test 3 material Flashcards
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
malnutrition
what is acute malnutrition time frame
less than 3 months
what is chronic malnutrition time frame
greater than 3 months
what is the continental divide for secretions in the nonobstructed GI tract
Ligament of Treitz
Bleeding sources proximal to the Ligament of Treitz can present with ______
hematemesis
distal will rarely present with hematemesis
Bleeding sources distal to the Ligament of Treitz will present with
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
Brisk proximal to the ligament of treitz bleeds can also present with
melena or frank blood per rectum
GI bleeding is common or uncommon in the pediatric population
uncommon
UGI bleeds differentials
lesions of the GI mucosa
esophageal varices secondary to liver disease
infectious colitis
what is the most common cause of colonic bleeding worldwide
infectious colitis
in countries with good water supplies, what accounts for the majority of lower GI bleeds
colon polyps allergic colitis anal fissures UC (ulcerative colitis) CD (Crohns Disease)
lower GI bleeding
infant who is fed cows milk or soy based formula
may have allergic colitis
lower GI bleeding
in someone with recent antibiotic therapy
C-Diff toxin induced colitis
history of dry heaves followed by hematemesis or melena suggests
Mallory-Weiss tear
Recent illness with GI bleeding may lead you to suspect
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
Ingestion of NSAIDS with gi bleed may lead you to
gastritis
duodenitis
ileal lesion
R colonic lesions
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
liver disease history - inherited A1 antitrypsin deficiency and hep B may be transmitted vertically at birth
IBD
intestinal cancer
The complaint of heartburn in older child or adolescent or a BRUE like symptom in in infant with GI bleed suggests
UGI source such as
esophagitis
gastritis
ulcer
urgency to defecate or tenesmus (incomplete defacation)
GI bleed
colitis
delayed passage of meconium or constipation in infancy can be symptoms of
CF or HD (bollick 440)
Being on abx and no enteral nutrition will have what complication
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
pertinent physical exam findings for GI bleeding
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
palpable moveable rectal mass might identify
polyps
blood in vomit or stool in the newborn may be from
the mother ingesting commercial dyes (#2 and #3), blueberries, beets, bismuth) - > red tinted or colored stool but may look like blood
what test should be considered in pt presenting with significant UGI bleeding
urgent upper endoscopy
only after stabilized
what test should be considered in pt with bright red lower GI bleeding
Conoloscopy
only after stabilized
GI bleed, pt hemodynamically unstable what can you adminishter
NS
LR
PRBCs
pt kept NPO
An endoscopy allows for
visualization
cauterization
biopsy
test for H. Pylori
med used in management of bleeding esophageal varices, why
octreotide - decrease CVP (central venous pressure) before endoscopic intervention
if variceal bleeding is not controlled by endoscopic and/or tamponade intervention what should be considered
Transjugular intrahepatic portosystemic shunting (TIPS)
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
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
polyps are usually removed with
snare electrocautery during a colonoscopy
GI bleeding from Henoch -Schonlein purpura (HSP) and HUS usually resolves with
resolution of the disorders
patients with UGI bleeds when can the diet resume
within 24 hours
what are the UGI bleeds discharged on
PPI for gastritis
or B-Blocker (propanolol) for esophageal varices
close outpatient follow up by GI
discharge of patients with lower GI bleed depends on
etiology of the bleeding
underlying chronic illness
response to therapy
infant upper GI bleed think
hemorrhagic gastritis
stress ulcer
vascular malformation
reflux esophagitis
infant lower GI bleed think
infectious colitis midgut volvulus anal fissures necrotizing enterocolitis intussusception milk protein allergy hirschsprung disease lymphonodular hyperplasia
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
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
upper Gi bleed for older child and adolescent think
hemorrhagic gastritis stress ulcer gastric/duodenal ulcer esophageal varices mallory-weiss tear epistaxis reflux esophagitis
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
what antibiotic does the book mention can look like blood in stool
cefdinir
what test can tell you if its blood or something else
occult stool
vomiting blood is always ________ to the ligament of treitz
proximal
when upper GI bleeding is suspected, what may be placed and why
a ng and gastric contents aspirated for evidence of recent bleeding
what test is used in newborns to determine whether it is fetal or maternal blood present in stool
apt test (alkali denaturation test)
hematemesis in newborn
blood found in stomach on lavage
peptic disease
hematemesis or rectal bleeding in newborn
APT shows adult hemoglobin is present
cracked maternal nipples
ingested maternal blood
hematemesis or rectal bleeding in newborn
Bruising
coagulopathy
streaks of bloody mucus in stool in newborn
eosinophils in feces and in rectal mucosa
allergic colitis
rectal bleeding in newborn
sick infant with tender and distended abdomen
necrotizing enterocolitis
hematemesis in newborn
cystic mass in abdomen on imaging study
Duplication cyst
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)
infancy to older than 2 yrs old hematemesis rectal bleeding possible epigastric pain coffee ground emesis
peptic disease
infancy to > 2 yrs old
hematemesis
history or evidence of liver disease
esophageal varices
infancy to 2 yrs old rectal bleeding crampy pain abd distension abd mass
intussusception
infancy to > 2 yrs old
rectal bleeding
massive bright red bleeding
no pain
meckel diverticulum
infancy to >2 yrs old
rectal bleeding
bloody diarrhea
fever
bacterial enteritis
infancy to > 2 yrs old hematemesis rectal bleeding possible epigastric pain coffee ground emesis
NSAID injury
older than 2 rectal bleeding usually crampy pain poor weight gain diarrhea
inflammatory bowel disease
> 2 yrs old
rectal bleeding
history of antibiotic use
bloody diarrhea
psueudomembranous colitis
> 2 yrs old
rectal bleeding
painless
bright red blood in stool - not massive
juvenile polyp
> 2 yrs old
rectal bleeding
streaks of blood in stool
no other symptoms
Nodular lymphoid hyperplasia
> 2 yrs old
hematemesis
bright red or coffee ground emesis
follows retching
Mallory-Weiss syndrome
>2 yrs old rectal bleeding thrombocytopenia anemia uremia
Hemolytic uremic syndrome (HUS)
> 2 yrs old
rectal bleeding
dilated external veins
blood with wiping
hemorrhoids
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
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
tests to evaluate rectal bleeding with formed stools
external and digital rectal examination sigmoidoscopy or colonoscopy meckel scan mesenteric arteriogram video capsule endoscopy
evaluation for hematemesis if endoscopy is not available
barium upper GI series
Evaluation of bleeding with pain and vomiting (Bowel obstruction)
abd x ray series
pneumatic or contrast enema
upper GI series
what scan is used to detect a meckel diverticulum
Meckel scan
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
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)
Blood in the diaper or toilet may be coming from the
urinary tract, vagina, or severe
diaper rash.
most common intra abdominal tumors are
neuroblastoma
Wilms tumor
2/3s of abdominal masses are due to
organomegaly
a history of bilious emesis or encopresis can lead to an assessment of
bowel obstruction
urinary excretion of ______ can lead to cola colored urine
bile salts
can present with acholic stools (pale)
obstruction of the biliary system
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
Jaundice can indicate _____ disease
liver
Pale skin can indicate
anemia
flushed rosy skin can be present in
sepsis
classic exanthems (diffuse rash) can be present with
viral infections
general appearance is ill-appearing, particularly with cachexia or FTT, _____ or _____ may be the cause
chronic infections
malignant disease
Masses in the RUQ most often involve the
liver
gallbladder
biliary tree
Epigastric masses can include both
epigastric hernias
diastasis recti
LUQ masses most often involve the
stomach
spleen
adrenal gland
kidney
Right and Left lower quadrant masses may be from
ovarian and fallopian processes or the intestines in orgin
suprapubic masses are most commonly
genitourinary in nature
Abd wall masses are either
superficial to the muscular layers or
their movement is coupled with the contraction of the abdominal musculature
_________ are most often observed when a very small child cries and it pops out
abd wall hernias
immobile masses are either
invasive tumors
masses that arise from the retroperitoneal organs
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)
Firmness, hardness, irregularity suggest either
tumor or
desmoplasia (scar)
Smoothness to a mass suggests an
encapsulated mass
Tympany indicates
gas such as a hollow viscus
Dullness indicates
fluid or a solid mass
A hernia is diagnosed with
physical exam
what kind of hematomas secondary to trauma are difficult to diagnose and why
rectus hematomas - hidden from view by rectus sheath
what kind of soft tissue tumors can be diagnosed on physical exam
fibromas and lipoma
fixed abd mass related to mesenteric fibromatosis or retroperitoneal sarcoma is diagnosed by
CT or MRI bc bowel gas often obscures retroperitoneal ultrasonography
in infants crying can lead to an ingestion of air ->
gastric distention which can cause vagal symptoms or resp sequelae
what makes gastric distension relatively easy to diagnose and treat
tympanic LUQ
response to NG
ingestion of hair and roughage can result in
bezoars
what 3 things can present with acute gastric distension with the inability to pass an NGT
congenital duplications
gastric tumors
gastric torsion
a exceedingly common disorder
presents with abd discomfort and a palpable mass
constipation
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)
mass in younger patients differential
intussusception duplications mesenteric cysts meconium pseudocysts bowel atresia malrotation with volvulus can occasionally present with an abd mass
bowel tumors that may present with a palpable mass
carcinoid
lymphoma
adenocarcinoma
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
multiple renal cysts can by caused by
polycystic kidney disease
multicystic dysplastic kidney disease
a large fluid filled cyst is present at the hilum, it can represent a
dilated renal pelvis with or without associate dyroureter
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
diffuse unilateral renal swelling can occur from
renal vein thrombosis
what type of tumor can present as a unilateral mass (kidney)
Wilms tumor
adrenal masses are most commonly ____ in origin
neoplastic
what is the most common pediatric adrenal tumor
neuroblastoma
what other endocrine tumor can occasionally be identified but rarely of sufficient size to produce a palpable mass
pheochromocytoma
in females _____ masses are extremely common
gynecologic
__________ cysts are a physiologic requirement for menstruation
small ovarian cysts (follicular)
benign ovarian masses include
dermoid cysts
mature teratomas
immature teratomas
germ cell tumors
what can occasionally produce a very edematous and swollen ovary that may occasionally present as a mass
torsion
the most common fallopian and uterine masses are
pregnancy (ectopic or intrauterine)
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
hematocolpos
the vagina is pooled with menstrual blood due to multiple factors leading to the blockage of menstrual blood flow
hydrometrocolpos
expanded fluid filled vaginal cavity with associated distention of the uterine cavity
hydrosalpinx
fallopian tube thats blocked with watery fluid
an enlarged spleen should suggest ____ or ____ until proven otherwise
hematologic disease
malignancy
splenomegaly - hematologic disease assoiciations
hereditary hemolytic anemias such as spherocytosis or elliptocytosis
sickle cell disease
hematologic malignancies associated with splenomegaly
leukemias
lymphomas
viral infections can be associated with splenomegaly
acute viral infection with
Epstein Barr virus (EBV) or
cytomegalovirus (CMV)
rheumatologic disease associated with splenomegaly
systemic lupus erythematosus
Langerhans cell histiocytosis
storage diseases associated with splenomegaly
Niemann-Pick
Gaucher disease
can cause significant hepatic edema and enlarged tender liver
Acute viral hepatitis
autoimmune hepatitis
metabolic disorders that can present with painless hepatomegaly
glycogen storage diseases
Wilson disease
congenital disorder that can cause painless hepatomegaly
Congenital hepatic fibrosis
cyst that can cause hepatomegaly
simple or biliary cysts
simple cyst in liver or polycystic liver disease can be diagnosed with
US
cysts that can be present anywhere along the biliary tree
biliary cysts or choledochal cysts
solid hepatic masses of vascular origin
hemangioma
lymphovascular malformations
solid hepatic masses of parenchymal origin
focal nodular hyperplasia
adenoma
neoplasia
The most common tumors in the younger patients (liver)
hepatoblastoma
most common liver tumors in the older pediatric patient
hepatocellular carcinoma
can produce diffuse neoplastic infiltration of the liver
lymphoma
acute liver congestion and hepatomegaly are associated with
vascular congestion such as in heart failure or Budd-Chiari syndrome
Congenital dilations of the biliary tract are classified as
choledochal cysts
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
pancreatic and biliary tract malignancies are common or rare in children
rare
what will you order for an abd mass to indicate infection, inflammation and anemia
CBC with Diff
what labs will you order for a abd mass to identify kidney disease
BUN and creatinine
what labs will you order for an abd mass to look at pancreatic disease
amylase and lipase
what labs will you order for an abd mass to look at liver function
liver function panel (LFTs)
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
what lab when evaluating an abd mass would be useful in identifying solid tumors
Uric acid
LDH
what radiographic test is used to identify an intestinal obstruction, fecal impaction and calcifications associated with tumor.
2 view x ray of abdomen
nonspecific
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
what test can be particularly useful in evaluating solid abd masses
CT scan with IV contrast
In addition to evaluating solid masses, CT with IV contrast can also see
vascular anatomy and presence of associated lymph nodes
What type of scan serves to help stage many cancers
CT with IV contrast
Masses of primary bowel or bladder are best seen with what study
fluoroscopic studies such as UGI, BE and voiding cystourethrogram
what type of contrast to bowel will produce significant artifact and prevent immediate subsequent CT scan
Enteral contrast administered to bowel
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 )
in benign abdominal masses an NGT is mandatory for all
perforations and obstructions
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
age of presentation for neuroblastoma
18 months, prevalence greatest in <4 years (85%)
most common extracranial tumor in children
neuroblastoma
Wilms tumor most common age of presentaion
1-5 yrs
most common malignant liver tumor
hepatoblastoma
what malignant tumor is associated with extreme prematurity and what age is the mean for diagnosis
Hepatoblastoma
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)
where are ganglion cells normally located
throughout the intestines from the mouth to the rectum
Hirschsprung disease (HD) is more prevalent in what gender
males (4 xs more than female)
short segment Hirschsprung disease (HD) what part of bowel is affected
rectosigmoid colon
long segment Hirschsprung disease (HD) what part of bowel is affected
rectosigmoid colon but also extends proximal to this point
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
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
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
children who are diagnosed with Hirschsprung disease (HD) at an older age typically have which type
shorter segment affected
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
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
diagnosis of Hirschsprung disease (HD) is made by what and confirmed how?
clinical picture and radiologic studies
confirmed by pathology from a rectal biopsy
Abd x ray for Hirschsprung disease (HD) will show what
large dilated loops of intestines and may have air fluid levels
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
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)
how is a BE performed
placing a small catheter into the rectum and instilling contrast into the colon then taking several radiographs
A BE would not be helpful in Hirschsprung disease (HD) for what population
neonates. May not have dilation of the colon yet
BE should be avoided if there are concerns for ______ or ______
perforation
enterocolitis
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
standard for definitive diagnosis of Hirschsprung disease (HD) with a sensitivity of 100% is a
rectal biopsy
what type of rectal biopsy can be done on neonates and infants in the diagnosis of Hirschsprung disease (HD)
suction rectal biopsy
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
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)
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
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
most common surgical technique for Hirschsprung disease (HD)
Transanal endorectal pull-through (TERPT) using the Swenson, Soave or Duhamel techniques
initial postop potential complications for TERPT
anastomotic leak bleeding bowel obstruction wound infection abscess stricture perianal excoriation
When can an anastomotic leak occur
anytime a surgeon is anastomosing 2 segments of bowel together.
symptoms of an anastomotic leak
fever
irritability
abd distension
An abscess may occur after a TERPT due to
poor hemostasis causing a hematoma that becomes infected
stricture of the sphincter may occur after a TERPT because
when retracting the sphincter muscle during surgery.
delayed passage of stool postop to TERPT
think stricture of the sphincter
how is stricture of the sphincter postop to TERPT fixed
gently dilating the anus with a lubricated hegar dilator
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
what needs to be monitored closely in the initial postop period following a TERPT
NG output vital signs urine output abd girth pain control
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
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.
symptoms of enterocolitis following a TERPT
fever
abd distension
explosive diarrhea
intervention for enterocolitis post TERPT
bowel decompression with rectal irrigations
broad spectrum IV abx followed by oral Flagyl
factors found to decrease risk of enterocolitis after TERPT
daily rectal irrigations or rectal dilations starting at 2 weeks post surgery
probiotic prophylaxis
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
are Hirschsprung disease (HD) kids ever able to establish normal bowel function
yes, but maybe later than other kids their age.
what are patients often prescribed for stooling issues with Hirschsprung disease (HD)
PEG 3350 (Miralax) or loperamide
severe -
antegrade continence enema
is Hirschsprung disease (HD) cured with surgery?
no, they will require close monitoring of bowel function, nutritional status and overall health for their lifetime
prognosis for Hirschsprung disease (HD) with short segment
good outcome with very few interventions required
Prognosis for Hirschsprung disease (HD) with total colon HD
may require multiple procedures and in rare cases and intestinal transplant
what type of obstruction is an illeus
functional - occurs when the peristalsis of the GI tract is impaired.
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
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
list the causes of functional bowel obstruction
abd surgery peritonitis sepsis trauma medications (opioids, anxiolytics) metabolic imbalances (hypokalemia, hyponatremia, hypomagnesemia, acidosis)
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)
symptoms of ileus
abd distension
absent or hypoactive bowel sounds due to lack of peristalsis
constant pain that worsens with increased bowel distension
with mechanical obstruction, bowel sounds may be
high pitched or hyperactive
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
vomiting proximal to the sphincter of Oddi will more likely be
non-bilious
bilious emesis represents an obstruction occurring beyond the
sphincter of Oddi
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
symptoms that may be present with resolution of POI are the passage of
flatus and stool
best indicator is tolerating a PO diet
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.
if there is significant gastric fluid loss with ileus, consider checking
electrolyte levels
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
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
NSAIDS post op
treats pain and inflammation
but promotes GI bleeding (side effect)
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.
postop return of function for the small bowel
12-24 hours
postop return of function for the stomach is
24-48 hours
postop return of function for the colon is
3-5 days
invagination of telescoping of the intestines involving the proximal portion of the bowel
intussusceptum
invagination of telescoping of the intestines involving the distal portion of the bowel
intussuscipiens
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
Currant jelly stool is an early or late sign of intussusception
very late
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
what are the 3 categories of intussusception
1) idiopathic
2) lead point
3) postsurgical
which category of intussusception is most commonly seen in infants and children
idiopathic
which type of intussusception often corresponds with viral gastroenteritis or an URI
idiopathic
what viral infections are associated with intussusception
adenovirus
rotavirus
HSV
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
what vaccine has resulted in 35 patients getting intussusception
Rotarix (approved vaccine for Rotavirus)
which type of intussusception has a identifiable cause in the intestinal mucosa
lead point intussusception
what ages does lead point intussusception affect
5-14 years
what are the most common causes of lead point intussusception
inverted Meckel diverticulum
polyps
duplication cyst
hemangiomas
what is the least common type of intussusception
postsurgical - can be VERY serious in infants and children
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
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
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
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.
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
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
care of nonoperative post reduction of intussusception
NPO for short time and clear liquids are introduced with diet progression as tolerated. send home
if recurrence of intussusception post reduction occurs
you can attempt re-reduction
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
how do you calculate normal urine output
1mL/kg/hr
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
who do patients follow up with post intussusception reduction
nonsurgical - PCP 1 week later
surgical - pediatric surgeon
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
can intussusception be prevented
no
abnormal rotation and fixation of the bowel during embryologic development.
malrotation
the classic form of malrotation is an
abnormal rotation of the duodenojejunal and decocolic loop and a high, medially positioned cecum
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
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)
incidence of malrotation is increased in children with what symptoms
heterotaxy
trisomies 13, 18, 21
Marfan
Prune-belly
what are some of the most common anatomic abnormalities associated with malrotation
diaphragmatic hernia
duodenal web
abdominal wall defects such as gastroschisis, omphalocele
when is malrotation diagnosed
60% before age 1
75% before age 5
however, malrotation and volvulus may both present in adulthood
presentation of malrotation in pediatric patient
no symptoms
intermittent symptoms
acute presentation
vomiting
abd pain
FTT
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
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
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
double bubble sign on radiograph indicates
duodenal obstruction
gasless abdomen may be appreciated in
volvulus
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)
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
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
prognosis for volvulus after Ladd procedure
obstruction from adhesions
outcomes variable from complete recovery to intestinal failure to death
Prognosis for pt with malrotation
excellent
resume normal daily activities
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
what gender is pyloric stenosis more prevalent in
first born males
some evidence of genetic association
maternal risk factors for pyloric stenosis are
hyperthyroidism quinolone antibiotic use smoking increased BMI intranasal decongestant use
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
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
olive sign think…
pyloric stenosis
spasmodic contraction of the pylorus with poorly coordinated gastric emptying
observed in what population
what is done
pylorospasm
neonates
resolves spontaneously with time
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
what does HPS stand for
hypertrophic pyloric stenosis
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
how is pyloric US confirmed
abdominal US
what is a string sign
elongated and thickened pyloric channel seen in pyloric stenosis
what is a beak sign
filling of the proximal pylorus seen in pyloric stenosis
what is a double shoulder sign
thickened pylorus compressing the antrum of the stomach (seen in pyloric stenosis)
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
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
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
when is the pyloric regimen more commonly prescribed
in infants with persistent emesis in the postop period
postop vomiting is due to
gastric distension and atony
majority of infants tolerate ad lib feeds post op. What is this?
volume of at least 60mL within 24-48 hrs of the operation
persistent vomiting beyond 72-96 hours postoperative pyloric stenosis repair may occur in cases of
incomplete pyloromyotomy
UGI series may be valuable to determine
pain control for postoperative pyloric stenosis
tylenol (usually sufficient bc area is infiltrated with local anesthetic)
monitor for what complications after repair of pyloric stenosis
surgical wound infection
incisional hernias
life threatening complications include
gastric mucosal tears
duodenal perforation
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
what qualifies infant for discharge after a pyloric stenosis repair
when they are tolerating 60mL for at least 2 consecutive feedings without emesis
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
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
partial or complete obstruction resulting from an anatomic cause, intraluminal or extraluminal.
mechanical
intraluminal or extraluminal cause of mechanical obstruction.
swallowed coin
intraluminal
intraluminal or extraluminal cause of mechanical obstruction.
hernia
extraluminal
intraluminal or extraluminal cause of mechanical obstruction.
intussusception
intraluminal
intraluminal or extraluminal cause of mechanical obstruction.
adhesion
extraluminal
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
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
consists of chewing food, allowing it to mix with oral secretions and liquid ingestions
mixing
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
first part of the small intestine is commonly known as the
duodenum
the remaining small intestine and the first portion of the colon is known as the
midgut
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
what organs and glands play a important role in GI physiology
liver
gallbladder
biliary tree
pancreas
what sphincter prevents reflux
upper esophageal sphincter
what kind of vomiting should never be accepted as a normal type of vomiting
bilious
Diagnostic abdominal labs
CBC with diff
UA
UPT
diagnostic abdominal labs
in setting of dehydration secondary to vomiting or diarrhea or suspicion of kidney disease
electrolytes
BUN
creatinine
labs for liver
LFTs
labs for pancreas
amylase
lipase
fecal studies in diarrhea
stool osmolarity
fecal leukocytes
fecal occult blood
ova and parasites (O&P)
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
fecal leukocytes are elevated in
acute colitis (particularly bacterial origin)
gross blood in stool is almost always indicative of
colitis
fecal occult blood tends to indicate
colitis or a bacterial toxin affecting small bowel
O& P is extremely helpful in what scenario
potential ingestion of contaminated water (very high specificity)
stool culture can evaluate for
shigella
C diff
Norovirus
Rotavirus
plain abd film positions
supine (most common)
upright in front of the radiographic plate
left lateral decubitus (left side down)
cross table views
stool has a characteristic appearance on an x ray from
the gas bubbles inside the stool
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
which view is inferior for detecting bowel perforation but can sometimes show free gas along the anterior abdominal wall
cross table lateral view
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
bacterial causes of gastroenteritis
E. Coli, staph, Campylobacter, salmonella, shigella, yersinia, C. Diff
common viral causes of gastroenteritis
rotavirus, adenovirus, coronavirus, parvovirus
what causes of gastroenteritis need abx
c.diff
shigella
salmonella
h. pylori
which causes of gastroenteritis is most likely to cause sepsis in < 3mos
shigella
salmonella
main cause of dysentery
shigella
gastroenteritis acquired by
via fecal-oral route, transmitted person-to-person, through contaminated food or water
s/s of gastroenteritis
fever, vomiting, diarrhea (watery, > 3x/day), recent antibiotic use (C. Diff), travel (especially internationally), dehydration (varying severity)
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
s/s neoplasm
weight loss, anorexia, fever, night sweats, easy bruising/bleeding.
bilious emesis, alcoholic stools, liver disease - jaundice, pale skin, cachexia, FTT, abdominal wall hernias - observe with vagal/bearing down
Bowel obstruction
what lab includes creatinine and BUN
chemistry
Benign masses think
assess for bowel obstruction, appendicitis, perforation, sepsis, ectopic pregnancy, torsion
what do you do for malignant tumors
admission, oncologic and surgical evaluation
what symptoms for milk protein allergy
blood in stool
diarrhea
can cause enterocolitis
IBD is most common in
Most common in >10 yo children
which IBD affects only the colon
UC
which IBD involves any part of the gut
CD
IBD is most common in what populations
jewish
IBD is linked to what antigen
human leukocyte antigen (HLA) subtypes
smoking _____ severity of CD and ______ risk for UC
Smoking INCREASES severity of CD and DECREASES the risk for UC
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
symptoms of Toxic megacolon
Fever Abdominal distension and pain Massively dilated colon Anemia Low serum albumin (fecal protein loss)
Subtle symptoms
Loss of appetite Crampy postprandial pain Poor growth Delayed puberty Fever Anemia Lethargy
Crohns
skip lesions associated with
crohns
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
to get a true diagnosis for IBD
endoscopy, biopsy and histology to differentiate CD from UC
fistulas are more associated with what IBD
Crohns
Crohns or UC?
malaise
fever
weight loss
common in Crohns
sometimes UC
Crohns or UC?
rectal bleeding
usual in UC
sometimes CD
Crohns or UC?
abd mass
common in CD
rare in UC
Crohns or UC?
abd pain
both
Crohns or UC?
perianal disease
Common in CD
rare in UC
ileal involvement
Crohns or UC?
CD
Crohns or UC?
strictures
common in CD
rare in UC
Crohns or UC?
fistula
common in CD
Crohns or UC?
skip lesions
CD
Crohns or UC?
transmural involvement
CD
Crohns or UC?
crypt abscesses
UC
Crohns or UC?
intestinal granulomas
CD
Crohns or UC?
risk of cancer
increased in CD
greatly increased in UC
Crohns or UC?
erythema nodosum
Common in CD
Crohns or UC?
mouth ulceration
CD
Crohns or UC?
osteopenia at onset
CD
Crohns or UC?
autoimmune hepatitis
UC
Crohns or UC?
sclerosing cholangitis
UC
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
celiac disease
commonly seen in
Seen in type 1 diabetics, thyroiditis, turners syndrome, and trisomy 21.
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
Diarrhea Pubertal delay Failure to thrive Abdominal bloating Irritability Decreased appetite Ascites (from hypoproteinemia)
Celiac
celiac disease monitoring
Careful monitoring of child’s growth curve and evaluation for reduced sub Q fat and abdominal distension are crucial.
celiac should be considered in any child with
Chronic abdominal complaints
Short stature
Poor weight gain
Delayed puberty
extraintestinal manifestations for celiac disease include
Osteopenia Arthritis Arthralgias Ataxia Dental enamel defects Elevated liver enzymes Dermatitis Herpetiformis Erythema nodosum
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.
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
risk factors for H. Pylori
Low socioeconomic status
Poor sanitation
Highest in developing countries
drugs increase risk for PUD
NSAIDS (ASA)
Tobacco use
Bisphosphonates
Potassium supplements
risk factors for PUD
drugs family history sepsis head trauma brain injury hypotension
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
alarm symptoms of PUD
Weight loss Hematemesis Melena , heme positive stools Chronic vomiting Microcytic anemia Nocturnal pain
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
currant jelly stools
intussusception
most common reason for abd surgery in children in US
appendicitis
Appendicitis can occur at any age but most common
10-12 yrs and males as opposed to females
fever (more common with perforation), decreased activity level, periumbilical pain with progression to RLQ pain, accompanied by anorexia, and eventually diarrhea
appendicitis
McBurney Point and rebound tenderness r/t
peritonitis associated with perforation of appendix
where is McBurney Point
R side of abdomen 1/3 of distance from anterior superior iliac spine to the umbilicus
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
Obturator sign
appendicitis
If appendix lies on the obturator internus muscle, pain may be present with internal rotation of the right thigh
Rovsing sign
appendicitis
Pain reported in the RLQ with palpation of the LLQ
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
Radiologic diagnostic for appendicitis
US
what is an US for appendicitis limited by
appendix position
bowel gas pattern
obesity (not recommended if BMI >25 in adults)
operator experience
what is the most sensitive test for appendicitis
CT
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
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
esophagus and trachea form within close proximity, can occur with VACTERL syndrome. communicating fistula from esophagus to trachea
Tracheoesophageal fistula
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:
diagnostic for transesophageal fistula
placement of OG tube + xray (will see it coil in the esophagus or stop), gas-less stomach on KUB, tracheobronchoscopy
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)
complications in
transesophageal fistula
esophageal stricture, esophageal dysmotility, GERD, tracheomalacia, vocal cord dysfunction
congenitally interrupted esophagus
Esophageal atresia
gassless abdomen on CXR can also suggest an
Esophageal atresia with proximal TEF
chronic reflux can develop into
Barrett esophagus
diarrhea < = 14 days with > 3 stools per day is what type
acute diarrhea
diarrhea > 14 days with > 3 stools per day is what
persistent diarrhea
diarrhea > 30 days > 3 stools per day
chronic diarrhea
Gastroenteritis lab to look at electrolytes
BMP
what labs for gastroenteritis
BMP
CBC with diff
stool cultures
O &P
first line therapy for travelers diarrhea in children is
Azithromycin
Antidiarrheal medications often contain what?
contributes to?
ASA
Reye syndrome
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
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)
Caloric calculation for enteral feeds
Breast milk—> 20kcals/oz
Formulas—>20kcals/oz (can fortify)
1oz = 30mL
Average baby needs—> 100kcal/kg/day (variable)
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.
wasting
Malnutrition initially results in wasting (deficiency in weight gain)
stunting
(deficiency in linear growth) that occurs after months of malnutrition, and head circumference is spared except with chronic, severe malnutrition.
Short stature with preserved weight =
endocrine etiology
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.
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
GI causes of FTT
Cystic fibrosis and other causes of pancreatic insufficiency
Celiac disease
Other malabsorption syndromes
Gastrointestinal reflux
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
infectious causes of FTT
HIV
Tuberculosis
Hepatitis
UTI, chronic sinusitis, parasitic infection
metabolic causes of FTT
THyroid disease
Adrenal or pituitary disease
Aminoaciduria, organic aciduria
Galactosemia
Neurologic causes of FTT
Cerebral palsy Hypothalamic and other CNS tumors Hypotonia syndromes Neuromuscular diseases Degenerative and storage diseases
renal causes of FTT
Chronic renal failure
Renal tubular acidosis
UTI
hematologic causes FTT
Sickle cell disease
Iron deficiency anemia
initial tests to evaluate FTT
CBC, iron deficiency anemia, lead toxicity, UA, urine culture, serum electrolytes to assess renal.
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
malnutrition-infection cycle:
Recurrent infections exacerbate malnutrition, leading to greater susceptibility to infection.
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.
children who live in psychological deprivation develop short stature with or without concomitant FTT or delayed puberty, a syndrome called
Psychosocial Short Stature
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
% of the LBM of infants and malnourished patients is water.
70
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
labs to order in dehydration
BUN (can increase with dehydration)
bicarb levels
blood pH
Na
anion gap (elevated in metabolic acidosis)
what lab indicates type of hydration
Na
dehydration type
most common in
Na 135-145
isonatremic
most common d/t gastroenteritis
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
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
oral rehydration pt gets
15mL/kg/hour or 60mL/kg/4hrs
sip volume per 5 min in oral dehydration
< 10kg 1mL/kg
10kg 10mL
For every additional 5kg, add: 5mL to a maximum of 50mL
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
tachycardia is present in what types of dehydration
moderate and severe
orthostatic hypotension is present in what type of dehydration
moderate
hypotension is present in what type of dehydration
severe
fontanelle is sunken in what type of dehydration
severe
respirations are deep in what type of dehydration
moderate
respirations are deep and rapid in what type of dehydration
severe
oliguria is in what type of dehydration
moderate
anuria and severe oliguria is seen in what type of dehydration
severe
what test greatest benefit is ability to distinguish blood vessels from ducts.
US dobbler B mode
standard of care to diagnose pyloric stenosis and intussusception or an obstructed, pus filled appendix.
US
test Extremely useful in evaluating the liver, biliary tree, and often head of pancreas.
US
reserved for either treatment or diagnostic uncertainty when the US cannot definitively diagnose pyloric stenosis or intussusception.
GI fluoroscopy
safest contrast agent
Safest with lowest sensitivity and specificity
Can be used to reduce intussusceptions.
air
contrast agent
Good sensitivity and specificity
Easily evacuate or excrete iodinated agents.
iodine based
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
Esophagram or gastrogram
Investigate anatomy for perforation and obstruction
Upper GI (imaging includes from swallowing to sm bowel) fluoroscopy
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
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
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
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
pancreatitis diagnostics
Elevated amylase & lipase o CRP o Hypocalcemia o Transient hypoglycemia o Hyperbilirubinemia o Increased LFTs o Hypoalbuminemia o US o CT
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
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)
Hypocalcemia (<9mg/dL) associated with
DiGeorge syndrome
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
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
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
Hypercalcemia (serum calcium >10 mg/dL)
associated with
williams syndrome
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
Hypercalcemia can result in
polyuria, renal calculi, and renal tubular dysfunction
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
chloride has a direct relationship with
sodium - if sodium is elevated, chloride is elevated
chloride has an inverse relationship with
bicarb
Hypochloremia is serum chloride of
<97 mmol/L
Hypochloremia is associated with
Bartter syndrome, CF, Bulimia nervosa, diuretic usage, removal of gastric secretions via NGT, and metabolic alkalosis
hypochloremia associated with metabolic alkalosis may (Rare) exhibit
arrhythmias, decreased respiratory effort, seizures in severe states
s/s hypochloremia
When associated with volume depletion or dehydration, may exhibit thirst, lethargy, tachycardia, tachypnea, and delayed cap refill
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
lab for hyperchloremia
> 108
presentation of hyperchloremia
often asymptomatic
may have Kussmaul respirations (especially in DKA); possible neurologic symptoms include lethargy, HA, and confusion
treatment of hyperchloremia
Address underlying cause and treat associated acidosis
Consider sodium bicarbonate IV if severe metabolic acidosis
hypomag lab value
<1.7
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
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
hypermag lab values
> 2.2
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
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
hypophosphatemia lab
<2.5
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
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
Hyperphosphatemia (serum phosphorus
> 4.1 mg/dL)
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
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
hypokalemia
(serum potassium <3.7 mEq/L)
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
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
hyper k levels
what level is a medical emergency
(serum potassium > 5.2 mEq/L) ** > 7mEq/L is a medical emergency**
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)
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
hyponatremia
<135
symptoms hyponatremia
Irritability N/V Poor feeding Lethargy Seizures Coma
causes hyponatremia
increased free water intake, excess water retention, increased Na losses, or combination
hyponatremia that develops over hours to days (<48hr
acute
more likely to produce cerebral edema and changes in neuro status
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)
hypernatremia
> 145
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)
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
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
toxic syndrome of what?
N/V, pallor, delayed jaundice-hepatic failure (72-96 hr)
acetaminophen
toxic syndrome of what?
Tachycardia, HTN, hyperthermia, psychosis and paranoia, seizures, mydriasis, diaphoresis, piloerection, aggressive behavior
Amphetamine, cocaine, and sympathomimetics
toxic syndrome of what?
Mania, delirium, fever, red dry skin, dry mouth, tachycardia, mydriasis, urinary retention
Anticholinergics
toxic syndrome of what?
HA, dizziness, coma, other symptoms affected
carbon monoxide
toxic syndrome of what?
Coma, convulsions, hyperpnea, bitter almond odor
cyanide
toxic syndrome of what?
Metabolic acidosis, hyperosmolarity, hypocalcemia, oxalate crystalluria
Ethylene glycol (antifreeze)
toxic syndrome of what?
Vomiting (bloody), diarrhea, hypotension, hepatic failure, leukocytosis,hyperglycemia, radiopaque pills on KUB, late intestinal stricture, Yersinia sepsis
Iron
toxic syndrome of what?
Coma, respiratory depression, hypotension, pinpoint pupils, bradycardia
Narcotics
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)
toxic syndrome of what?
Tachypnea, fever, lethargy, coma, vomiting, diaphoresis, alkalosis (early), acidosis (late)
Salicylates
toxic syndrome of what?
Coma, convulsions, mydriasis, hyperreflexia, arrhythmia (prolonged QT interval), cardiac arrest, shock
Cyclic antidepressants
A poisoned child can exhibit any one of six basic clinical patterns:
Coma Toxicity Metabolic acidosis Heart rhythm aberrations GI symptoms Seizures
used for gastric decontamination in toxicity/overdose/ingestion
Syrup of Ipecac Gastric Lavage Activated Charcoal Cathartics Whole-Bowel Irrigation
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
criterion to use gastric lavage
ingestion of potentially life threatening poison;
2.
procedure done within one hour of ingestion
complications of gastric lavage
aspiration pneumonia, laryngospasm, tension
pneumothorax, tachycardia, atrial/ventricular ectopy, mechanical injury
to the GI tract, hyper/hyponatremia, hypothermia
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
Most commonly used and most effective method of gastric
decontamination
activated charcoal
substances not absorbed well by activated charcoal
alcohols, acids, alkalis, hydrocarbons, iron,
potassium, magnesium, sodium, lithium salts
when should activated charcoal be given
within 1 hr of ingestion
adverse reactions to activated charcoal
vomiting
constipation
obstruction
aspiration
all rare
contraindications to using activated charcoal
unprotected airway, hydrocarbon and
caustic ingestion, non-intact GI tract
Increase GI transit time of ingested toxins
No evidence-based indications for routine use
cathartics
names of cathartics used in ingestion
Sorbitol, magnesium citrate, and magnesium sulfate
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
used in whole bowel irrigation to rapidly evacuates contents of GI tract within 2-6hrs post ingestion
PEG
indications for using PEG in ingestion (whole bowel irrigation)
ingestion of adult iron tablets, heavy metals, lithium, sustained release drug formulations
contraindications for using PEG in ingestion (whole bowel irrigation)
unprotected airway,hemodynamic instability, Ileus, bowel obstruction/
perforation, intractable vomiting, GI hemorrhage
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
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
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
antidote for tylenol overdose
Antidote N-acetylcysteine (NAC)
mucomyst is most effective if given within ___ hrs post ingestion
8
Food and Drug Administration (FDA)
tylenol overdose Treatment Regimens:
72 hour oral course (Acetadote)
21 hour IV course (mucomyst)
Children metabolize ethanol at a rate of
10-25 mg/dL/hr
alcohol ingestion in pediatrics symptoms
facial flushing, vomiting, diaphoresis, respiratory depression, seizures,
hypotension, hypothermia, and hypoglycemia
Estimated pediatric lethal dose alcohol
3.8mL/k 100% alcohol
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
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
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
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
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
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
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
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
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
Arrhythmias Often tachyarrhythmias; possibly fatal Impaired cardiac conduction Nausea and vomiting (often the first sign) Dizziness, HA, mental disturbances Shock
digoxin tox
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)
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
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
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
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
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
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
