7.hypoxic ischemic pdf - د. زياد

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Hypoxic ischemic

encephalopathy

Definitions

 Hypoxia/anoxia : denotes a partial or complete lack of oxygen, respectively, in

one or more tissues of the body, including the blood stream.

 Asphyxia : is the state in which pulmonary or placental gas exchange is

affected leading to progressive hypoxemia, which is severe enough to be
associated with acidosis.

 Ischemia : is a reduction in or cessation of blood flow that arises from

either systemic hypotension, cardiac arrest, or occlusive vascular disease.

 Asphyxia impaired gas exchange with both decreased oxygen and

increased carbon dioxide resulting in acidosis. Clinical features are
variable. Term and preterm infants suffer different lesions and outcomes

 Term infants=Neuronal injury.
 Preterm infants=White matter injury
 Is a term used to designate the clinical and neuropathological findings of

an encephalopathy that occurs in a infant who has experienced a
significant episode of intrapartum asphyxia

Etiology:

Interruption of maternal-fetal exchange.

 Systemic (maternal): cardiopulmonary arrest, eclampsia, hypovolumic

shock, trauma.

 Uterus: Uterine rupture
 Placenta: Abruption
 Cord: compression, rupture, knot

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Pathophysiology

HIE sequence=Primary Energy Failure.

 Hypoxemia and Hypercarbia.
 Acidosis and hypoxemia further impair cerebral autoregulation

perfusion pressures fall.

 Decreased brain perfusion (Ischemia)
 Oxygen deficiency anaerobic metabolism which requires more glucose.
 Increased lactic acid and increased hydrogen ions.
 Tissue acidosis.
 Direct neuronal damage= cell death

Incidence of HIE

 2-4% of Term infants.

20% associated with primarily antepartum events. (Maternal hypotension,
IUGR, maternal diabetes).
35% associated with intrapartum events. (cord prolapse, traumatic delivery,
placental abruption).
35% associated with a combination of antepartum and intrapartum events.
10% are associated with postnatal events. (cardiac failure, pulmonary failure).

Clinical Presentation of HIE

Stage 1



Hyperalertness, Decreased sleep



Uninhibited reflexes



Excessive reaction to stimuli



Weak suck but normal tone



Sympathetic overactivity - Eyes wide open, decreased blinking, mydriasis.



EEG normal



Duration less than 24 hours



Good prognosis - No long-term neurologic sequelae

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Stage 2



Lethargy or obtundation (ie, delayed and incomplete response sensory stimuli)



Mild hypotonia



Suppressed primitive reflexes



Seizures



Lethargy



Parasympathetic activation with miosis (even on dim light), heart rate less
than 120 beats per minute, increased peristalsis, and copious secretions)

Stage 3



Stupor response only to strong stimuli with withdrawal or decerebrate posturing only



Rarely coma



Severe hypotonia (ie, flaccidity)



Suppression of deep tendon and primitive (ie, Moro, tonic neck,
oculocephalic, suck) reflexes



Suppression of brainstem reflexes (corneal or gag)



Clinical seizures less frequent than stage 2



Deep, periodic EEG pattern with high amplitude and frequency of bursts
less than every 6-12 seconds, very-low voltag or isoelectric EEG



Major neurologic sequelae, including microcephaly, mental retardation,
CP, seizures.

Prognosis

based on apgar score

 Score at 1, 5 minutes does not give prognosis indicator
 The longer the score remains lower, the greater its significance
 0-3 at 5min , CP risk app. 1%
 may be increased to 9%if for 15min
 dramatic rise to 57% CP risk if for 20min

Outcomes

 Mild encephalopathy: will generally do well.
 Moderate encephalopathy:

1. 10% risk of death. 2. 30% risk of disabilities.

 Severe encephalopathy:

1. 60% risk of death. 2. Many if not all survivors are handicapped.

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HIE Effects on other Organ Systems

 Cardiovascular: Tricuspid insufficiency, myocardial necrosis, CHF,

ventricular dysfunction, and shock.

 Renal: Oliguria, acute tubular or cortical necrosis and renal failure.
 Liver: Liver failure, elevated ammonia and indirect bilirubin, decreased

clotting factors at 3-4 days of life.

 GI: Delayed NEC, hemorrhage.
 Resp: PPHN, depression, hemorrhage, edema, respiratory distress
 Hematologic: Thrombocytopenia from shortened platelet survival.
 Metabolic: hypo/hyperglycemia, hypocalcemia, hyponatremia,

hyperkalemia.

Diagnosis of HIE

 Obstetric History.
 Poor adaptation at birth which requires resuscitation.
 Low apgar score, need for assisted ventilation.
 Development of encephalopathy. (Seizure activity).
 Evidence of multisystem organ failure.
 Measures of impaired placental gas exchange.
 Cord pH or early venous/arterial pH .

Management

 Prevention.
 Insure physiological oxygen and acid-base balance
 Maintain environmental temp and humidity
 Correct caloric, fluid and electrolyte disturbances
 Maintain blood volume and hemostasis
 Treat infection
 Neuro-resus measures to reduce cerebral oedema ineffective
 Seizure treated with phenobarbital, or lorazepam