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test 3 material Flashcards

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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
what test should be considered in pt presenting with significant UGI bleeding
urgent upper endoscopy only after stabilized
26
what test should be considered in pt with bright red lower GI bleeding
Conoloscopy only after stabilized
27
GI bleed, pt hemodynamically unstable what can you adminishter
NS LR PRBCs pt kept NPO
28
An endoscopy allows for
visualization cauterization biopsy test for H. Pylori
29
med used in management of bleeding esophageal varices, why
octreotide - decrease CVP (central venous pressure) before endoscopic intervention
30
if variceal bleeding is not controlled by endoscopic and/or tamponade intervention what should be considered
Transjugular intrahepatic portosystemic shunting (TIPS)
31
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)
nuclear medicine tagged RBC bleeding study or a angiogram with selective vessel embolization
32
this may help identify a radiographically silent lesion or one beyond the reach of the conventional upper or lower endoscope
single or double balloon enteroscopy
33
polyps are usually removed with
snare electrocautery during a colonoscopy
34
GI bleeding from Henoch -Schonlein purpura (HSP) and HUS usually resolves with
resolution of the disorders
35
patients with UGI bleeds when can the diet resume
within 24 hours
36
what are the UGI bleeds discharged on
PPI for gastritis or B-Blocker (propanolol) for esophageal varices close outpatient follow up by GI
37
discharge of patients with lower GI bleed depends on
etiology of the bleeding underlying chronic illness response to therapy
38
infant upper GI bleed think
hemorrhagic gastritis stress ulcer vascular malformation reflux esophagitis
39
infant lower GI bleed think
``` infectious colitis midgut volvulus anal fissures necrotizing enterocolitis intussusception milk protein allergy hirschsprung disease lymphonodular hyperplasia ```
40
young child upper gi bleed think
``` hemorrhagic gastritis stress ulcer gastric/duodenal ulcer esophageal varices mallory-weiss tear epistaxis reflux esophagitis foreign body toxic ingestion ```
41
young child lower gi bleed think
``` 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 ```
42
upper Gi bleed for older child and adolescent think
``` hemorrhagic gastritis stress ulcer gastric/duodenal ulcer esophageal varices mallory-weiss tear epistaxis reflux esophagitis ```
43
lower GI bleed or older child and adolescent think
``` 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 ```
44
what antibiotic does the book mention can look like blood in stool
cefdinir
45
what test can tell you if its blood or something else
occult stool
46
vomiting blood is always ________ to the ligament of treitz
proximal
47
when upper GI bleeding is suspected, what may be placed and why
a ng and gastric contents aspirated for evidence of recent bleeding
48
what test is used in newborns to determine whether it is fetal or maternal blood present in stool
apt test (alkali denaturation test)
49
hematemesis in newborn | blood found in stomach on lavage
peptic disease
50
hematemesis or rectal bleeding in newborn APT shows adult hemoglobin is present cracked maternal nipples
ingested maternal blood
51
hematemesis or rectal bleeding in newborn | Bruising
coagulopathy
52
streaks of bloody mucus in stool in newborn | eosinophils in feces and in rectal mucosa
allergic colitis
53
rectal bleeding in newborn | sick infant with tender and distended abdomen
necrotizing enterocolitis
54
hematemesis in newborn | cystic mass in abdomen on imaging study
Duplication cyst
55
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
volvulus (twisting or knotting of the GI tract causing an obstruction - most commonly due to a birth defect called a malrotation)
56
``` infancy to older than 2 yrs old hematemesis rectal bleeding possible epigastric pain coffee ground emesis ```
peptic disease
57
infancy to > 2 yrs old hematemesis history or evidence of liver disease
esophageal varices
58
``` infancy to 2 yrs old rectal bleeding crampy pain abd distension abd mass ```
intussusception
59
infancy to > 2 yrs old rectal bleeding massive bright red bleeding no pain
meckel diverticulum
60
infancy to >2 yrs old rectal bleeding bloody diarrhea fever
bacterial enteritis
61
``` infancy to > 2 yrs old hematemesis rectal bleeding possible epigastric pain coffee ground emesis ```
NSAID injury
62
``` older than 2 rectal bleeding usually crampy pain poor weight gain diarrhea ```
inflammatory bowel disease
63
> 2 yrs old rectal bleeding history of antibiotic use bloody diarrhea
psueudomembranous colitis
64
>2 yrs old rectal bleeding painless bright red blood in stool - not massive
juvenile polyp
65
>2 yrs old rectal bleeding streaks of blood in stool no other symptoms
Nodular lymphoid hyperplasia
66
>2 yrs old hematemesis bright red or coffee ground emesis follows retching
Mallory-Weiss syndrome
67
``` >2 yrs old rectal bleeding thrombocytopenia anemia uremia ```
Hemolytic uremic syndrome (HUS)
68
>2 yrs old rectal bleeding dilated external veins blood with wiping
hemorrhoids
69
tests for evaluation of GI bleeding | all patients get
``` 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
70
what tests ordered to evaluate bloody diarrhea
stool culture - looking for c-diff sigmoidoscopy (looks at rectum and lower part of large intestine (colon))or colonoscopy CT with contrast
71
tests to evaluate rectal bleeding with formed stools
``` external and digital rectal examination sigmoidoscopy or colonoscopy meckel scan mesenteric arteriogram video capsule endoscopy ```
72
evaluation for hematemesis if endoscopy is not available
barium upper GI series
73
Evaluation of bleeding with pain and vomiting (Bowel obstruction)
abd x ray series pneumatic or contrast enema upper GI series
74
what scan is used to detect a meckel diverticulum
Meckel scan
75
what is a mesenteric arteriogram
special x ray of the blood vessels (arteries) in the abd to show where the artery is blocked or bleeding
76
what does video capsule endoscopy show
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)
77
Blood in the diaper or toilet may be coming from the
urinary tract, vagina, or severe | diaper rash.
78
most common intra abdominal tumors are
neuroblastoma | Wilms tumor
79
2/3s of abdominal masses are due to
organomegaly
80
a history of bilious emesis or encopresis can lead to an assessment of
bowel obstruction
81
urinary excretion of ______ can lead to cola colored urine
bile salts
82
can present with acholic stools (pale)
obstruction of the biliary system
83
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
renal pathology
84
Jaundice can indicate _____ disease
liver
85
Pale skin can indicate
anemia
86
flushed rosy skin can be present in
sepsis
87
classic exanthems (diffuse rash) can be present with
viral infections
88
general appearance is ill-appearing, particularly with cachexia or FTT, _____ or _____ may be the cause
chronic infections | malignant disease
89
Masses in the RUQ most often involve the
liver gallbladder biliary tree
90
Epigastric masses can include both
epigastric hernias | diastasis recti
91
LUQ masses most often involve the
stomach spleen adrenal gland kidney
92
Right and Left lower quadrant masses may be from
ovarian and fallopian processes or the intestines in orgin
93
suprapubic masses are most commonly
genitourinary in nature
94
Abd wall masses are either
superficial to the muscular layers or | their movement is coupled with the contraction of the abdominal musculature
95
_________ are most often observed when a very small child cries and it pops out
abd wall hernias
96
immobile masses are either
invasive tumors | masses that arise from the retroperitoneal organs
97
Tenderness to the mass suggests a
recent change (such as hemorrhage that lead to acute increase in volume of the mass placing tension on the capsule)
98
Firmness, hardness, irregularity suggest either
tumor or | desmoplasia (scar)
99
Smoothness to a mass suggests an
encapsulated mass
100
Tympany indicates
gas such as a hollow viscus
101
Dullness indicates
fluid or a solid mass
102
A hernia is diagnosed with
physical exam
103
what kind of hematomas secondary to trauma are difficult to diagnose and why
rectus hematomas - hidden from view by rectus sheath
104
what kind of soft tissue tumors can be diagnosed on physical exam
fibromas and lipoma
105
fixed abd mass related to mesenteric fibromatosis or retroperitoneal sarcoma is diagnosed by
CT or MRI bc bowel gas often obscures retroperitoneal ultrasonography
106
in infants crying can lead to an ingestion of air ->
gastric distention which can cause vagal symptoms or resp sequelae
107
what makes gastric distension relatively easy to diagnose and treat
tympanic LUQ | response to NG
108
ingestion of hair and roughage can result in
bezoars
109
what 3 things can present with acute gastric distension with the inability to pass an NGT
congenital duplications gastric tumors gastric torsion
110
a exceedingly common disorder | presents with abd discomfort and a palpable mass
constipation
111
infectious and inflammatory diseases of the bowel that can produce a mass
abscesses from a perforated appendix Meckel diverticulum phlegmons from Crohn Disease (CD) palpable lead pipe colon from ulcerative colitis (UC)
112
mass in younger patients differential
``` intussusception duplications mesenteric cysts meconium pseudocysts bowel atresia malrotation with volvulus can occasionally present with an abd mass ```
113
bowel tumors that may present with a palpable mass
carcinoid lymphoma adenocarcinoma
114
in most cases a palpable kidney represents what? | what population can this be a normal finding
obstructive kidney disease parenchymal kidney disease infants the kidney is occasionally palpable
115
multiple renal cysts can by caused by
polycystic kidney disease | multicystic dysplastic kidney disease
116
a large fluid filled cyst is present at the hilum, it can represent a
dilated renal pelvis with or without associate dyroureter
117
bilat findings of a large fluid filled cyst is present at the hilum can suggest
bladder outflow obstruction such as posterior urethral valves or neurogenic bladder
118
diffuse unilateral renal swelling can occur from
renal vein thrombosis
119
what type of tumor can present as a unilateral mass (kidney)
Wilms tumor
120
adrenal masses are most commonly ____ in origin
neoplastic
121
what is the most common pediatric adrenal tumor
neuroblastoma
122
what other endocrine tumor can occasionally be identified but rarely of sufficient size to produce a palpable mass
pheochromocytoma
123
in females _____ masses are extremely common
gynecologic
124
__________ cysts are a physiologic requirement for menstruation
small ovarian cysts (follicular)
125
benign ovarian masses include
dermoid cysts mature teratomas immature teratomas germ cell tumors
126
what can occasionally produce a very edematous and swollen ovary that may occasionally present as a mass
torsion
127
the most common fallopian and uterine masses are
pregnancy (ectopic or intrauterine)
128
these fallopian and uterine masses can lead to accumulation of serum or menses and a large palpable pelvic mass
obstruction of the fallopian tube at the isthmus (hydrosalpinx) uterus at the cervix vagina at the hymen hydrometrocolpos hematocolpos
129
hematocolpos
the vagina is pooled with menstrual blood due to multiple factors leading to the blockage of menstrual blood flow
130
hydrometrocolpos
expanded fluid filled vaginal cavity with associated distention of the uterine cavity
131
hydrosalpinx
fallopian tube thats blocked with watery fluid
132
an enlarged spleen should suggest ____ or ____ until proven otherwise
hematologic disease | malignancy
133
splenomegaly - hematologic disease assoiciations
hereditary hemolytic anemias such as spherocytosis or elliptocytosis sickle cell disease
134
hematologic malignancies associated with splenomegaly
leukemias | lymphomas
135
viral infections can be associated with splenomegaly
acute viral infection with Epstein Barr virus (EBV) or cytomegalovirus (CMV)
136
rheumatologic disease associated with splenomegaly
systemic lupus erythematosus | Langerhans cell histiocytosis
137
storage diseases associated with splenomegaly
Niemann-Pick | Gaucher disease
138
can cause significant hepatic edema and enlarged tender liver
Acute viral hepatitis | autoimmune hepatitis
139
metabolic disorders that can present with painless hepatomegaly
glycogen storage diseases | Wilson disease
140
congenital disorder that can cause painless hepatomegaly
Congenital hepatic fibrosis
141
cyst that can cause hepatomegaly
simple or biliary cysts
142
simple cyst in liver or polycystic liver disease can be diagnosed with
US
143
cysts that can be present anywhere along the biliary tree
biliary cysts or choledochal cysts
144
solid hepatic masses of vascular origin
hemangioma | lymphovascular malformations
145
solid hepatic masses of parenchymal origin
focal nodular hyperplasia adenoma neoplasia
146
The most common tumors in the younger patients (liver)
hepatoblastoma
147
most common liver tumors in the older pediatric patient
hepatocellular carcinoma
148
can produce diffuse neoplastic infiltration of the liver
lymphoma
149
acute liver congestion and hepatomegaly are associated with
vascular congestion such as in heart failure or Budd-Chiari syndrome
150
Congenital dilations of the biliary tract are classified as
choledochal cysts
151
Acquired dilation of the biliary tree can occur secondary to
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
152
pancreatic and biliary tract malignancies are common or rare in children
rare
153
what will you order for an abd mass to indicate infection, inflammation and anemia
CBC with Diff
154
what labs will you order for a abd mass to identify kidney disease
BUN and creatinine
155
what labs will you order for an abd mass to look at pancreatic disease
amylase and lipase
156
what labs will you order for an abd mass to look at liver function
liver function panel (LFTs)
157
what lab would you order for an abd mass that is nonspecific but is sensitive for significant illness
albumin hypoalbuminemia is what you would be looking for
158
what lab when evaluating an abd mass would be useful in identifying solid tumors
Uric acid | LDH
159
what radiographic test is used to identify an intestinal obstruction, fecal impaction and calcifications associated with tumor.
2 view x ray of abdomen nonspecific
160
what can be used to identify the origin of an abdominal mass and differentiate between solid and cystic
US not definitive but can guide you in the selection of further imaging and/or labs
161
what test can be particularly useful in evaluating solid abd masses
CT scan with IV contrast
162
In addition to evaluating solid masses, CT with IV contrast can also see
vascular anatomy and presence of associated lymph nodes
163
What type of scan serves to help stage many cancers
CT with IV contrast
164
Masses of primary bowel or bladder are best seen with what study
fluoroscopic studies such as UGI, BE and voiding cystourethrogram
165
what type of contrast to bowel will produce significant artifact and prevent immediate subsequent CT scan
Enteral contrast administered to bowel
166
What scans are used for hepatobiliary and pancreatic disease (masses)
US and CT are not helpful for these Traditionally (HIDA) hepatobiliary imino-diacetic acid increasingly more common is MRCP (magnetic resonance cholangiopancreatography )
167
in benign abdominal masses an NGT is mandatory for all
perforations and obstructions
168
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)
``` IV NG drainage abx support for septic shock surgical consult ```
169
age of presentation for neuroblastoma
18 months, prevalence greatest in <4 years (85%)
170
most common extracranial tumor in children
neuroblastoma
171
Wilms tumor most common age of presentaion
1-5 yrs
172
most common malignant liver tumor
hepatoblastoma
173
what malignant tumor is associated with extreme prematurity and what age is the mean for diagnosis
Hepatoblastoma
174
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
Hirschsprung disease (HD)
175
where are ganglion cells normally located
throughout the intestines from the mouth to the rectum
176
Hirschsprung disease (HD) is more prevalent in what gender
males (4 xs more than female)
177
short segment Hirschsprung disease (HD) what part of bowel is affected
rectosigmoid colon
178
long segment Hirschsprung disease (HD) what part of bowel is affected
rectosigmoid colon but also extends proximal to this point
179
genetic role in Hirschsprung disease (HD) what gene?
there is familial occurrence in up to 20% of these cases and they are usually the long segment Hirschsprung disease (HD) RET gene
180
what is the classic presentation for Hirschsprung disease (HD)
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
181
Presenting age of Hirschsprung disease (HD)
can present at any age but most are diagnosed in the neonatal period diagnosis after 2yrs old is very rare
182
children who are diagnosed with Hirschsprung disease (HD) at an older age typically have which type
shorter segment affected
183
children diagnosed at an older age with Hirschsprung disease (HD) usually present with what symptoms
long and tenuous history of constipation, malnutrition, FTT and chronic abd distension
184
if missed in the neonatal period infants often present with Hirschsprung disease (HD) at what point?
when they transition from breast milk to formula or when solid foods are introduced
185
diagnosis of Hirschsprung disease (HD) is made by what and confirmed how?
clinical picture and radiologic studies confirmed by pathology from a rectal biopsy
186
Abd x ray for Hirschsprung disease (HD) will show what
large dilated loops of intestines and may have air fluid levels
187
after Hirschsprung disease (HD) is suspected on an abd x ray, what would be the next test to order
Barium enema - this would not be diagnostic but identifies who will require a more invasive evaluation
188
what will the barium enema show in Hirschsprung disease (HD)
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)
189
how is a BE performed
placing a small catheter into the rectum and instilling contrast into the colon then taking several radiographs
190
A BE would not be helpful in Hirschsprung disease (HD) for what population
neonates. May not have dilation of the colon yet
191
BE should be avoided if there are concerns for ______ or ______
perforation | enterocolitis
192
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.
Anorectal manometry - measures resting anal sphincter pressure. In older children, it can assess for the sensation of being full
193
standard for definitive diagnosis of Hirschsprung disease (HD) with a sensitivity of 100% is a
rectal biopsy
194
what type of rectal biopsy can be done on neonates and infants in the diagnosis of Hirschsprung disease (HD)
suction rectal biopsy
195
most common problems with suction rectal biopsy in the diagnosis of Hirschsprung disease (HD)
inadequate sample or sample taken too close to to the sphincter. must be done 2cm above anus
196
what type of rectal biopsy is done on an older child
full thickness rectal biopsy - must be sutured closed. requires general anesthesia. poses the highest risk but most accurate (bleeding, infection, scar)
197
initial treatment of Hirschsprung disease (HD)
IV fluid resuscitation bowel decompression via NGT rectal irrigations abx if enterocolitis or sepsis is a concern rectal irrigations (taught to caregivers) surgical intervention
198
when might surgical intervention be held for correction of Hirschsprung disease (HD)
if child is able to tolerate a diet without abd distension, may wait for adequate weight gain and bowel decompression prior to intervening surgically
199
most common surgical technique for Hirschsprung disease (HD)
Transanal endorectal pull-through (TERPT) using the Swenson, Soave or Duhamel techniques
200
initial postop potential complications for TERPT
``` anastomotic leak bleeding bowel obstruction wound infection abscess stricture perianal excoriation ```
201
When can an anastomotic leak occur
anytime a surgeon is anastomosing 2 segments of bowel together.
202
symptoms of an anastomotic leak
fever irritability abd distension
203
An abscess may occur after a TERPT due to
poor hemostasis causing a hematoma that becomes infected
204
stricture of the sphincter may occur after a TERPT because
when retracting the sphincter muscle during surgery.
205
delayed passage of stool postop to TERPT
think stricture of the sphincter
206
how is stricture of the sphincter postop to TERPT fixed
gently dilating the anus with a lubricated hegar dilator
207
when do you usually see perianal excoriation in the postop period following TERPT and what is done
once the pt starts stooling. over time the patients stooling pattern returns to normal
208
what needs to be monitored closely in the initial postop period following a TERPT
``` NG output vital signs urine output abd girth pain control ```
209
common long term complications following a TERPT (pg 474)
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
210
what happens with enterocolitis following a TERPT
inflammation of the lining of the colon or small intestines. As it progresses, it erodes in the lining of the intestines -> becomes infected.
211
symptoms of enterocolitis following a TERPT
fever abd distension explosive diarrhea
212
intervention for enterocolitis post TERPT
bowel decompression with rectal irrigations broad spectrum IV abx followed by oral Flagyl
213
factors found to decrease risk of enterocolitis after TERPT
daily rectal irrigations or rectal dilations starting at 2 weeks post surgery probiotic prophylaxis
214
what collaborative resources are important to involve in a pt care that has Hirschsprung disease (HD)
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
215
are Hirschsprung disease (HD) kids ever able to establish normal bowel function
yes, but maybe later than other kids their age.
216
what are patients often prescribed for stooling issues with Hirschsprung disease (HD)
PEG 3350 (Miralax) or loperamide severe - antegrade continence enema
217
is Hirschsprung disease (HD) cured with surgery?
no, they will require close monitoring of bowel function, nutritional status and overall health for their lifetime
218
prognosis for Hirschsprung disease (HD) with short segment
good outcome with very few interventions required
219
Prognosis for Hirschsprung disease (HD) with total colon HD
may require multiple procedures and in rare cases and intestinal transplant
220
what type of obstruction is an illeus
functional - occurs when the peristalsis of the GI tract is impaired.
221
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
Ileus
222
3 phases of a postop ileus and what is the cause
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
223
list the causes of functional bowel obstruction
``` abd surgery peritonitis sepsis trauma medications (opioids, anxiolytics) metabolic imbalances (hypokalemia, hyponatremia, hypomagnesemia, acidosis) ```
224
causes of mechanical bowel obstruction
Postop adhesions hematoma intussusception distal intestinal obstruction syndrome Malrotation with volvulus tumors bezoar Congenital abnormalities (duodenal atresia, duodenal web, annular pancreas, jejunoileal atresia)
225
symptoms of ileus
abd distension absent or hypoactive bowel sounds due to lack of peristalsis constant pain that worsens with increased bowel distension
226
with mechanical obstruction, bowel sounds may be
high pitched or hyperactive
227
what is typically a late sign of ileus and is preceded with abd distension and accumulation of GI fluids
vomiting the higher the obstruction, the more frequent the emesis episodes may be
228
vomiting proximal to the sphincter of Oddi will more likely be
non-bilious
229
bilious emesis represents an obstruction occurring beyond the
sphincter of Oddi
230
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 _____
longer | POI
231
symptoms that may be present with resolution of POI are the passage of
flatus and stool best indicator is tolerating a PO diet
232
whats diagnostic for ileus
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.
233
if there is significant gastric fluid loss with ileus, consider checking
electrolyte levels
234
Preop measures that can aid in minimizing POI
minimizing fasting prior to surgery (2 hours for liquids, 6 hours for food) avoidance of preop medications including anxiolytics
235
what postop care practices may aid in the resolution of POI (post op ileus)
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
236
NSAIDS post op
treats pain and inflammation | but promotes GI bleeding (side effect)
237
treatment for a symptomatic ileus
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
postop return of function for the small bowel
12-24 hours
239
postop return of function for the stomach is
24-48 hours
240
postop return of function for the colon is
3-5 days
241
invagination of telescoping of the intestines involving the proximal portion of the bowel
intussusceptum
242
invagination of telescoping of the intestines involving the distal portion of the bowel
intussuscipiens
243
what leads to intussusception
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
Currant jelly stool is an early or late sign of intussusception
very late
245
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
intussusception
246
what are the 3 categories of intussusception
1) idiopathic 2) lead point 3) postsurgical
247
which category of intussusception is most commonly seen in infants and children
idiopathic
248
which type of intussusception often corresponds with viral gastroenteritis or an URI
idiopathic
249
what viral infections are associated with intussusception
adenovirus rotavirus HSV
250
what is thought to link a viral infection to intussusception
the virus leads to hypertrophy of Peyer patches (lymph node in the intestines) which might act as a lead point causing the intussusception
251
what vaccine has resulted in 35 patients getting intussusception
Rotarix (approved vaccine for Rotavirus)
252
which type of intussusception has a identifiable cause in the intestinal mucosa
lead point intussusception
253
what ages does lead point intussusception affect
5-14 years
254
what are the most common causes of lead point intussusception
inverted Meckel diverticulum polyps duplication cyst hemangiomas
255
what is the least common type of intussusception
postsurgical - can be VERY serious in infants and children
256
when should postsurgical intussusception be on your differential
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
classic symptoms of intussusception
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
diagnostics for intussusception
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
if the intussusception is not reduced on the first attempt utilizing contrast/air/saline enema what should you do
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
Contrast/air/saline enema is less likely to work for reducing intussusception when
symptoms have been greater than 3 days, age older than 3 years, rectal bleeding, abdominal distention and a palpable abdominal mass is present
261
when is surgical intervention required for an intussusception and is it time sensitive?
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
care of nonoperative post reduction of intussusception
NPO for short time and clear liquids are introduced with diet progression as tolerated. send home
263
if recurrence of intussusception post reduction occurs
you can attempt re-reduction
264
care of pt after surgical reduction of intussusception
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
how do you calculate normal urine output
1mL/kg/hr
266
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
nonsurgical 24 hours 6 months
267
who do patients follow up with post intussusception reduction
nonsurgical - PCP 1 week later surgical - pediatric surgeon
268
Most morbidity and mortality related to intussusception is related to _____ secondary to _______ which can lead to _____ and _____
delayed diagnosis and treatment secondary to intestinal ischemia which can lead to IF(intestinal failure) and small bowel transplant
269
can intussusception be prevented
no
270
abnormal rotation and fixation of the bowel during embryologic development.
malrotation
271
the classic form of malrotation is an
abnormal rotation of the duodenojejunal and decocolic loop and a high, medially positioned cecum
272
when malrotation is present and the midgut twists in a clockwise direction around the SMA leading to occlusion of the SMA
Volvulus (if not addressed quickly, bowel necrosis rapidly ensues
273
the incidence of malrotation is not known because the _____ of people with this disorder are _____
majority asymptomatic (may occur in as many as 1% of the population)
274
incidence of malrotation is increased in children with what symptoms
heterotaxy trisomies 13, 18, 21 Marfan Prune-belly
275
what are some of the most common anatomic abnormalities associated with malrotation
diaphragmatic hernia duodenal web abdominal wall defects such as gastroschisis, omphalocele
276
when is malrotation diagnosed
60% before age 1 75% before age 5 however, malrotation and volvulus may both present in adulthood
277
presentation of malrotation in pediatric patient
no symptoms intermittent symptoms acute presentation vomiting abd pain FTT
278
most common presentation of malrotation is that of
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
symptoms of a volvulus
bilious emesis initially appear non-toxic becomes ill appearing in the presence of ischemic bowel develop a firm, distended abdomen hypovolemia shock death
280
diagnostics of malrotation/volvulus
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
double bubble sign on radiograph indicates
duodenal obstruction
282
gasless abdomen may be appreciated in
volvulus
283
How is malrotation and volvulus fixed
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
surgical care of pt with volvulus repair
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
what other organ sometimes gets removed during a Lad procedure and why
appendix because its on the L side which may confuse future health care providers causing them to miss an appendicitis
286
prognosis for volvulus after Ladd procedure
obstruction from adhesions outcomes variable from complete recovery to intestinal failure to death
287
Prognosis for pt with malrotation
excellent | resume normal daily activities
288
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
pyloric stenosis
289
what gender is pyloric stenosis more prevalent in
first born males some evidence of genetic association
290
maternal risk factors for pyloric stenosis are
``` hyperthyroidism quinolone antibiotic use smoking increased BMI intranasal decongestant use ```
291
what is the hallmark symptoms of pyloric stenosis
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
how does pyloric stenosis progress
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
olive sign think...
pyloric stenosis
294
spasmodic contraction of the pylorus with poorly coordinated gastric emptying observed in what population what is done
pylorospasm neonates resolves spontaneously with time
295
Gastroesophageal reflux (GER) is on the differential with pyloric stenosis. what same and different symptom might you see
may also have weight loss | projectile vomiting is uncommon
296
what does HPS stand for
hypertrophic pyloric stenosis
297
what electrolyte imbalances might be seen in HPS (hypertrophic pyloric stenosis) what about pH what else might be elevated
hypochloremic hypokalemic metabolic alkalosis unconjugated hyperbilirubinemia r/t transient impairment of glucuronyl transferase activity
298
how is pyloric US confirmed
abdominal US
299
what is a string sign
elongated and thickened pyloric channel seen in pyloric stenosis
300
what is a beak sign
filling of the proximal pylorus seen in pyloric stenosis
301
what is a double shoulder sign
thickened pylorus compressing the antrum of the stomach (seen in pyloric stenosis)
302
how is pyloric stenosis fixed?
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
bicarb levels should be less than _____mEq/L for infants prior to surgery. Why?
30 | because infants with metabolic alkalosis are at high risk for resp depression when recovering from anesthesia
304
what is the pyloric regimen
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
when is the pyloric regimen more commonly prescribed
in infants with persistent emesis in the postop period
306
postop vomiting is due to
gastric distension and atony
307
majority of infants tolerate ad lib feeds post op. What is this?
volume of at least 60mL within 24-48 hrs of the operation
308
persistent vomiting beyond 72-96 hours postoperative pyloric stenosis repair may occur in cases of
incomplete pyloromyotomy UGI series may be valuable to determine
309
pain control for postoperative pyloric stenosis
tylenol (usually sufficient bc area is infiltrated with local anesthetic)
310
monitor for what complications after repair of pyloric stenosis
surgical wound infection incisional hernias life threatening complications include gastric mucosal tears duodenal perforation
311
what should be closely monitored in infants post op after pyloric stenosis repair
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
what qualifies infant for discharge after a pyloric stenosis repair
when they are tolerating 60mL for at least 2 consecutive feedings without emesis
313
education to give caregiver for discharge after pyloric stenosis repair
caregiver should return for fever greater than 101.5 rectal, persistent emesis, abd pain or any signs or symptoms of wound infection
314
when does the pt need to follow up after a pyloric stenosis repair
follow up with PCP in 1 week for wound evaluation and weight check and surgeon in 2 weeks
315
partial or complete obstruction resulting from an anatomic cause, intraluminal or extraluminal.
mechanical
316
intraluminal or extraluminal cause of mechanical obstruction. swallowed coin
intraluminal
317
intraluminal or extraluminal cause of mechanical obstruction. hernia
extraluminal
318
intraluminal or extraluminal cause of mechanical obstruction. intussusception
intraluminal
319
intraluminal or extraluminal cause of mechanical obstruction. adhesion
extraluminal
320
what is the physiologic response to an partial obstruction
enhances secretion and motility proximal to the level of obstruction in an attempt to push the offending obstruction open and overcome the blockage
321
due to the physiologic response to a partial obstruction at the level of an ostomy or distal bowel can present with both
diarrhea like increased output and proximal distention, nausea and vomiting
322
consists of chewing food, allowing it to mix with oral secretions and liquid ingestions
mixing
323
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)
Propulsion
324
first part of the small intestine is commonly known as the
duodenum
325
the remaining small intestine and the first portion of the colon is known as the
midgut
326
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
hindgut
327
what organs and glands play a important role in GI physiology
liver gallbladder biliary tree pancreas
328
what sphincter prevents reflux
upper esophageal sphincter
329
what kind of vomiting should never be accepted as a normal type of vomiting
bilious
330
Diagnostic abdominal labs
CBC with diff UA UPT
331
diagnostic abdominal labs in setting of dehydration secondary to vomiting or diarrhea or suspicion of kidney disease
electrolytes BUN creatinine
332
labs for liver
LFTs
333
labs for pancreas
amylase | lipase
334
fecal studies in diarrhea
stool osmolarity fecal leukocytes fecal occult blood ova and parasites (O&P)
335
diarrhea should be ____ to serum. if its not, what might have happened
isotonic improper collecting - scooping poop from toilet water faking diarrhea...pouring water into poop to make it look like diarrhea
336
fecal leukocytes are elevated in
acute colitis (particularly bacterial origin)
337
gross blood in stool is almost always indicative of
colitis
338
fecal occult blood tends to indicate
colitis or a bacterial toxin affecting small bowel
339
O& P is extremely helpful in what scenario
potential ingestion of contaminated water (very high specificity)
340
stool culture can evaluate for
shigella C diff Norovirus Rotavirus
341
plain abd film positions
supine (most common) upright in front of the radiographic plate left lateral decubitus (left side down) cross table views
342
stool has a characteristic appearance on an x ray from
the gas bubbles inside the stool
343
what x ray and what views/technique is best for looking for a bowel perforation
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
which view is inferior for detecting bowel perforation but can sometimes show free gas along the anterior abdominal wall
cross table lateral view
345
which x ray view is the least sensitive for bowel perforation
standard supine view (can show the falciform ligament or bowel outline, suggesting free gas
346
bacterial causes of gastroenteritis
E. Coli, staph, Campylobacter, salmonella, shigella, yersinia, C. Diff
347
common viral causes of gastroenteritis
rotavirus, adenovirus, coronavirus, parvovirus
348
what causes of gastroenteritis need abx
c.diff shigella salmonella h. pylori
349
which causes of gastroenteritis is most likely to cause sepsis in < 3mos
shigella | salmonella
350
main cause of dysentery
shigella
351
gastroenteritis acquired by
via fecal-oral route, transmitted person-to-person, through contaminated food or water
352
s/s of gastroenteritis
fever, vomiting, diarrhea (watery, > 3x/day), recent antibiotic use (C. Diff), travel (especially internationally), dehydration (varying severity)
353
treatment of gastroenteritis
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
s/s neoplasm
weight loss, anorexia, fever, night sweats, easy bruising/bleeding.
355
bilious emesis, alcoholic stools, liver disease - jaundice, pale skin, cachexia, FTT, abdominal wall hernias - observe with vagal/bearing down
Bowel obstruction
356
what lab includes creatinine and BUN
chemistry
357
Benign masses think
assess for bowel obstruction, appendicitis, perforation, sepsis, ectopic pregnancy, torsion
358
what do you do for malignant tumors
admission, oncologic and surgical evaluation
359
what symptoms for milk protein allergy
blood in stool diarrhea can cause enterocolitis
360
IBD is most common in
Most common in >10 yo children
361
which IBD affects only the colon
UC
362
which IBD involves any part of the gut
CD
363
IBD is most common in what populations
jewish
364
IBD is linked to what antigen
human leukocyte antigen (HLA) subtypes
365
smoking _____ severity of CD and ______ risk for UC
Smoking INCREASES severity of CD and DECREASES the risk for UC
366
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 ```
Colitis
367
symptoms of Toxic megacolon
``` Fever Abdominal distension and pain Massively dilated colon Anemia Low serum albumin (fecal protein loss) ```
368
Subtle symptoms ``` Loss of appetite Crampy postprandial pain Poor growth Delayed puberty Fever Anemia Lethargy ```
Crohns
369
skip lesions associated with
crohns
370
labs for IBD
``` 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
to get a true diagnosis for IBD
endoscopy, biopsy and histology to differentiate CD from UC
372
fistulas are more associated with what IBD
Crohns
373
Crohns or UC? malaise fever weight loss
common in Crohns sometimes UC
374
Crohns or UC? rectal bleeding
usual in UC sometimes CD
375
Crohns or UC? abd mass
common in CD rare in UC
376
Crohns or UC? abd pain
both
377
Crohns or UC? perianal disease
Common in CD rare in UC
378
ileal involvement Crohns or UC?
CD
379
Crohns or UC? strictures
common in CD rare in UC
380
Crohns or UC? fistula
common in CD
381
Crohns or UC? skip lesions
CD
382
Crohns or UC? | transmural involvement
CD
383
Crohns or UC? crypt abscesses
UC
384
Crohns or UC? intestinal granulomas
CD
385
Crohns or UC? risk of cancer
increased in CD greatly increased in UC
386
Crohns or UC? | erythema nodosum
Common in CD
387
Crohns or UC? | mouth ulceration
CD
388
Crohns or UC? osteopenia at onset
CD
389
Crohns or UC? autoimmune hepatitis
UC
390
Crohns or UC? sclerosing cholangitis
UC
391
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.
Celiac disease
392
celiac disease | commonly seen in
Seen in type 1 diabetics, thyroiditis, turners syndrome, and trisomy 21.
393
PUD treatment
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
``` Diarrhea Pubertal delay Failure to thrive Abdominal bloating Irritability Decreased appetite Ascites (from hypoproteinemia) ```
Celiac
395
celiac disease monitoring
Careful monitoring of child’s growth curve and evaluation for reduced sub Q fat and abdominal distension are crucial.
396
celiac should be considered in any child with
Chronic abdominal complaints Short stature Poor weight gain Delayed puberty
397
extraintestinal manifestations for celiac disease include
``` Osteopenia Arthritis Arthralgias Ataxia Dental enamel defects Elevated liver enzymes Dermatitis Herpetiformis Erythema nodosum ```
398
lab and imaging for celiac
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
treatment of celiac
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
risk factors for H. Pylori
Low socioeconomic status Poor sanitation Highest in developing countries
401
drugs increase risk for PUD
NSAIDS (ASA) Tobacco use Bisphosphonates Potassium supplements
402
risk factors for PUD
``` drugs family history sepsis head trauma brain injury hypotension ```
403
clinical manifestations of PUD
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
alarm symptoms of PUD
``` Weight loss Hematemesis Melena , heme positive stools Chronic vomiting Microcytic anemia Nocturnal pain ```
405
Laboratory and imaging studies: | PUD
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
currant jelly stools
intussusception
407
most common reason for abd surgery in children in US
appendicitis
408
Appendicitis can occur at any age but most common
10-12 yrs and males as opposed to females
409
fever (more common with perforation), decreased activity level, periumbilical pain with progression to RLQ pain, accompanied by anorexia, and eventually diarrhea
appendicitis
410
McBurney Point and rebound tenderness r/t
peritonitis associated with perforation of appendix
411
where is McBurney Point
R side of abdomen 1/3 of distance from anterior superior iliac spine to the umbilicus
412
what is psoas sign
appendicitis Concomitant irritation of the psoas muscle and associated pain will be present with passive extension of flexion of the RLE
413
Obturator sign
appendicitis If appendix lies on the obturator internus muscle, pain may be present with internal rotation of the right thigh
414
Rovsing sign
appendicitis Pain reported in the RLQ with palpation of the LLQ
415
diagnostic labs for appendicitis
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
Radiologic diagnostic for appendicitis
US
417
what is an US for appendicitis limited by
appendix position bowel gas pattern obesity (not recommended if BMI >25 in adults) operator experience
418
what is the most sensitive test for appendicitis
CT
419
Acute appendicitis (non-perforated) treat
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
treatment of perforated appenicitis
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
esophagus and trachea form within close proximity, can occur with VACTERL syndrome. communicating fistula from esophagus to trachea
Tracheoesophageal fistula
422
en utero polyhydramnios (excessive amniotic fluid), small/absent gastric bubble on US, newborn signs excessive salivation, choking, difficulty swallowing, cyanotic/resp distress with feedings
Tracheoesophageal fistula:
423
diagnostic for transesophageal fistula
placement of OG tube + xray (will see it coil in the esophagus or stop), gas-less stomach on KUB, tracheobronchoscopy
424
treatment for | transesophageal fistula
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
complications in | transesophageal fistula
esophageal stricture, esophageal dysmotility, GERD, tracheomalacia, vocal cord dysfunction
426
congenitally interrupted esophagus
Esophageal atresia
427
gassless abdomen on CXR can also suggest an
Esophageal atresia with proximal TEF
428
chronic reflux can develop into
Barrett esophagus
429
diarrhea < = 14 days with > 3 stools per day is what type
acute diarrhea
430
diarrhea > 14 days with > 3 stools per day is what
persistent diarrhea
431
diarrhea > 30 days > 3 stools per day
chronic diarrhea
432
Gastroenteritis lab to look at electrolytes
BMP
433
what labs for gastroenteritis
BMP CBC with diff stool cultures O &P
434
first line therapy for travelers diarrhea in children is
Azithromycin
435
Antidiarrheal medications often contain what? contributes to?
ASA Reye syndrome
436
how to calculate hourly rates of maintenance fluids
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
how to calculate daily maintenance fluids
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
Caloric calculation for enteral feeds
Breast milk---> 20kcals/oz Formulas--->20kcals/oz (can fortify) 1oz = 30mL Average baby needs---> 100kcal/kg/day (variable)
439
In FTT there are specific growth charts for what genetic conditions
There are specific growth charts for genetic conditions such as Down syndrome and Turner syndrome that should be used accordingly.
440
wasting
Malnutrition initially results in wasting (deficiency in weight gain)
441
stunting
(deficiency in linear growth) that occurs after months of malnutrition, and head circumference is spared except with chronic, severe malnutrition.
442
Short stature with preserved weight =
endocrine etiology
443
The distinct difference between FTT and malnutrition is that FTT does not
provide an assessment of the severity, duration, or mechanism for poor growth that characterizes the child’s nutritional status.
444
environmental causes of FTT
``` Emotional deprivation Rumination Child maltreatment Maternal depression Poverty Poor feeding techniques Improper formula preparation Improper mealtime environment Unusual parental nutritional beliefs ```
445
GI causes of FTT
Cystic fibrosis and other causes of pancreatic insufficiency Celiac disease Other malabsorption syndromes Gastrointestinal reflux
446
congenital /anatomic
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
infectious causes of FTT
HIV Tuberculosis Hepatitis UTI, chronic sinusitis, parasitic infection
448
metabolic causes of FTT
THyroid disease Adrenal or pituitary disease Aminoaciduria, organic aciduria Galactosemia
449
Neurologic causes of FTT
``` Cerebral palsy Hypothalamic and other CNS tumors Hypotonia syndromes Neuromuscular diseases Degenerative and storage diseases ```
450
renal causes of FTT
Chronic renal failure Renal tubular acidosis UTI
451
hematologic causes FTT
Sickle cell disease | Iron deficiency anemia
452
initial tests to evaluate FTT
CBC, iron deficiency anemia, lead toxicity, UA, urine culture, serum electrolytes to assess renal.
453
FTT kids have more occurances of
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
malnutrition-infection cycle:
Recurrent infections exacerbate malnutrition, leading to greater susceptibility to infection.
455
Re-feeding syndrome
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
children who live in psychological deprivation develop short stature with or without concomitant FTT or delayed puberty, a syndrome called
Psychosocial Short Stature
457
Signs and symptoms: Psychosocial Short Stature
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
% of the LBM of infants and malnourished patients is water.
70
459
s/s of dehydration
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
labs to order in dehydration
BUN (can increase with dehydration) bicarb levels blood pH Na anion gap (elevated in metabolic acidosis)
461
what lab indicates type of hydration
Na
462
dehydration type most common in Na 135-145
isonatremic most common d/t gastroenteritis
463
dehydration type most common in Na >145
hypernatremic d/t balance shifts and lead loss of brain hydration leads to shear force injuries such as subdural or hemorrhage
464
dehydration type most common in Na <135 present in
hyponatremic fluid loss d/t diarrhea/sweat present with seizures, noncardiogenic edema, resp distress or cerebral herniation
465
oral rehydration pt gets
15mL/kg/hour or 60mL/kg/4hrs
466
sip volume per 5 min in oral dehydration
< 10kg 1mL/kg 10kg 10mL For every additional 5kg, add: 5mL to a maximum of 50mL
467
IV rehydration
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
tachycardia is present in what types of dehydration
moderate and severe
469
orthostatic hypotension is present in what type of dehydration
moderate
470
hypotension is present in what type of dehydration
severe
471
fontanelle is sunken in what type of dehydration
severe
472
respirations are deep in what type of dehydration
moderate
473
respirations are deep and rapid in what type of dehydration
severe
474
oliguria is in what type of dehydration
moderate
475
anuria and severe oliguria is seen in what type of dehydration
severe
476
what test greatest benefit is ability to distinguish blood vessels from ducts.
US dobbler B mode
477
standard of care to diagnose pyloric stenosis and intussusception or an obstructed, pus filled appendix.
US
478
test Extremely useful in evaluating the liver, biliary tree, and often head of pancreas.
US
479
reserved for either treatment or diagnostic uncertainty when the US cannot definitively diagnose pyloric stenosis or intussusception.
GI fluoroscopy
480
safest contrast agent Safest with lowest sensitivity and specificity Can be used to reduce intussusceptions.
air
481
contrast agent Good sensitivity and specificity Easily evacuate or excrete iodinated agents.
iodine based
482
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
Barium
483
Esophagram or gastrogram | Investigate anatomy for perforation and obstruction
``` Upper GI (imaging includes from swallowing to sm bowel) fluoroscopy ```
484
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.
lower GI fluoroscopy
485
CT with contrast helps identify
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
reasons to use MRI
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
pancratitis s/s
``` 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
pancreatitis diagnostics
``` Elevated amylase & lipase o CRP o Hypocalcemia o Transient hypoglycemia o Hyperbilirubinemia o Increased LFTs o Hypoalbuminemia o US o CT ```
489
treatment pancreatitis
``` 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
liver and renal labs
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
Hypocalcemia (<9mg/dL) associated with
DiGeorge syndrome
492
s/s hypocalcemia
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
treatment of sympomatic hypocalcemia, acute
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
chronic hypocalcemia, subacute or chronic repletion
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
Hypercalcemia (serum calcium >10 mg/dL) associated with
williams syndrome
496
severe hypercalcemia s/s
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
Hypercalcemia can result in
polyuria, renal calculi, and renal tubular dysfunction
498
treatment of hypercalcemia
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
chloride has a direct relationship with
sodium - if sodium is elevated, chloride is elevated
500
chloride has an inverse relationship with
bicarb
501
Hypochloremia is serum chloride of
<97 mmol/L
502
Hypochloremia is associated with
Bartter syndrome, CF, Bulimia nervosa, diuretic usage, removal of gastric secretions via NGT, and metabolic alkalosis
503
hypochloremia associated with metabolic alkalosis may (Rare) exhibit
arrhythmias, decreased respiratory effort, seizures in severe states
504
s/s hypochloremia
When associated with volume depletion or dehydration, may exhibit thirst, lethargy, tachycardia, tachypnea, and delayed cap refill
505
treatment hypochloremia
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
lab for hyperchloremia
>108
507
presentation of hyperchloremia
often asymptomatic | may have Kussmaul respirations (especially in DKA); possible neurologic symptoms include lethargy, HA, and confusion
508
treatment of hyperchloremia
Address underlying cause and treat associated acidosis | Consider sodium bicarbonate IV if severe metabolic acidosis
509
hypomag lab value
<1.7
510
presentation of hypomag
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
treat hypomag
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
hypermag lab values
>2.2
513
presentation of hypermag
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
treat hypermag
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
hypophosphatemia lab
<2.5
516
presentation happens at severe level <1
``` 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
treatment of hypophosphatemia
Parental repletion is indicated with potassium or sodium phosphate Subacute or gradual onset of symptoms Replace with potassium or sodium phosphate enteral supplements
518
Hyperphosphatemia (serum phosphorus
>4.1 mg/dL)
519
s/s hyperphosphatemia
``` Altered mental status Tetany, weakness, paresthesias Fatigue Cramping Laryngospasm Neuromuscular irritability Cardiac arrhythmias Chronic hyperphosphatemia may result in calcium deposits in soft tissue ```
520
treatment hyperphosphatemia
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
hypokalemia
(serum potassium <3.7 mEq/L)
522
presentation hypok
``` 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
treat hypo k
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
hyper k levels | what level is a medical emergency
(serum potassium > 5.2 mEq/L) ** > 7mEq/L is a medical emergency**
525
presentation of hyper k
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
tretment hyper k
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
hyponatremia
<135
528
symptoms hyponatremia
``` Irritability N/V Poor feeding Lethargy Seizures Coma ```
529
causes hyponatremia
increased free water intake, excess water retention, increased Na losses, or combination
530
hyponatremia that develops over hours to days (<48hr
acute | more likely to produce cerebral edema and changes in neuro status
531
treatment of hyponatremia
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
hypernatremia
>145
533
etiology of hypernatremia
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
symptoms of hypernatremia
``` 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
mgmt of hypernatremia
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
toxic syndrome of what? N/V, pallor, delayed jaundice-hepatic failure (72-96 hr)
acetaminophen
537
toxic syndrome of what? Tachycardia, HTN, hyperthermia, psychosis and paranoia, seizures, mydriasis, diaphoresis, piloerection, aggressive behavior
Amphetamine, cocaine, and sympathomimetics
538
toxic syndrome of what? Mania, delirium, fever, red dry skin, dry mouth, tachycardia, mydriasis, urinary retention
Anticholinergics
539
toxic syndrome of what? HA, dizziness, coma, other symptoms affected
carbon monoxide
540
toxic syndrome of what? Coma, convulsions, hyperpnea, bitter almond odor
cyanide
541
toxic syndrome of what? Metabolic acidosis, hyperosmolarity, hypocalcemia, oxalate crystalluria
Ethylene glycol (antifreeze)
542
toxic syndrome of what? Vomiting (bloody), diarrhea, hypotension, hepatic failure, leukocytosis,hyperglycemia, radiopaque pills on KUB, late intestinal stricture, Yersinia sepsis
Iron
543
toxic syndrome of what? Coma, respiratory depression, hypotension, pinpoint pupils, bradycardia
Narcotics
544
toxic syndrome of what? Miosis, salivation, urination, diaphoresis, lacrimation, bronchospasm (bronchorrhea), muscle weakness and fasciculations, emesis, defecation, coma, confusion, pulmonary edema, bradycardia
Cholinergics (organophosphates, nicotine)
545
toxic syndrome of what? Tachypnea, fever, lethargy, coma, vomiting, diaphoresis, alkalosis (early), acidosis (late)
Salicylates
546
toxic syndrome of what? Coma, convulsions, mydriasis, hyperreflexia, arrhythmia (prolonged QT interval), cardiac arrest, shock
Cyclic antidepressants
547
A poisoned child can exhibit any one of six basic clinical patterns:
``` Coma Toxicity Metabolic acidosis Heart rhythm aberrations GI symptoms Seizures ```
548
used for gastric decontamination in toxicity/overdose/ingestion
``` Syrup of Ipecac Gastric Lavage Activated Charcoal Cathartics Whole-Bowel Irrigation ```
549
contraindications to syrup of ipecac
``` Age less than 6 months Impaired gag reflex Impending coma or seizures Hydrocarbon Ingestion Caustic Ingestions (acid, alkalis) Ingestion of sharp foreign bodies ```
550
criterion to use gastric lavage
ingestion of potentially life threatening poison; 2. procedure done within one hour of ingestion
551
complications of gastric lavage
aspiration pneumonia, laryngospasm, tension pneumothorax, tachycardia, atrial/ventricular ectopy, mechanical injury to the GI tract, hyper/hyponatremia, hypothermia
552
contraindications for gastric lavage
ingestion of caustics, ingestion of hydrocarbons with high risk for aspirations, unprotected airway, in stable patient, or at risk for GI bleed
553
Most commonly used and most effective method of gastric | decontamination
activated charcoal
554
substances not absorbed well by activated charcoal
alcohols, acids, alkalis, hydrocarbons, iron, | potassium, magnesium, sodium, lithium salts
555
when should activated charcoal be given
within 1 hr of ingestion
556
adverse reactions to activated charcoal
vomiting constipation obstruction aspiration all rare
557
contraindications to using activated charcoal
unprotected airway, hydrocarbon and | caustic ingestion, non-intact GI tract
558
Increase GI transit time of ingested toxins | No evidence-based indications for routine use
cathartics
559
names of cathartics used in ingestion
Sorbitol, magnesium citrate, and magnesium sulfate
560
contraindications for using cathartics in ingestion
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
used in whole bowel irrigation to rapidly evacuates contents of GI tract within 2-6hrs post ingestion
PEG
562
indications for using PEG in ingestion (whole bowel irrigation)
ingestion of adult iron tablets, heavy metals, lithium, sustained release drug formulations
563
contraindications for using PEG in ingestion (whole bowel irrigation)
unprotected airway,hemodynamic instability, Ileus, bowel obstruction/ perforation, intractable vomiting, GI hemorrhage
564
early manifestations of tylenol ingestion
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
adults when to seek emergent evaluation after tylenol overdose
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
age less than 6 for when to get med attention after tylenol overdose
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
antidote for tylenol overdose
Antidote N-acetylcysteine (NAC)
568
mucomyst is most effective if given within ___ hrs post ingestion
8
569
Food and Drug Administration (FDA) | tylenol overdose Treatment Regimens:
72 hour oral course (Acetadote) | 21 hour IV course (mucomyst)
570
Children metabolize ethanol at a rate of
10-25 mg/dL/hr
571
alcohol ingestion in pediatrics symptoms
facial flushing, vomiting, diaphoresis, respiratory depression, seizures, hypotension, hypothermia, and hypoglycemia
572
Estimated pediatric lethal dose alcohol
3.8mL/k 100% alcohol
573
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
iron overdose
574
toxic dose iron
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
management of toxic dose of iron
``` 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
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
salicylate tox
577
mgmt of Salicylate tox
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
Recreational use of inhaled hydrocarbons is a significant health issue in pediatrics
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
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
Hydrocarbons/Kerosene
580
``` 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: ```
Hydrocarbons/Kerosene | inhaled
581
management of care in Hydrocarbons/Kerosene
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
``` Arrhythmias Often tachyarrhythmias; possibly fatal Impaired cardiac conduction Nausea and vomiting (often the first sign) Dizziness, HA, mental disturbances Shock ```
digoxin tox
583
monitor and treat dig tox
``` 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
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
CCB tox symptoms
585
mgmt and treat CCB tox
``` 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
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
BB tox
587
evaluate and treat BB tox
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
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
TCAs
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eval and mgmt TCA tox
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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