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Flashcards in GI Deck (186):
1

describe the initial steps of digestion

1. Digestion starts with food being crushed and mashed into smaller pieces in the mouth.
2. Amylase from the salivary glands begins the breakdown of carbohydrates.
3. The food bolus is swallowed and propelled through the esophagus through the lower esophageal sphincter and into the stomach
4. Digestion of fats starts in the stomach with lipase from gastric glands being secreted.
5. Protein digestion begins when pepsin and HCL denature the proteins to produce large peptide fragments and some free amino acids.

2

Where do fats, proteins, and carbs start being digested

1. carbs- mouth from amylase in saliva
2. fats- stomach with lipase from gastric glands
3. Proteins- stomach w/ pepsin and HCL

3

It is that about ___ after you start to eat, that your body initiates a gastro-colic reflex where your colon, rectum and anus are stimulated to evacuate.

15-20 minutes

4

Where are vitamin B1, B2, B3, B5, B6, folic acid, vitamin C, zinc and iron absorbed

-Vitamins B1, B5, B6 are absorbed in the jejunum and ileum.

-Vitamins B2, and B3 are absorbed throughout the small intestine.

-Folic Acid absorbed in the proximal jejunum.

-Vitamin C absorbed in the distal small intestine.

-Iron is absorbed primarily in the proximal intestine.

-Zinc is absorbed mainly in the ileum.

5

describe digestion in the SI

1. fats are combined with bile salts and pancreatic lipase to create small, mixed micelles which are ultimately absorbed into the enterocytes and through to the lacteals. Fat soluble vitamins are absorbed this way (A,D, E, K)
2. protein digestion in the duodenum
3. starches are broken down into smaller components by pancreatic amylase

6

describe protein digestion in the duodenum

1. Cholecystokinin is released which stimulates the pancreas to release protease zymogens (aka proenzymes) and the intestinal cells to release enterokinase.
2. Enterokinase converts trypsinogen to its active form—trypsin.
3. Trypsin activates more trypsinogen, chymotrypsinogen, proelastase and procarboxypeptidase A and B into their active forms. These enzymes are responsible for cleaving certain AA bonds thus creating smaller peptide chains that can be better absorbed.
4. These peptide chains are further broken down by the brush border enzymes into single, di and tripeptides which are then transported in to the enterocyte.
5. Intracellular peptidases will continue to convert these small peptides into individual amino acids that will be absorbed into the circulatory system.

7

describe starch break down in the SI

Starches are broken down into smaller components by pancreatic amylase. These disaccharides are further broken down by brush border enzymes such as lactase, sucrase, maltase, isomaltase, and trehalase and then transported into the cell. Highest activity of these enzymes in the proximal intestine.

8

Chronic abdominal pain is abdominal pain lasting longer than ___

6 months

9

HPI questions that will help you sort through your differential diagnosis when seeing a child for chronic abdominal pain

1. Stooling pattern. How often are they stooling? What does the stool look like? Do they see blood and/or mucous in the stool? You’ll also want to know if stooling makes the pain better or worse?
2. You’ll want to ask about the location of the pain.
3. Are there signs that indicate something organic is taking place—vomiting, weight loss/weight gain, fevers, waking at night because of pain or symptoms, etc?
4. Does food make the pain better/worse? Does stress seem to exacerbate the pain?

10

PMH questions to help you assess abdominal pain

1. Did the child pass meconium within the first 48 hours?
2. Does the child have other associated medical conditions that increase the risk of certain GI diseases—atopy (allergies/asthma/eczema), cystic fibrosis, diabetes, down’s syndrome, etc?
3. Is the child on medications that can contribute to abdominal pain, and/or diarrhea and constipation (iron, antibiotics, antidepressants, ADHD meds, psych meds, etc)?
4. What kind of surgeries has the child had—imperforate anus repair, tethered cord release, spina bifida, intestinal resections, etc?

11

Fhx questions to ask to help you asses abdominal pain

1. Is there a family history of other GI conditions?
2. Atopic family history?
3. Autoimmune family history?

12

2 main GI conditions you'll see in infants

1. GERD
2. Milk protein intolerance

13

Who do we see milk protein intolerance most commonly in

-in infants anywhere from 1-2 weeks of age to about 9-10 months of age.
-Typically it occurs in breastfed infants who present with fussiness anytime throughout the day and not just in the evenings.

14

Presentation of milk protein intolerance

1. fussiness anytime throughout the day- not just PM
2. Bright red blood or mucous in their stools
3. Growing well- eating and gaining weight appropriately

15

what is milk protein intolerance due to?

-a combination of insufficient secretion of zymogens from the pancreas leading to incomplete protein digestion and an immature, leaky gut in the infant. The poorly digested proteins irritate the lining of the intestinal tract causing pain when the infant eats

16

tx of milk protein intolerance

1. includes educating the family that this is a self-limiting condition (4-10 months of age)
2. Maternal elimination diet can help
3. If soy formula does not change the condition, you can do a 2 week trial of a semi-elemental formula like Nutramigen or Alimentum where the proteins are more hydrolyzed. (not liked as much by infants so transition by milking)
4. If the child is still highly fussy, you can try a two week trial of elemental formula such as EleCare and Neocate

17

describe the prognosis of milk protein intolerance

-Self-limiting
-As the child grows and matures, the pancreas will reach adult secretory levels by a year of age and the tight junctions between the cells will work more effectively.
-Parents typically start to see improvement around 4-6 months of age but some kids can take up to 10 months for improvement in their symptoms.

18

describe how maternal elimination diet can help milk protein intolerance

-Start with a two week trial of eliminating one food at a time—dairy first, then soy and finally peanuts. If no improvement is seen after eliminating those three foods, you can do a trial of a soy formula for 2 weeks.

*Unfortunately 50% of kids that react to breast milk or regular formula will also react to soy.

19

One of the most common causes of chronic abdominal pain in kids is

constipation

20

define constipation

-a delay or difficulty in defecation present for 2 or more weeks. The average child will stool 1-2 times a day unless they are in the first few weeks of life where they can stool 1-4 times a day.

21

what are the peak times of constipation occurence

1. 6 months of age with the introduction of solids
2. 1-2 years of age with the introduction of cow’s milk
3. 3-5 years of age with the challenge of kids not wanting to stool at school

22

You will want to make sure the child passed meconium within the first ___ or you are likely dealing with a condition other than chronic constipation

48 hours

23

Red flags for other abdominal conditions that are not constipation/encopresis

1. not passing meconium in 1st 48 hrs
2. fever
3. vomiting
4. failure to thrive
5. anal stenosis
6. tight empty rectum on PE
7. abdominal distention

24

The North American Pediatric Gastroenterology, Hepatology and Nutrition association recommends one treatment regimen for kids UNDER a year of age with chronic retentive constipation:

1. Education: explain the process of constipation
2. Diet: can introduce 2-4 oz of sorbitol containing fruit juice into diet or feed pureed prunes
3. Medication: If diet and education are not helpful, consider a trial of an osmotic laxative like Lactulose or Karo syrup (1-2 tablespoons QD-BID—titrating to achieve soft pudding consistency stools)
-Can add in ½ dropper of Little Tummies laxative if necessary for 2 weeks if child is very retentive

25

The North American Pediatric Gastroenterology, Hepatology and Nutrition association recommends one treatment regimen For kids OVER 1 year of age with chronic retentive constipation:

1. Education: explain the process of constipation and that treatment will be a long term process (4-6 months minimum)
2. Diet: decrease milk intake; increase fiber (5+ age); increase clear fluids
3. Behavioral changes: toilet time 15-20 min after meals
4. Medication: If diet and education are not helpful, consider a trial of Lactulose or Miralax (1/2 capful/1 tablespoon-1 capful/2 tablespoons dissolved in 4-10 oz of clear fluid) QD to BID
-Can add in 1 dropper of Little Tummies laxative or ½-1 square of Chocolate Ex-lax QD to BID if necessary for 2 weeks-2 months

26

Be fairly aggressive in your treatment of constipation. The reason why is the possibility of a child developing ___

encopresis aka fecal incontinence

27

what is encopresis

-Defined as involuntary passage of fecal material in the underwear; typically the child has anywhere from 3-8 bowel movements in their underwear that they can’t control
-Due to long standing chronic retentive constipation that has gone untreated or undertreated

28

tx of Encopresis

1. Education: explain the process of constipation and that treatment will be a long term process (4-6 months minimum but more likely a year); explain soiling is NOT voluntary
2. Diet: increase fiber (5gm+ age); increase fluids; this is going to be the long term management plan
3. Behavioral changes: toilet time 15-20 min after meals
4. Disimpaction—remove impaction with enema followed by a bowel clean out over a 2 day period (bowel clean out consists of a clear liquid diet, Miralax 4 times a day and ExLax twice a day until the stool comes out clear liquid)
5. Medication: Following bowel clean out, give Miralax (1 capful/2 tablespoons dissolved in 6-8 oz of clear fluid BID)
-Also add in 1-2 squares of Chocolate Ex-lax BID for 2 months then wean but continue on Miralax for another 6-12 months

29

what is celiac disease

-an autoimmune response to the gluten protein in wheat.
-The gluten triggers an antibody response in the proximal small intestine resulting in inflammation and destruction of the villi.
-The villous atrophy leads to a loss of absorptive surface and intestinal enzymes frequently leading to malabsorption and diarrhea.

*an underlying cause of chronic abdominal pain

30

sx of celiac disease

Wide range of sx
1. anything from asymptomatic results found on screening tests
2. bloating
3. abdominal pain
4. failure to thrive with diarrhea

31

what should you do if you suspect celiac disease

1. order a Tissue Transglutaminase Antibody blood test and also get a serum IgA level.
-If the TTG level is elevated, it is suggestive of Celiac Disease, but it is recommended to confirm the diagnosis with an upper endoscopy given the long term risks of untreated or poorly treated Celiac Disease (osteoporosis, intestinal lymphoma, infertility)

32

long term risks of untreated or poorly treated Celiac Disease

1. Osteoporosis
2. Intestinal lymphoma
3. infertility

33

tx for Celiac disease

Strict gluten free diet

34

Causes of chronic abdominal pain

1. constipation/encopresis
2. Celiac disease
3. IBD (Crohns, UC)
4. Functional abdominal pain (IBS)

35

what are the 2 types of IBD and describe their similarities

Chron's and ulcerative colitis

1. Both are autoimmune disorders
2. There can be some exam findings that will make you more suspicious for this diagnosis—anal tags or perianal fistulas
3. Typically you will see changes in the CBC indicative of anemia and you will see elevated ESR and CRP
4. Both diseases are diagnosed with endoscopy
5. Both are treated with steroids, immune modulators, and nutrition;
6. Both are periodically monitored by pediatric GI specialists

36

Who and WHAT does Crohn's disease effect

-Affects preteens through adults
-5 to 10 new cases per 100,000 individuals/year

-Affects any part of GI tract from mouth to anus
-PATCHY disease: most often effects terminal ileum, ileum and cecum and the colon

37

sx of Crohn's Disease

1. Abdominal pain (can wake from sleep)
2. weight loss
3. Diarrhea
4. Hematochezia
5. Growth failure
6. Extraintestinal manifestations (like delayed puberty)

38

who and WHAT does Ulcerative colitis effect

-Affects preteens to adults (peak incidence 15-25 yo)
-2.05-3.67/100, 000 per year in children

-Affects only the colon
-Diffuse, CONTINUOUS process starting at the rectum and extending more proximally into the colon

39

Active UC is characterized by

diffuse and continuous edema, erythema, friability, and ulceration

40

Sx of UC

1. Abdominal pain
2. weight loss
3. fevers
4. bloody, mucousy diarrhea
5. nocturnal diarrhea
6. Growth failure
7. Extraintestinal manifestations (like delayed puberty

41

Definition of Functional abdominal pain (IBS)

MUST INCLUDE:
1. Episodic or continuous abdominal pain
2. No evidence of an inflammatory, anatomic, metabolic or neoplastic process that explains the subject’s sx
3. Some loss of daily functioning
4. Additional somatic symptoms such as headache, limb pain or difficulty sleeping


42

IBS cannot include what sx

1. Persistent RUQ or RLQ pain
2. dysphagia
3. persistent vomiting
4. GI blood loss
5. nocturnal diarrhea
6. family hx of IBD, celiac dz, or PUD
7. pain that wakes the child from sleep
8. arthritis
9. perirectal disease
10. involuntary weight loss
11. deceleration of linear growth
12. delayed puberty
13. unexplained fever

43

who does IBS affect

Children school aged to adolescents

44

Features of IBS

1. no discernible pattern
2. nothing seems to consistently make it better or worse
3. the child continues to grow and develop appropriately

45

what is IBS caused by

visceral hypersensitivity

46

IBS is a dx of exclusion. Before you can diagnose it, what screening labs must be normal?

Screening labs: CBC, CRP, ESR, TTG, IgA, CMP, GGT, and UA

47

tx of IBS

1. Education: explain what condition the patient has
2. Symptomatic:
-increased fiber and fluids;
-antispasmodics (Levsin subligual or Bentyl 10 mg QD-QID daily);
-can consider Tricyclic antidepressant—amitriptyline (10-20 mg daily);
-stress management and relaxation techniques

48

define nausea and regurgitation

Nausea - a sensation of impending emesis

Regurgitation - the return of small amounts of food or secretions to the hypopharynx -food is brought back to the mouth without abdominal and diaphragmatic muscular activity

*Emesis rarely occurs without nausea

49

define emesis and retching

Emesis (a.k.a. “vomiting”) - forceful expulsion of stomach contents through an open glottis

Retching (a.k.a. “dry heaves”) - same mechanism as vomiting but glottis remains closed

*Emesis rarely occurs without nausea

50

The approach to acute nausea and vomiting is based on three key questions:

1. Is immediate therapy needed due to the consequences of nausea and vomiting regardless of the underlying cause?
2. Are empiric treatment and reassurance sufficient?
3. Is expeditious work-up required to establish the cause?- Is this a more serious problem, like an anatomical issue, that requires emergent intervention?

51

common causes of vomiting in neonates

1. GERD
2. Pyloric stenosis
3. Necrotizing enterocolitis*
4. Malrotation w/ volvulus
5. Hirschsprung disease
6. Atresias*, stenoses
7. Metabolic disorders*
8. Feeding intolerance

*unique to neonatal period
*Others, such as pyloric stenosis, Hirschsprung disease, and malrotation may be picked up outside of the neonatal period, typically in early infancy.

52

Common causes of vomiting in infants

1. GERD*
2. Gastroenteritis*
3. Anatomic
4. Intussusception
5. Rumination
6. Nutrient intolerances
7. Overfeeeding
8. Munchausen syndrome by proxy

*most common

53

Common causes of vomiting in childhood

1. Gastroenteritis
2. Infection
3. Peptic ulcer/GERD
4. Cyclic vomiting
5. Psychogenic
6. Toxic ingestion- should be considered in any child who has the motor skills to place objects in the mouth
7. Intracranial mass

54

Common causes of vomiting in adolescene

1. Gastroenteritis
2. Peptic ulcer/GERD
3. Psychogenic
4. Intracranial mass
5. Cyclic vomiting
6. Bulimia
7. Pregnancy
8. Drugs of abuse
9. Suicide attempt

*pschyogenic causes become more prominent

55

Bilious vomiting in the first months of life suggests

anatomical obstruction or other serious condition

56

With vomiting in neonates and infants it is important to:

1. take it seriously
2. Distinguish vomiting from regurgitation
3. Bilious versus non-bilious

57

"For bilious vomiting, I give ____. It has never failed in the worst cases of persistent bilious vomiting. It can be repeated in half an hour if really necessary. The results are immediate.”

one teaspoonful of table salt

58

how to distinguish vomiting vs reguritation

Vomiting would likely be of larger volume and would certainly be forceful.

59

cause of bilious vomiting in older children

bilious vomiting can occur with any syndrome with repeated bouts of vomiting. As food is expelled, all that remains in the GI tract is saliva and bile

60

cause of bilious vomiting in neonatal or early infancy period

-malrotation with or without volvulus
-intussusception

61

what is a malrotation

-a developmental error in the formation of the G.I. tract in which the intestine does not complete its normal rotational pattern of fetal development
-incomplete rotation of the intestine during fetal development

62

Malrotation can cause symptoms of __ or __ and makes the intestine susceptible to volvulus.

incomplete or intermittent obstruction

63

what happens with volvulus

the large intestine wraps around a segment of the small intestine causing obstructive symptoms and ischemia.
-Volvulus can be intermittent and resolve spontaneously but can also be persistent and lead within hours to strangulation of the bowel.

64

how does malrotation present

1. Usually presents in neonatal period with bilious emesis
2. Infants and children may present with failure to thrive, signs of intermittent obstruction characterized by intermittent episodes of severe abdominal pain
3. Malrotation can be missed in infancy and is occasionally not picked up until adolescence or later in life (25-50% of adolescents w/ malrotation are asymptomatic)

65

how do you diagnose malrotation

US or barium enema

66

tx of malrotation

surgical

67

how does malrotation with volvulus typically present

1. severe abdominal pain,
2. unremitting vomiting
3. presents as an acute small bowel obstruction

*Life threatening surgical emergency

68

complications of malrotation with volvulus

1. Significant bowel necrosis can result from compression of superior mesenteric artery
2. high risk of short bowel syndrome
3. Life threatening surgical emergency

69

what is intussusception

-Prolapse (telescoping) of one portion of bowel into adjacent segment, most commonly terminal ileum near the ileocecal junction
-Compression--> swelling-> obstruction

70

What is the presentation of intussusception

1. neonate period: Most common at 3-12 months,
2. 3:1 mal predominance
3. abdominal pain
4. vomiting (bilious or non-bilious)
5. currant jelly stools (50%)

71

Dx and Tx of intussusception

barium enema or air enema: both are diagnostic AND therapeutic

72

prognosis of intussusception

Prognosis is strongly correlated with duration before reduction
-Complicated cases require surgical treatment

73

what is currant jelly stool

Mucus from the inflamed segment of intestine mixed with blood causes the currant jelly stool

*seen 50% of time w/ intussusception

74

Non-bilious vomiting causes

1. intussusception
2. GERD
3. Pyloric stenosis
4. acute appendicitis

75

Presentation of pyloric stenosis (IHPS)

1. 4:1 male predominance
2. vomiting usually at 2-4 weeks of age, progresses to projectile vomiting
3. Vomiting is immediately post-prandial and infant will feed following emesis (“hungry vomiter”)
4. undernourished infant w/ hypocholoremic metabolic alkalosis (rarely seen now)
5. presents first 2 months of life
6. "olive sign"- palpable pylorus

76

what is the cause of pyloric stenosis (IHPS)

-Positive family history in 13%, first born 30%

-caused by hypertrophy of the muscles that make up the pylorus.
-As the hypertrophy increases over a span of several weeks the nature of the vomiting progresses

77

Dx of pyloric stenosis (IHPS)

abdominal US

78

tx of pyloric stenosis (IHPS)

1. Correction of fluid/electrolyte imbalance
2. followed by surgery (pyloromyotomy)

79

what is GERD

Passage of gastric contents into the esophagus due to transient relaxation of the LES (lower esophageal sphincter)
-

80

Presentation of GERD in neonates and infants

1. Postprandial regurgitation (rarely vomiting)
2. May have irritability
3. feeding aversion
4. back arching

81

How do you dx GERD in neonates and infants

*often a clinical diagnosis in which you will take an empirical treatment approach
-can use prolonged monitoring of esophageal pH to diagnose

82

tx of GERD in neonates and infants

-typically self-limiting, resolves 6-12 months
2. smaller feedings at frequent intervals
3. positioning w/ the head of the crib elevated
4. Meds:
-H2-receptor blockers: e.g ranitidine (Zantac)
-Proton pump inhibitors: e.g. omeprazole (Prilosec)
-Antacids(e.g. Al hydroxide) not recommended at this age

83

Presentation of GERD in children

1. chest pain
2. epigastric pain
3. dysphagia
4. heart burn
5. food impaction
6. vomiting
7. cough

84

Dx of GERD in children

Although the diagnosis is often made clinically, the gold standard for diagnosis is esophageal pH in conjunction with a symptom diary.

85

Management of GERD in children

1. thickened feedings
2. poistioning can help in younger children
3. Older kids- weight reduction and dietary modification
4. Meds:
-H2-receptor blockers e.g ranitidine (Zantac)
-Proton pump inhibitors e.g. omeprazole (Prilosec)
-Surgical: Nissen fundoplication

86

what is the most common cause of acute abdomen in children

acute appendicitis

87

Presentation of acute appendicitis depends on

age

88

Classic presentation of acute appendicitis

1. adolescents (age 13+):
2. anorexia
3. periumbilical pain migrating to the RLQ
4. non-bilious vomiting, preceded by pain.

*. If there are prolonged bouts of vomiting, the vomitus can become bile-stained.

89

Neonatal presentation of acute appendicitis

1. birth - 30 d
2. Abdominal distention
3. vomiting

90

infant presentation of acute appendicitis

1. 30 d - 2 y
2. Vomiting
3. inconsolability
4. fever
5. Diarrhea not uncommon in first 2-3 months of life.

91

preschool presentation of acute appendicitis

1. 2-5 y
2. Vomiting is often the first symptom and frequently PRECEDES abdominal pain,
3. fever present in most, but not all patients.

92

school age presentation of acute appendicitis

1. 6-12 y
2. Abdominal pain and vomiting are present, but the
3. typical migration of periumbilical pain to RLQ may not occur.
4. Diarrhea, constipation, and dysuria can confuse the diagnosis

93

PE of classic acute appendicitis

1. RLQ tenderness
2. guarding
3. rebound tenderness
4. fever

94

PE of acute appendicitis in neonates (birth -30d)

1. Abdominal distention is common.
2. Hypothermia,
3. hypotension,
4. respiratory distress may also be seen.

95

PE of acute appendicitis in infants (30d-2yrs)

1. Fever
2. diffuse abdominal tenderness (due to rupture) are the most common physical findings

96

PE of acute appendicitis in preschool to adult

classic signs

-RLQ tenderness
-guarding
-rebound tenderness
-fever

97

How do you score the pediatric appendicitis score (PAS)

1. Anorexia: 1 point
2. Nausea or vomiting: 1 point
3. Migration of pain: 1 point
4. Fever > 38º C (100.5º F): 1 point
5. Tenderness with cough, percussion, or hopping: 2 points
6. Right-lower-quadrant tenderness: 2 points
7. WBC count > 10,000 cells/mm3: 1 point
8. PMNs plus band forms > 7500 cells/mm3: 1 point

-Mean score 7= appendicitis
-pts w/o appendicitis had a mean score of 1.9
-score of 3-6 was indeterminate for appendicitis

98

Labs for of acute appendicitis

1. WBC is elevated and/or left-shifted in most (~96%) children with acute appendicitis. Poor specificity!
2. CRP may provide useful information but currently not well-validated.
3. Urinalysis: Should be part of the work-up but…Caveat: 7-25 % of children with acute appendicitis have pyuria on urine dip. NOT useful for rule out!
4. Recommended labs: WBC, urinalysis, hCG for postmenarchal females.

99

Imaging for acute appendicitis and when would you do it?

1. US or CT

-Children with a typical clinical presentation or PAS of 7 or greater: Consult with a pediatric surgeon BEFORE obtaining imaging

-Children with a low likelihood of appendicitis or a low PAS (1-2)can be managed without imaging and followed closely

100

diarrhea is defined as

an increase in frequency, fluidity, or volume of bowel movements.

101

Etiologies of diarrhea

1. Infectious**
2. Intolerances (formula, lactose, carbohydrate, protein)
3. Irritable bowel syndrome (IBS)
4. Inflammatory bowel disease (IBD)
5. Medication use (e.g. antibiotics)
6. Laxative abuse
7. Toxic ingestion

102

AAP defines acute gastroenteritis as

“diarrheal disease of rapid onset, with or without accompanying symptoms and signs such as nausea, vomiting, fever, or abdominal pain.”*

103

causes of acute gastroenteritis

viral, bacterial, parastic

104

Management of acute gastroenteritis

*Supportive
-Rehydration, refeeding, attention to volume status

* antidiarrheal agents are generally not recommended

105

In developing countries, diarrheal illnesses account for an estimated 4-5 million deaths per year in children __

under 5 years

106

___ alone is believed to cause over 500,000 deaths per year in children under the age of 5.

Rotavirus

*causes acute gastroenteritis

107

Common Viral pathogens and the duration of illness

1. Rotavirus- avg 6 days, range 1-10d
2. Enteric adenoviruses- avg 11d, range 1-22d
3. Astrovirus- avg 5 d, range 1-5 d
4. Torovirus- avg 5 d, range 1-5 d
5. Norwalk-Like- avg 2 d, range 1-4 d

*With the exception of adenoviruses most viral pathogens cause brief bouts of illness lasting less than one week.

108

The most common viral agent associated with severe diarrhea in infants and children

Rotavirus-- affects villi of SI

109

describe the presentation of rotavirus

1. 48 hour incubation, followed by:
2. vomiting,
3. mild fever,
4. then voluminous, watery diarrhea
5. peak in winter months (Nov-May) -- but now w/ vx pattern is less reliable
6. peak in infants under 2yrs (3-15months)

*The presentation of rotavirus gastroenteritis is similar to other viral gastroenteritides.

110

complications of rotavirus gastroenteritis

1. severe dehydration
2. death

Stool bicarb loss may lead to metabolic acidosis

111

describe the spread of rotavirus

fecal-oral route

-survives hours no the hands, days on environmental fomits

112

how do you dx rotavirus gastroenteritis

Clinical diagnosis if minimal or mild dehydration, no culture or other testing needed

*viral testing is often performed to monitor outbreaks.

113

tx of all viral gastroenteritis

1. Estimate degree of hydration
2. Rehydration is mainstay of therapy
3. AAP recommends AGAINST the use of antiemetics or antidiarrheals in acute gastroenteritis
4. Continue breast-feeding and re-initiate solid foods as as soon as rehydration is complete
5. The BRAT diet: Has NOT been shown to be more effective than normal diet, instead feed a normal diet as tolerated BUT can be used

114

what is the BRAT diet

Bananas, rice, applesauce, toast

115

How to prevent rotavirus gastroenteritis

1. Hygiene: Hand-washing with soap and water probably not sufficient; **alcohol-based gels recommended
2. Asymptomatic children should be isolated from symptomatic children, if possible
3. **RotaTeq: human-bovine reassortant vaccine approved by FDA and recommended by AAP for routine childhood immunization in 2006. Oral vaccine to be administered at 2, 4 and 6 months.
4. Rotarix: attenuated human vaccine approved in 2008. Oral vaccine, administered in two doses at 2 and 4 months.

* Immunization: RotaShield vaccine pulled from the market in 1999 following several cases of intussusception.

116

the most common bacterial pathogens causing diarrhea

1. Salmonella
2. Aeromonas
3. Plesimonas
4. Yersinia enterocolitica
5. C difficile
6. Listeria
7. E Coli, E Coli 0157:H7
8. Shigella

117

presentation of bacterial gastroenteritis depends on

causative organism

118

common presentation of gastroenteritis

*Depends on organism

Bloody stools common (50%), usually with more frequent, small-volume bowel movements, vomiting less common

-Febrile, non-bloody diarrhea: Usually viral
-Afebrile, non-bloody: Usually viral
-Febrile, bloody diarrhea: Usually bacterial
-Afebrile, bloody diarrhea: Usually bacterial, consider non-infectious source

119

w/u of gastroenteritis

1. History and exam should first focus on determining if patient is seriously ill and assessing hydration status
2. Stool culture and smear for WBCs, ova and parasites

120

sources of salmonella

foodborne (poultry, raw eggs)

121

describe the presentation of salmonella

1. Incubation of 6-72 hrs,
2. followed by abrupt onset N/V,
3. crampy abd pain,
4. then watery diarrhea,
5. sometimes blood and mucus
6. Duration: 5 days to months (chronic)

122

tx of salmonella

1. Supportive.
2. Antibiotics may prolong course not recommended unless pt is immune-compromised or has evidence of bacteremia or meningitis
3. Antibiotic treatment with cefotaxime or ceftriaxone if bacteremia or meningitis is present or immuno-compromised host.

123

presentation of Shigella

1. Uncommon before 3-6 months of age. Younger patients typically have more severe disease
2.Abrupt onset cramps,
3. urgency,
4. fever,
5. chills,
6. malaise,
7. diarrhea
8. Stool often with blood, mucus
9. Peak: SUMMER months
10. duration 5 days

124

how is shigella spread

fecal-oral transmission

*HIGHLY contagious

125

tx of shigella

1. Antibiotics:
Trimethoprim/sulfamethoxazole (TMP/SMX), Cefixime, ceftriaxone.
2. Supportive measures.

126

sources of E. Coli 0157:H7

uncooked meats, unpasteurized fruit juice, contaminated water

127

Presentation of E. coli

1. sever crampy, bloody diarrhea
2. risk for hemolytic uremic syndrome (HUS)
3. More common in children under age 4

128

Tx of E. coli

1. supportive

*Abx may actually worsen prognosis

129

sources of Giardia lamblia

1. infected feces
2. contaminated drinking water or food
3. recreational pools
4. children and employees at day care centers
5. animal hosts: beaver

130

The most common protozoan-caused diarrhea in North America

Giardia lamblia

131

describe the presentation of giardia

1. incubation 1-2+ weeks
2. Malodorous, greasy diarrhea, usually without blood.
2. Can cause chronic diarrhea
3. malaise,
4. other GI symptoms: Vomiting

132

dx of Giardia

stool O and P testing

133

tx of Giardia

Metronidazole 15mg/kg for 10 days

134

___ medications are ineffective and possibly even dangerous for smaller children for gastroenteritis .

True antidiarrheal

ex. kaopectate, loperamide, tincture of opium, diphenoxylate with atropine

135

meds to help with acute gastroenteritis

1. Cholestyramine (Questran) helps to bind the stools to decrease diarrhea. Rx: Questran 1/3 packet mixed with food TID until formed stools

2. Promethazine (Phenergan) suppositories: They work for vomiting, but potential for respiratory depression and toxicity when used in younger kids. Contraindicated under age 2

136

how can you dx dehydration by parental report

1. Vomiting, diarrhea, or decreased oral intake is useful but non-specific
2. Urine and stool output is very subjective
3. Normal tear production is useful in excluding moderate to severe dehydration

137

PE to assess dehydration

1. Change in body weight before and after rehydration is the standard method for diagnosis
2. To identify dehydration before treatment, many factors can be used but most are not helpful in isolation. The most useful individual signs are:
-Increased capillary refill time
-Abnormal skin turgor
-Abnormal respiratory pattern

138

Clinical dehydration scales based on a combination of factors are much better predictors than any individual factor. 4 factors predicted dehydration:

1. cap refill over 2 sec
2. absence of tears
3. dry mucous membranes
4. ill general appearance

139

Labs to assess dehydration

1. BUN
2. Creatinine
3. BUN/Creatinine ratio
4. Urine specific gravity

*NONE of the above are useful in diagnosing dehydration in children!

**IT IS A CLINICAL DX AND MUST NOT BE FALSELY REASSURED BY LABS

140

describe the use of skin turgor in assessing dehydration

Pinch a fold of skin on the lateral abdomen for 2 seconds and release.

-Normal: skin recoils immediately
-Moderate: Skin recoils within 2 seconds
-Severe: Skin is slow to recoil (over 2sec), “tenting”

*Do not perform on the hand!

141

describe the use of capillary refill in assessing dehydration

Squeeze and blanch the nail bed and count time to reperfusion.

-Normal: less than 2 seconds
-Moderate: greater than 2 seconds (2-4 sec)
-Severe: prolonged or no refill

*Performed on the sternum in neonates

142

clinical presentation of dehydration

1. sucken eyes and cheeks
2. decreased skin turgor
3. sunken fontanelle
4. few or no tears
5. dry mouth or tongue
6. sunken abdomin

143

General Signs of Mild dehydration

-Wt. loss: 3-5%
-Mental status: well, alert
-Thirst: drinks normally, might refuse liquids

144

General signs of moderate dehydration

-Wt. loss: 6-10%
-Mental status: normal, fatigued or restless, irritable
-Thirst: thirsty, eager to drink

145

General signs of severe dehydration

-Wt. loss: 11-15%
-Mental status: apathetic, lethargic, unconscious
-Thirst: drinks poorly or unable to drink

146

hemodynamic signs of mild dehydration

-Pulse: normal
-Cap refill: 2-3sec
-BP: nl
-Perfusion: nl

147

hemodynamic signs of moderate dehydration

-Pulse: slight increase
-Cap refill: 3-4 sec
-BP: nl
-Perfusion: nl

148

hemodynamic signs of severe dehydration

-Pulse: tachy
-Cap refill: over 4 sec
-BP: low (emergency)
-Perfusion: circulatory collapse

149

Assessment of fluid loss of mild dehydration

-UO: mild oliguria
-Tears: decreased
-Urine specific gravity: over 1.020

150

Assessment of fluid loss of moderate dehydration

-UO: oliguria
-Tears: decreased
-Urine specific gravity: over 1.020

151

Assessment of fluid loss of severe dehydration

-UO: anuria
-Tears: absent
-Urine specific gravity: anuria

152

7 Principles of fluid replacement

1. Oral rehydration solution (ORS) should be used
2. Oral rehydration should be performed rapidly (within 3-4 hours
3. Age-appropriate, unrestricted diet is recommended as soon as dehydration is corrected
4. For breastfed infants, nursing should be continued
5. For formula-fed infants, diluted formula is not recommended, special formula usually is not necessary
6. Additional ORS should be given for ongoing losses through diarrhea
7. No unnecessary laboratory tests or medications should be administered

153

Fluid Replacement in Children with Gastroenteritis: Caveats

1. IV Fluids not recommended in mild or moderate dehydration unless the child is not able to take ORT
2. ORT is recommended in severe dehydration only if the patient is clinically stable, alert, and taking ORT well

154

Fluid replacement solutions are a combination of

water, sugar, and salt in proportions that approach the osmolarity of body fluids

155

Sugars in the appropriate proportion are an important component of rehydration fluids because of

cellular glucose/solute co-transport, which increases the rate of rehydration.

156

___ are appropriately formulated for rehydration.
___ are not. Why

Pedialyte and other rehydration solutions
*osmolarity ~250milliosmoles/L

Sodas and other beverages like apple juice
~2-3x the osmolarity of rehydration solutions

*those beverages can worsen dehydration and their use in the setting of acute gastroenteritis should be strongly discouraged

157

The basic principle of IV fluid replacement is __ followed by __

volume resuscitation followed by rehydration

158

describe volume resuscitation

Start with Lactated Ringer’s solution or NS at 20ml/kg IV over one hour

159

describe rehydration after volume resuscitation

*if electrolytes normal:
-Then administer ORT at 100 ml/kg over 3-4 hours if tolerated OR
-D5 ¼ NS IVF with 20 mEq/L potassium over 3-4 hours OR if significant stool loss
-D5 ½ NS with 20 mEq/L potassium to replace losses on top of maintanence levels

160

what is the recommended ORS and IV fluids for MILD dehydration in children w/ gastroenteritis

ORS:
-50ml/kg over 3-4 hrs

IV fluids:
-not recommended

161

what is the recommended ORS and IV fluids for MODERATE dehydration in children w/ gastroenteritis

ORS:
-100 ml/kg over 3-4 hours

IV fluids:
-not recommended

162

what is the recommended ORS and IV fluids for SEVERE dehydration in children w/ gastroenteritis

ORS:
-100-150 ml/kg over 3-4 hours

IV fluids:
-20 ml/kg bolus over one hour

163

what is the recommended ORS and IV fluids for ON-GOING LOSSES dehydration in children w/ gastroenteritis

ORS:
-10 ml/kg for each stool or emesis

IV fluids:
-10 ml/kg for each stool or emesis

164

describe the Holliday-Segar Method to calculate maintenance fluids

you first determine the total milliliters per day and then calculate milliliters per hour to determine the rate of IV flow. For example a 10 kg child would need 10x100 or 1000 mL of IV fluids per day or 40 mL per hour.

165

a pt that weights 3-10kgs needs how many ml/day and ml/hr of IV fluids?

ml/day: 100ml/kg

ml/hr: 4ml/kg/hr

166

a pt that weights 10-20kgs needs how many ml/day and ml/hr of IV fluids?

ml/day: 1000 + 50(wt-10kg)

ml/hr: 40 + 2(wt-10kg)

167

a pt that weights over 20kgs needs how many ml/day and ml/hr of IV fluids?

ml/day: 1500 + 20(wt- 20kg)

ml/hr: 60 + (wt-20kg)

168

Calculating Maintenance Fluids:Holliday-Segar Method Simplified for home ORT

Infants: 1 oz/hour
Toddlers: 2 oz/hour
Older children: 3 oz/hour

169

when should a child be hospitalized for fluid managment

1. Caregivers cannot provide adequate care at home;
2. Substantial difficulties exist in administrating ORT, including intractable vomiting, ORS refusal, or inadequate ORS intake;
3. Concern exists for other possible illnesses complicating the clinical course;
4. ORS treatment fails, including worsening diarrhea or dehydration despite adequate volumes;
5. Severe dehydration (over 9% of body weight) exists;
6. Social or logistical concerns exist that might prevent return evaluation, if necessary, or
7. Such factors as young age, unusual irritability or drowsiness, progressive course of symptoms, or uncertainty of diagnosis exist that might indicate a need for close observation.

170

Such factors as: _____ that might indicate a need for close observation.

1. young age
2. unusual irritability or
3. drowsiness,
4. progressive course of symptoms, or
5. uncertainty of diagnosis exist

171

CBC may provide evidence for

1. inflammation (WBC and platelet count)
2. poor nutrition or bleeding (Hemoglobin, RBC volume, reticulocyte counts)
3. infection (WBC and differential)

172

__, __, __, and __ help w/ define hydration status

UA
BUN
serum electrolytes
creatinine

173

___ pain results when autonomic nerves within the gut detect injury, transmitting sensation by nonmyelinated fibers

Visceral

174

The pain is vague, dull, slow in onset, and poorly localized

visceral pain

175

__ pain results when overlying body structures are injured.

somatic

somatic structures include the parietal peritoneum, fascia, muscles, and skin of the abdominal wall

176

lab tests for infection or inflammation

CBC
CRP
ESR

177

lab tests for biliary or liver disease

AST
ALT
GGT
Bilirubin

178

lab tests for pancreatitis

amylase
lipase

179

lab tests for UTI, bleeding due to stone, trauma, or obstruction

UA

180

when is plain flat or upright abdominal film best

-Bowel obstruction
-appendiceal fecalith
-free intraperitoneal air
-kidney stones

181

when is CT scan best

-intra-abdominal or pelvic abscess
-appendicitis
-crohs
-pancreatitis
-gallstones
-kidney stones

182

when is barium enema best

intussusception
-malrotation

183

when is US best

Gallstones
-appendcitis
-intussusception
-pancreatitits
-kidney stone

184

when is upper endoscopy best

-suspected peptic ulcer or eosphagitis

185

to determine if diarrhea is osmotic or secretory the ___ is calculate

osmotic gaps

Osmoticgap =290-2 ([Na+] + [K+])

Secretory= less than 50
Osmotic= over 50, indicates malabsored substances other than electrolyte account for fecal osmolarity

186

Having E. Coli O157:H puts you at risk for

HUS