Asphyxia is a Greek word which means “stopping of the pulse”, a condition due to lack of oxygen in respired air, resulting in impending or actual cessation of apparent life. There is wide variation in the definition of asphyxia in medical literature. The American Academy of Pediatrics Committee on fetus and newborn has therefore suggested the following essential criteria for defining a case of Hypoxic Ischemic Encephalopathy.

Table: Essential criteria for perinatal asphyxia Prolonged metabolic or mixed academia (pH < 7.00) on an umbilical cord arterial blood sample. Persistence of an Apgar score of 0-3 for >5 minutes. Clinical neurological manifestations e.g., seizure, hypotonia, coma or hypoxic-ischemic encephalopathy in the immediate neonatal period. Evidence of multi-organ system dysfunction in the immediate neonatal period
Table: Multi-organ system dysfunction in perinatal asphyxia
C.N.S. Pulmonary Renal Metabolic Gastrointestinal Hematologic Death	Hypoxic ischemic, encephalopathy, cerebral edema, neonatal seizure, long-term neurologic sequelae. Primary pulmonary hypertension, meconium aspiration, surfactant disruption. Oliguria, acute renal failure. Metabolic acidosis, hypoglycemia, hypocalcaemia, hyponatremia. Necrotizing enterocolitis, hepatic dysfunction. Thrombocytopenia, disseminated intravascular coagulation

Role of intrapartum fetal monitoring :

There is definite role of monitoring the fetus during intrapartum period, which would enable obstetricians for timely intervention and immediate delivery. This also gives enough time for the neonatologists for timely preparedness. The fetal movement count is an important tool, which has a sensitivity of 12-50% and specificity of 91-97%. The non stress test has a sensitivity of 14-59% and specificity of 79-97%. The fetal biophysical profile has typical positive likelihood ratio of 2.5-27.4 and negative likelihood ratio of 0.2-0.9. Fetal heart rate monitoring is a simple tool and abnormal pattern is indicative of a sensitivity of 70% and specificity of 80%. Fetal scalp blood pH monitoring is by far he best indicator of fetal hypoxia but is an invasive and difficult procedure, which has a sensitivity of 31% and specificity of 93%.

HYPOXIC ISCHAEMIC ENCEPHALOPATHY (HIE)

This is a characteristic neurological syndrome that occurs in newborn babies due to lack of oxygen (hypoxia) and lack of perfusion (ischemia). In term babies the syndrome occurs after a period of perinatal asphyxia and is also called post asphyxial encephalopathy (PAE). In preterm babies the insult most often is postnatal and affects the periventricular white matter whereas in term babies, the damage commonly occurs in cerebral cortex.

Classification of severity of HIE (Levene)

Features Consciousness Tone Seizure Sucking/Respiration

Mild Irritability Hypotonic No Spontaneous

Moderate Lethargy Marked Yes Poor suck

Severe Comatose Severe Prolonged Unable to suck & maintain spontaneous respiration

Management in the labour room –

As soon as the baby is born all efforts should be made to do immediate resuscitative measures as per NRP guidelines, which is adapted by National Neonatology Forum of India.

Nursery management –

The baby should be transferred to neonatal nursery with oxygen if required and preferably under a preheated radiant warmer or in a transport incubator. In the nursery, repeat initial assessment including BP, pulse oximetry and glucose estimation.

Supportive care –

Maintenance of temperature by keeping under radiant warmer, perfusion by appropriate fluid therapy, oxygenation, normal metabolic state and control of seizures are the hallmarks of successful management of perinatal asphyxia.

Oxygenation –

Oxygenation should be maintained at normal level by constant monitoring with a pulse oximeter and if facilities are available by ABC monitoring. Hyper oxygenation and aminophylline are contraindicated since both can decrease cerebral blood flow.

Management of seizures –

Most of the episode of seizures associated with asphyxia settles on its own and does not require any anticonvulsant. However if the seizure persists for more than three episodes per hour for s duration of more than three minutes, then phenobarbitone is the drug of choice. A loading dose of phenobarbitone in the dose of 20 mg/kg is recommended followed by maintenance dose of 5-6 mg/kg body wt. If the seizure is not controlled by phenobarbitone, phenytoin may be added. In refractory seizure, midazolam infusion or lorazepam or in its absence diazepam may be tried. However, diazepam should be avoided. The role of newer antiepileptics in neonatal seizures is debatable and sufficient evidence for their use is lacking at the present time. Most of the anticonvulsants can be tapered and withdrawn at the time of discharge. Some of the cases with persistent seizures need further evaluation in the form of EEC, CT, MRI and evoked visual and auditory responses. Based on the investigations and neurological status of the child, a decision on continuation of antiepileptic is decided. There is no indication of steroids or mannitol in the management of cerebral edema associated with asphyxia since the edema is cytotoxic in nature, which will resolve with careful fluid management and proper maintenance of BP and peripheral perfusion.

Hypoglycemia, Hypocalcemia and Hyponatremia –

In asphyxia usually 10% glucose drips which is started as initial maintenance fluid is sufficient in most of the cases. However in symptomatic hypoglycemia, bolus dose is required. Symptomatic hypocalcemia needs correction. In persistent hypocalcemia, serum magnesium level is to be obtained. Hyponatremia should be anticipated and prevented by restriction of fluid administration.

Shock –

Hypovolemic shock is treated with bolus dose of normal saline, ringer lactate, plasma or whole blood may be given at the dose of 10 ml/kg body weight. In cardiogenic shock administration of dopamine 5-20 microgram/kg/minute is administered. In case of no response to dobutamine in the same doses schedule is tried. Routine CVP monitoring is not required but in case of refractory shock, an umbilical catheter is placed and advanced to atria for monitoring of CVP.

Renal complication –

Daily monitoring of urine output, body weight and renal function tests should be carried out. Estimation of electrolytes e.g., sodium and potassium is essential. In prerenal failure bolus dose of normal saline or ringer lactate is given in the dose of 10-20 ml/kg body weight in 1-2 hours. If there is intrinsic renal failure, fluid restriction is done with 40 ml/kg body weight per day plus urine output. Careful evaluation of electrolyte would decide about the fluid management. Dopamine in the dose of 2.5-5.0 microgram/kg/minute may be administered to increase renal blood flow. If serum potassium is high, supplemental potassium is withheld. Potassium is started only after neonate stars passing adequate urine. In case serum potassium exceeds 6 meq/dl, lasix, calcium, sodium bicarbonate, glucose/insulin drip may be required. In severe intrinsic renal failure due to acute tubular necrosis, peritoneal dialysis is indicated. However, PD is rarely required in post asphyxial renal involvement in newborn.

Sepsis –

The screening for sepsis should be undertaken in all cases of asphyxia e.g., complete blood examination, micro ESR, CRP, immature neutrophil count urine culture and sensitivity, chest x-ray and blood culture. Most of the patients with asphyxia would require to be kept under antibiotic cover with ampicillin and gentamicin combination as first line drug.

Feeding –

Most of the cases of severe asphyxia would have bowel ischemia and increase chances of development of neonatal necrotizing enterocolitis. It is recommended to withhold enteral feeding for 5-7 days.

Other supportive measures include transfusion of blood products as and when indicated specially if DIC sets in.

Mechanical ventilation –

If the baby is not able to maintain normal respiration and blood gas level with oxygen, mechanical ventilatory support may be needed. However, it is to be noted that while on ventilation care should be taken not to hyperventilate and wash out carbon dioxide. Hypocapnia can lead to cerebral ischemia and infarcts whereas hypercapnea can lead to increased cerebral perfusion and worsen cerebral edema. However, mild hypercarbia with pco2 level of 40-45 mm of Hg is recommended.

Table : Potential therapeutic strategies

Blockade of free radical generation. Scavenging of oxygen free radicals Substrate manipulation Blockade of secondary metabolites or inflammatory mediators. Blockade of platelet adhesion. Inhibition of excitatory amino acids.

Management of perinatal asphyxia is mainly symptomatic and supportive. There is abundance of potential treatment options in the management of ischemia and reperfusion injury following perinatal asphyxia. The stumbling block is that most of the drugs need to be administered either prophylactically or very early in the disease because of very short window period in newborn babies. Among the drugs allopurinol, magnesium sulphate and nimodepine needs further trial. There is a very great potential for high dose phenobarbitone in severe hypoxic-ischemic injury and needs further evaluation in Indian set up. Role of hypothermia should be evaluated by well-controlled multicentric studies. At present all these drugs are to be considered to be of experimental in nature and should not be used for management.

Maha Neocon 2005 - Conference Abstracts.Pediatric Oncall [serial online] 2006 [cited 15 February 2006(Supplement 2)];3. Available from:
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