Clinical case study pharmacy


The case of Sarah as stated with the symptoms (underweight, her skin is not pink like a healthy baby but is ashen gray, has poor muscle tone and is not active like other infants, looking listless and is not feeding well, a distended abdomen) could be a suspected case of Necrotizing enterocolitis (NEC).

NEC is the most common acquired acute gastro-intestinal illness in the neonatal period affects about 5% of infants with birthweight ≤1,500 g and typically is characterized by abdominal distension, bloody stools and pneumatosis intestinalis. NEC accounts for 15% of deaths in premature babies weighing less than 1500 grams. Overall death from those babies with NEC is 25%. The actual spectrum of illness ranges from mild cases of feeding intolerance and bdominal distension to severe cases characterized by intestinal necrosis, perforation, and septic shock. In the premature infant, NEC usually occurs a week to ten days after the initiation of feedings. In the term baby, NEC occurs within one to four days of life if feeding is started on day one. The risk of NEC is less with later gestational age. Very few unfed infants develop NEC. One theory which connects feeding to bowel mucosa damage involves the overgrowth of bacteria when provided with a carbohydrate source. The digestion of the lactose in formula by premature infant is incomplete and the residual ferments (has a chemical change) that encourages growth of bacteria that cause inflammation. Origins of infections can be summarized under the following:

Origin of infections before birth

Infections in preterm infants may originate in utero (Schrag & Schuchat, 2005). In particular, intraamniotic bacterial infections in relation to premature rupture of membranes may cause preterm birth followed by a severe threat of immediate postnatal sepsis and/or meningitis. Another cause of infections of which the origin can be found in severe intrauterine growth retardation (IUGR) caused by poor placental function during the second and last trimester of fetal development which may be traced to intrauterine infections.

Origin of infections related to the gastrointestinal tract

Severe infections in preterm infants often originate from the gastrointestinal (GI) tract because of the developmental immaturity of the gut. Most times, the gut wall is not yet fully mature, and the ultimately tight junctions between the mucosal cell layers are still open, permitting bacteria from the intestinal lumen to penetrate into the interstitium or vascular system causing sepsis (Caicedo & Schanler, 2005). The process of gut maturation is influenced not only by the gestational age but also by the effect of administrating enteral feeding late or early by so-called gavage feeding using an indwelling plastic probe. Over the last 10–15 y, the concept of minimal enteral trophic feeding has been introduced into clinical practice: the early start of enteral feeding in small quantities (maximal 12–24 mL · kg–1 · d–1) in ventilated preterm infants during the period of parenteral feeding to enhance the gut function and with the intention to enable full enteral feeding sooner after birth (Tyson & Kennedy, 2005). It remains very difficult, however, to collect sufficient clinical evidence for the validity of the concept of minimal enteral feeding.

Origin of infections related to the neonatal intensive care unit (NICU) environment

There are available literatures on the development of the intestinal microflora of preterm infants and the factors influencing its environment (Westerbeek et al., 2006). Most studies show that the intestinal bacterial colonization with beneficial bacteria is delayed in preterm infants. Therefore, the number of potentially pathogenic bacteria is high. The widespread use of antibiotics at the neonatal intensive care unit (NICU) or wrong administration of antibiotics by parent (mother) which shas a negative effect on the development of the intestinal microflora. Many preterm infants receive prophylactic antibiotics at birth. Over the period 1998–2000, a surveillance study on nosocomial infections was performed at our NICU (Van der Zwet, 2007). During 50% of the admission time, at least 1 antibiotic was administered to the preterm infants. The risk of sepsis was negatively related to birth weight: <1000 g birth weight, 31% risk of sepsis; 1000–1500 g birth weight, 28% risk of sepsis; and 1550–2500 g birth weight, 4% risk of sepsis. Apart from low birth weight, another high-risk factor for sepsis in preterm infants is the use of total parenteral nutrition mixtures (Van der Zwet et al., 2005).

In the case of the infant Sarah, it can be seen that it was the abuse of antibiotics by her mother during pregnancy that led to her being infected before birth. It was a clear case of numerous use of  antibiotics which where self administered by her mother, that had a negative effect on the microflora of Sarah’s intestine. This led to the development and colonization of pathogenic bacteria causing infection to her bowels.

The infant Sarah will have to undergo some clinical test and diagnosis to confirm that she is suffering from NEC. The findings will look like the presentations summarized below:

Clinical Findings will present any of the following; Abdominal distension, abdominal tenderness or redness, feeding residuals, often bilious, absent bowel sounds, gross or occult blood in stool, bluish discoloration of abdominal wall, non-specific signs (temperature instability, glucose instability, lethargy, apnea/bradycardia, hypotension).

Radiographic Findings (in order of severity) will present the following; Non-specific bowel dilatation, thickening of bowel wall, fixed, dilated loop (unchanged on >1 radiograph), pneumatosis intestinalis (small gas bubbles in bowel wall, almost always associated

with dilated bowel loops), portal venous gas, free intraperitoneal gas (indicative of intestinal perforation).

Laboratory Findings will include; Thrombocytopenia, metabolic acidosis (poor prognostic sign), abnormally ↑ or ↓ WBC, left shift of WBC (toward immature precursors), neutropenia, and evidence of DIC.

A further diagnosis will be carried out to determine the stage of NEC in Sarah using the Bell’s criteria. There are three stages of NEC which can be presented with the following symptoms:

Stage 1. Suspected NEC: gastric residuals, abdominal distension, occult or gross blood

in stool, x-ray normal to mild distension, temperature instability, apnea, bradycardia.

Stage 2. Definite NEC: mild to moderate systemic illness, absent bowel sounds, abdominal tenderness, pneumatosis intestinalis or portal venous gas, metabolic acidosis, ↓ platelets.

Stage 3. Advanced NEC: severely ill, marked distension, signs of peritonitis, hypotension, metabolic & respiratory acidosis, DIC, pneumoperitoneum if bowel perforation present.

The management and treatment of the infant Sarah will be carried out depending on the stage of NEC diagnosed as shown below:

Suspected NEC (this can be done to keep Sarah’s life longer); Make NPO, start maintenance IV fluids, obtain baseline KU,serial abdominal examinations will be performed, culture urine & CSF if systemic signs, consider stool culture, R/O surgical cause of distension, observe closely for worsening, if improvement occurs, consider cautious feeding in 3d, test all stools for occult blood, consider gastric decompression, CBC, platelets & blood culture, consider starting antibiotics.

Definite/Advanced NEC; Consult will be obtained with Pediatric Surgery, NPO for at least 7-10d, IV fluids: Because of “third spacing,” Sarah may require fluid resuscitation to

improve bowel perfusion (e.g., D5-Lactated Ringer’s at 150 mL/kg per 24 h), urine output will be followed closely; renal failure is common due to hypoperfusion, gastric decompression (Replogle tube to low, continuous suction), abdominal radiographs (AP & cross table lateral q6-8h) to look for perforation, endotracheal intubation and assisted ventilation as needed, circulatory support: arterial blood pressure will be monitored and maintain in normal range with volume expanders and dopamine (Dobutamine is less effective in infants and may actually cause hypotension, blood culture and start of antibiotics: ampicillin & gentamicin for 7-10d (Anaerobic coverage is usually not necessary unless infant is several weeks old), follow CBC, platelets, PT, PTT, fibrinogen; replace clotting factors products prn, frequent measurements of arterial pH and blood gas tensions, correct metabolic acidosis, frequent measurements of electrolytes; watch for hyperkalemia.

Surgical Consideration; Operative intervention is indicated for bowel perforation, evidence of necrotic bowel (fixed loop, metabolic acidosis, DIC, shock), or progressively worsening

clinical condition despite intensive medical management, a peritoneal drain may be inserted in extremely ill infants to delay or avoid laparotomy, if NEC develops in a baby with PDA, begin medical management and consider urgent operative closure of PDA. Indomethacin will not be given to Sarah if it is suspected or definite NEC.

Sarah’s condition can be seen as a suspected case of NEC. Though diagnosis would have to be carried out to ascertain the level it has affected the infant Sarah according to the stages shown above. The management and treatment will then be carried out based on the severity.

Finally, Sarah’s mother will be advised to be careful if she gets pregnant again. She will be advised on the general prevention strategies to avoid future NEC as follows: Intestinal priming (gut stimulation feedings): dilute, low volume feedings to stimulate GI mucosal development, advance feedings slowly in small preterm infants, she will not advance feedings if there are gastric residuals, especially if bile stained, fresh human milk appears to be protective against NEC, she will not feed infants with PDA, UAC, or UVC, she give enteral feedings during and for 48-72h after indomethacin,  she will minimize antibiotic use and abuse, as they alter intestinal flora and select for resistant species, epidemiologic controls: cohorting of multiple cases (possible infectious cause), antenatal glucocorticoids for lung maturation also accelerate intestinal maturation, suggested possible future approaches: enteral IgG/IgA, formula acidification, anaerobic bacterial supplementation (bifidobacteria).


Caicedo, R. A., Schanler, R.J., LI, N. & Neu, J. (2005) The developmental intestinal ecosystem: implications for the infant. Pediatr Res.58:625–8.

Schrag, S. & Schuchat, A. (2005) Prevention of neonatal sepsis. Clin Perinatol.32:601–15.

Tyson, J. E. & Kennedy, K. A. (2005) Trophic feeding for parenterally fed infants. Cochrane Database Syst Rev. 3:CD000504.

Van der Zwet, W.C. (2007) Epidemiology and prevention of nosocomal infection in the neonatal intensive care unit [dissertation]. Amsterdam: Vrije Universiteit.

Van der Zwet, W.C., Kaiser, A. M., Van Elburg, R.M.,  Berkhof, J., Fetter, W. P., Parlevliet, G. A. & Vandenbroucke-Grauls, C. M. (2005) Nosocomial infections in a Dutch neonatal intensive care unit: SS. 61:300–11.

Westerbeek, E.A., Van den Berg, A., Lafeber, H.N., Knol, J., Fetter, W. P.& Van Elburg, R. M. (2006) The intestinal bacterial colonisation in preterm infants: A review of the literature. Clin Nutr. 25:361–8.


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