PERINATAL ASPHYXIA (07-06-2011)

Views:
 
Category: Education
     
 

Presentation Description

No description available.

Comments

By: drusmanshah (16 month(s) ago)

please send me a copy . i shall be thankful to u .. usman unums32@yahoo.com

By: drbadal30sbmc (18 month(s) ago)

sir i need ur suefactant presentation . plz send it to my mail. drbadal30@ yahoo. com

By: nadeem2sahibzada (18 month(s) ago)

your adress is not recognised.send your request on nadeem2sahibzada@gmail.com

 

By: jlborro (22 month(s) ago)

can i request for a copy (jborro3@yahoo.com)

By: abdelmohsen1 (32 month(s) ago)

Could u please mail the presentation of genetic counsiling to me I am AbdelMohsen Mostafa Egypt (abdelmohsen1@hotmail.com) all thanks

By: nadeem2sahibzada (33 month(s) ago)

brother ! i am out station this time.i will mail you both the presentations soon Inshaallah.

See all

Presentation Transcript

PERINATAL ASPHYXIA:

PERINATAL ASPHYXIA Dr.Nadeem-Ur-Rasool DCH Trainee

DEFINITIONS:

DEFINITIONS ASPHYXIA :- Lack of Oxygen due to failure of initiation of breathing. HYPOXEMIA :- ↓ Oxygenation of the blood HYPOXIA :- ↓ Oxygen supply to the tissues. HYPERCAPNIA :- Impairment in the exchang of respiratory gases.

Cont…...….:

Cont…...…. ISCHEMIA :- Decreased blood flow to cells\organs insufficient to maintain their function. PERINATAL ASPHYXIA \ HIE :- Impaired blood gas exchange during intrapartum period.If persists leads to progressive hypoxemia & hypercapnia with metabolic acidosis that may result in ischemic encephalopathy.

Cont……...:

Cont……... NEONATAL ENCEPHALOPATHY :- Disturbed neurologic functions …. difficulity in maintaining respiration,hypotonia,altered level of consciousness,reflexes,seizures&poor feeding.Does not imply HIE.HIE is a subset of NE.

PERINATAL ASPHYXIA:

PERINATAL ASPHYXIA Criteria required to define an acute intrapartum event include; Evidence of metabolic acidosis in fetal blood. Early onset of severe or moderate NE in infants born at ≥34 wks gestation. Exclusion of other identifiable etiologies……… ..trauma , coagulation disorders , infections or genetic disorders.

CAUSES :

CAUSES MATERNAL CAUSES Placental Insuffiency ( hypertension,pr-eclempsia,eclampsia,renal failure) Diabetes Chronic Lung Disease Hypotension Pelvic Abnormality Abnormal myometrial contractility (Obstructed Labor) Use of anaesthetics

Cont…...…:

Cont…...… FETAL CAUSES Abnormal lie \ presentation Cephalopelvic disproportion Postmaturity Placental infarction Placental seperation Placentitis Antepartum hemorrhage Cord prolapse \ Cord compression

Cont…..…..:

Cont…..….. NEONATAL CAUSES Airway obstruction (mucus plug \ blood clot) Aspiration pneumonia Choanal atresia Diaphragmatic hernia Depressed respiratory center (Prolonged labor \ anaesthetics )

PATHOPHYSIOLOGY:

PATHOPHYSIOLOGY Oxygen is essential for normal functioning of body cells \ organs. The Pathology depends upon the organ affected & severity of insult. Organ system involvement is usually * CNS 72% (most frequently involved) * Renal 42% * Cardiac 29% * GIT 29% * Pulmonary 26%

Cont…..….:

Cont…..…. ↓ Oxygen (Asphyxia) is followed by * Metabolic Acidosis * Hypoglycemia * Hypotension * Alteration in cerebral blood flow

Cont….:

Cont…. ↑ Glycolysis results in ↑ lactate levels High energy phosphate concentrations ↓

Cont…..…..:

Cont…..….. Energy dependent ionic pumps fails resulting in * ↓ in normal intracellular potassium due to leakage. * Influx of sodium,chloride & calcium into cells

Cont….:

Cont…. Membrane depolarization occurs leading to release of the exitotoxic neurotransmitters (glutamate & Aspartate ) which activate N-methyl-D- aspartate receptors which plays a critical role in neuronal demage .

Cont……….:

Cont………. Major circulatory changes during asphyxia are: * Loss of cerebrovascular autoregulation (Cerebral blood flow becomes “Pressure Passive”) * Initial increase in CBF (2 nd ry to redistributin of cardiac output , initial systemic HTN, loss of cerebro -vascular auto-regulation , local accumulation of vasodilator factors i.e H*.K*, adenosine,prostaglandin ) ↓

Cont….:

Cont…. * In prolonged asphyxia…. ↓ In cardiac output, hypotension, ↓ CBF. * Post-asphyxia… persistance state of vasoparalysis & cerebral hypremia ……. severity correlates with severity of insult.

Cont……….:

Cont………. In CNS decreased cerebral oxygenation & hypo-perfusion in combination with metabolic changes increased capillary permeability resulting in fluid leaks…cerebral edema & cell death. Full term infants show cortical necrosis & para-sagittal ischemic injury resulting in focal & multifocal cortical infarcts producing focal seizures & hemiplegia .

Cont…….:

Cont……. In Preterm infants…. Periventricular leukomalacia,basal ganglia demage & IVH occurs. The majority of neuronal disintegration occurs after termination of the asphyxial insult. (due to persistence of abnormal energy metabolism & low ATP levels)

STAGES OF HIE:

STAGES OF HIE Stage 1 : Hyperalertness,uninhibited Moro & stretch reflexes lasting < 24 hours. Stag 2 : Progressive obtundation,hypotonia , ↓ spontaneous movements with or without seizures. Stage 3 : Stuporous & flaccid with depressed brain stem responces & have seizures.

Multiple Organ Involvement:

Multiple Organ Involvement CVS : shock,hypotension,tricuspid insufficiency,myocardial necrosis,CCF,ventricular dysfunction RENAL : Oliguria \ anuria,acte tubular or cortical necrosis, renal failure. HEPATIC : ↑ ammonia & indirect bilirubin , ↓ clotting factors at 3-4 days of age in mod. To severe asphyxia . ↓

Cont…..….:

Cont…..…. GIT : Paralytic ileus , NEC. LUNGS : RDS , Pul.Hemorrhage , shock lung , pul.hypertension HAEMATOLOGIC : Thrombocytopenia,DIC . METABOLIC : Acidosis , hypoglycemia , hypocalcemia , hyponatremia ,SIADH.

INCIDENCE:

INCIDENCE Is usually related to gestational age & birth weight . incidence is higher in premature. In developed countries is 1-2 % and in pakistan is 3.3%.

DIAGNOSIS:

DIAGNOSIS No specific blood test to diagnose perinatal asphyxia. Fetal acidemia …fetal arterial ph <7 Umbilical artery PO 2 levels.( not predictive of adverse outcome) Apgar score… poor tool for assessing asphyxia. FHR

Cont….:

Cont…. EEG CT.. (assessment of diffuse cortical neuronal injury,brain calcifications, haemorrhagic lesions) MRI.. (technique of choice.periventricular white matter injury,arterial infarction,brain malformations,HIE )

MANAGEMENT:

MANAGEMENT Prevention….optimal management. Immediate resuscitation. Maintenance of adequate ventilation. Maintenance of adequate Oxygenation.

Cont….:

Cont…. Maintenance of adequate perfusion. Correction of metabolic acidosis. Maintenance of normal serum glucose level. Control of seizures.

Cont…..:

Cont….. Prevention of cerebral edema…* fluid restriction, * mannitol (0.5-1g/kg/dose, * avoide steroids. Maintenance of fluid & electrolyte balance.. *Monitor urine output , should be more than 1 ml/kg/hr. * a single dose of theophylline within 1 st h of life in term HIE pts. May improve renal function.

Cont…..:

Cont….. Maintenance of thermoneutral environment. Pharmacologic agents. * Mg* * agents to prevent free O 2 redical formation ( allupurinol,inhibitors of nitric oxide production) * Ca* channel blockers All these pharmacological agents remain investigational

Cont…….….:

Cont…….…. PROGNOSIS Most survivors do not have major sequelae .

Cont….:

Cont…. Long term neurologic sequelae can be predicted on basis of; * severity of the encephalopathy. * presence of neonatal seizures … esp. in 1 st 12h after birth. * an abnormal MRI .. obtained in 1 st 24-72 h. * severity & duration of EEG abnormalities. * microcephaly at 3 months of age or an abnormal neurologic exam at 12 months of age.

Cont….….:

Cont….…. Nondisabled survivors of moderate HIE have ; *delayed skills in reading , spelling. *difficulties with attention. * difficulties in short term recall