Necrotizing Enterocolitis in an Asphyxiated Premature Infant

Sunarka, Hamid H, Sudaryat S

(Department of Child Health, Medical School, University of Udayana/ Central General Hospital, Denpasar)

Abstract A case of NEC in a six days old asphyxiated premature infant was reported. The diagnosis was based on predisposing factors including low weight infant, severe ash- pyxia, her mother sufferef from fever and premature rupture of the amniotic membrans more than 24 hours. Clinical features include abdominal distention with discoloration of the abdominal wall, vomiting bloody stool, sclerema, temperature instability, jaundice, and respiratory distres. Plain abdominal X ray examination showed significant intestinal distention, and hiponatremia. The patient was treated with supportive therapy and sur­ gical intervention was not done because the poor condition of the patient. The prognosis of NEC depend on the severity of disease, with mortality rate varies from 0 to 64%. The prognosis of our case is not good and on January 28, 1904 she died. [Paediatr Indones 1996;36:126 131]

mon final pathway of necrosis and in­ flammation of the neonatal intestine.3 Introduction The incidence of NEC varies from one center to another. In 1985 the child Necrotizing enterocolitis (NEC) is mainly a Health Department Medical School of In­ disease of low birth-weight infant and es­ donesia University/Cipto Mangunkusu- pecially common among infant weighing mo Hospital was reported 3 cases of 1500 grams or less at birth.1 It is most NEC.4 In the united States, from recent common serious disease of the gastroin­ surveys involving 31 centers, the inci­ testinal tract.2 NEC is a disease with mul­ dence of NEC was 1.1 per 1000 livebirths tifactorial etiology leading to the one com- and 24 per 1000 admission to the neona­ tal intensive care unit.1 In the United Accepted for publication: March 22, 1996 Author's address: Kingdom, the average reporting rate of Sunarka, MD, Department of Child Health, Medical School, definite cases of NEC was 0.3 per 1000 University of Indonesia, Jakarta Sunarka, et al 127

livebirths, ranging from 9.5 per 1000 in observed. On chest inspection the tho­ neonates weighing <1000 g at birth to 0.2 racic movement was symmetric on both per 1000 in neonate weighing >2500 g at sides, and subcostal retraction was ob­ birth. Another population study, carried served. On auscultation the first and sec­ out in the Netherlands, reported NEC in ond heart sounds were regular, no 6% of livebirths who were very low birth murmurs were heard, and breath sounds weight (VLBW) and/or < 32 weeks were bronchovesicular, no crackle and no gestation.3 wheezing. The abdomen was distended The purpose of this paper in to report a with discoloration of the whole abdominal case of necrotizing enterocolitis in order wall and the inguinal region, peristalsis to remind us o f this problem. were diminished and the liver and spleen could not be palpable. The extremities were pale, sclerema was present, and no cyanosis. Report of the Case The laboratory investigation revealed tlie following result: HB 10.4 g/dl, WBC DN, an Indonesian girl, aged six days was 10.400/cmm, hematocrit 30% and blood admitted on January 23rd, 1994 at the sugar' 85 mg/dl. Liquor: NOnne and Child Health Department of Denpasar Bandy negative, cells 0/cmrn and glucose Central General Hospital. She was bom 50.3 mg/dl. The blood culture on Janu­ vaginally at Kasih Ibu Maternity Hospital ary 24, 1994 was negative. The results of on January 17, 1994 at a gestational age serum electrolytes: Sodium 117.8 of 29 weeks and birth weight of 1500 mrnol/1, Potassium 6.46 mmol/1, Chlo­ grams. Her mother suffered from fever ride meq/1 and calcium 9.0 mg/dl. BUN and premature rupture of tire amniotic 23.8 mg/ 100ml and serum creatinine 0.0 membranes more than 24 hours. Apgar mg/ 100ml. Plain abdominal X-rays film score was 3 at 1 minute and 4 at 5 min­ showed significant intestinal distention utes. No history of earlier oral feeding af­ with signs of ileus and positive foot ball ter birth. At 5 days of age she suddenly sign. The radiologist's interpretation sug­ became lethargic, mildly jaundiced, with gest a pattern supporting NEC. abdominal distention, vomiting, respira­ The working diagnosis was NEC. The tory distress, and bloody stool. patient was put in a incubator with na­ On January 23ed, 1994 the baby was sogastric decompression and intermittent referred to Denpasar- Central General suction and oral feeding was withheld. Hospital. Physical examination on admis­ The patient was heated with intravenous sion revealed lethargy, hypotonia, poor feeding, started by using half-strength peripheral circulation, jaundice Kramer aminofusin, diluted with 10% dextrose grade 3 with a body weight of 1400 solution at tire rate of 150 cc/kg body grams, the heart rate 144/minute. The weight/day which is equivalent of 75 respiratory rate 64/minute irregular, the cal/kg body weight/day, Ampicillin 75 rectal temperature 36.4oC. The major mg and Gentamycine 7.5 mg twice daily fontanel was flat and signs of anemia was intravenously, transfusion of 15 cc whole 128 Necrotizing enterocolitis in an asphyxiated premature infant

blood/day for 3 days. Hyponatremia cor­ maternal disorder (e.g., toxemia, infec­ rection by using sodium chloride 3% 12 tion).3'46 Hypoxia or ischemic injury of cc intravenously. bowel wall, direct injury to the mucosal On January 25, 1994 the patient be­ wall by hyper-osmolar feeding and infec­ came lethargic with heart rate tion with gram negative microorganism 160/minute, respiratory rate 44/minute have been suggested as étiologie factors.6 with frequent attack of apnea and rectal The current most acceptable theory of the temperature was 36oC. The abdominal pathogenesis is hypoxia which evokes a distention was increased and peristaltic reflex resulting redistribution of blood, sounds were absent. The patient was re­ shunted away from less vulnerable or­ ferred to the Department of Surgery gans like the mesenteric, the renal and where it was diagnosed as paralytic ileus the peripheral vascular bed to first class with NEC as the possible underlying organs (the brain and the heart) which cause. Surgical intervention was not per­ would suffer irreversible damage if de­ formed because of the poor condition of prived of adequate perfusion.3,4,7 The mu­ the patient. On January 28, 1994 at cosal cells, which are highly sensitive to 08.00 PM the patient was somnolent with ischemia, stop secreting protective mu­ a heart rate of 118/minute irregular, res­ cous, and hence proteolytic autodigestion piratory rat 28/minute irregular with re­ of mucosa occurs.6,8 current apnea period and at 20.30 PM Once the integrity of mucosa is broken, the patient died. it will be invaded by gas forming micro or­ ganism. Bacteria are absorbed into the lymphatic and into the radices of the por­ Discussion tal venous system, leading to overwhelm­ ing sepsis and death.6 The predisposing NEC is commonly thought o f as occurring factors for our case were found that low in the premature infant, usually in the birth weight infant (birth-weight 1500 first one to two weeks of life. Indeed, 75% grams) with severe asphyxia, her mother to 95% of cases of NEC occur in infants of suffered from fever and premature rup­ less than 38 weeks gestation, and with ture of the amniotic membrane for more onset typically at 4 to 6 days of age.5 In than 24 hours. our case, she was bom from a mother The diagnosis of NEC based on clinical with a gestational age of 29 weeks and features: systemic manifestation include onset of clinical signs of NEC at 5 days of recurrent apnea and bradycardia, leth­ age. ^ argy, hypotonia, poor peripheral circula­ The etiology of NEC is still obscure and tion, temperature instability, jaundice, is considered to be multifactorial with respiratory distress, sclerema and meta­ many predisposing factors including low bolic acidosis. Gastorintestinal manifesta­ weight infants, particularly prematurity, tions include abdominal distention, poor asphyxia, bottle feeding, hyperviscosity, feeding, pre-gavage residue, vomiting dis­ umbilical catheterization, premature rup­ coloration of the abdominal wall and ture of the amniotic membranes and blood in stool.13,6 But all these clinical Sunarka, et al 129 manifestation might not be present in many neonatal unit, an indication for each case.6 In our case the clinical mani­ surgical intervention.3 In our case the festation we found were lethargy, hypoto­ plain abdominal x-ray film showed signifi­ nia, apnea, poor peripheral circulation, cant intestinal distention with flues. jaundice, sclerema, abdominal distention, Laboratory features: Blood studies will of­ vomiting, blood in stool, discoloration of ten reveal, thrombocytopenia, persistent abdominal wall and inguinal region and metabolic acidosis, and severe refractory temperature instability. Munit6 found ab­ hyponatremia. The are the most common dominal distention and prolonged gastric triad and help to confirm the diagnosis.11 emptying were always present in each Microbiology examination, only 30-40% of case. Apnea, cyanosis and sclerema were neonates with NEC have positive bacte­ seen among severe cases. In any authors rial culture of blood, stool or peritoneal opinion, a neonate with diarrhea, espe­ fluid.3 In our case we found hyponatre­ cially of low birth weight, who has abdo­ mia but culture of blood was negative. minal distention, a positive guaiac test Treatment of NEC include supportive and positive reducing substances in the therapy and operative intervention.'3,12 stool with nonspecific radiological find­ Supportive therapy includes cessation of ings in the x-ray should be heated as a enteral feeding, nasogastric decompres­ NEC (6). Radiology: Abdominal x-rays sion with intermittent suction. Parenteral have an important role in established the nutrition should be initiated through a diagnosis of NEC and evaluating the se­ peripheral vein as soon as possible, with verity and extent of the disease. No­ the aim of providing 75-110 cal/kg/day specific radiological findings which once both amino acid solutions and in­ frequently accompany or precede the ap­ tralipid are tolerated, correction of electr o­ pearance of pneumatosis intestinalis, is a lyte and acid-base balance and if pathognomic sign of NEC, which is short­ hypotension develops resuscitation with lived, and usually disappear within 12 blood or plasma,1,4,12 Parenteral antibiot­ hours,.10 Although the radiological hall­ ics are started usually a combination of a mark of NEC is pneumatosis intestinalis, penicillin and an aminoglycoside such as this may be absent in 14-17% of definite gentamicin.1,3 Alternatively, one of tire NEC cases.3 Abdominal radiograph will third generation cephalosporins such as often reveal an abnormal gas pattern con­ cefotaxime is used in some neonatal sistent with flues, gaseous distention, units.3 If abdominal perforation has oc­ foamy pattern and asymmetric of gas pat­ curred, coverage for anaerobic bacteria tern portal or hepatic venous air, and should be added, Usually clindamycin is pneumoperitoneum.3-611 On the other used for this purpose.12 Operative inter­ hand, asymmetry of gas pattern is associ­ vention is indicated in stage HI (advance), ated with NEC only about 30% of cases. NEC, vary among neonqtal units but Pneumoperitonium occurs in 10-30% of have include pneumoperitoneum, local­ cases and develops most frequently early ized abdominal mass, portal vein gas and in the course of the disease. Portal vein clinical deterioration despite medical gas is a sign of advance disease, and in therapy.1,3 Surgery usually consist of the 130 Necrotizing enterocolitis in an asphyxiated premature infant resection of gangrenous or perforated in­ benign disorder can be distinguished testine and either extériorisation of the from NEC. ends in an enterostomy or primary The prognosis of NEC depends on the anastomosis.3 The management of our severity of the disease. The mortality rate case only supportive therapy by cessation of NEC varies from 0 to 64%. Survival for of enteral feeding, institution of par­ patients treated conservatively, who obvi­ enteral nutrition, administration of anti­ ously have a less advanced diseases is biotic intravenously, correction of from 60% to 90%. Currently the survival electrolyte and blood transfusion. Surgi­ rate after operation (stage El) is 50% to cal intervention was not performed be­ 77% in North America.711 The survival cause the poor condition of patient. rate reported for VLBW neonates with NEC must be distinguished from disor­ NEC have a range from 61% to 88%.11 ders as follow:311 Risk factors for death include female sex, 1. Pneumonia and sepsis are common in early onset among those who are VLBW, this population and frequently associ­ abnormal bleeding, thrombocytopenia, ated with an abdominal ilues. The ab­ DIC, positive blood culture especially with dominal distention and tenderness gram negative bacteria, and need for characteristic of NEC will be absent, surgery.3 The incidence of complication however. such as intestinal stricture among NEC 2. Surgical abdominal catastrophes in­ survivors varied from 14% to 42%.1,3 The clude malrotation with obstruction strictures are in the large bowel in 75% (complete or intermittent), malrotation and multiple in one third of cases.1 Due with mid gut volvulus, intususception, to some risk factors for death was found ulcer diathesis gastric perforation and in this case such as abnormal bleeding, mesenteric vessel thrombosis. The birth weight 1500 grams, female and clinical presentation of these disorder need for surgery we concluded the prog­ may overlap with that of NEC. Occa­ nosis o f our case is not good. sionally the diagnosis is made only at Prevention of NEC is the ultimate goal. the time of exploratory laparotomy. Prevention of prematurity will reduce the 3. Infectious enterocolitis is rare in the incidence of NEC but this goal will not be population, but must be considered if achieved in this century.3,12 Attention diarrhea is present. These children must be given to the early diagnosis and lack of any other systemic or enteric prompt treatment of perinatal and neona­ signs of NEC. tal conditions which predispose to the de­ 4. Feeding intolerance is common but an velopment of NEC predominantly ill-defined problem in the premature through tile hypoxic-ischemic injury infant. Differentiation of this problem pathway,3 also prophylaxis with enteral from NEC is difficult at times. Cau­ antibiotics.12 Althoug breast milk does not tious evaluation by withholding en­ offer absolute protection against NEC, teral feedings and administering intra­ multicenter study has proven efficacy of venous fluids and antibiotics for 72 breast milk in reducing the risk of the de­ hours may be indicated until this velopment NEC.3 Sunarka, et al 131

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