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Colic Clinical Presentation

  • Author: Prashant G Deshpande, MD; Chief Editor: Carmen Cuffari, MD  more...
Updated: Sep 03, 2015


Colic remains a diagnosis of exclusion.

Crying by infants with or without colic is mostly observed during evening hours and peaks at the age of 6 weeks. The cause of this diurnal rhythm is not known. The amount of crying is not related to an infant's sex; the mother's parity; or the parents' socioeconomic status, education, or ages.

On acoustic analysis, colicky crying differs from regular crying. Compared with regular crying, colicky crying is more variable in pitch, more turbulent or dysphonic, and has a higher pitch. Mothers of infants with colic, unlike mothers of infants without colic, rate the cries as more urgent, discomforting, arousing, aversive, and irritating than usual.

Obtain a detailed history about the timing, the amount of crying, and the family's daily routine. The benign nature of colic should be emphasized.

Rule out causes of excessive crying in an infant, such as having hair in the eye, strangulated hernia, otitis, and sepsis.



Perform physical examination to confirm normalcy. Infants with colic often have accelerated growth. Weight gain is typical, whereas failure to thrive should make one suspicious about the diagnosis of colic.



GI causes may include but are not limited to gastroesophageal reflux, overfeeding, underfeeding, milk protein allergy, and early introduction of solids. Parental anxiety and parental stress has been a subject of many studies. Postpartum depression may lead to stress in parents, which may be transferred to the infant, resulting in excess crying.

Other causes include inexperienced parents or incomplete or no burping after feeding. Incorrect positioning after feeding may contribute to excessive crying. Note that colic is not limited to the first-born child, casting doubt on the theory about inexperienced parenting as the etiologic factor.

Recent epidemiologic evidence suggests that exposure to cigarette smoke and its metabolites may be related to colic. Maternal smoking and exposure to nicotine replacement therapy (NRT) during pregnancy may be associated with colic.[3] In one study, prenatal nicotine exposure was associated with an elevated risk for infantile colic in offspring. This was true both in women who smoked during pregnancy and those who used nicotine replacement therapy compared with unexposed women. Partners’ smoking was not associated with infantile colic after adjustment for maternal smoking.[4]

Some evidence has linked persistent crying in young infants to food allergy.[5] An association between colic and cow's milk allergy (CMA) has been postulated.[6] Data from one study suggested an association between low birth weight and increased incidence of colic.[7]

Some reports have focused on intestinal microflora and its association with colic.[8] Lower counts of intestinal lactobacilli were observed in infants with colic compared with infants without colic.[9]

The results of a Dutch study that followed the temporal development of intestinal microbiota from birth to approximately 100 days in 24 infants suggested that early differences in the development and composition of gut flora may be at the root of infant colic.[13, 14] At 2 weeks, babies later diagnosed with colic had significantly less microbial diversity and stability than their healthy counterparts, as well as more than twice the abundance of proteobacteria and significantly reduced levels of Bacteroidetes. These differences were all seen in the first month of life, before the colic peak, and usually disappeared by 3 to 4 months of age, when colic usually resolves.

Contributor Information and Disclosures

Prashant G Deshpande, MD Attending Pediatrician, Department of Pediatrics, Christ Hospital Medical Center and Hope Children's Hospital; Assistant Clinical Professor of Pediatrics, Midwestern University

Prashant G Deshpande, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Telemedicine Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Stefano Guandalini, MD Founder and Medical Director, Celiac Disease Center, Chief, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, University of Chicago Medical Center; Professor, Department of Pediatrics, Section of Gastroenterology, Hepatology and Nutrition, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

Stefano Guandalini, MD is a member of the following medical societies: American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, North American Society for the Study of Celiac Disease

Disclosure: Received consulting fee from AbbVie for consulting.

Chief Editor

Carmen Cuffari, MD Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Prometheus Laboratories for speaking and teaching; Received honoraria from Abbott Nutritionals for speaking and teaching.

Additional Contributors

Chris A Liacouras, MD Director of Pediatric Endoscopy, Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia; Associate Professor of Pediatrics, University of Pennsylvania School of Medicine

Chris A Liacouras, MD is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

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