be present.
Here you see signs of edema/infarction in the R basal Ganglia.

29. MRI

30. Diffusion-weighted MRI

31. Spectroscopy Metabolites in the Brain
Classic area to look for damage with HIE is the basal ganglia.
“Doublet peak of lactate”

32. Spectroscopy

33. EEG
-Amplitude-integrated EEG (aEEG)
-8- or 16-channel neonatal EEG

35. Near-infrared spectroscopy(NIRS)
A recent study has assessed the correlation between measurements of cerebral perfusion by NIRS and by MRI in full-term infants with HIE treated with hypothermia. A high correlation has been found between the two tools regarding brain perfusion measurements in term infants with severe encephalopathy.

36. Evoked Potentials
BAEPs
VEPs
SEPs
FVEPs

37. When comparing FVEPs and VEPs, some studies showed SEPs to be superior in the prediction of neurodevelopmental outcome. Because the predictive value within the first 6 hours after birth was noted to be similar for aEEG and evoked potentials, aEEG is preferred because of easy access, application, and interpretation.

38. Heart evaluations
Evidence of myocardial dysfunction was present in all the 50 newborns who had suffered from moderate and severe birth asphyxia. Myocardial status were dependent on the degree of asphyxia. Myocardial dysfunction detected by Doppler ultrasonography has been shown to occur in many asphyxiated newborn infants. Early diagnosis and treatment of these cases reduced mortality in moderate asphyxia to zero and in severe asphyxia to 40% in the present study .

39. . In 10 newborns who suffered from moderate asphyxia, myocardial status was as follows: respiratory distress in eight (80%) cardiac murmur in two (20%), cardiomegaly on X-ray was present in three (30%) and ischemic changes in form of ST, T changes in ECG in all. Shock and CHF were absent. Of 40 cases of severe birth asphyxia features observed were shock in four (10%) CHF in nine (22.5%) respiratory distress in 40 (100%) cardiac murmur in 40 (100%) ischemic changes inform of ST depression, abnormal Q and T waves in 40 (100%) cardiomegaly in 28 (70%).

40. پایان دکتر رویا طاهری تفتی فوق تخصص نوزادان
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