USMLE forum
 
Archives
Step 1
Step 2 CK
Step 2 CS
Matching & Residency
Step 3
 
Forum
 
 
  <<   < *  Step 2 CK  *  2006 Archives  *   >   >>  

* try this one!
 #83405  
  eric88 - 04/13/06 11:50
 
  A 30-year-old white primigravida asks you about the benefits and drawbacks of corticosteroid therapy for premature labor at 30 weeks gestation. Which one of the following statements is most accurate?


A. Therapy will decrease the risk of neonatal necrotizing enterocolitis.

B. Weekly corticosteroid injections until 34 weeks gestation is the standard regimen to prevent respiratory distress syndrome.

C. Therapy is associated with a higher rate of neonatal intraventricular hemorrhage.

D. Therapy is associated with a higher rate of persistent patent ductus arteriosus.

E. Therapy decreases the risk of respiratory distress syndrome but not total neonatal mortality
 
Report Abuse

* Re:try this one!
#303579
  alibi - 04/13/06 14:38
 
 

Home | Specialties | Resource Centers | CME | PDA | Contributor Recruitment

April 13, 2006

Articles Images CME Advanced Search Consumer Health Link to this site

You are in: eMedicine Specialties > Pediatrics > Neonatology


Necrotizing Enterocolitis
Last Updated: November 25, 2002 Rate this Article
Email to a Colleague
Get CME/CE for article

Synonyms and related keywords: NEC, inflammation of the intestinal tissues, enteral feeding, sepsis

AUTHOR INFORMATION Section 1 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography




Author: Shelley C Springer, MD, MBA, MSc, Neonatologist, Assistant Professor of Pediatrics, Department of Pediatrics, University of Wisconsin, Madison
Coauthor(s): David J Annibale, MD, Director of Fellowship Training Program in Neonatal-Perinatal Medicine, Associate Professor, Department of Pediatrics, Medical University of South Carolina


Shelley C Springer, MD, MBA, MSc, is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, Minnesota Medical Association, National Perinatal Association, and South Carolina Medical Association

Editor(s): Oussama Itani, MD, Medical Director of Neonatology, Borgess Medical Center, Clinical Assistant Professor, Department of Pediatrics and Human Development, Michigan State University; Robert Konop, PharmD, Director, Clinical Account Management, Ancillary Care Management; David A Clark, MD, Chairman, Professor, Department of Pediatrics, Albany Medical College; Carol L Wagner, MD, Associate Professor, Department of Pediatrics, Division of Neonatology, Medical University of South Carolina; and Neil N Finer, MD, Director, Division of Neonatology, Professor, Department of Pediatrics, University of California at San Diego

Disclosure





INTRODUCTION Section 2 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography



Background: Necrotizing enterocolitis (NEC) is the most common gastrointestinal medical and/or surgical emergency occurring in neonates. With mortality rates approaching 50% in infants who weigh less than 1500 g, NEC represents a significant clinical problem. Although, it is more common in premature infants, it can also be observed in term babies. Despite intensive study over the past 30 years, its etiology remains elusive.


Pathophysiology: NEC affects the gastrointestinal tract and, in severe cases, can have profound systemic impact.

Initial symptoms may be subtle and can include the following:


Feeding intolerance

Delayed gastric emptying

Abdominal distention and/or tenderness

Ileus/decreased bowel sounds

Abdominal wall erythema (advanced stages)

Hematochezia
Systemic signs can include the following:


Apnea

Lethargy

Decreased peripheral perfusion

Shock (in advanced stages)

Cardiovascular collapse

Bleeding diathesis (consumption coagulopathy)
Nonspecific laboratory abnormalities can include the following:


Hyponatremia

Metabolic acidosis

Thrombocytopenia

Leukopenia and leukocytosis with left shift

Neutropenia

Prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), decreasing fibrinogen, rising fibrin split products (in cases of consumption coagulopathy)
Although the exact etiology is still unknown, research suggests that it is multifactorial; ischemia and/or reperfusion injury may play a role. Cases that cluster in epidemics suggest an infectious etiology; however, a single causative organism has not been identified. Organisms isolated from stool cultures from affected babies are also isolated from healthy babies. Therefore, no single organism has been identified as the culprit responsible for triggering the disease. Some experimental work suggests that translocation of intestinal flora across an incompetent mucosa may play a role in spreading disease and systemic involvement. Such a mechanism would account for the apparent protection breastfed infants have against fulminant NEC.

Animal model research studies have shed light on the pathogenesis of this disease. Regardless of the triggering mechanisms, the resultant outcome is significant inflammation of the intestinal tissues and the release of inflammatory mediators (eg, leukotrienes, tumor necrosis factor, platelet-activating factor), which lead to variable degrees of intestinal damage.


Frequency:


In the US: Frequency varies from nursery to nursery without correlation with season or geographic location. Outbreaks of NEC seem to follow an epidemic pattern within nurseries, suggesting an infectious etiology even though a specific causative organism is unknown.
Population studies conducted in the United States over the past 25 years indicate a relatively stable incidence, ranging from 0.3-2.4 cases per 1000 live births. Because more premature babies are surviving, expecting an increase in the overall incidence of NEC is reasonable.

Internationally: Population-based studies from other countries suggest an attack rate similar to the United States.
Mortality/Morbidity:

The mortality rate ranges from 10-44% in infants weighing less than 1500 g, compared to 0-20% mortality rate for babies weighing more than 2500 g. Extremely premature infants (1000 g) are particularly vulnerable, with reported mortality rates of 40-100%. One study compared mortality rates for term versus preterm infants and reported rates of 4.7% for term infants and 11.9% for premature babies.
Survivors can have significant short-term and long-term morbidities. Patients with medical NEC (see Bell stage II under Medical Care) must remain on nothing by mouth (NPO) for protracted periods, compromising the nutrition that is essential for a premature infant. Many of these babies have difficult IV access; the need for prolonged parenteral nutrition requires placing central venous catheters, which have attendant risks and complications of their own. Prolonged hyperalimentation and the absence of enteral nutrition can cause cholestasis and direct hyperbilirubinemia.
Patients with significant disease can develop strictures, which require surgical intervention and further compromise successful enteral feeding. Patients who are severely affected require intestinal resection. In rare cases, the entire intestine can be involved, precluding surgical intervention. Depending on the location and extent of the bowel removed, long-term morbidities can include the need for colostomy, repeated surgical procedures, prolonged parenteral nutrition, poor nutrition, malabsorption syndromes, failure to thrive, and multiple hospitalizations.
Race: Some studies indicate higher frequency in black babies than in white babies, but other studies show no difference based on race.

Sex: Most studies indicate that male and female babies are affected equally. However, the higher incidence of neonatal sepsis and meningitis reported for male infants suggests otherwise.

Age:

NEC clearly predominates in premature infants, with incidence inversely related to birth weight and gestational age. Although specific numbers range from 4% to more than 40%, infants weighing less than 1000 g at birth have the highest attack rates. This rate drops dramatically to 3.8 per 1000 live births for infants weighing 1501-2500 g at birth. Similarly, rates decrease profoundly for infants born after 35-36 weeks' postconceptional age.
Average age at onset in premature infants seems to be related to postconceptional age, with babies born earlier developing NEC at a later chronologic age. One study reported the average age of onset as 20.2 days for babies born less than 30 weeks' estimated gestational age (EGA), 13.8 days for babies born at 31-33 weeks' EGA, and 5.4 days for babies born after 34 weeks' gestation.
Term infants develop NEC much earlier, with the average age of onset occurring within the first week of life or sometimes occurring within the first 1-2 days of life.




CLINICAL Section 3 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography



History:

NEC is more common in preterm infants.
Epidemiologic studies demonstrate that antecedent history is usually the same for term as well as preterm babies. However, demographics, risk factors, typical patient characteristics, and clinical course differ significantly.
Term baby
Typically the term baby is much younger than the afflicted preterm baby, with published series reporting median age of onset from 1-3 days of life
The affected term neonate is usually systemically ill with other conditions, such as birth asphyxia, respiratory distress, congenital heart disease, metabolic abnormalities, or has a history of abnormal fetal growth pattern.
Maternal risk factors that reduce fetal gut flow, such as placental insufficiency from chronic disease or maternal cocaine abuse, can increase the baby's risk.
Premature baby
Premature babies are at risk for several weeks, with the age of onset inversely related to gestational age at birth.
Patients are typically advancing on enteral feedings or may have achieved full-volume feeds when symptoms develop.
Presenting symptoms may include subtle signs of feeding intolerance that progress over several days, subtle systemic signs that may be reported enigmatically by the nursing staff as "acting different," and fulminant systemic collapse.
Symptoms of feeding intolerance can include abdominal distention/tenderness, delayed gastric emptying as evidenced by gastric residuals, and vomiting (occasionally).
Systemic symptoms can progress insidiously to include increased apnea and bradycardia, lethargy, and temperature instability representing the primary manifestation(s).
Patients with fulminant NEC present with profound apnea, rapid cardiovascular and hemodynamic collapse, and shock.
The baby's feeding history can help increase the index of suspicion for early NEC. Babies who are breastfed have a lower incidence of NEC than formula-fed babies.


Rapid advancement of formula feeding has been associated with an increased risk of NEC (McKeown, 1992).
Physical:

The pertinent physical findings in patients who develop NEC can be primarily gastrointestinal, primarily systemic, indolent, fulminant, or any combination of these. A high index of clinical suspicion is essential to minimize potentially significant morbidity or mortality.
Gastrointestinal signs can include any or all of the following:
Increased abdominal girth
Visible intestinal loops
Obvious abdominal distention and decreased bowel sounds
Change in stool pattern
Hematochezia
A palpable abdominal mass
Erythema of the abdominal wall
Systemic signs can include any of the following:
Respiratory failure
Decreased peripheral perfusion
Circulatory collapse
With insidious onset, the severity of derangement may be mild, whereas patients with fulminant disease can present with severe clinical abnormalities.
Several characteristic laboratory findings occur (see Lab Studies).
If abdominal signs are present, surgical consultation may be advisable. Disease progression ranges from indolent to fulminant, and early involvement of surgical colleagues can be helpful, especially if appropriate surgical care requires transfer to another facility.
DIFFERENTIALS Section 4 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography



Acidosis, Metabolic
Acidosis, Respiratory
Apnea of Prematurity
Bacteremia
Candidiasis
Coarctation of the Aorta
Enteroviral Infections
Gastroesophageal Reflux
Hirschsprung Disease
Hospital-Acquired Infections
Hypoplastic Left Heart Syndrome
Intestinal Malrotation
Intestinal Volvulus
Meningitis, Bacterial
Neonatal Sepsis
Omphalitis
Prematurity
Urinary Tract Infection
Volvulus



Other Problems to be Considered:

Spontaneous intestinal perforation (SIP): Not infrequently, free air is noted on an abdominal radiograph of a premature infant, either as an incidental finding on imaging performed for other reasons or during an initial evaluation for abdominal pathology. SIP can be distinguished from NEC by its lack of systemic involvement, absence of other clinical signs common to bowel perforation, and higher rate of survival (Shorter, 1999). SIP is further distinguished by its earlier onset in babies of smaller birthweight and more extreme prematurity (Adderson, 1998). Associations have been identified between SIP and indomethacin (Shorter, 1999), dexamethasone (Stark, 2001), and systemic candidiasis (Adderson, 1998).

Quick Find
Author Information
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous
Pictures
Bibliography

Click for related images.

Related Articles
Acidosis, Metabolic

Acidosis, Respiratory

Apnea of Prematurity

Bacteremia

Candidiasis

Coarctation of the Aorta

Enteroviral Infections

Gastroesophageal Reflux

Hirschsprung Disease

Hospital-Acquired Infections

Hypoplastic Left Heart Syndrome

Intestinal Malrotation

Intestinal Volvulus

Meningitis, Bacterial

Neonatal Sepsis

Omphalitis

Prematurity

Urinary Tract Infection

Volvulus




Continuing Education
CME available for this topic. Click here to take this CME.


Patient Education
Click here for patient education.







WORKUP Section 5 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography




Lab Studies:


Initial presentation usually includes subtle signs of feeding intolerance, such as gastric residuals, abdominal distention, and/or grossly bloody stools. Abdominal imaging studies are crucial at this stage. Laboratory studies are pursued if the abdominal studies are worrisome or the baby is manifesting any systemic signs.
Complete blood count with manual differential to look for signs of infection, anemia, and thrombocytopenia is usually repeated at least every 6 hours if the patient continues to deteriorate.
White blood cell count: Marked elevation may be worrisome (<20,000 depending on whether treatment includes systemic steroids for lung disease), but leukopenia (<5000) is even more concerning. Although elevated mature and/or immature neutrophil counts may not be good indicators of neonatal sepsis after the first 3 days of life, moderate neutropenia (absolute neutrophil count [ANC] <1500) strongly suggests evolving sepsis.
Red blood cell count: Premature infants are prone to anemia from iatrogenic blood draws as well as anemia of prematurity; however, blood loss from hematochezia and/or a developing consumptive coagulopathy can manifest as an acute decrease in hematocrit.
Platelet count: Platelets are an acute phase reactant, and thrombocytosis can represent physiologic stress to an infant, but acute NEC is more commonly associated with thrombocytopenia (<100,000). Thrombocytopenia may become more profound and alarming in severe cases that become complicated with consumption coagulopathy. Consumption coagulopathy is characterized by prolonged prothrombin time (PT), prolonged activated partial thromboplastin time (aPTT), and decreasing fibrinogen and increasing fibrin degradation products concentrations
Blood culture: Drawing a blood culture is recommended before beginning antibiotics in any patient presenting with any signs/symptoms of sepsis or NEC. Although blood cultures do not grow any organisms in most cases of NEC, sepsis is one of the major conditions that mimic NEC and it should be considered in the differential diagnosis. Therefore, identification of a specific organism can aid and guide further therapy.
Serum electrolytes can show some characteristic abnormalities. Obtain a panel of basic electrolytes during the initial evaluation, followed serially at least every 6 hours depending on the acuity of the patient's condition.
Serum sodium: Hyponatremia is a worrisome sign that can suggest the initial stages of a developing capillary leak. Depending on the baby's age and feeding regimen, baseline sodium levels may be low-normal or subnormal, but an acute decrease (<130 mEq/dL) is alarming and heightened vigilance is warranted.
Metabolic acidosis: Low serum bicarbonate (<20) in a baby with a previously normal acid-base status also is concerning.
Arterial blood gasses
Depending on presentation acuity and the baby's respiratory status, an arterial blood gas can reveal whether the baby needs respiratory support and the developing acid-base status.
Acute acidosis with baseline carbon dioxide pressure is worrisome (as is apnea). Metabolic acidosis results from decreased cardiac output (as in cardiovascular collapse and shock), leading to poor perfusion of peripheral tissues and lactic acidosis.
An arterial blood sample is a convenient way to simultaneously obtain a blood culture, CBC, serum electrolytes, and ABG for the initial evaluation (note that arterial blood has a lower yield for demonstrating bacteremia than venous blood). Depending on presentation acuity, inserting a peripheral arterial line while peripheral perfusion and intravascular volume is still good may be prudent. This peripheral arterial line facilitates serial blood sampling and invasive blood pressure monitoring that is essential if the baby's condition deteriorates.
Imaging Studies:


The mainstay of diagnostic imaging is abdominal radiography. An anteroposterior (AP) abdominal radiograph and a left lateral decubitus radiograph (left side down) are essential for initially evaluating any baby with abdominal signs. Perform these abdominal radiographs serially at 6-hour or greater intervals, depending on presentation acuity and the preferences of the attending medical team, including any involved surgeons.
Characteristic findings on an AP abdominal radiograph include an abnormal gas pattern, dilated loops, and thickened bowel walls (suggesting edema/inflammation). Serial radiographs help assess disease progression. A fixed and dilated loop that persists over several examinations is especially worrisome.
Radiographs can sometimes reveal scarce or absent intestinal gas, which is more worrisome than diffuse distention that changes over time.
Pneumatosis intestinalis is a radiologic sign pathognomonic of NEC. It appears as a characteristic train-track lucency configuration within the bowel wall. Intramural air bubbles represent extravasated air from within the intestinal lumen. Analysis of gas aspirated from these air bubbles reveals that it consists primarily of hydrogen, suggesting that these are caused by bacterial fermentation of undigested intraluminal substrates. Carbohydrate (often lactose) fermentation by intestinal flora yields hydrogen and carbon dioxide and a series of short-chain organic acids, which can promote inflammation.
Abdominal free air is ominous and usually requires emergency surgical intervention (see Spontaneous intestinal perforation under Other Problems to be Considered). The presence of abdominal free air can be difficult to discern on a flat radiograph, which is why decubitus radiographs are recommended at every evaluation. The football sign is characteristic of intraperitoneal air on a flat plate and manifests as a subtle oblong lucency over the liver shadow. It represents the air bubble that has risen to the most anterior aspect of the abdomen in a baby lying in a supine position and can be demonstrated by left lateral decubitus imaging.
Portal gas is a subtle and transient finding that was originally thought to be ominous when detected but is now considered less ominous. Portal gas, which is not usually captured in serial radiographs, appears as linear branching areas of decreased density over the liver shadow and represents air present in the portal venous system. Portal gas is much more dramatically observed on ultrasonography (see below).
Ascites is a late finding that usually develops some time after perforation when peritonitis is present. Ascites is observed on an AP radiograph as centralized bowel loops that appear to be floating on a background of density. It is better appreciated on ultrasonography.
Left side down (left lateral) decubitus radiography allows the detection of intraperitoneal air, which rises above the liver shadow (right side up) and can be visualized easier than on other views. Obtain this view with every AP examination until progressive disease is no longer a concern.
Abdominal ultrasonography is a relatively new technology for evaluating suspected NEC in neonates.
Advantages

Available at bedside

Noninvasive imagery of intra-abdominal structures
Disadvantages

Limited availability at some medical centers

Requires extensive training to discern subtle ultrasonographic appearance of some pathologies
With abdominal ultrasonography, a skilled physician can identify a larger amount of diagnostic information faster and with less risk to the baby than with the current standard evaluation methods.
Abdominal air (easily observed on ultrasonography and in grossly distended patients) can interfere with assessing intra-abdominal structures.
Ultrasonography can be used to identify areas of loculation and/or abscess consistent with a walled-off perforation when patients with indolent NEC have scarce gas or a fixed area of radiographic density.
Ultrasonography is excellent for distinguishing fluid from air, so ascites can be identified and quantified. Serial examinations can be used to monitor the progression of ascites as a marker for the disease course.
Portal air can be easily observed as bubbles present in the venous system. This finding has been termed informally the "champagne sign" because of its similar appearance to a champagne flute.
Recent data suggest that ultrasonographic assessment of major splanchnic vasculature can help in the differential diagnosis of NEC from other more benign and emergent disorders.
The orientation of the superior mesenteric artery in relationship to the superior mesenteric vein can provide information regarding the possibility of a malrotation with a subsequent volvulus. If a volvulus is present, the artery and vein are twisted and, at some point in their courses, their orientation switches. This abnormality can be detected, even if the rotation is 360 degrees, if the full path of the vessels can be observed.
Doppler study of the splanchnic arteries early in the course of NEC can help distinguish developing NEC from benign feeding intolerance in a mildly symptomatic baby.
A clinical study from Europe and a recent small series in the United States demonstrate markedly increased peak flow velocity (>1.00) of arterial blood flow in the celiac and superior mesenteric arteries in early NEC. Such a finding at the presentation of symptoms can further aid in diagnosis and therapy, potentially sparing those individuals at low risk for NEC from unnecessary interventions.
Procedures:


Upper GI (with or without) small bowel follow-through
This procedure is a definitive way to diagnose the presence or absence of intestinal volvulus.
Always consider intestinal volvulus if bilious vomiting is present, especially in the term infant.
Because the presence of volvulus is a surgical emergency, it is an important diagnosis to exclude in a neonate with abdominal symptoms.
Perform before contrast enema because the presence of contrast in the colon can obscure pertinent findings.
Contrast enema
This procedure is a definitive way to diagnose a distal obstruction.
Always use a water-soluble contrast agent because of the risk of perforation. Contrast enemas are contraindicated in the presence of perforation. Consider carefully the clinical risks and benefits before undertaking this evaluation in the unstable and/or acutely ill infant.
Contrast enema findings are important for the differential diagnosis of intestinal abnormalities because distal obstructions, such as meconium plug, small left colon syndrome, and Hirschsprung disease, may cause symptoms in the baby without fulminant systemic collapse.
Rectal biopsy
This procedure is the criterion standard for diagnosing Hirschsprung disease.
This biopsy is a pediatric surgical procedure that is performed either as a bedside suction biopsy or as an open biopsy.
Ganglion cells in the biopsied specimen definitively rule out the diagnosis. The absence of cells, while suspicious for disease, merely may be the result found in the particular specimen obtained and is not 100% conclusive.
Placement of a peripheral arterial line may be helpful at the beginning of the patient's evaluation to facilitate serial arterial blood sampling and invasive monitoring.
If the baby is deteriorating rapidly, with apnea and/or signs of impending circulatory and respiratory collapse, airway control and initiation of mechanical ventilation is indicated.
Abdominal decompression
Decompression is essential at the first sign of abdominal pathology.

If possible, use a large-bore catheter with multiple side holes to prevent vacuum attachment to the stomach mucosa.

Set the catheter for low continuous suction and monitor output.

If copious amounts of gastric/intestinal secretions are removed, consider IV replacement with a physiologically similar solution, such as lactated Ringer solution.
Paracentesis

Ascites can develop during fulminant NEC and can compromise respiratory function. Remove ascites using intermittent paracentesis.

Ultrasonographic guidance can facilitate paracentesis.

After completing the procedure, significant fluid shifts between the intravascular and extravascular spaces are possible, so avoid removing large amounts of fluid at one time.
Place an intra-abdominal drain as an alternative to laparotomy if the baby is not a surgical candidate.
Histologic Findings: Inspecting the affected bowel reveals mucosal ischemia, progressing to cell death and sloughing. Necrosis can be limited to the mucosal layer, observed radiographically as pneumatosis, or it can affect the full wall, resulting in perforation with subsequent peritonitis. Necrotic and/or perforated intestine must be resected.
TREATMENT Section 6 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography




Medical Care:

Diagnosis of NEC is based on clinical suspicion supported by findings on radiologic as well as laboratory studies. Treatment of NEC depends on the degree of bowel involvement and severity of its presentation. Objective staging criteria developed by Bell have been widely adopted or modified to help tailor therapy according to disease severity.
Bell stage I - Suspected disease
Stage IA

Mild nonspecific systemic signs such as apnea, bradycardia, and temperature instability are present.

Mild intestinal signs such as increased gastric residuals and mild abdominal distention are present.

Radiographic findings can be normal or can show some mild nonspecific distention.

Treatment is NPO with antibiotics for 3 days.
Stage IB

Diagnosis is the same as IA, with the addition of grossly bloody stool.

Treatment is NPO with antibiotics for 3 days.
Bell stage II - Definite disease

Stage IIA

Patient is mildly ill.

Diagnostic signs include the mild systemic signs present in stage IA.

Intestinal signs include all of the signs present in stage I, with the addition of absent bowel sounds and abdominal tenderness.

Radiographic findings show ileus and/or pneumatosis intestinalis. This diagnosis is sometimes referred to colloquially as medical NEC.

Treatment includes NPO and antibiotics for 7-10 days.

Stage IIB

Patient is moderately ill.

Diagnosis requires all of stage I signs plus the systemic signs of moderate illness, such as mild metabolic acidosis and mild thrombocytopenia.

Abdominal examination reveals definite tenderness, perhaps some erythema or other discoloration, and/or right lower quadrant mass.

Radiographs show portal venous gas with or without ascites.

Treatment is NPO and antibiotics for 14 days.
Bell stage III - Represents advanced NEC with severe illness that has a high likelihood of progressing to surgical intervention

Stage IIIA

Patient has severe NEC with an intact bowel.

Diagnosis requires all of the above conditions, with the addition of hypotension, bradycardia, respiratory failure, severe metabolic acidosis, coagulopathy, and/or neutropenia.

Abdominal examination shows marked distention with signs of generalized peritonitis.

Radiographic examination reveals definitive evidence of ascites.

Treatment involves NPO for 14 days, fluid resuscitation, inotropic support, ventilator support, and paracentesis.

Stage IIIB

This stage is reserved for the severely ill infant with perforated bowel observed on radiograph.

Free air visible on abdominal radiograph indicates surgery. Surgical treatment includes resecting the affected portion of the bowel, which may be extensive. Initially, an ileostomy with a mucous fistula is typically performed, with reanastomosis performed later. Strictures may occur, with or without a history of surgical intervention, which may require surgical treatment.

If the patient is extremely small and sick, he/she may not have the stability to tolerate laparotomy. If free air develops in such a patient, consider inserting a peritoneal drain under local anesthesia in the nursery. Two retrospective reviews of the use of peritoneal drains as initial therapy for perforated bowel concluded that, while most patients ultimately require open laparotomy, initial peritoneal drainage may allow systemic stabilization and recovery in the smallest, sickest infants until they become better surgical candidates (Ahmed, 1998; Rovin, 1999).

Surgical Care:

Any patient requiring surgical intervention and many of those patients not progressing to surgery require protracted courses of parenteral nutrition and intravenous antibiotics.
Secure central venous access is optimal for ensuring uninterrupted delivery of antibiotics and nutrition as well as maximizing nourishment with central venous formulations.
Some units successfully use percutaneously inserted central venous catheters (PCVCs), while other units prefer surgically placed central lines such as Broviac catheters. Both types carry an increased risk of infection, particularly if they are used to administer lipids.
Consultations: Consult with a pediatric surgeon at the earliest suspicion of developing NEC. This may require transferring the patient to another facility where such services are available.

Diet:

When NEC is suspected, enteral feedings are withheld and parenteral nutrition is initiated. Centrally delivered formulations with maximal nutritional components are preferred (see Surgical Care). Enteral feedings can be restarted 10-14 days after findings on abdominal radiographs normalize in the case of nonsurgical NEC. Reinitiating enteral feeds in postsurgical babies may take longer and may also depend on issues such as the extent of surgical resection, timing of reanastomosis, and preference of the consulting surgical team.
Because of the high incidence of postsurgical strictures, some clinicians prefer to evaluate intestinal patency via contrast studies prior to initiating enteral feeds. When feeds are restarted, formulas containing casein hydrolysates, medium-chain triglycerides, and safflower/sunflower oils (Pregestimil/Nutramigen) may be better tolerated and absorbed than standard infant formulas.

MEDICATION Section 7 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography



Pharmacologic therapy includes agents to treat the developing disease and those to provide supportive and symptomatic relief.


Drug Category: Antimicrobial agents -- Although no definitive infectious etiology is known to cause NEC, clinical consensus finds that antibiotic treatment is appropriate for the threat of sepsis. Broad-spectrum parenteral therapy is initiated at the onset of symptoms after collecting blood, spinal fluid, and urine for culture. Antibacterial coverage for gram-positive and gram-negative organisms is essential, with the addition of anaerobic coverage for infants older than 1 week who show radiologic disease progression. Antifungal therapy should be considered for premature infants with a history of recent or prolonged antibacterial therapy or for babies who continue to deteriorate clinically and/or hematologically despite adequate antibacterial coverage.

Although any combination of drugs can be employed, one frequently used regimen includes vancomycin, cefotaxime, and clindamycin or metronidazole. This combination provides broad gram-positive coverage (including staphylococcal species), excellent gram-negative coverage (with the exception of pseudomonads), and anaerobic coverage.Drug Name
Vancomycin (Lyphocin, Vancocin, Vancoled) -- Provides excellent gram-positive coverage, including methicillin-resistant Staphylococcus species and Streptococcus species. Blocks bacterial cell wall synthesis. The parenteral formulation is widely bioavailable throughout all body tissues and fluids, including cerebrospinal fluid. Recommended for empiric use in patients with central lines, VP shunts, and for those with probable staphylococcal or streptococcal infection. Enteral administration for Clostridium difficile intoxication.
Adult Dose Severe infections: 2-4 g/d IV
Mild-to-moderate infections: 1-2 g/d IV
Pediatric Dose Dosage depends on gestational age, postnatal age, and birthweight
<7 days, <1200 g: 15 mg/kg/d IV qd
>7 days, >2000 g: 60 mg/kg/d IV divided q6-8h
Contraindications Documented hypersensitivity
Interactions Concurrent administration with anesthetic agents can cause erythema, hypotension, and hypothermia; concurrent administration of other ototoxic or nephrotoxic drugs, including loop diuretics and aminoglycosides
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Use caution with compromised renal function; monitor trough levels (5-10 mcg/mL) and adjust regimen to maintain safe and effective serum levels
Drug Name
Cefotaxime (Claforan) -- Broad-spectrum third-generation cephalosporin with excellent nonpseudomonal gram-negative coverage at the expense of gram-positive effects. Safety profile is more favorable than aminoglycosides. Penetrates cerebrospinal fluid to treat meningitis.
Adult Dose 1-2 g IV/IM q6-8h
Pediatric Dose Varies with weight and postnatal age
<1 month, <1200 g: 50 mg/kg/dose IV/IM q12h
>7 days, >2000 g: 50 mg/kg/dose IV/IM q6h
Contraindications Documented hypersensitivity
Interactions Probenecid may increase cefotaxime levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Adjust dose in severe renal impairment; has been associated with severe colitis
Drug Name
Clindamycin (Cleocin) -- Inhibits bacterial protein synthesis and is bacteriostatic or bacteriocidal depending on drug concentration and organism. Coverage includes anaerobes commonly found in the intestinal tract and many staphylococcal and streptococcal species.
Adult Dose 600-1200 mg IV/IM q6-8h
Pediatric Dose Dependent on weight and postnatal age
Parenteral recommendation range:
<7 days, <2000 g: 10 mg/kg/d IV divided q12h; not to exceed 4.8 g/d
>7 days, >2000 g: 20 mg/kg/d IV divided q6h; not to exceed 4.8 g/d
Contraindications Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
Interactions Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Dosage may require adjustment if patient has hepatic impairment; overgrowth of Clostridium difficile and associated development of pseudomembranous colitis can occur; C difficile infection has been associated with the development of postinflammatory adhesions and/or stricture (Freeman, 1999); metronidazole also has anaerobic coverage and may be an acceptable substitute
Drug Category: Antifungal agents -- Their mechanism of action may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide, which is toxic to the fungal cell.
If antifungal therapy is warranted, fluconazole can be initiated. Fluconazole is less toxic than amphotericin B, which is substituted if no clinical response to fluconazole occurs or if evidence of microbiological resistance is present.Drug Name
Fluconazole (Diflucan) -- Antifungal agent with good activity against Candida albicans. Associated with less toxicity and easier to administer than amphotericin B; however, fluconazole-resistant candidal species are being isolated with increasing frequency. Can be administered enterally or parenterally.
Adult Dose 200-800 mg PO/IV qd
Pediatric Dose Dependent on EGA and postnatal age
29 weeks' EGA and <14 d postnatal: 5-6 mg/kg/dose PO/IV q72h
Term and age >14 d: 3-6 mg/kg/d PO/IV qd
Contraindications Documented hypersensitivity
Interactions Levels may increase with hydrochlorothiazide; fluconazole levels may decrease with chronic coadministration of rifampin; coadministration of fluconazole may decrease phenytoin clearance; inhibits CYP2C19 and CYP3A4; may increase concentrations of theophylline, tolbutamide, glyburide, and glipizide; effects of anticoagulants may increase with fluconazole coadministration; increases in cyclosporine concentrations may occur when administered concurrently
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Use caution in impaired renal function, dosage may require adjustment; monitor liver enzymes and liver function tests during protracted therapy; discontinue use if clinical signs of hepatic failure develop
Drug Category: Vasopressors -- Babies with serious illness may progress to shock and require pharmacologic blood pressure support.Drug Name
Dopamine (Intropin) -- An adrenergic agonist that increases blood pressure by stimulating alpha-adrenergic vascular receptors resulting in vasoconstriction. Has some inotropic effects via beta1 cardiac receptors and, at low doses, increases glomerular filtration via renal dopaminergic receptors. Useful for babies with hypotension not responsive to volume repletion.
May be mixed in dextrose so that glucose delivery is not compromised.
Adult Dose 1-5 mcg/kg/min IV; not to exceed 30 mcg/kg/min
Pediatric Dose 1-20 mcg/kg/min IV; titrate to effect
Contraindications Documented hypersensitivity; pheochromocytoma; ventricular fibrillation
Interactions Phenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects of dopamine
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Extravasation can cause tissue necrosis, treat with phentolamine as quickly as possible after the event; correct hypovolemia before infusion
Drug Name
Dobutamine (Dobutrex) -- Adrenergic agonist with specific effects on beta1-receptors in the heart, resulting in increased contractility. Has minimal alpha-adrenergic activity. Can be used for babies in shock, usually adjunctively with dopamine, to increase cardiac output.
May be mixed in dextrose so that glucose delivery is not compromised.
Adult Dose 1-20 mcg/kg/min IV
Pediatric Dose Administer as in adults
Contraindications Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis; atrial fibrillation or flutter
Interactions Beta-adrenergic blocking agents antagonize effects; general anesthetics may increase toxicity
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Hypovolemic state should be corrected before using this drug
Drug Name
Epinephrine (Adrenaline) -- Nonspecific adrenergic agonist that stimulates alpha-, beta1-, and beta2-receptors. Can be used to support blood pressure in severe hypotension refractory to other treatment modalities.
Pediatric Dose 0.1-1 mcg/kg/min IV
Contraindications Documented hypersensitivity; cardiac arrhythmias or angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; do not use during labor (may delay second stage of labor)
Interactions Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in hypertension, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias
Drug Name
Naloxone (Narcan) -- Opioid receptor blocker. Experimental evidence suggests that it may increase blood pressure for babies in shock, perhaps by blocking the binding of endogenously produced endorphins released in sepsis, particularly from gram-negative organisms.
Pediatric Dose Bolus dose: 0.1 mg/kg IV
For continuous IV infusion, administer a test dose as above, observe for magnitude and duration of effect, and calculate continuous dose appropriately
Reported dosage range 2.5-160 mcg/kg/h IV
Contraindications Documented hypersensitivity; opioid addiction in baby or mother if baby is <7 d
Interactions Blocks the effects of narcotic analgesics and those of endogenous endorphins that may be involved in intrinsic pain relief pathways
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in cardiovascular disease; naloxone may precipitate withdrawal symptoms in patients addicted to opiates
Drug Category: Volume expanders -- Patients with severe illness may experience fluid shifts to the extracellular space, resulting in intravascular depletion requiring expansion.Drug Name
Albumin (5% and 25%) -- Used to increase intravascular oncotic pressure in hypovolemia and helps mobilize fluids from the interstitial to the intravascular space. Concentration can be either 5% (5 g/100 mL) or 25% (25 g/100 mL), depending on the desired effect.
Pediatric Dose Typical dose: 0.5-1 g/kg
Use 5% to replete the intravascular space
Use 25% to move fluid from the extravascular to the intravascular space
Contraindications Documented hypersensitivity; severe anemia; cardiac failure
Interactions None reported
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions If the patient has an ongoing capillary leak, exogenous albumin also moves into the interstitium; administer IV slowly, rapid administration can cause fluid shifts, exacerbating the risk of intraventricular hemorrhage in premature neonates; carries all of the risks and restrictions associated with administering blood products; protein load may exacerbate renal insufficiency, a potential complication of septic shock
Drug Name
Sodium chloride 0.9% (Normal saline, NS, Isotonic saline) -- Can be used as a volume expander and be as effective as albumin in acute hypovolemia.
Pediatric Dose 10-20 mL/kg IV infused over 30 min
Contraindications Fluid retention; hypernatremia; cardiac failure
Interactions None reported
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in congestive heart failure, hypertension, edema, liver cirrhosis, renal insufficiency, and sodium toxicity
Drug Name
Fresh frozen plasma -- Used as a volume expander, especially helpful for patients with concomitant coagulopathy.
Pediatric Dose 10-15 mL/kg IV infused over 1 h
Contraindications Documented hypersensitivity
Interactions None reported
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Carries all of the risks and restrictions associated with administering blood products
Drug Category: Opioid analgesics -- Although difficult to assess, premature infants presumably experience pain with severe illness and invasive procedures. Narcotic analgesics are safe and effective in premature infants and have a long history of clinical experience.Drug Name
Morphine sulfate (Duramorph, Astramorph) -- Opioid analgesic with a long history of safe and effective use in neonates. Inhibits ascending pain pathways by binding to the opiate receptors in the CNS. Causes generalized CNS depression. It is used for sedation and analgesia.
Adult Dose Starting dose: 0.1 mg/kg IV/IM/SC
Maintenance dose: 5-20 mg/70 kg IV/IM/SC q4h; titrate to control pain and to tolerable adverse effects
Pediatric Dose Administer as a bolus or a continuous infusion
Bolus: Start >0.01 mg/kg IV q2-4h prn; not to exceed 0.1 mg/kg q1h
Continuous infusion: >0.01 mg/kg/h IV; titrate upward until desired effect is achieved
Contraindications Documented hypersensitivity; hypotension; potentially compromised airway when establishing rapid airway control would be difficult
Interactions Other CNS depressants (eg, drugs typically not used in neonates) can potentiate the adverse effects of morphine; naloxone reverses morphine
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Causes respiratory depression/apnea at higher doses; use only preservative-free preparations in neonates; may cause systemic hypotension secondary to histamine release; prolonged use causes physiologic dependence and abrupt cessation can cause severe neonatal abstinence syndrome
Drug Name
Fentanyl (Sublimaze) -- Opioid analgesic 50-100 times more potent than morphine; mechanism of action and indications for use are similar; has less hypotensive effects than morphine because of minimal-to-no associated histamine release.
Administered bolus IV or as a continuous infusion. Because of small volumes used in neonates for bolus administration, it is not usually cost-effective to administer bolus.
Pediatric Dose Bolus dose: 1-4 mcg/kg/dose slow IV push
Continuous infusion: 0.5-1 mcg/kg/h IV; titrate to desired effect
If used during ECMO, higher doses can be anticipated, typically 1-5 mcg/kg/h initially
Because of tachyphylaxis, dose may need to be increased during the ECMO run, with doses as high as 20 mcg/kg/h reported by day 7 of treatment
Contraindications Documented hypersensitivity; hypotension; potentially compromised airway when establishing rapid airway control would be difficult
Interactions Other CNS depressants (eg, drugs not typically used in neonates) and MAOIs may potentiate adverse effects; naloxone reverses fentanyl
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Rapid IV administration may result in chest wall rigidity, severely compromising ability to ventilate the baby; higher doses are associated with respiratory depression/apnea; should be administered by qualified health care professionals trained in the use of general anesthetic agents; patient should be closely monitored, dose should be titrated, and lowest effective dose should be used; prolonged use (>5 d continuous infusion) results in physiologic dependence and abrupt cessation precipitates neonatal abstinence syndrome
FOLLOW-UP Section 8 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography





Further Inpatient Care:


Prolonged parenteral nutrition is essential to optimize the baby's nutrition while the gastrointestinal tract is allowed enough time for recovery and return to normal functioning. Central venous access is essential to facilitate parenteral delivery of adequate calories and nutrients to the recovering premature baby to minimize catabolism and promote growth.
Prolonged central venous access may be associated with an increased incidence of nosocomial infection, predominately with skin flora such as coagulase-negative Staphylococcus species. A high degree of clinical suspicion must be maintained to detect the subtle signs of such infection as early as possible.
Parenteral administration of lipid formulations via central venous catheters is also associated with an increased incidence of catheter-related sepsis.
Lipids coat the catheter's interior, allowing ingress of skin flora through the catheter lumen. A high degree of clinical suspicion is required for early detection of such an infection.
If line infection is suspected, obtain a blood culture through the central line. Antibiotics effective against skin flora (eg, vancomycin) should be administered through the line. Obtain another central line blood culture if the results of the first culture are positive. Persistently positive line cultures require removing the central line.
Prolonged parenteral nutrition may be associated with cholestasis and direct hyperbilirubinemia. This condition resolves gradually following initiation of enteral feeds.
Prolonged broad-spectrum antibacterial therapy increases the premature infant's risk for fungal sepsis.
Almost all premature infants demonstrate fungal colonization of the intestinal tract. Antibacterial therapy inhibits normal gut flora and allows fungal overgrowth caused by the absence of normal bacterial inhibition. Although prophylactic antifungal therapy reduces the incidence of fungal colonization in premature infants, it does not reduce the incidence of fungal sepsis. Therefore, it is not a recommended standard practice in the management of the preterm neonates
As with other systemic infections in this patient population, clinical signs of fungal sepsis can be subtle and nonspecific. Delay in detection and treatment of fungal sepsis can allow the formation of fungal balls intraocularly, in the kidney, and/or in the heart. This complication carries a high mortality rate and morbidity including blindness, obstructive renal failure, and endocarditis. A high index of suspicion for fungal infection must be maintained when a baby on broad-spectrum antibacterials develops signs of systemic infection.
Further Outpatient Care:


If a baby goes home with a colostomy, parents need thorough instruction regarding the baby's care. Having the parent(s) room with the baby at the hospital for several days prior to discharge is advisable so that they can learn and demonstrate adequate caregiving skills.
Babies who have undergone intestinal resection may experience short-gut syndrome (see Short-gut syndrome under Complications). These babies require vigilant nutritional regimens to maintain adequate calories and vitamins for optimum growth and healing.
Transfer:


In the acute phase, patients with progressive NEC require pediatric surgical consultation. During refeeding, patients with or without previous surgical history may demonstrate signs of obstruction requiring surgical evaluation and/or intervention. Transfer the patient to a facility offering pediatric surgical expertise, if it is not available at the current location.
Deterrence/Prevention:


Breastfed babies have a lower incidence of NEC than formula-fed babies (Lucas, 1990; Eyal, 1982).
Much anecdotal evidence exists about the role of feeding regimens in the etiology of NEC. Clinical research does not demonstrate definitive evidence for either causation or prevention. Although conventional wisdom recommends slow initiation and advancement of enteral feeds for premature infants, random trials do not show an increased incidence for babies in whom feeds have been started early in life versus after 2 weeks' chronologic age (Berseth, 1992; Meetze, 1992). In 1992, McKeown et al reported that rapid increase in feeding volume (>20 mL/kg/d) was associated with higher risk of NEC. However, in 1999, Rayyis et al showed no difference in NEC Bell stage greater than or equal to II in patients advanced at 15 mL/kg/d compared with those advanced at 35 mL/kg/d. Systematic review published by the Cochrane Collaboration in 1999 reported no effect on NEC of rapid feeding advancement for low–birth weight infants.
Because early presentation of NEC can be subtle, high clinical suspicion is important when evaluating any infant with signs of feeding intolerance or other abdominal pathology. In general, continuing to feed a baby with developing NEC worsens the disease.
Complications:


Approximately 75% of all patients survive. Of those patients who survive, 50% develop a long-term complication. The 2 most common complications are intestinal stricture and short-gut syndrome.
Intestinal strictures
This complication can develop in infants with or without a preceding perforation.
Incidence is 25-33%.
Although the most likely location for acute disease is the terminal ileum, strictures most commonly involve the left side of the colon.
Symptoms of feeding intolerance and bowel obstruction typically occur 2-3 weeks after recovery from the initial event.
The presence and location of the obstruction is diagnosed using barium enema; surgical resection of the affected area is required. Many surgeons routinely perform barium enemas in their patients before bowel reanastomosis so that all necessary surgical intervention can be performed at one time.
Short-gut syndrome
This is a malabsorption syndrome resulting from removal of excessive or critical portions of small bowel necessary for absorption essential nutrients from intestinal lumen.
Symptoms are most profound in babies who either have lost most of their small bowel or have lost a smaller portion that includes the ileocecal valve.

Loss of small bowel can result in malabsorption of nutrients as well as fluids and electrolytes.

The neonatal gut will grow and adapt over time, but long-term studies suggest that this growth may take as long as 2 years to occur. During that time, maintenance of an anabolic and complete nutritional state is essential for the growth and development of the baby. This is achieved by parenteral provision of adequate vitamins, minerals, and calories; appropriate management of gastric acid hypersecretion; and monitoring for bacterial overgrowth. The addition of appropriate enteral feedings during this time is important for gut nourishment and remodeling.
MISCELLANEOUS Section 9 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography




Medical/Legal Pitfalls:


Following hospital discharge, caring for premature infants has shifted away from neonatologists at regionalized centers to general pediatricians and other health care providers in the community. Adequate interaction between subspecialists and community physicians and formulation of well-communicated health care plans for these vulnerable babies are crucial to serve their best interest, to optimize their health outcome, and to minimize the opportunities for malpractice law suits.
Failure to recognize signs of NEC early enough to effect timely transfer to a tertiary care facility offering pediatric surgery could expose the clinician to medicolegal liability if the baby has a poor outcome as a result. Timely communication with parents and education are crucial to prevent lawsuits in case of unfortunate outcome.
Special Concerns:


As with all neonatal care, the risks and benefits of various clinical approaches must be considered carefully. As many as 50% of all premature infants manifest feeding intolerance during their hospital course, but less than one fourth of those infants develop NEC.
Cessation of feeding and initiation of broad-spectrum antibiotics in every baby with feeding intolerance impedes proper nutrition and exposes the baby to unnecessary antibacterials that may predispose to fungemia. On the other hand, failure to intervene appropriately for the baby with early NEC may exacerbate the disease and worsen the outcome. Clearly, managing this population requires a high degree of clinical suspicion for possible untoward events, tempered by cautious watching and waiting.
PICTURES Section 10 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography



Caption: Picture 1. Necrotizing enterocolitis. Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
View Full Size Image
eMedicine Zoom View (Interactive!)
Picture Type: X-RAY
Caption: Picture 2. Necrotizing enterocolitis. Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
View Full Size Image
eMedicine Zoom View (Interactive!)
Picture Type: X-RAY
Caption: Picture 3. Necrotizing enterocolitis. Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
View Full Size Image
eMedicine Zoom View (Interactive!)
Picture Type: X-RAY
Caption: Picture 4. Necrotizing enterocolitis. Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
View Full Size Image
eMedicine Zoom View (Interactive!)
Picture Type: X-RAY
Caption: Picture 5. Necrotizing enterocolitis. Pneumoperitoneum. Photo courtesy of the Department of Pathology, Cornell University Medical College.
View Full Size Image
eMedicine Zoom View (Interactive!)
Picture Type: X-RAY
Caption: Picture 6. Necrotizing enterocolitis. Resected portion of necrotic bowel. Photo courtesy of the Department of Pathology, Cornell University Medical College.
View Full Size Image
eMedicine Zoom View (Interactive!)
Picture Type: Photo
Caption: Picture 7. Necrotizing enterocolitis. Micrograph of mucosal section showing transmural necrosis. Photo courtesy of the Department of Pathology, Cornell University Medical College.
View Full Size Image
eMedicine Zoom View (Interactive!)
Picture Type: Photo
Caption: Picture 8. Necrotizing enterocolitis. Normal (top) versus necrotic section of bowel. Photo courtesy of the Department of Pathology, Cornell University Medical College.
View Full Size Image
eMedicine Zoom View (Interactive!)
Picture Type: Photo
Caption: Picture 9. Necrotizing enterocolitis. Histologic section of mucosal wall demonstrating pneumatosis. Photo courtesy of the Department of Pathology, Cornell University Medical College.
View Full Size Image
eMedicine Zoom View (Interactive!)
Picture Type: Photo
Caption: Picture 10. Necrotizing enterocolitis. Histologic section of bowel mucosa showing regeneration of normal cellular architecture. Photo courtesy of the Department of Pathology, Cornell University Medical College.
View Full Size Image
eMedicine Zoom View (Interactive!)
Picture Type: Photo
BIBLIOGRAPHY Section 11 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography





Adderson EE, Pappin A, Pavia AT: Spontaneous intestinal perforation in premature infants: a distinct clinical entity associated with systemic candidiasis. J Pediatr Surg 1998 Oct; 33(10): 1463-7[Medline].
Ahmed T, Ein S, Moore A: The role of peritoneal drains in treatment of perforated necrotizing enterocolitis: recommendations from recent experience. J Pediatr Surg 1998 Oct; 33(10): 1468-70[Medline].
Avila-Figueroa C, Goldmann DA, Richardson DK: Intravenous lipid emulsions are the major determinant of coagulase- negative staphylococcal bacteremia in very low birth weight newborns. Pediatr Infect Dis J 1998 Jan; 17(1): 10-7[Medline].
Berseth CL, Abrams SA: Special gastrointestinal concerns. In: Taeusch W, Ballard RA, eds. Avery's Diseases of the Newborn. 7th ed. Philadelphia, Pa: WB Saunders Co; 1998: 965-970.
Berseth CL: Effect of early feeding on maturation of the preterm infant's small intestine. J Pediatr 1992 Jun; 120(6): 947-53[Medline].
Eyal F, Sagi E, Arad I: Necrotising enterocolitis in the very low birthweight infant: expressed breast milk feeding compared with parenteral feeding. Arch Dis Child 1982 Apr; 57(4): 274-6[Medline].
Freeman J, Wilcox MH: Antibiotics and Clostridium difficile. Microbes Infect 1999 Apr; 1(5): 377-84[Medline].
Hartman GE, Boyajian MJ, Choi SS, et al: General surgery. In: Neonatology: Pathophysiology & Management of the Newborn. 5th ed. Philadelphia, Pa: Lippincott; 1999: 1005-1044.
Kanto WP Jr, Hunter JE, Stoll BJ: Recognition and medical management of necrotizing enterocolitis. Clin Perinatol 1994 Jun; 21(2): 335-46[Medline].
Kennedy KA, Tyson JE, Chamnanvanakij S: Rapid versus slow rate of advancement of feedings for promoting growth and preventing necrotizing enterocolitis in parenterally fed low-birth-weight infants. Cochrane Database Syst Rev 2000; (2): CD001241[Medline].
Lucas A, Cole TJ: Breast milk and neonatal necrotising enterocolitis. Lancet 1990 Dec 22-29; 336(8730): 1519-23[Medline].
McKeown RE, Marsh TD, Amarnath U: Role of delayed feeding and of feeding increments in necrotizing enterocolitis. J Pediatr 1992 Nov; 121(5 Pt 1): 764-70[Medline].
Meetze WH, Valentine C, McGuigan JE: Gastrointestinal priming prior to full enteral nutrition in very low birth weight infants. J Pediatr Gastroenterol Nutr 1992 Aug; 15(2): 163-70[Medline].
Nash PL: Naloxone and its use in neonatal septic shock. Neonatal Netw 1990 Jun; 8(6): 29-34[Medline].
Rayyis SF, Ambalavanan N, Wright L: Randomized trial of "slow" versus "fast" feed advancements on the incidence of necrotizing enterocolitis in very low birth weight infants. J Pediatr 1999 Mar; 134(3): 293-7[Medline].
Rovin JD, Rodgers BM, Burns RC: The role of peritoneal drainage for intestinal perforation in infants with and without necrotizing enterocolitis. J Pediatr Surg 1999 Jan; 34(1): 143-7[Medline].
Shorter NA, Liu JY, Mooney DP: Indomethacin-associated bowel perforations: a study of possible risk factors. J Pediatr Surg 1999 Mar; 34(3): 442-4[Medline].
Stark AR, Carlo WA, Tyson JE: Adverse effects of early dexamethasone in extremely-low-birth-weight infants. National Institute of Child Health and Human Development Neonatal Research Network. N Engl J Med 2001 Jan 11; 344(2): 95-101[Medline].
Stoll BJ: Epidemiology of necrotizing enterocolitis. Clin Perinatol 1994 Jun; 21(2): 205-18[Medline].
Taketomo CK, Hodding JH, Kraus DM: Pediatric Dosage Handbook. 6th ed. Hudson, Ohio: Lexi-Comp, Inc; 1999.

NOTE:
Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER


Necrotizing Enterocolitis excerpt

About Us | Privacy | Terms of Use | Contact Us | Advertise | Institutional Subscribers



We subscribe to the
HONcode principles of the
Health On the Net Foundation © 1996-2006 by WebMD.
All Rights Reserved.

 
Report Abuse

* Re:try this one!
#303682
  att - 04/13/06 16:59
 
  what a huge article!who is going to read it????  
Report Abuse

* Re:try this one!
#303787
  alibi - 04/13/06 19:47
 
  I am sorry, but I did.  
Report Abuse

* Re:try this one!
#303802
  april17 - 04/13/06 20:12
 
  according to UW, Corticoids use dec risk of NColitis, Intraventrical hemorrhage & RDS  
Report Abuse

[<< First]     [< Prev]     Page 2 of 2          

[<<First]   [<Prev]  ... Message ...  [Next >]   [Last >>]
 

 

 

Google
  Web USMLEforum.com
 

Step 1 Step 2 CK Step 2 CS Matching & Residency Step 3
USMLE Forum ArchivesUSMLE LinksUSMLE Forum Home