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Essentials of Acute Care > test 3 material > Flashcards

test 3 material Flashcards

1
Q

an imbalance between nutrient requirements and intake that results in cumulative deficits of energy, protein, or micronutrients that can negatively affect growth, development or other relevant outcomes

A

malnutrition

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2
Q

what is acute malnutrition time frame

A

less than 3 months

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3
Q

what is chronic malnutrition time frame

A

greater than 3 months

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4
Q

what is the continental divide for secretions in the nonobstructed GI tract

A

Ligament of Treitz

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5
Q

Bleeding sources proximal to the Ligament of Treitz can present with ______

A

hematemesis

distal will rarely present with hematemesis

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6
Q

Bleeding sources distal to the Ligament of Treitz will present with

A

melena (stool that has the appearance and consistency of liquid tar - black and offensive in odor), maroon colored stool, red bloody stool, red blood streaked stool, guaiac positive stool

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7
Q

Brisk proximal to the ligament of treitz bleeds can also present with

A

melena or frank blood per rectum

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8
Q

GI bleeding is common or uncommon in the pediatric population

A

uncommon

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9
Q

UGI bleeds differentials

A

lesions of the GI mucosa
esophageal varices secondary to liver disease
infectious colitis

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10
Q

what is the most common cause of colonic bleeding worldwide

A

infectious colitis

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11
Q

in countries with good water supplies, what accounts for the majority of lower GI bleeds

A 
colon polyps
allergic colitis
anal fissures
UC (ulcerative colitis)
CD (Crohns Disease)
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12
Q

lower GI bleeding

infant who is fed cows milk or soy based formula

A

may have allergic colitis

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13
Q

lower GI bleeding

in someone with recent antibiotic therapy

A

C-Diff toxin induced colitis

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14
Q

history of dry heaves followed by hematemesis or melena suggests

A

Mallory-Weiss tear

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15
Q

Recent illness with GI bleeding may lead you to suspect

A

HUS (hemolytic uremic syndrome) - caused by toxins released by e.coli - causes acute reaction of hemolytic anemia. byproduct of the hemolyzed RBCs cause renal failure

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16
Q

Ingestion of NSAIDS with gi bleed may lead you to

A

gastritis
duodenitis
ileal lesion
R colonic lesions

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17
Q

A family history of IBD, intestinal cancers at an early age, or liver disease with GI bleed may lead you to think of your differentials

A

liver disease history - inherited A1 antitrypsin deficiency and hep B may be transmitted vertically at birth

IBD

intestinal cancer

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18
Q

The complaint of heartburn in older child or adolescent or a BRUE like symptom in in infant with GI bleed suggests

A

UGI source such as
esophagitis
gastritis
ulcer

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19
Q

urgency to defecate or tenesmus (incomplete defacation)

GI bleed

A

colitis

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20
Q

delayed passage of meconium or constipation in infancy can be symptoms of

A

CF or HD (bollick 440)

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21
Q

Being on abx and no enteral nutrition will have what complication

A

it will kill the intestinal tracks vit K producing bacteria. this will cause the pt PTT to rise, resulting in coagulopathy. Add Ng suction to this and you can have a UGI bleed from the NG tube suction induced mucosal injury

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22
Q

pertinent physical exam findings for GI bleeding

A

oxygen sats
tachycardia
postural changes in pulse and BP
hypotension
skin, conjunctivae or nail beds pale
rectal exam for hemorrhoids, tears, or other perianal disease
melena or bright red blood in the digital exam suggests source of blood

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23
Q

palpable moveable rectal mass might identify

A

polyps

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24
Q

blood in vomit or stool in the newborn may be from

A

the mother ingesting commercial dyes (#2 and #3), blueberries, beets, bismuth) - > red tinted or colored stool but may look like blood

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25
Q

what test should be considered in pt presenting with significant UGI bleeding

A

urgent upper endoscopy

only after stabilized

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26
Q

what test should be considered in pt with bright red lower GI bleeding

A

Conoloscopy

only after stabilized

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27
Q

GI bleed, pt hemodynamically unstable what can you adminishter

A

NS
LR
PRBCs

pt kept NPO

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28
Q

An endoscopy allows for

A

visualization
cauterization
biopsy
test for H. Pylori

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29
Q

med used in management of bleeding esophageal varices, why

A

octreotide - decrease CVP (central venous pressure) before endoscopic intervention

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30
Q

if variceal bleeding is not controlled by endoscopic and/or tamponade intervention what should be considered

A

Transjugular intrahepatic portosystemic shunting (TIPS)

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31
Q

in patients with significant GI bleeding whom an upper endoscopy and colonoscopy have failed to show the source of bleeding (if the loss of blood is brisk enough to detect)

A

nuclear medicine tagged RBC bleeding study

or a angiogram with selective vessel embolization

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32
Q

this may help identify a radiographically silent lesion or one beyond the reach of the conventional upper or lower endoscope

A

single or double balloon enteroscopy

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33
Q

polyps are usually removed with

A

snare electrocautery during a colonoscopy

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34
Q

GI bleeding from Henoch -Schonlein purpura (HSP) and HUS usually resolves with

A

resolution of the disorders

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35
Q

patients with UGI bleeds when can the diet resume

A

within 24 hours

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36
Q

what are the UGI bleeds discharged on

A

PPI for gastritis
or B-Blocker (propanolol) for esophageal varices

close outpatient follow up by GI

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37
Q

discharge of patients with lower GI bleed depends on

A

etiology of the bleeding

underlying chronic illness

response to therapy

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38
Q

infant upper GI bleed think

A

hemorrhagic gastritis
stress ulcer
vascular malformation
reflux esophagitis

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39
Q

infant lower GI bleed think

A 
infectious colitis
midgut volvulus
anal fissures
necrotizing enterocolitis
intussusception
milk protein allergy
hirschsprung disease
lymphonodular hyperplasia
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40
Q

young child upper gi bleed think

A 
hemorrhagic gastritis
stress ulcer
gastric/duodenal ulcer
esophageal varices
mallory-weiss tear
epistaxis
reflux esophagitis
foreign body
toxic ingestion
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41
Q

young child lower gi bleed think

A 
infectious colitis
midgut volvulus
anal fissures
hemorrhoid
ulcer
polyps
hemolytic-uremic syndrome
juvenile polyp
pseudomembranous colitis
inflammatory bowel disease
Henoch Schonlein purpura
Meckel diverticulum
Ischemic colitis
intussusception
angiodysplasia
graft vs host disease
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42
Q

upper Gi bleed for older child and adolescent think

A 
hemorrhagic gastritis
stress ulcer
gastric/duodenal ulcer
esophageal varices
mallory-weiss tear
epistaxis
reflux esophagitis
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43
Q

lower GI bleed or older child and adolescent think

A 
infectious colitis
anal fissures
hemorrhoid
ulcer
polyps
juvenile polyp
inflammatory bowel disease
Henoch -Schonlein Purpura
Meckel diverticulum
Hemolytic -uremic syndrome
Bacterial enteritis
Angiodysplasia
graft vs host disease
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44
Q

what antibiotic does the book mention can look like blood in stool

A

cefdinir

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45
Q

what test can tell you if its blood or something else

A

occult stool

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46
Q

vomiting blood is always ________ to the ligament of treitz

A

proximal

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47
Q

when upper GI bleeding is suspected, what may be placed and why

A

a ng and gastric contents aspirated for evidence of recent bleeding

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48
Q

what test is used in newborns to determine whether it is fetal or maternal blood present in stool

A

apt test (alkali denaturation test)

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49
Q

hematemesis in newborn

blood found in stomach on lavage

A

peptic disease

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50
Q

hematemesis or rectal bleeding in newborn
APT shows adult hemoglobin is present
cracked maternal nipples

A

ingested maternal blood

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51
Q

hematemesis or rectal bleeding in newborn

Bruising

A

coagulopathy

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52
Q

streaks of bloody mucus in stool in newborn

eosinophils in feces and in rectal mucosa

A

allergic colitis

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53
Q

rectal bleeding in newborn

sick infant with tender and distended abdomen

A

necrotizing enterocolitis

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54
Q

hematemesis in newborn

cystic mass in abdomen on imaging study

A

Duplication cyst

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55
Q

hematemesis in newborn
hematochezia (passage of fresh blood through anus usually in or with stools - think lower gi bleed or a brisk upper gi bleed)
acute, tender distended abdomen

A

volvulus (twisting or knotting of the GI tract causing an obstruction - most commonly due to a birth defect called a malrotation)

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56
Q 
infancy to older than 2 yrs old
hematemesis
rectal bleeding possible
epigastric pain
coffee ground emesis
A

peptic disease

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57
Q

infancy to > 2 yrs old
hematemesis
history or evidence of liver disease

A

esophageal varices

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58
Q 
infancy to 2 yrs old
rectal bleeding
crampy pain
abd distension
abd mass
A

intussusception

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59
Q

infancy to > 2 yrs old
rectal bleeding
massive bright red bleeding
no pain

A

meckel diverticulum

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60
Q

infancy to >2 yrs old
rectal bleeding
bloody diarrhea
fever

A

bacterial enteritis

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61
Q 
infancy to > 2 yrs old
hematemesis
rectal bleeding possible
epigastric pain
coffee ground emesis
A

NSAID injury

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62
Q 
older than 2
rectal bleeding usually
crampy pain
poor weight gain
diarrhea
A

inflammatory bowel disease

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63
Q

> 2 yrs old
rectal bleeding
history of antibiotic use
bloody diarrhea

A

psueudomembranous colitis

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64
Q

> 2 yrs old
rectal bleeding
painless
bright red blood in stool - not massive

A

juvenile polyp

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65
Q

> 2 yrs old
rectal bleeding
streaks of blood in stool
no other symptoms

A

Nodular lymphoid hyperplasia

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66
Q

> 2 yrs old
hematemesis
bright red or coffee ground emesis
follows retching

A

Mallory-Weiss syndrome

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67
Q 
>2 yrs old
rectal bleeding
thrombocytopenia
anemia
uremia
A

Hemolytic uremic syndrome (HUS)

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68
Q

> 2 yrs old
rectal bleeding
dilated external veins
blood with wiping

A

hemorrhoids

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69
Q

tests for evaluation of GI bleeding

all patients get

A 
CBC and platelet count
coagulation tests (PT/PTT)
tests for liver dysfunction (AST, ALT, GGT, bilirubin)
occult blood test of stool or vomitus
Blood type and crossmatch

abd x ray series

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70
Q

what tests ordered to evaluate bloody diarrhea

A

stool culture - looking for c-diff
sigmoidoscopy (looks at rectum and lower part of large intestine (colon))or colonoscopy
CT with contrast

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71
Q

tests to evaluate rectal bleeding with formed stools

A 
external and digital rectal examination
sigmoidoscopy or colonoscopy
meckel scan 
mesenteric arteriogram
video capsule endoscopy
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72
Q

evaluation for hematemesis if endoscopy is not available

A

barium upper GI series

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73
Q

Evaluation of bleeding with pain and vomiting (Bowel obstruction)

A

abd x ray series
pneumatic or contrast enema
upper GI series

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74
Q

what scan is used to detect a meckel diverticulum

A

Meckel scan

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75
Q

what is a mesenteric arteriogram

A

special x ray of the blood vessels (arteries) in the abd to show where the artery is blocked or bleeding

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76
Q

what does video capsule endoscopy show

A

shows inside of small intestine that is not easily reached with more traditional endoscopy procedures

used to find cause of GI bleeding
diagnose inflammatory bowel diseases such as Crohns disease, cancer, celiac disease, polyps

also looks at esophagus (esophageal varices)

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77
Q

Blood in the diaper or toilet may be coming from the

A

urinary tract, vagina, or severe

diaper rash.

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78
Q

most common intra abdominal tumors are

A

neuroblastoma

Wilms tumor

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79
Q

2/3s of abdominal masses are due to

A

organomegaly

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80
Q

a history of bilious emesis or encopresis can lead to an assessment of

A

bowel obstruction

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81
Q

urinary excretion of ______ can lead to cola colored urine

A

bile salts

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82
Q

can present with acholic stools (pale)

A

obstruction of the biliary system

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83
Q

changes in the character of urine or the urinating experience (frequency, urgency, dysuria, decrease UO, dribbling or accidents) can be the presentation of a ____ pathology

A

renal pathology

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84
Q

Jaundice can indicate _____ disease

A

liver

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85
Q

Pale skin can indicate

A

anemia

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86
Q

flushed rosy skin can be present in

A

sepsis

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87
Q

classic exanthems (diffuse rash) can be present with

A

viral infections

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88
Q

general appearance is ill-appearing, particularly with cachexia or FTT, _____ or _____ may be the cause

A

chronic infections

malignant disease

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89
Q

Masses in the RUQ most often involve the

A

liver
gallbladder
biliary tree

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90
Q

Epigastric masses can include both

A

epigastric hernias

diastasis recti

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91
Q

LUQ masses most often involve the

A

stomach
spleen
adrenal gland
kidney

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92
Q

Right and Left lower quadrant masses may be from

A

ovarian and fallopian processes or the intestines in orgin

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93
Q

suprapubic masses are most commonly

A

genitourinary in nature

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94
Q

Abd wall masses are either

A

superficial to the muscular layers or

their movement is coupled with the contraction of the abdominal musculature

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95
Q

_________ are most often observed when a very small child cries and it pops out

A

abd wall hernias

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96
Q

immobile masses are either

A

invasive tumors

masses that arise from the retroperitoneal organs

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97
Q

Tenderness to the mass suggests a

A

recent change (such as hemorrhage that lead to acute increase in volume of the mass placing tension on the capsule)

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98
Q

Firmness, hardness, irregularity suggest either

A

tumor or

desmoplasia (scar)

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99
Q

Smoothness to a mass suggests an

A

encapsulated mass

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100
Q

Tympany indicates

A

gas such as a hollow viscus

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101
Q

Dullness indicates

A

fluid or a solid mass

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102
Q

A hernia is diagnosed with

A

physical exam

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103
Q

what kind of hematomas secondary to trauma are difficult to diagnose and why

A

rectus hematomas - hidden from view by rectus sheath

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104
Q

what kind of soft tissue tumors can be diagnosed on physical exam

A

fibromas and lipoma

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105
Q

fixed abd mass related to mesenteric fibromatosis or retroperitoneal sarcoma is diagnosed by

A

CT or MRI bc bowel gas often obscures retroperitoneal ultrasonography

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106
Q

in infants crying can lead to an ingestion of air ->

A

gastric distention which can cause vagal symptoms or resp sequelae

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107
Q

what makes gastric distension relatively easy to diagnose and treat

A

tympanic LUQ

response to NG

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108
Q

ingestion of hair and roughage can result in

A

bezoars

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109
Q

what 3 things can present with acute gastric distension with the inability to pass an NGT

A

congenital duplications
gastric tumors
gastric torsion

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110
Q

a exceedingly common disorder

presents with abd discomfort and a palpable mass

A

constipation

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111
Q

infectious and inflammatory diseases of the bowel that can produce a mass

A

abscesses from a perforated appendix

Meckel diverticulum

phlegmons from Crohn Disease (CD)

palpable lead pipe colon from ulcerative colitis (UC)

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112
Q

mass in younger patients differential

A 
intussusception
duplications
mesenteric cysts
meconium pseudocysts
bowel atresia
malrotation with volvulus can occasionally present with an abd mass
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113
Q

bowel tumors that may present with a palpable mass

A

carcinoid
lymphoma
adenocarcinoma

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114
Q

in most cases a palpable kidney represents what?

what population can this be a normal finding

A

obstructive kidney disease
parenchymal kidney disease

infants the kidney is occasionally palpable

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115
Q

multiple renal cysts can by caused by

A

polycystic kidney disease

multicystic dysplastic kidney disease

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116
Q

a large fluid filled cyst is present at the hilum, it can represent a

A

dilated renal pelvis with or without associate dyroureter

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117
Q

bilat findings of a large fluid filled cyst is present at the hilum can suggest

A

bladder outflow obstruction such as posterior urethral valves or neurogenic bladder

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118
Q

diffuse unilateral renal swelling can occur from

A

renal vein thrombosis

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119
Q

what type of tumor can present as a unilateral mass (kidney)

A

Wilms tumor

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120
Q

adrenal masses are most commonly ____ in origin

A

neoplastic

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121
Q

what is the most common pediatric adrenal tumor

A

neuroblastoma

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122
Q

what other endocrine tumor can occasionally be identified but rarely of sufficient size to produce a palpable mass

A

pheochromocytoma

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123
Q

in females _____ masses are extremely common

A

gynecologic

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124
Q

__________ cysts are a physiologic requirement for menstruation

A

small ovarian cysts (follicular)

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125
Q

benign ovarian masses include

A

dermoid cysts
mature teratomas
immature teratomas
germ cell tumors

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126
Q

what can occasionally produce a very edematous and swollen ovary that may occasionally present as a mass

A

torsion

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127
Q

the most common fallopian and uterine masses are

A

pregnancy (ectopic or intrauterine)

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128
Q

these fallopian and uterine masses can lead to accumulation of serum or menses and a large palpable pelvic mass

A

obstruction of the fallopian tube at the isthmus (hydrosalpinx)

uterus at the cervix

vagina at the hymen

hydrometrocolpos
hematocolpos

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129
Q

hematocolpos

A

the vagina is pooled with menstrual blood due to multiple factors leading to the blockage of menstrual blood flow

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130
Q

hydrometrocolpos

A

expanded fluid filled vaginal cavity with associated distention of the uterine cavity

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131
Q

hydrosalpinx

A

fallopian tube thats blocked with watery fluid

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132
Q

an enlarged spleen should suggest ____ or ____ until proven otherwise

A

hematologic disease

malignancy

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133
Q

splenomegaly - hematologic disease assoiciations

A

hereditary hemolytic anemias such as spherocytosis or elliptocytosis

sickle cell disease

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134
Q

hematologic malignancies associated with splenomegaly

A

leukemias

lymphomas

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135
Q

viral infections can be associated with splenomegaly

A

acute viral infection with
Epstein Barr virus (EBV) or
cytomegalovirus (CMV)

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136
Q

rheumatologic disease associated with splenomegaly

A

systemic lupus erythematosus

Langerhans cell histiocytosis

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137
Q

storage diseases associated with splenomegaly

A

Niemann-Pick

Gaucher disease

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138
Q

can cause significant hepatic edema and enlarged tender liver

A

Acute viral hepatitis

autoimmune hepatitis

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139
Q

metabolic disorders that can present with painless hepatomegaly

A

glycogen storage diseases

Wilson disease

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140
Q

congenital disorder that can cause painless hepatomegaly

A

Congenital hepatic fibrosis

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141
Q

cyst that can cause hepatomegaly

A

simple or biliary cysts

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142
Q

simple cyst in liver or polycystic liver disease can be diagnosed with

A

US

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143
Q

cysts that can be present anywhere along the biliary tree

A

biliary cysts or choledochal cysts

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144
Q

solid hepatic masses of vascular origin

A

hemangioma

lymphovascular malformations

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145
Q

solid hepatic masses of parenchymal origin

A

focal nodular hyperplasia
adenoma
neoplasia

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146
Q

The most common tumors in the younger patients (liver)

A

hepatoblastoma

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147
Q

most common liver tumors in the older pediatric patient

A

hepatocellular carcinoma

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148
Q

can produce diffuse neoplastic infiltration of the liver

A

lymphoma

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149
Q

acute liver congestion and hepatomegaly are associated with

A

vascular congestion such as in heart failure or Budd-Chiari syndrome

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150
Q

Congenital dilations of the biliary tract are classified as

A

choledochal cysts

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151
Q

Acquired dilation of the biliary tree can occur secondary to

A

obstruction

including gallbladder hydrops from chronic cystic duct obstruction and biliary ductal dilation due to obstruction from gallstone disease or biliary strictures

or from pancreatic head masses

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152
Q

pancreatic and biliary tract malignancies are common or rare in children

A

rare

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153
Q

what will you order for an abd mass to indicate infection, inflammation and anemia

A

CBC with Diff

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154
Q

what labs will you order for a abd mass to identify kidney disease

A

BUN and creatinine

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155
Q

what labs will you order for an abd mass to look at pancreatic disease

A

amylase and lipase

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156
Q

what labs will you order for an abd mass to look at liver function

A

liver function panel (LFTs)

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157
Q

what lab would you order for an abd mass that is nonspecific but is sensitive for significant illness

A

albumin

hypoalbuminemia is what you would be looking for

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158
Q

what lab when evaluating an abd mass would be useful in identifying solid tumors

A

Uric acid

LDH

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159
Q

what radiographic test is used to identify an intestinal obstruction, fecal impaction and calcifications associated with tumor.

A

2 view x ray of abdomen

nonspecific

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160
Q

what can be used to identify the origin of an abdominal mass and differentiate between solid and cystic

A

US

not definitive but can guide you in the selection of further imaging and/or labs

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161
Q

what test can be particularly useful in evaluating solid abd masses

A

CT scan with IV contrast

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162
Q

In addition to evaluating solid masses, CT with IV contrast can also see

A

vascular anatomy and presence of associated lymph nodes

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163
Q

What type of scan serves to help stage many cancers

A

CT with IV contrast

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164
Q

Masses of primary bowel or bladder are best seen with what study

A

fluoroscopic studies such as UGI, BE and voiding cystourethrogram

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165
Q

what type of contrast to bowel will produce significant artifact and prevent immediate subsequent CT scan

A

Enteral contrast administered to bowel

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166
Q

What scans are used for hepatobiliary and pancreatic disease (masses)

A

US and CT are not helpful for these

Traditionally (HIDA) hepatobiliary imino-diacetic acid

increasingly more common is
MRCP (magnetic resonance cholangiopancreatography )

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167
Q

in benign abdominal masses an NGT is mandatory for all

A

perforations and obstructions

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168
Q

treatment for benign abd masses associated with emergent evaluation (appendicitis, colitis with pending perforation, biliary tract with cholangitis and sepsis and potential ovarian torsion or ectopic pregnancy)

A 
IV
NG drainage
abx
support for septic shock
surgical consult
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169
Q

age of presentation for neuroblastoma

A

18 months, prevalence greatest in <4 years (85%)

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170
Q

most common extracranial tumor in children

A

neuroblastoma

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171
Q

Wilms tumor most common age of presentaion

A

1-5 yrs

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172
Q

most common malignant liver tumor

A

hepatoblastoma

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173
Q

what malignant tumor is associated with extreme prematurity and what age is the mean for diagnosis

A

Hepatoblastoma

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174
Q

absence of ganglion cells (aganglionosis) of the enteric nerve plexus of the intestines (aganglionosis begins at the anus and continues proximally)

results in the ABSENT peristalsis in the affected bowel and causes a functional intestinal obstruction.

also a loss of rectosphincter reflexes - internal sphincter does not relax to allow stool to be evacuated

A

Hirschsprung disease (HD)

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175
Q

where are ganglion cells normally located

A

throughout the intestines from the mouth to the rectum

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176
Q

Hirschsprung disease (HD) is more prevalent in what gender

A

males (4 xs more than female)

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177
Q

short segment Hirschsprung disease (HD) what part of bowel is affected

A

rectosigmoid colon

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178
Q

long segment Hirschsprung disease (HD) what part of bowel is affected

A

rectosigmoid colon but also extends proximal to this point

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179
Q

genetic role in Hirschsprung disease (HD)

what gene?

A

there is familial occurrence in up to 20% of these cases and they are usually the long segment Hirschsprung disease (HD)

RET gene

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180
Q

what is the classic presentation for Hirschsprung disease (HD)

A

failure to pass muconium in the first 8 hours of life

bilious emesis

abd distention

FTT

Sepsis

may have visible bowel loops with peristalsis

rectal exam may reveal a spastic rectum with no stool in the rectal vault - the rectal exam may cause the pt to have explosive diarrhea

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181
Q

Presenting age of Hirschsprung disease (HD)

A

can present at any age but most are diagnosed in the neonatal period

diagnosis after 2yrs old is very rare

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182
Q

children who are diagnosed with Hirschsprung disease (HD) at an older age typically have which type

A

shorter segment affected

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183
Q

children diagnosed at an older age with Hirschsprung disease (HD) usually present with what symptoms

A

long and tenuous history of constipation, malnutrition, FTT and chronic abd distension

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184
Q

if missed in the neonatal period infants often present with Hirschsprung disease (HD) at what point?

A

when they transition from breast milk to formula or when solid foods are introduced

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185
Q

diagnosis of Hirschsprung disease (HD) is made by what and confirmed how?

A

clinical picture and radiologic studies

confirmed by pathology from a rectal biopsy

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186
Q

Abd x ray for Hirschsprung disease (HD) will show what

A

large dilated loops of intestines and may have air fluid levels

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187
Q

after Hirschsprung disease (HD) is suspected on an abd x ray, what would be the next test to order

A

Barium enema - this would not be diagnostic but identifies who will require a more invasive evaluation

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188
Q

what will the barium enema show in Hirschsprung disease (HD)

A

dilation of the colon, which is normal ganglionic colon followed by a funnel shaped area (transition zone) ->this is where the colon has some ganglion cells but not enough -> will show an area of dilation that narrows into the aganglionic bowel (wont be dilated)

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189
Q

how is a BE performed

A

placing a small catheter into the rectum and instilling contrast into the colon then taking several radiographs

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190
Q

A BE would not be helpful in Hirschsprung disease (HD) for what population

A

neonates. May not have dilation of the colon yet

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191
Q

BE should be avoided if there are concerns for ______ or ______

A

perforation

enterocolitis

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192
Q

screening tool for Hirschsprung disease (HD) but not definitive however less invasive then the rectal biopsy and highly sensitive (up to 80%). also used in developing bowel continence in children with HD.

A

Anorectal manometry - measures resting anal sphincter pressure. In older children, it can assess for the sensation of being full

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193
Q

standard for definitive diagnosis of Hirschsprung disease (HD) with a sensitivity of 100% is a

A

rectal biopsy

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194
Q

what type of rectal biopsy can be done on neonates and infants in the diagnosis of Hirschsprung disease (HD)

A

suction rectal biopsy

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195
Q

most common problems with suction rectal biopsy in the diagnosis of Hirschsprung disease (HD)

A

inadequate sample or sample taken too close to to the sphincter. must be done 2cm above anus

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196
Q

what type of rectal biopsy is done on an older child

A

full thickness rectal biopsy - must be sutured closed. requires general anesthesia. poses the highest risk but most accurate (bleeding, infection, scar)

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197
Q

initial treatment of Hirschsprung disease (HD)

A

IV fluid resuscitation

bowel decompression via NGT

rectal irrigations

abx if enterocolitis or sepsis is a concern

rectal irrigations (taught to caregivers)

surgical intervention

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198
Q

when might surgical intervention be held for correction of Hirschsprung disease (HD)

A

if child is able to tolerate a diet without abd distension, may wait for adequate weight gain and bowel decompression prior to intervening surgically

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199
Q

most common surgical technique for Hirschsprung disease (HD)

A

Transanal endorectal pull-through (TERPT) using the Swenson, Soave or Duhamel techniques

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200
Q

initial postop potential complications for TERPT

A 
anastomotic leak
bleeding
bowel obstruction
wound infection
abscess
stricture
perianal excoriation
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201
Q

When can an anastomotic leak occur

A

anytime a surgeon is anastomosing 2 segments of bowel together.

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202
Q

symptoms of an anastomotic leak

A

fever
irritability
abd distension

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203
Q

An abscess may occur after a TERPT due to

A

poor hemostasis causing a hematoma that becomes infected

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204
Q

stricture of the sphincter may occur after a TERPT because

A

when retracting the sphincter muscle during surgery.

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205
Q

delayed passage of stool postop to TERPT

A

think stricture of the sphincter

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206
Q

how is stricture of the sphincter postop to TERPT fixed

A

gently dilating the anus with a lubricated hegar dilator

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207
Q

when do you usually see perianal excoriation in the postop period following TERPT and what is done

A

once the pt starts stooling. over time the patients stooling pattern returns to normal

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208
Q

what needs to be monitored closely in the initial postop period following a TERPT

A 
NG output
vital signs
urine output
abd girth
pain control
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209
Q

common long term complications following a TERPT (pg 474)

A

anal stenosis or stricture
bowel incontinence (nerve damage or poor sphincter tone)
constipation (common after pull through procedure - must work with surgeon to establish effective bowel regimen)
enterocolitis - highest morbidity and mortality!!

rare
impotence
urinary dysfunction
retained aganglionic segment

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210
Q

what happens with enterocolitis following a TERPT

A

inflammation of the lining of the colon or small intestines. As it progresses, it erodes in the lining of the intestines -> becomes infected.

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211
Q

symptoms of enterocolitis following a TERPT

A

fever
abd distension
explosive diarrhea

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212
Q

intervention for enterocolitis post TERPT

A

bowel decompression with rectal irrigations

broad spectrum IV abx followed by oral Flagyl

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213
Q

factors found to decrease risk of enterocolitis after TERPT

A

daily rectal irrigations or rectal dilations starting at 2 weeks post surgery

probiotic prophylaxis

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214
Q

what collaborative resources are important to involve in a pt care that has Hirschsprung disease (HD)

A

dietician ->weight gain can be difficult for families

social worker -> help the family cope with the diagnosis and provide them with necessary resources

gastroenterology - to help with complex stooling issues

surgery - for repair

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215
Q

are Hirschsprung disease (HD) kids ever able to establish normal bowel function

A

yes, but maybe later than other kids their age.

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216
Q

what are patients often prescribed for stooling issues with Hirschsprung disease (HD)

A

PEG 3350 (Miralax) or loperamide

severe -
antegrade continence enema

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217
Q

is Hirschsprung disease (HD) cured with surgery?

A

no, they will require close monitoring of bowel function, nutritional status and overall health for their lifetime

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218
Q

prognosis for Hirschsprung disease (HD) with short segment

A

good outcome with very few interventions required

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219
Q

Prognosis for Hirschsprung disease (HD) with total colon HD

A

may require multiple procedures and in rare cases and intestinal transplant

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220
Q

what type of obstruction is an illeus

A

functional - occurs when the peristalsis of the GI tract is impaired.

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221
Q

There is a failure of normal flow of chyme through the intestinal lumen from intestinal immotility in the absence of an obstructing lesion. bowel becomes distended and fluid and air accumulate due to the bowels inability to reabsorb GI fluids and oral intake

A

Ileus

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222
Q

3 phases of a postop ileus and what is the cause

A

1) neurological
2) inflammatory
3) resolution of vasal activation

following surgery there is more sympathetic stimulation from pain and tissue trauma than parasympathetic stimulation which results in decreased GI motility

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223
Q

list the causes of functional bowel obstruction

A 
abd surgery
peritonitis
sepsis
trauma
medications (opioids, anxiolytics) 
metabolic imbalances (hypokalemia, hyponatremia, hypomagnesemia, acidosis)
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224
Q

causes of mechanical bowel obstruction

A

Postop adhesions

hematoma

intussusception

distal intestinal obstruction syndrome

Malrotation with volvulus

tumors

bezoar

Congenital abnormalities (duodenal atresia, duodenal web, annular pancreas, jejunoileal atresia)

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225
Q

symptoms of ileus

A

abd distension

absent or hypoactive bowel sounds due to lack of peristalsis

constant pain that worsens with increased bowel distension

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226
Q

with mechanical obstruction, bowel sounds may be

A

high pitched or hyperactive

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227
Q

what is typically a late sign of ileus and is preceded with abd distension and accumulation of GI fluids

A

vomiting

the higher the obstruction, the more frequent the emesis episodes may be

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228
Q

vomiting proximal to the sphincter of Oddi will more likely be

A

non-bilious

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229
Q

bilious emesis represents an obstruction occurring beyond the

A

sphincter of Oddi

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230
Q

the more distal the location of the operative intervention and the greater the bowel manipulation, the _______ it should be anticipated the patient will exhibit signs of _____

A

longer

POI

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231
Q

symptoms that may be present with resolution of POI are the passage of

A

flatus and stool

best indicator is tolerating a PO diet

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232
Q

whats diagnostic for ileus

A

first is abdominal radiograph - the bowel becomes distended and as air and fluid accumulate and air fluid levels become visible as would also be seen with a mechanical obstruction.

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233
Q

if there is significant gastric fluid loss with ileus, consider checking

A

electrolyte levels

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234
Q

Preop measures that can aid in minimizing POI

A

minimizing fasting prior to surgery (2 hours for liquids, 6 hours for food)

avoidance of preop medications including anxiolytics

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235
Q

what postop care practices may aid in the resolution of POI (post op ileus)

A

early ambulation
enteral feeding
chewing gum (promotes vagal stimulation)
pain control (minimizes sympathetic stim) - use of other classes of analgesics as opioids slows gastric motility

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236
Q

NSAIDS post op

A

treats pain and inflammation

but promotes GI bleeding (side effect)

237
Q

treatment for a symptomatic ileus

A

bowel rest
decompression with NGT to low intermittent suction or gravity

replacement of fluids lost in gastric content and electrolytes replacement (ie) 0.45 NS with 20mEq KCL/L

Parenteral nutrition should be individualized - recent guidelines are to start within the first week if enteral nutrition cannot be started or for severely malnourished patients or those at risk for nutritional deterioration

for most patients this resolves on its own with time.

238
Q

postop return of function for the small bowel

A

12-24 hours

239
Q

postop return of function for the stomach is

A

24-48 hours

240
Q

postop return of function for the colon is

A

3-5 days

241
Q

invagination of telescoping of the intestines involving the proximal portion of the bowel

A

intussusceptum

242
Q

invagination of telescoping of the intestines involving the distal portion of the bowel

A

intussuscipiens

243
Q

what leads to intussusception

A

The mesentery of the intussusceptum is compressed and the swelling of the bowel wall leads to the obstruction. Venous engorgement and ischemia of the intestinal mucosa causes bleeding followed by an outpouring of mucous which may result in “currant jelly” stool

244
Q

Currant jelly stool is an early or late sign of intussusception

A

very late

245
Q

one of the most common causes of bowel obstruction in children and occurs most commonly in the ileocecal region. 90% of cases reported in children less than 3 years old with the peak being 3-12 mos of age

A

intussusception

246
Q

what are the 3 categories of intussusception

A

1) idiopathic
2) lead point
3) postsurgical

247
Q

which category of intussusception is most commonly seen in infants and children

A

idiopathic

248
Q

which type of intussusception often corresponds with viral gastroenteritis or an URI

A

idiopathic

249
Q

what viral infections are associated with intussusception

A

adenovirus
rotavirus
HSV

250
Q

what is thought to link a viral infection to intussusception

A

the virus leads to hypertrophy of Peyer patches (lymph node in the intestines) which might act as a lead point causing the intussusception

251
Q

what vaccine has resulted in 35 patients getting intussusception

A

Rotarix (approved vaccine for Rotavirus)

252
Q

which type of intussusception has a identifiable cause in the intestinal mucosa

A

lead point intussusception

253
Q

what ages does lead point intussusception affect

A

5-14 years

254
Q

what are the most common causes of lead point intussusception

A

inverted Meckel diverticulum

polyps

duplication cyst

hemangiomas

255
Q

what is the least common type of intussusception

A

postsurgical - can be VERY serious in infants and children

256
Q

when should postsurgical intussusception be on your differential

A

this should be on your differential for any postsurgical patient showing signs of obstruction in the early postop period after abdominal and thoracic operations

257
Q

classic symptoms of intussusception

A

crampy abd pain
emesis
bloody stool
mass in the RLQ (only seen in 20-60%)

pain forces the child to retract their legs to their chest, lasts for a few min, followed by relaxation and a period of lethargy

progresses to appearing more ill
express bloody stool as the bowels blood flow becomes compromised

258
Q

diagnostics for intussusception

A

Abd radiograph - lack sensitivity - may see a RUQ soft tissue density with absence of colonic gas

nonsurgical reduction by contrast/air/saline enema is diagnostic and can reduce it nonsurgically.
—–100% accurate in diagnostic and 80-90% success rate for reduction (declines the longer the duration of symptoms). Fluoroscopy is used to assess that the medium fully refluxes into the small intestine

259
Q

if the intussusception is not reduced on the first attempt utilizing contrast/air/saline enema what should you do

A

a second or third attempt may be performed in 2-6 hours as long as the patient is stable. After the 3rd try it is unlikely to work and will need to be surgically reduced.

260
Q

Contrast/air/saline enema is less likely to work for reducing intussusception when

A

symptoms have been greater than 3 days, age older than 3 years, rectal bleeding, abdominal distention and a palpable abdominal mass is present

261
Q

when is surgical intervention required for an intussusception and is it time sensitive?

A

if the enema reductions fails (after 3rd attempt)

if the patient becomes unstable

perforation is noted

yes, by the time surgery is required, intestinal blood supply has become compromised and it is considered emergent

262
Q

care of nonoperative post reduction of intussusception

A

NPO for short time and clear liquids are introduced with diet progression as tolerated. send home

263
Q

if recurrence of intussusception post reduction occurs

A

you can attempt re-reduction

264
Q

care of pt after surgical reduction of intussusception

A

NPO for longer periods of time
slow advancement of an age appropriate diet
receive IV fluids
IV abx

monitor hydration status by HR and urine output which should be 1mL/kg/hr

pain management

265
Q

how do you calculate normal urine output

A

1mL/kg/hr

266
Q

recurrence of intussusception is more common with _______ reduction and most commonly occurs in the first _____ hours after the procedure up, with most recurrence occurring within ___ months of the initial diagnosis

A

nonsurgical
24 hours
6 months

267
Q

who do patients follow up with post intussusception reduction

A

nonsurgical - PCP 1 week later

surgical - pediatric surgeon

268
Q

Most morbidity and mortality related to intussusception is related to _____ secondary to _______ which can lead to _____ and _____

A

delayed diagnosis and treatment secondary to intestinal ischemia which can lead to IF(intestinal failure) and small bowel transplant

269
Q

can intussusception be prevented

A

no

270
Q

abnormal rotation and fixation of the bowel during embryologic development.

A

malrotation

271
Q

the classic form of malrotation is an

A

abnormal rotation of the duodenojejunal and decocolic loop and a high, medially positioned cecum

272
Q

when malrotation is present and the midgut twists in a clockwise direction around the SMA leading to occlusion of the SMA

A

Volvulus (if not addressed quickly, bowel necrosis rapidly ensues

273
Q

the incidence of malrotation is not known because the _____ of people with this disorder are _____

A

majority
asymptomatic

(may occur in as many as 1% of the population)

274
Q

incidence of malrotation is increased in children with what symptoms

A

heterotaxy

trisomies 13, 18, 21

Marfan

Prune-belly

275
Q

what are some of the most common anatomic abnormalities associated with malrotation

A

diaphragmatic hernia
duodenal web
abdominal wall defects such as gastroschisis, omphalocele

276
Q

when is malrotation diagnosed

A

60% before age 1

75% before age 5

however, malrotation and volvulus may both present in adulthood

277
Q

presentation of malrotation in pediatric patient

A

no symptoms
intermittent symptoms
acute presentation

vomiting
abd pain
FTT

278
Q

most common presentation of malrotation is that of

A

a neonate discharged home that later develops bilious emesis. (initially clear, then bilious when the bowel becomes obstructed) then bloody stool with bowel ischemia

279
Q

symptoms of a volvulus

A

bilious emesis
initially appear non-toxic
becomes ill appearing in the presence of ischemic bowel

develop a firm, distended abdomen
hypovolemia
shock
death

280
Q

diagnostics of malrotation/volvulus

A

abd films - may suggest a bowel obstruction with presence of air fluid levels

Abd US may show evidence of a malrotation

Upper GI series shows absence of a typical duodenal “C loop” with the duodenum instead of remaining on the R side of the abdomen. Abnormal placement of the cecum on follow through (or by contrast enema) confirms the diagnosis

standard for diagnosis is UGI study

US may reveal an abnormal SMA and superior mesenteric vein orientation

CT scan may indicate “swirl sign” - considered diagnostic

281
Q

double bubble sign on radiograph indicates

A

duodenal obstruction

282
Q

gasless abdomen may be appreciated in

A

volvulus

283
Q

How is malrotation and volvulus fixed

A

surgical intervention

considered controversial to surgically repair all malrotations if incidental finding (most surgeons will advocate for a Ladd procedure bc there is no way to tell if they will or will not develop a life threatening volvulus)

284
Q

surgical care of pt with volvulus repair

A

elective may be done outpatient
ng tube to decompress bowel function resumes

symptomatic usually require

fluid resuscitation

correction of electrolyte abnormalities

have blood products ready for surgery

pt who require second look surgery may require ICU, mechanical vent, vasopressors, coagulopathies, fluid/electrolyte imbalances
may need parenteral nutrition

285
Q

what other organ sometimes gets removed during a Lad procedure and why

A

appendix because its on the L side which may confuse future health care providers causing them to miss an appendicitis

286
Q

prognosis for volvulus after Ladd procedure

A

obstruction from adhesions

outcomes variable from complete recovery to intestinal failure to death

287
Q

Prognosis for pt with malrotation

A

excellent

resume normal daily activities

288
Q

the circumferential muscle of the pyloric sphincter becomes hypertrophied, resulting in elongation and obliteration of the pyloric channel. Abnormal innervations leads to failure of pyloric muscle relaxation. eventually there is a high grade gastric outlet obstruction, with compensatory dilation, hypertrophy and hyperperistalsis of the stomach

A

pyloric stenosis

289
Q

what gender is pyloric stenosis more prevalent in

A

first born males

some evidence of genetic association

290
Q

maternal risk factors for pyloric stenosis are

A 
hyperthyroidism
quinolone antibiotic use
smoking
increased BMI
intranasal decongestant use
291
Q

what is the hallmark symptoms of pyloric stenosis

A

nonbilious, projectile and progressive emesis 30-60 min after feeding starting between 2-6 weeks of age and can occur as late as 3 months of age

infant may express persistent hunger with weight loss and dehydration

olive sign - hypertrophied pylorus in the midepigastrium may be appreciated

292
Q

how does pyloric stenosis progress

A

early in the course vomiting is intermittent

As gastric outlet obstruction develops, vomiting becomes more continuous

infant may express persistent hunger with weight loss and dehydration

293
Q

olive sign think…

A

pyloric stenosis

294
Q

spasmodic contraction of the pylorus with poorly coordinated gastric emptying

observed in what population

what is done

A

pylorospasm

neonates

resolves spontaneously with time

295
Q

Gastroesophageal reflux (GER) is on the differential with pyloric stenosis. what same and different symptom might you see

A

may also have weight loss

projectile vomiting is uncommon

296
Q

what does HPS stand for

A

hypertrophic pyloric stenosis

297
Q

what electrolyte imbalances might be seen in HPS (hypertrophic pyloric stenosis)

what about pH

what else might be elevated

A

hypochloremic
hypokalemic
metabolic alkalosis

unconjugated hyperbilirubinemia r/t transient impairment of glucuronyl transferase activity

298
Q

how is pyloric US confirmed

A

abdominal US

299
Q

what is a string sign

A

elongated and thickened pyloric channel seen in pyloric stenosis

300
Q

what is a beak sign

A

filling of the proximal pylorus seen in pyloric stenosis

301
Q

what is a double shoulder sign

A

thickened pylorus compressing the antrum of the stomach (seen in pyloric stenosis)

302
Q

how is pyloric stenosis fixed?

A

surgical repair
non emergent
prior to anesthesia, infants should be hemodynamically stable with appropriate VS, normal electrolytes and urine output of at least 1mL/kg/hr
appropriate bicarb levels

303
Q

bicarb levels should be less than _____mEq/L for infants prior to surgery. Why?

A

30

because infants with metabolic alkalosis are at high risk for resp depression when recovering from anesthesia

304
Q

what is the pyloric regimen

A

ad lib feeds started 4 hours post op after pyloric repair or pyloric regimen is used….

initial feed is 15mL of Pedialyte

1 hr later is 30 mL of Pedialyte

2 hrs later is 1/2 strength formula 30 mL or breastfeed for 2 min

2 hr later is full strength formula 30 mL or breastfeed for 2 min

3 hr later full strength formula 45mL or breastfeed for 5 min

3 hr later full strength formula 60 mL or breastfeed for 7 min

3 hr later Ad lib feeds

305
Q

when is the pyloric regimen more commonly prescribed

A

in infants with persistent emesis in the postop period

306
Q

postop vomiting is due to

A

gastric distension and atony

307
Q

majority of infants tolerate ad lib feeds post op. What is this?

A

volume of at least 60mL within 24-48 hrs of the operation

308
Q

persistent vomiting beyond 72-96 hours postoperative pyloric stenosis repair may occur in cases of

A

incomplete pyloromyotomy

UGI series may be valuable to determine

309
Q

pain control for postoperative pyloric stenosis

A

tylenol (usually sufficient bc area is infiltrated with local anesthetic)

310
Q

monitor for what complications after repair of pyloric stenosis

A

surgical wound infection
incisional hernias

life threatening complications include
gastric mucosal tears
duodenal perforation

311
Q

what should be closely monitored in infants post op after pyloric stenosis repair

A

tachycardia because it is an early sign of peritonitis secondary to perforation

elevated core temp is another sign that a mucosal tear may exist

312
Q

what qualifies infant for discharge after a pyloric stenosis repair

A

when they are tolerating 60mL for at least 2 consecutive feedings without emesis

313
Q

education to give caregiver for discharge after pyloric stenosis repair

A

caregiver should return for fever greater than 101.5 rectal, persistent emesis, abd pain or any signs or symptoms of wound infection

314
Q

when does the pt need to follow up after a pyloric stenosis repair

A

follow up with PCP in 1 week for wound evaluation and weight check and surgeon in 2 weeks

315
Q

partial or complete obstruction resulting from an anatomic cause, intraluminal or extraluminal.

A

mechanical

316
Q

intraluminal or extraluminal cause of mechanical obstruction.

swallowed coin

A

intraluminal

317
Q

intraluminal or extraluminal cause of mechanical obstruction.

hernia

A

extraluminal

318
Q

intraluminal or extraluminal cause of mechanical obstruction.

intussusception

A

intraluminal

319
Q

intraluminal or extraluminal cause of mechanical obstruction.

adhesion

A

extraluminal

320
Q

what is the physiologic response to an partial obstruction

A

enhances secretion and motility proximal to the level of obstruction in an attempt to push the offending obstruction open and overcome the blockage

321
Q

due to the physiologic response to a partial obstruction at the level of an ostomy or distal bowel can present with both

A

diarrhea like increased output and proximal distention, nausea and vomiting

322
Q

consists of chewing food, allowing it to mix with oral secretions and liquid ingestions

A

mixing

323
Q

the act of initiating a swallowing reflex whereby the food bolus will be handed from somatic control (chewing) over to autonomic control (the enteric nervous system responsible for the remainder of the GI tract)

A

Propulsion

324
Q

first part of the small intestine is commonly known as the

A

duodenum

325
Q

the remaining small intestine and the first portion of the colon is known as the

A

midgut

326
Q

all structures that receive blood from the inferior mesenteric artery or pelvic arteries which includes the remaining transverse colon, descending and sigmoid colon, intra-abdominal rectum, extraperitoneal rectum and anus

A

hindgut

327
Q

what organs and glands play a important role in GI physiology

A

liver
gallbladder
biliary tree
pancreas

328
Q

what sphincter prevents reflux

A

upper esophageal sphincter

329
Q

what kind of vomiting should never be accepted as a normal type of vomiting

A

bilious

330
Q

Diagnostic abdominal labs

A

CBC with diff
UA
UPT

331
Q

diagnostic abdominal labs

in setting of dehydration secondary to vomiting or diarrhea or suspicion of kidney disease

A

electrolytes
BUN
creatinine

332
Q

labs for liver

A

LFTs

333
Q

labs for pancreas

A

amylase

lipase

334
Q

fecal studies in diarrhea

A

stool osmolarity
fecal leukocytes
fecal occult blood
ova and parasites (O&P)

335
Q

diarrhea should be ____ to serum. if its not, what might have happened

A

isotonic

improper collecting - scooping poop from toilet water

faking diarrhea…pouring water into poop to make it look like diarrhea

336
Q

fecal leukocytes are elevated in

A

acute colitis (particularly bacterial origin)

337
Q

gross blood in stool is almost always indicative of

A

colitis

338
Q

fecal occult blood tends to indicate

A

colitis or a bacterial toxin affecting small bowel

339
Q

O& P is extremely helpful in what scenario

A

potential ingestion of contaminated water (very high specificity)

340
Q

stool culture can evaluate for

A

shigella
C diff
Norovirus
Rotavirus

341
Q

plain abd film positions

A

supine (most common)

upright in front of the radiographic plate

left lateral decubitus (left side down)

cross table views

342
Q

stool has a characteristic appearance on an x ray from

A

the gas bubbles inside the stool

343
Q

what x ray and what views/technique is best for looking for a bowel perforation

A

upright chest x ray after 2 min of standing has the maximum sensitivity for free gas suggesting perforation

left lateral decubitus has better sensitivity than other radiographic views bc it causes free gas to rise around the liver, enhancing the ease of distinguishing it from surrounding bowel gas

344
Q

which view is inferior for detecting bowel perforation but can sometimes show free gas along the anterior abdominal wall

A

cross table lateral view

345
Q

which x ray view is the least sensitive for bowel perforation

A

standard supine view (can show the falciform ligament or bowel outline, suggesting free gas

346
Q

bacterial causes of gastroenteritis

A

E. Coli, staph, Campylobacter, salmonella, shigella, yersinia, C. Diff

347
Q

common viral causes of gastroenteritis

A

rotavirus, adenovirus, coronavirus, parvovirus

348
Q

what causes of gastroenteritis need abx

A

c.diff
shigella
salmonella
h. pylori

349
Q

which causes of gastroenteritis is most likely to cause sepsis in < 3mos

A

shigella

salmonella

350
Q

main cause of dysentery

A

shigella

351
Q

gastroenteritis acquired by

A

via fecal-oral route, transmitted person-to-person, through contaminated food or water

352
Q

s/s of gastroenteritis

A

fever, vomiting, diarrhea (watery, > 3x/day), recent antibiotic use (C. Diff), travel (especially internationally), dehydration (varying severity)

353
Q

treatment of gastroenteritis

A

stool studies if refractory to treatment, oral rehydration therapy preferably with oral rehydration solutions (pedialyte) - instruct parents to provide an extra 2-4oz of rehydration for each episode of vomiting/diarrhea in the infant, probiotics

354
Q

s/s neoplasm

A

weight loss, anorexia, fever, night sweats, easy bruising/bleeding.

355
Q

bilious emesis, alcoholic stools, liver disease - jaundice, pale skin, cachexia, FTT, abdominal wall hernias - observe with vagal/bearing down

A

Bowel obstruction

356
Q

what lab includes creatinine and BUN

A

chemistry

357
Q

Benign masses think

A

assess for bowel obstruction, appendicitis, perforation, sepsis, ectopic pregnancy, torsion

358
Q

what do you do for malignant tumors

A

admission, oncologic and surgical evaluation

359
Q

what symptoms for milk protein allergy

A

blood in stool
diarrhea
can cause enterocolitis

360
Q

IBD is most common in

A

Most common in >10 yo children

361
Q

which IBD affects only the colon

A

UC

362
Q

which IBD involves any part of the gut

A

CD

363
Q

IBD is most common in what populations

A

jewish

364
Q

IBD is linked to what antigen

A

human leukocyte antigen (HLA) subtypes

365
Q

smoking _____ severity of CD and ______ risk for UC

A

Smoking INCREASES severity of CD and DECREASES the risk for UC

366
Q

Diarrhea
Blood and mucous in the stool
Urgency
Tenesmus-sensation of incomplete emptying after defecation

Severe: wakens at night to pass stool

Toxic megacolon is LIFE-THREATENING 
Fever
Abdominal distension and pain
Massively dilated colon 
Anemia
Low serum albumin (fecal protein loss)
Extraintestinal manifestations:
Sclerosing cholnitis
Arthritis 
Uveitis
Pyoderma gangrenosum
erythema nodosum (EN) -erythematous lesions
A

Colitis

367
Q

symptoms of Toxic megacolon

A 
Fever
Abdominal distension and pain
Massively dilated colon 
Anemia
Low serum albumin (fecal protein loss)
368
Q

Subtle symptoms

Loss of appetite 
Crampy postprandial pain
Poor growth
Delayed puberty 
Fever
Anemia
Lethargy
A

Crohns

369
Q

skip lesions associated with

A

crohns

370
Q

labs for IBD

A 
CBC with diff
ESR - is elevated in 80% of CD and 40% of UC
CRP - inflammation
Albumin
AST, ALT, GGT for hepatic involvement

stool studies

371
Q

to get a true diagnosis for IBD

A

endoscopy, biopsy and histology to differentiate CD from UC

372
Q

fistulas are more associated with what IBD

A

Crohns

373
Q

Crohns or UC?

malaise
fever
weight loss

A

common in Crohns

sometimes UC

374
Q

Crohns or UC?

rectal bleeding

A

usual in UC

sometimes CD

375
Q

Crohns or UC?

abd mass

A

common in CD

rare in UC

376
Q

Crohns or UC?

abd pain

A

both

377
Q

Crohns or UC?

perianal disease

A

Common in CD

rare in UC

378
Q

ileal involvement

Crohns or UC?

A

CD

379
Q

Crohns or UC?

strictures

A

common in CD

rare in UC

380
Q

Crohns or UC?

fistula

A

common in CD

381
Q

Crohns or UC?

skip lesions

A

CD

382
Q

Crohns or UC?

transmural involvement

A

CD

383
Q

Crohns or UC?

crypt abscesses

A

UC

384
Q

Crohns or UC?

intestinal granulomas

A

CD

385
Q

Crohns or UC?

risk of cancer

A

increased in CD

greatly increased in UC

386
Q

Crohns or UC?

erythema nodosum

A

Common in CD

387
Q

Crohns or UC?

mouth ulceration

A

CD

388
Q

Crohns or UC?

osteopenia at onset

A

CD

389
Q

Crohns or UC?

autoimmune hepatitis

A

UC

390
Q

Crohns or UC?

sclerosing cholangitis

A

UC

391
Q

Injury to the mucosa of the small intestines caused by ingestion of gluten (protein component) from wheat, rye, barley, and related grains.
Severe: causes malabsorption and malnutrition.

A

Celiac disease

392
Q

celiac disease

commonly seen in

A

Seen in type 1 diabetics, thyroiditis, turners syndrome, and trisomy 21.

393
Q

PUD treatment

A

H. pylori present- multidrug regimen (twice daily for 1-2 weeks)
omeprazole -clarithromycin-metronidazole
omeprazole -amoxicillin- clarithromycin
omeprazole - amoxicillin-metronidazole

Bismuth effective against h. Pylori and can be considered

Tetracycline AVOID IN CHILDREN <8 YEARS OLD

Non h.pylori- PPI (can also try H2 receptor antagonist)

Typically heal in 4-8 weeks in 80% of patients

esophagitis - requires 4-5 months of PPI treatment for optimal healing

394
Q 
Diarrhea
Pubertal delay
Failure to thrive 
Abdominal bloating 
Irritability
Decreased appetite
Ascites (from hypoproteinemia)
A

Celiac

395
Q

celiac disease monitoring

A

Careful monitoring of child’s growth curve and evaluation for reduced sub Q fat and abdominal distension are crucial.

396
Q

celiac should be considered in any child with

A

Chronic abdominal complaints
Short stature
Poor weight gain
Delayed puberty

397
Q

extraintestinal manifestations for celiac disease include

A 
Osteopenia
Arthritis
Arthralgias 
Ataxia
Dental enamel defects
Elevated liver enzymes
Dermatitis Herpetiformis
Erythema nodosum
398
Q

lab and imaging for celiac

A

IgA antiendomysial antibody and IgA tissue transglutaminase antibody
Total serum IgA (for accuracy of tests).
Endoscopic small bowel biopsy-essential to confirm diagnosis (should be done when still ingesting gluten).
Villous atrophy (short or absent vili)
Mucosal inflammation
Crypt hyperplasia
Increased number of intraepithelial lymphocytes
Repeat biopsies to confirm response to treatment (several months later).
Rule out labs to also order when celiac suspicion:
CBC, calcium, phosphate, vitamin D, iron, total protein and albumin, liver function tests.

399
Q

treatment of celiac

A

Complete elimination of gluten from diet
Consult dietician/ support groups helpful
Most patients respond clinically within a few weeks
Weight gain
Improved appetite
Improved overall sense of well-being
Histological improvement takes several months to normalize

400
Q

risk factors for H. Pylori

A

Low socioeconomic status
Poor sanitation
Highest in developing countries

401
Q

drugs increase risk for PUD

A

NSAIDS (ASA)
Tobacco use
Bisphosphonates
Potassium supplements

402
Q

risk factors for PUD

A 
drugs
family history
sepsis
head trauma
brain injury
hypotension
403
Q

clinical manifestations of PUD

A

Recurrent burning epigastric and retrosternal pain → esophagitis
Duodenal ulcers-pain several hours after eating, awakens pt at night
Eating relieves pain
Gastric ulcers- aggravated by eating resulting in weight loss
GI bleeding can occur in either
Reported relief with antacids or acid blockers

404
Q

alarm symptoms of PUD

A 
Weight loss 
Hematemesis 
Melena , heme positive stools 
Chronic vomiting 
Microcytic anemia 
Nocturnal pain
405
Q

Laboratory and imaging studies:

PUD

A

Endoscopy - can also test for h pylori during procedure (urease test or presence histologically on tissue)

Noninvasive: h. Pylori fecal antigen and 13C urea breath test

406
Q

currant jelly stools

A

intussusception

407
Q

most common reason for abd surgery in children in US

A

appendicitis

408
Q

Appendicitis can occur at any age but most common

A

10-12 yrs and males as opposed to females

409
Q

fever (more common with perforation), decreased activity level, periumbilical pain with progression to RLQ pain, accompanied by anorexia, and eventually diarrhea

A

appendicitis

410
Q

McBurney Point and rebound tenderness r/t

A

peritonitis associated with perforation of appendix

411
Q

where is McBurney Point

A

R side of abdomen 1/3 of distance from anterior superior iliac spine to the umbilicus

412
Q

what is psoas sign

A

appendicitis
Concomitant irritation of the psoas muscle and associated pain will be present with passive extension of flexion of the RLE

413
Q

Obturator sign

A

appendicitis

If appendix lies on the obturator internus muscle, pain may be present with internal rotation of the right thigh

414
Q

Rovsing sign

A

appendicitis

Pain reported in the RLQ with palpation of the LLQ

415
Q

diagnostic labs for appendicitis

A

WBC
ANC
CRP

CBC - leukocytosis with WBC >10,000-15,000 and bandemia

CMP - evaluate for dehydration, liver abnormalities

urinalysis - r/o UTI

upt

416
Q

Radiologic diagnostic for appendicitis

A

US

417
Q

what is an US for appendicitis limited by

A

appendix position
bowel gas pattern
obesity (not recommended if BMI >25 in adults)
operator experience

418
Q

what is the most sensitive test for appendicitis

A

CT

419
Q

Acute appendicitis (non-perforated) treat

A

Administer antibiotics

Antibiotic coverage targeted toward bacterial flora in the appendix (E. coli, streptococcus group milleri, anaerobes, and pseudomonas aeruginosa)

appendectomy (within 6-24 hours while receiving IV abx and fluids

420
Q

treatment of perforated appenicitis

A

Nonoperative management

Antibiotic therapy is generally prescribed for 5-7 days depending on patient response.

Ceftriaxone and Flagyl for perforated appendix have proven to be adequate

Interventional radiology abscess drainage, if feasible

Consider placement of a percutaneous inserted venous catheter (PICC) at the time of abscess drainage

Prolonged ileus may require parenteral nutrition

Interval appendectomy approx 6-8 weeks later

Operative management

child does not improve with nonoperative management (remains febrile, persistent pain), operative management indicated

421
Q

esophagus and trachea form within close proximity, can occur with VACTERL syndrome. communicating fistula from esophagus to trachea

A

Tracheoesophageal fistula

422
Q

en utero
polyhydramnios (excessive amniotic fluid), small/absent gastric bubble on US,

newborn signs
excessive salivation, choking, difficulty swallowing, cyanotic/resp distress with feedings

A

Tracheoesophageal fistula:

423
Q

diagnostic for transesophageal fistula

A

placement of OG tube + xray (will see it coil in the esophagus or stop), gas-less stomach on KUB, tracheobronchoscopy

424
Q

treatment for

transesophageal fistula

A

minimize pulmonary aspiration, NPO, IV fluids, broad-spectrum antibiotics, surgical repair and closure of the fistula (can require “spit fistula” if esophagus is unable to be attached to the stomach and gastrostomy tube)

425
Q

complications in

transesophageal fistula

A

esophageal stricture, esophageal dysmotility, GERD, tracheomalacia, vocal cord dysfunction

426
Q

congenitally interrupted esophagus

A

Esophageal atresia

427
Q

gassless abdomen on CXR can also suggest an

A

Esophageal atresia with proximal TEF

428
Q

chronic reflux can develop into

A

Barrett esophagus

429
Q

diarrhea < = 14 days with > 3 stools per day is what type

A

acute diarrhea

430
Q

diarrhea > 14 days with > 3 stools per day is what

A

persistent diarrhea

431
Q

diarrhea > 30 days > 3 stools per day

A

chronic diarrhea

432
Q

Gastroenteritis lab to look at electrolytes

A

BMP

433
Q

what labs for gastroenteritis

A

BMP
CBC with diff
stool cultures
O &P

434
Q

first line therapy for travelers diarrhea in children is

A

Azithromycin

435
Q

Antidiarrheal medications often contain what?

contributes to?

A

ASA

Reye syndrome

436
Q

how to calculate hourly rates of maintenance fluids

A

4:2:1 rule used to calculate HOURLY rate of fluids

0-10kg—>4mL/kg/hr (first 10kg)

10-20kg—> 2mL/kg/hr (second 10kg)

> 20kg—>1 mL/kg/hr (any weight in excess of 20kg)

Simple rule if >20 kg is 40 mL/hr + patients weight in kg = hourly infusion rate

437
Q

how to calculate daily maintenance fluids

A

100: 50: 20 rule used to calculate DAILY maintenance fluids

0-10 kg—>100 mL/kg/day (first 10kg)

10-20 kg—> 50 mL/kg/day (second 10kg)

> 20 kg—> 20 mL/kg/day(any weight in excess of 20kg)

438
Q

Caloric calculation for enteral feeds

A

Breast milk—> 20kcals/oz
Formulas—>20kcals/oz (can fortify)
1oz = 30mL
Average baby needs—> 100kcal/kg/day (variable)

439
Q

In FTT there are specific growth charts for what genetic conditions

A

There are specific growth charts for genetic conditions such as Down syndrome and Turner syndrome that should be used accordingly.

440
Q

wasting

A

Malnutrition initially results in wasting (deficiency in weight gain)

441
Q

stunting

A

(deficiency in linear growth) that occurs after months of malnutrition, and head circumference is spared except with chronic, severe malnutrition.

442
Q

Short stature with preserved weight =

A

endocrine etiology

443
Q

The distinct difference between FTT and malnutrition is that FTT does not

A

provide an assessment of the severity, duration, or mechanism for poor growth that characterizes the child’s nutritional status.

444
Q

environmental causes of FTT

A 
Emotional deprivation
Rumination
Child maltreatment
Maternal depression
Poverty
Poor feeding techniques
Improper formula preparation
Improper mealtime environment
Unusual parental nutritional beliefs
445
Q

GI causes of FTT

A

Cystic fibrosis and other causes of pancreatic insufficiency
Celiac disease
Other malabsorption syndromes
Gastrointestinal reflux

446
Q

congenital /anatomic

A

Chromosomal abnormalities, genetic syndromes
Congenital heart disease
Gastrointestinal abnormalities (e.g., pyloric stenosis, malrotation)
Vascular rings
Upper airway obstruction
Dental caries
Congenital immunodeficiency syndromes

447
Q

infectious causes of FTT

A

HIV
Tuberculosis
Hepatitis
UTI, chronic sinusitis, parasitic infection

448
Q

metabolic causes of FTT

A

THyroid disease
Adrenal or pituitary disease
Aminoaciduria, organic aciduria
Galactosemia

449
Q

Neurologic causes of FTT

A 
Cerebral palsy
Hypothalamic and other CNS tumors
Hypotonia syndromes
Neuromuscular diseases
Degenerative and storage diseases
450
Q

renal causes of FTT

A

Chronic renal failure
Renal tubular acidosis
UTI

451
Q

hematologic causes FTT

A

Sickle cell disease

Iron deficiency anemia

452
Q

initial tests to evaluate FTT

A

CBC, iron deficiency anemia, lead toxicity, UA, urine culture, serum electrolytes to assess renal.

453
Q

FTT kids have more occurances of

A

more otitis media, respiratory and GI infections.

stool sample for culture and ova and parasites for the child with diarrhea, abdominal pain, malodorous stools

454
Q

malnutrition-infection cycle:

A

Recurrent infections exacerbate malnutrition, leading to greater susceptibility to infection.

455
Q

Re-feeding syndrome

A

changes in serum electrolyte concentrations and the associated complications. Changes typically affect phosphorus, potassium, calcium, pulmonary, or neurological problems.
Patients with marasmus, kwashiorkor, and anorexia nervosa, and those who experience prolonged fasting are at risk for re-feeding syndrome.
Can be avoided by slow institution of nutrition, close monitoring of serum electrolytes during the initial days of feeding, and prompt replacement of depleted electrolytes.

456
Q

children who live in psychological deprivation develop short stature with or without concomitant FTT or delayed puberty, a syndrome called

A

Psychosocial Short Stature

457
Q

Signs and symptoms:

Psychosocial Short Stature

A

polyphagia , polydipsia
Hoarding and stealing of food
Gorging and vomiting
Children usually depressed and socially withdrawn
Affected children usually have endocrine dysfunction with decreased growth hormone secretion and a mutated response to exogenous growth hormone
Rapid improvement if child removed from adverse environment
Prognosis depends on age at diagnosis and degree of psychological trauma

458
Q

% of the LBM of infants and malnourished patients is water.

A

70

459
Q

s/s of dehydration

A

Poor skin turgor indicates loss of interstitial fluid
Tachycardia and delayed cap refill indicates body’s compensation for maintaining perfusion.
Mottled skin
Sunken fontanel
Sunken eyes
Increased RR/HR

460
Q

labs to order in dehydration

A

BUN (can increase with dehydration)

bicarb levels

blood pH

Na

anion gap (elevated in metabolic acidosis)

461
Q

what lab indicates type of hydration

A

Na

462
Q

dehydration type

most common in

Na 135-145

A

isonatremic

most common d/t gastroenteritis

463
Q

dehydration type

most common in

Na >145

A

hypernatremic

d/t balance shifts and lead loss of brain hydration leads to shear force injuries such as subdural or hemorrhage

464
Q

dehydration type

most common in

Na <135

present in

A

hyponatremic

fluid loss d/t diarrhea/sweat

present with seizures, noncardiogenic edema, resp distress or cerebral herniation

465
Q

oral rehydration pt gets

A

15mL/kg/hour or 60mL/kg/4hrs

466
Q

sip volume per 5 min in oral dehydration

A

< 10kg 1mL/kg
10kg 10mL
For every additional 5kg, add: 5mL to a maximum of 50mL

467
Q

IV rehydration

A

20mL/kg fluid bolus repeated until restoration of fluid volume, normal perfusion, LOC improves, and decreased capillary refill time

60mL/kg in the first hour

Use LR or NaCl 0.9%

If history is suggestive of hyperchloremic dehydration LR is preferred

Maintenance fluid either D5 NS or D5 LR

468
Q

tachycardia is present in what types of dehydration

A

moderate and severe

469
Q

orthostatic hypotension is present in what type of dehydration

A

moderate

470
Q

hypotension is present in what type of dehydration

A

severe

471
Q

fontanelle is sunken in what type of dehydration

A

severe

472
Q

respirations are deep in what type of dehydration

A

moderate

473
Q

respirations are deep and rapid in what type of dehydration

A

severe

474
Q

oliguria is in what type of dehydration

A

moderate

475
Q

anuria and severe oliguria is seen in what type of dehydration

A

severe

476
Q

what test greatest benefit is ability to distinguish blood vessels from ducts.

A

US dobbler B mode

477
Q

standard of care to diagnose pyloric stenosis and intussusception or an obstructed, pus filled appendix.

A

US

478
Q

test Extremely useful in evaluating the liver, biliary tree, and often head of pancreas.

A

US

479
Q

reserved for either treatment or diagnostic uncertainty when the US cannot definitively diagnose pyloric stenosis or intussusception.

A

GI fluoroscopy

480
Q

safest contrast agent

Safest with lowest sensitivity and specificity
Can be used to reduce intussusceptions.

A

air

481
Q

contrast agent
Good sensitivity and specificity
Easily evacuate or excrete iodinated agents.

A

iodine based

482
Q

contrast agent

Viscous and sticky
Optimal sensitivity and specificity
Disadvantage in setting of perforation, will coat any body cavity and be impossible to completely remove

A

Barium

483
Q

Esophagram or gastrogram

Investigate anatomy for perforation and obstruction

A 
Upper GI (imaging includes from swallowing to sm bowel)
fluoroscopy
484
Q

Barium enema is the most useful study of the colon and rectum.
Frequently therapeutic and evacutes inspissated or thickened stool and can reduce and ileocecal intussusception.

A

lower GI fluoroscopy

485
Q

CT with contrast helps identify

A

Blood vessels from other fluid filled tubes

In areas of inflammation the enhanced blood flow means higher IV contrast and can help identify regional inflammation

Clearance of iodinated contrast via kidneys allows delayed images in which urine-filled structures can be distinguished from surrounding fluid-filled tubes and pockets

486
Q

reasons to use MRI

A

Radiation free imaging technique

Helpful in evaluation of solid organs (liver, kidney, and adrenal)

Noninvasive technique for imaging the biliary tree particularly in gallstone disease

Pelvic MRI helpful in evaluating complex gynecologic disease

487
Q

pancratitis s/s

A 
Fever
o   Ab pain
o   Nausea
o   Vomiting
o   Anorexia
o   Uncommon
o   Back pain
o   Altered loc
o   Kidney failure
o   Hypotension
o   Ascites
o   Pleural effusions
o   Fluid retention
488
Q

pancreatitis diagnostics

A 
Elevated amylase & lipase
o   CRP
o   Hypocalcemia
o   Transient hypoglycemia
o   Hyperbilirubinemia
o   Increased LFTs
o   Hypoalbuminemia
o   US
o   CT
489
Q

treatment pancreatitis

A 
Mostly supportive
o   IVF à generous
o   Pain manage
o   Manage metabolic complications
o   Pancreatic rest
o   NJ feedings
o   Remove pancreas – severe chronic cases
490
Q

liver and renal labs

A

CBC
Reticulocyte count
Blood smear examination
Albumin, total protein
Prothrombin time (PT)/ Partial thrombin time (PTT)
Alanine aminotransferase (ALT)/ Aspartate aminotransferase (AST)
Alkaline phosphatase
Gamma-glutamyl transpeptidase (GGT)
Electrolytes
Blood urea nitrogen (BUN)
Viral serologies: HsAg, anti HbsAg, anti HB Core, hepatitis C, anti HAV, HIV, EBV (Epstein-Barr virus), CMV (cytomegalovirus), hepatitis D (if possible HBsAg)
Ceruloplasmin level
Iron, total iron binding capacity, ferritin
Antinuclear antibody (ANA), antimicrosomal antibody (AMA), anti LKM1 (Anti-liver, kidney, microsomal 1 antibody), SMA ( smooth muscle antibody)
Toxicology screen (acetaminophen level)

491
Q

Hypocalcemia (<9mg/dL) associated with

A

DiGeorge syndrome

492
Q

s/s hypocalcemia

A

Can include neuromuscular irritability, Chvostek sign, confusion, irritability, laryngospasm, muscle cramps, numbness and tingling, paresthesia and weakness, seizures, tetany and Trousseau sign
ECG changes include sinus tachycardia, long QT interval and AV block
Evidence of myocardial irritability with severe hypocalcemia
can include hypotension and bradycardia

493
Q

treatment of sympomatic hypocalcemia, acute

A

Parental calcium replacement:

Calcium chloride (10-20 mg/kg/dose) given through central venous catheter only

Calcium gluconate (100 mg/kg/dose) given through either PIV or central venous catheter

494
Q

chronic hypocalcemia, subacute or chronic repletion

A

Enteral supplements such as calcium carbonate, citrate, calcium gluconate, glubionate, lactate, along with vitamin D supplements and 1, 25-dihydroxy vitamin D for patients unable to convert vitamin D

495
Q

Hypercalcemia (serum calcium >10 mg/dL)

associated with

A

williams syndrome

496
Q

severe hypercalcemia s/s

A

less severe can be asymtpomatic

GI signs of nausea, anorexia, constipation, neurologic signs such as anxiety, depression, HA, lethargy, hypotonia, seizures, and coma. Cardiac arrhythmias include shortened QT interval, sinus bradycardia, first-degree heart block, and ventricular tachycardia

497
Q

Hypercalcemia can result in

A

polyuria, renal calculi, and renal tubular dysfunction

498
Q

treatment of hypercalcemia

A

Identification and treatment of underlying disease

Hydration with NS (often 2-3 times maintenance rate)

Hypercalcemia may cause increased urinary output, resulting in dehydration Increased urinary sodium excretion enhances calcium excretion

Diuresis with loop diuretics, which aids in calcium excretion

o Avoid thiazide diuretics that reduce calcium excretion

Glucocorticoids-reduce effects and level of vitamin D

Only calcitonin for rapid correction of calcium or if hypercalcemia is refractory to hydration and diuresis

Bisphosphonates have become the mainstay of rapid treatment of severe hypercalcemia

If severe or refractory, hemodialysis may be indicated

499
Q

chloride has a direct relationship with

A

sodium - if sodium is elevated, chloride is elevated

500
Q

chloride has an inverse relationship with

A

bicarb

501
Q

Hypochloremia is serum chloride of

A

<97 mmol/L

502
Q

Hypochloremia is associated with

A

Bartter syndrome, CF, Bulimia nervosa, diuretic usage, removal of gastric secretions via NGT, and metabolic alkalosis

503
Q

hypochloremia associated with metabolic alkalosis may (Rare) exhibit

A

arrhythmias, decreased respiratory effort, seizures in severe states

504
Q

s/s hypochloremia

A

When associated with volume depletion or dehydration, may exhibit thirst, lethargy, tachycardia, tachypnea, and delayed cap refill

505
Q

treatment hypochloremia

A

First address known causes, including fluid resuscitation, and add potassium-sparing diuretics or acetazolamide to reduce reabsorption of bicarbonate
Chloride repletion: can be replaced with sodium, potassium, and ammonium chloride compositions. Arginine chloride or hydrochloric acid can be used for severe Hypochloremia- related seizures, arrhythmias, or respiratory depression

506
Q

lab for hyperchloremia

A

> 108

507
Q

presentation of hyperchloremia

A

often asymptomatic

may have Kussmaul respirations (especially in DKA); possible neurologic symptoms include lethargy, HA, and confusion

508
Q

treatment of hyperchloremia

A

Address underlying cause and treat associated acidosis

Consider sodium bicarbonate IV if severe metabolic acidosis

509
Q

hypomag lab value

A

<1.7

510
Q

presentation of hypomag

A

GI: anorexia, N/V
Neuro: depression, malaise, nonspecific psychiatric symptoms, hyperreflexia, seizures, paresthesias, ataxia, tetany, decreased DTRs, weakness, paralysis, muscle weakness, delirium, carpopedal spasm, and clonus
Cardiac: ECG changes, atrial or ventricular ectopy, torsades de pointes, and long QT interval
Endocrine: Hyperglycemia can occur if hypomagnesemia is related to insulin resistance

511
Q

treat hypomag

A

Severe, acute management:
Magnesium sulfate or magnesium chloride (if torsades de pointe rhythm noted)
Consider potassium repletion, particularly if refractory
Mild, subacute management:
o Magnesium gluconate, oxide, or sulfate

512
Q

hypermag lab values

A

> 2.2

513
Q

presentation of hypermag

A

Neuro: Impairment of the neuromuscular junction; hypotonia, decreased DTRs, weakness, paralysis, CNS depression, lethargy, and confusion
Cardiac: Altered vascular tone, hypotension, flushing, possible ECG changes (prolonged PR, QRS, or QT intervals), heart block
GI: Abdominal cramping, N/V
Respiratory failure can occur in severe cases

514
Q

treat hypermag

A

Cessation of magnesium intake
Monitoring of renal function and support of cardiovascular and respiratory function
Parental calcium supplements (calcium chloride or calcium gluconate) for heart block
Removal of magnesium with volume expansion, forced diuresis, loop diuretics, dialysis if life-threatening or exchange transfusion if life-threatening and unable to perform dialysis

515
Q

hypophosphatemia lab

A

<2.5

516
Q

presentation happens at severe level <1

A 
Neurologic signs of confusion, irritability, coma, muscle weakness, paresthesias, seizures, and apnea in VLBW infants
Hemolytic anemia
Hypoxia
Impaired granulocyte activity
Thrombocytopenia
Rhabdomyolysis
Myocardia depression
Rickets (chronic)
Treatment
517
Q

treatment of hypophosphatemia

A

Parental repletion is indicated with potassium or sodium phosphate
Subacute or gradual onset of symptoms
Replace with potassium or sodium phosphate enteral supplements

518
Q

Hyperphosphatemia (serum phosphorus

A

> 4.1 mg/dL)

519
Q

s/s hyperphosphatemia

A 
Altered mental status
Tetany, weakness, paresthesias
Fatigue
Cramping
Laryngospasm
Neuromuscular irritability
Cardiac arrhythmias
Chronic hyperphosphatemia may result in calcium deposits in soft tissue
520
Q

treatment hyperphosphatemia

A

Restrict dietary intake of phosphorus (protein restriction)
Phosphate binders which include sevelamer hydrochloride, lanthanum carbonate, calcium carbonate, or aluminum hydroxide
If cell lysis with normal renal function, forced diuresis with NS and osmotic diuretic such as mannitol
Consider dialysis if severe and underlying poor renal function; dialysis may be of limited effectiveness

521
Q

hypokalemia

A

(serum potassium <3.7 mEq/L)

522
Q

presentation hypok

A 
Often no symptoms
Diastolic dysfunction, HTN, or ventricular arrhythmias in patient with heart disease, heart failure, or left ventricular hypertrophy
ECG changes can include delayed depolarization, flat or absent T waves, long QT, prolonged QRS, ST changes, and the presence of U waves
Cramping
Decreased perfusion
Fatigue
Ileus
Impaired insulin release
Impaired muscle contraction, paralysis
Polyuria
523
Q

treat hypo k

A

Identification of cause
Potassium repletion
Acute, risk for arrhythmia
Calculate electrolyte deficiency to minimize risk of hyperkalemia with treatment
o Potassium chloride 0.5-1 mEq/kg/dose IV; maximum 20 mEq/dose; central administration is preferred and cardiac monitoring required
Subacute, chronic repletion
Potassium chloride, phosphate, or bicarb enteral supplement, based on etiology

524
Q

hyper k levels

what level is a medical emergency

A

(serum potassium > 5.2 mEq/L) ** > 7mEq/L is a medical emergency**

525
Q

presentation of hyper k

A

ECG changes: most commonly peaked T waves, low-voltage P waves, prolonged PR and QRS interval, ST changes, AV block, ventricular tachycardia and fibrillation, loss of PR interval, merging of QRS, and T waves to produce a sine wave pattern, asystole
Neuro: muscle weakness, paresethias, and tetany with sever hyperkalemia (> 9 mEq/L)

526
Q

tretment hyper k

A

Evaluate for accuracy of the laboratory sample (may be falsely elevated with hemolysis, thrombocytosis, or leukocytosis)
Remove all exogenous potassium sources
Hyperkalemia with ECG changes:
o Administer calcium chloride or calcium gluconate IV for membrane stabilization
o Administer IV insulin and glucose (e.g., D25 or D50), IV sodium bicarb, inhaled ß-agonists (e.g., albuterol); all temporarily shifts of potassium intracellulary
o Diuretics, if normal renal function (results in potassium removal)
o Cation exchange resin, such as sodium polystyrene sulfonate (exchanges potassium for sodium in the GI tract, resulting in potassium removal)
o Hemodialysis, If refractory to conventional therapy or with renal failure

527
Q

hyponatremia

A

<135

528
Q

symptoms hyponatremia

A 
Irritability
N/V
Poor feeding
Lethargy
Seizures
Coma
529
Q

causes hyponatremia

A

increased free water intake, excess water retention, increased Na losses, or combination

530
Q

hyponatremia that develops over hours to days (<48hr

A

acute

more likely to produce cerebral edema and changes in neuro status

531
Q

treatment of hyponatremia

A

If pt presents with seizures, the serum sodium must be acutely raised to 125mEq/L to stop seizure activity
Total mEq Na+ to raise sodium to target level = 0.6 x (weight in kg) x (target Na+ - measured Na+)
To raise serum Na+ levels the calculated amount of hypertonic saline should be administered over 15-20min to gain rapid control over seizures
1.2ml/kg aliquot of 3% NaCl will raise serum sodium level by 1mEq/L
If hypertonic Na unavailable – use 20ml/kg bolus of NS
Once acute correction completed, raise sodium more slowly:
10-12mEq/L in 24hrs or 0.5-1mEq/L/hr
Strict I&O
Urine specific gravity
Serum electrolytes
Serum osmolality
Daily weights
If serum Na and osmolality raised too rapidly the resulting water shift can lead to neuro complications (intracranial bleeding)

532
Q

hypernatremia

A

> 145

533
Q

etiology of hypernatremia

A

excessive Na intake, loss of free water
Risk Factors = Those who cannot signal thirst, infants, small children, developmental delay, decreased LOC, critical illness, Na+ bicarbonate administration, concentrated formula, water loss (diarrhea, Diabetes insipidus)

534
Q

symptoms of hypernatremia

A 
High pitched cry
Lethargy
Seizures
Fever
Renal failure
Rhabdomyolysis
Infants – can mimic infection and sepsis
Permanent CNS dysfunction can occur when Na >165-175mEq/L
535
Q

mgmt of hypernatremia

A

Essential to treat slowly and carefully!
If free water administered would travel to place of highest osmolality (cells) and cause the cells to swell → cerebral edema
If pt has signs of shock administer isotonic crystalloid by bolus (20ml/kg) until perfusion is adequate
Once stable estimated the fluid deficit and plan to replace over 48-72hr while proving maintenance fluids and replacement of ongoing losses (ex. Diarrhea)
Generally serum Na should decrease at rate no faster than 0.5-1mEq/L/hr or 10-12mEq/L in 24hr
If pt hypervolemic and hypernatremic → loop diuretics and decreased Na

536
Q

toxic syndrome of what?

N/V, pallor, delayed jaundice-hepatic failure (72-96 hr)

A

acetaminophen

537
Q

toxic syndrome of what?

Tachycardia, HTN, hyperthermia, psychosis and paranoia, seizures, mydriasis, diaphoresis, piloerection, aggressive behavior

A

Amphetamine, cocaine, and sympathomimetics

538
Q

toxic syndrome of what?

Mania, delirium, fever, red dry skin, dry mouth, tachycardia, mydriasis, urinary retention

A

Anticholinergics

539
Q

toxic syndrome of what?

HA, dizziness, coma, other symptoms affected

A

carbon monoxide

540
Q

toxic syndrome of what?

Coma, convulsions, hyperpnea, bitter almond odor

A

cyanide

541
Q

toxic syndrome of what?

Metabolic acidosis, hyperosmolarity, hypocalcemia, oxalate crystalluria

A

Ethylene glycol (antifreeze)

542
Q

toxic syndrome of what?

Vomiting (bloody), diarrhea, hypotension, hepatic failure, leukocytosis,hyperglycemia, radiopaque pills on KUB, late intestinal stricture, Yersinia sepsis

A

Iron

543
Q

toxic syndrome of what?

Coma, respiratory depression, hypotension, pinpoint pupils, bradycardia

A

Narcotics

544
Q

toxic syndrome of what?

Miosis, salivation, urination, diaphoresis, lacrimation, bronchospasm (bronchorrhea), muscle weakness and fasciculations, emesis, defecation, coma, confusion, pulmonary edema, bradycardia

A

Cholinergics (organophosphates, nicotine)

545
Q

toxic syndrome of what?

Tachypnea, fever, lethargy, coma, vomiting, diaphoresis, alkalosis (early), acidosis (late)

A

Salicylates

546
Q

toxic syndrome of what?

Coma, convulsions, mydriasis, hyperreflexia, arrhythmia (prolonged QT interval), cardiac arrest, shock

A

Cyclic antidepressants

547
Q

A poisoned child can exhibit any one of six basic clinical patterns:

A 
Coma
Toxicity
Metabolic acidosis
Heart rhythm aberrations
GI symptoms
Seizures
548
Q

used for gastric decontamination in toxicity/overdose/ingestion

A 
Syrup of Ipecac
Gastric Lavage
Activated Charcoal
Cathartics
Whole-Bowel Irrigation
549
Q

contraindications to syrup of ipecac

A 
Age less than 6 months
Impaired gag reflex
Impending coma or seizures
Hydrocarbon Ingestion
Caustic Ingestions (acid, alkalis)
Ingestion of sharp foreign bodies
550
Q

criterion to use gastric lavage

A

ingestion of potentially life threatening poison;
2.
procedure done within one hour of ingestion

551
Q

complications of gastric lavage

A

aspiration pneumonia, laryngospasm, tension
pneumothorax, tachycardia, atrial/ventricular ectopy, mechanical injury
to the GI tract, hyper/hyponatremia, hypothermia

552
Q

contraindications for gastric lavage

A

ingestion of caustics, ingestion of hydrocarbons with
high risk for aspirations, unprotected airway, in stable patient, or at risk
for GI bleed

553
Q

Most commonly used and most effective method of gastric

decontamination

A

activated charcoal

554
Q

substances not absorbed well by activated charcoal

A

alcohols, acids, alkalis, hydrocarbons, iron,

potassium, magnesium, sodium, lithium salts

555
Q

when should activated charcoal be given

A

within 1 hr of ingestion

556
Q

adverse reactions to activated charcoal

A

vomiting
constipation
obstruction
aspiration

all rare

557
Q

contraindications to using activated charcoal

A

unprotected airway, hydrocarbon and

caustic ingestion, non-intact GI tract

558
Q

Increase GI transit time of ingested toxins

No evidence-based indications for routine use

A

cathartics

559
Q

names of cathartics used in ingestion

A

Sorbitol, magnesium citrate, and magnesium sulfate

560
Q

contraindications for using cathartics in ingestion

A

absent bowel sounds, recent abdominal
trauma, recent bowel surgery, intestinal obstruction/perforation, dehydration,
hypotension, significant electrolyte, imbalance, renal failure,
heart block, <12months of age

561
Q

used in whole bowel irrigation to rapidly evacuates contents of GI tract within 2-6hrs post ingestion

A

PEG

562
Q

indications for using PEG in ingestion (whole bowel irrigation)

A

ingestion of adult iron tablets, heavy metals, lithium, sustained release drug formulations

563
Q

contraindications for using PEG in ingestion (whole bowel irrigation)

A

unprotected airway,hemodynamic instability, Ileus, bowel obstruction/
perforation, intractable vomiting, GI hemorrhage

564
Q

early manifestations of tylenol ingestion

A

Nausea, vomiting, malaise, sweating
Progression to hepatic injury as early as 2-3 days
Right upper quadrant pain and tenderness
Liver enzymes begin increasing 24-36 hrs after overdose
Maximal liver injury peaks 3-5 days
Jaundice, coagulopathy, encephalopathy
Recovery, if occurs, is complete within 5-7 days

565
Q

adults when to seek emergent evaluation after tylenol overdose

A

10gm or 200mg/kg (whichever is less) per 24 hrs
6 gm or 150mg/kg (whichever is less) per 24 hr period for
48 hr or longer

566
Q

age less than 6 for when to get med attention after tylenol overdose

A

Dose >200mg/kg in 24 hr period
Dose >150mg/kg per 24 hr period for the preceding 48 hrs
Dose >100mg/kg per 24 hour period for 72 hours or longer

567
Q

antidote for tylenol overdose

A

Antidote N-acetylcysteine (NAC)

568
Q

mucomyst is most effective if given within ___ hrs post ingestion

A

8

569
Q

Food and Drug Administration (FDA)

tylenol overdose Treatment Regimens:

A

72 hour oral course (Acetadote)

21 hour IV course (mucomyst)

570
Q

Children metabolize ethanol at a rate of

A

10-25 mg/dL/hr

571
Q

alcohol ingestion in pediatrics symptoms

A

facial flushing, vomiting, diaphoresis, respiratory depression, seizures,
hypotension, hypothermia, and hypoglycemia

572
Q

Estimated pediatric lethal dose alcohol

A

3.8mL/k 100% alcohol

573
Q

Early signs and symptoms: occur 4-6 hours after ingestion
Nausea, vomiting, diarrhea
Progression of symptoms include:
Metabolic acidosis, coma, hypotension, shock, hepatic failure, coagulopathy,
seizures, death
Later complications
Bowel obstruction or stricture

A

iron overdose

574
Q

toxic dose iron

A

Toxic Dose:
Observe at home for ingestion of chewable multivitamin with iron,
carbonyl iron formulations or polysaccharide iron complexes, regardless of dose
Refer to ER for >40mg/kg of elemental iron (adult ferrous salt formulations)
Toxicity at > 60mg/kg

575
Q

management of toxic dose of iron

A 
Orogastric Lavage
Supportive Care
Deferoxamine methylate (DFO)
Acts as chelating agent, binds to free iron and forms ferrioxamine
Dose: 15mg/kg/hr IV infusion
576
Q

Wide anion gap metabolic acidosis, respiratory alkalosis (not always in children), hypokalemia,
hypoglycemia
Nausea, vomiting, hematemesis, gastric pain, tinnitus/impaired hearing, tachypnea, tachycardia,
dehydration, fever
Serious toxicity: delirium, seizures, coma, rhabdomyolysis, non cardiac pulmonary edema,
increased cranial pressure, arrhythmias, asystole
Reye’s Syndrome – chronic administration of aspirin during viral illness

A

salicylate tox

577
Q

mgmt of Salicylate tox

A

ER referral for ingestion
>150mg/kg or 6.5gm of ASA equivalent
Gastrointestinal Decontamination
Activated Charcoal
Seizure management with IV benzodiazepines
Fluid and Electrolyte corrections
Sodium Bicarbonate 1-2mEq/kg IV to correct acidosis
Alkalization of Urine – IVF (D5W with NaHC03 and KCL run at 2x maintenance)
Correct hypoglycemia

578
Q

Recreational use of inhaled hydrocarbons is a significant health issue in pediatrics

A

Inhalants are the second most widely used illicit drug class among adolescents
Low cost, accessible
Most pressurized aerosolized agents can be abused
Propellants used in most aerosolized materials are hydrocarbons
Performed through huffing, sniffing, or bagging
Recognition and treatment remains challenging for caregivers and health care providers

579
Q

Liquid ingestion (most commonly an unintentional ingestion)
Most common injury is aspiration with resultant pneumonitis
Lower viscosity agents causing greater injury because of their distribution
Injury to the epithelial tissue of the respiratory tract results in:
Inflammation and bronchospasm
Poor O2 exchange
Atelectasis
Pneumonitis
Contact with alveolar membranes results in :
Hemorrhage
Edema
Surfactant inactivation
Leukocyte invasion
Vascular thrombosis
ome agents can cause renal and bone marrow toxicity
Methemoglobinemia

A

Hydrocarbons/Kerosene

580
Q 
Absorption across the pulmonary vascular bed
Side effects noted to 15-30 minutes after inhalation
Two primary systems are impacted
Cardiac
Arrhythmias
Increased O2 demand
Acute myocardial infarction
CNS
Renal tubular acidosis
Hypokalemia
Hyperchloremia
Frostbite/Burns
Face, trachea, esophagus
Bone marrow damage/ Aplastic anemia
Leukemia
Toxic hepatitis
Highly lipid soluble; crosses the blood-brain barrier
Chronic use results in cerebral atrophy and neuropsychological changes
Management:
A

Hydrocarbons/Kerosene

inhaled

581
Q

management of care in

Hydrocarbons/Kerosene

A

Monitoring
VS
Respiratory status
Can progress to respiratory failure quickly (aspiration of liquid hydrocarbons)
Chest radiograph findings often lag behind clinical symptoms
Evaluations of serum electrolytes , renal function , hepatic function
Treatment
ABCs
Aggressive supportive care
Active removal of agent is contraindicated unless highly toxic hydrocarbon ingested
Avoid use of catecholamines, inotropic agents, and bronchodilators due to myocardial
sensitization of catecholamines
Use amiodarone to treat arrhythmias (inhalants)
Correct electrolytes

582
Q 
Arrhythmias
Often tachyarrhythmias; possibly fatal
Impaired cardiac conduction
Nausea and vomiting (often the first sign)
Dizziness, HA, mental disturbances
Shock
A

digoxin tox

583
Q

monitor and treat dig tox

A 
Monitoring
Electrolyte levels
Especially serum potassium
Continuous EKG
BP
Treatment
Aggressive supportive care
Atropine can be used for bradycardia
Antidote is Digoxin Immune Fab (Digibind)
584
Q

Cardiovascular
Hypotension, bradycardia, bradyarrhythmias
Conduction abnormalities of sinoatrial/atrioventricular
(SA/AV) node, idioventricular arrhythmias
Shock
Death
Other effects
Altered mental status, seizures
Respiratory depression
Hyperglycemia
Bowel ischemia
Verapamil and diltiazem can result in cardiac failure

A

CCB tox symptoms

585
Q

mgmt and treat CCB tox

A 
Monitoring
BP
EKG
Blood glucose levels
Treatment
Aggressive supportive care
Fluid resuscitation for hypotension
Atropine for symptomatic bradycardia
Calcium, IV
High-dose insulin may improve hypotension
Glucagon may help improve cardiac contractility and conduction
IV lipid administration may act as a :lipid sink” for absorbing lipophilic drugs
586
Q

WIdely variable depending on the amount ingested and the specific drug that was ingested
Ranges from asymptomatic to cardiac arrest
Most patients become symptomatic within 2 hours after ingestion, except in the case of extended
release medications in which symptomatology can be delayed for up to 24 hours
Most common presentations are:
Bradycardia
Hypotension
Ventricular dysrhythmias can be associated with the ingestion of 𝛃-Blockers with MSA properties
Seizures and neurologic sequelae can occur if patient experiences severe hypotension or if
medication ingested possesses lipophilicity

A

BB tox

587
Q

evaluate and treat BB tox

A

Diagnostic Evaluation
Accurate history
Name of agent ingested
Approximation of number of pills ingested and concentration
Approximate time of ingestion
Possibility of co-ingestion
Any interventions performed prior to seeking assistance
EKG
Serum electrolytes
Urine and serum toxicology screen
Acetaminophen and salicylate levels to evaluate for co-ingestion
Management
Depends on the amount ingested and patient symptomatology
First, evaluate airway, breathing, and circulation
Consider activated charcoal (1g/kg/dose) if within 1 hour of ingestion
Fluid bolus (NS 20 mL/kg) for hypotension
Atropine, IV, for bradycardia
Glucagon infusion for moderate to severe ingestions
Sodium bicarbonate if the 𝛃-Blocker ingested possess MSA properties
Helps to prevent dysrhythmias

588
Q

Agitation, delirium
Mydriasis
Dry mouth
Tachycardia, HTN
Warm dry skin
Fever
Urinary retention
Decreased bowel sounds
can cause profound hypotension by 𝞪-adrenergic blockade
Respiratory failure and coma can occur by CNS depressant effect
Cardiac conduction abnormalities
Result of sodium channel blockage in the myocardium
Widened QRS complex and prolonged QT interval on EKG
Life-threatening dysrhythmias, including ventricular tachycardia or fib

A

TCAs

589
Q

eval and mgmt TCA tox

A

Diagnostic Evaluation
Can be detected on serum drug screen testing
Diagnosis is typically made based on history of TCA use or presence in the home and the anti-
cholinergic clinical manifestations
Management
Acute airway management may be necessary because of respiratory failure from CNS de-
pression
Seizures management
Benzodiazepines
EKG abnormalities and dysrhythmias
Sodium bicarbonate
Goal of achieving an arterial pH of 7.45-7.55
Sodium bicarbonate is thought to act in two ways
Sodium loading may overcome TCA blockage of myocardial sodium
channels
Increasing pH may increase protein binding of TCA, resulting in a
reduction of free drug in the serum
Hypotension
Inotropic agents
Norepinephrine often preferred

Essentials of Acute Care (9 decks)

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