File - FHT PICU Internship Site
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PICU
RENAL/GI/ENDO
Overview of Anatomy and Physiology
The esophagus,
stomach, large and
small intestine, aided
by the liver,
gallbladder and
pancreas convert the
nutritive components
of food into energy
and break down the
non-nutritive
components into
waste to be excreted.
Congenital
Acquired
1.
Cleft Lip and Cleft
Palate
GER
2.
Pyloric stenosis
3.
Biliary atresia
Appendicitis
4.
Hirschsprung’s
disease
Celiac
disease
CCRN FOCUS
Acute abdominal trauma
Acute GI Hemorrhage
Bowel infection/Obstruction/Perforation (nec, mesenteric ischemia,
adhesions
GER
GI Abnormalities (omphalocele, gastrochisis, volvulus, Hirsh. Disease,
malrotation, intussusception
GI Surgeries
Hepatic Failure (portal HTN, cirrhosis, biliary atresia, esophageal varices
Malnutrition/malabsorption
Hirschsprung Disease
Also
called congenital aganglionic
megacolon
Mechanical obstruction from inadequate
motility of intestine
Incidence: 1 in 5000 live births; more
common in males and in Down syndrome
Absence of ganglion cells in colon
Hirschsprung Disease
Clinical Manifestations
of Hirschsprung Disease
Aganglionic
segment usually includes
the rectum and proximal colon
Accumulation of stool with distention
Failure of internal anal sphincter to
relax
Enterocolitis may occur
What to look for?
–
In a neonate, history commonly reveals a
failure to pass meconium and stool within the
first 24 to 48 hours after birth. On inspection, the
infant may have abdominal distention and
easily palpable stool masses. When stool does
pass through, its liquid or ribbon like.
Diagnostic Evaluation
X-ray,
barium
enema
Confirm
diagnosis with
rectal biopsy
Therapeutic Management
Surgery
Two
stages
Temporary ostomy
Second stage “pull-through”
procedure
Question
Justin, is a 4 month
old patient with
Trisomy 21 admitted
with a new diagnosis
of Hirschsprung’s
disease. You would
expect to see the
following on exam….
1. Jaundice, increased
direct bilirubin
2. Foul, ribbon like stools
Jaundice increased
ammonia
4. Increased PT and PTT
followed by
hematechezis
Intussusception
Telescoping
or
invagination
of one
portion of
intestine into
another
Intussusception
Invagination
causes inflammation and
swelling at the affected site. Edema
eventually causes obstruction and necrosis
from occlusion of the blood supply to the
bowel
http://www.youtube.com/watch?v=Ex6ax
VN8TWM
What are you looking for?
Hx-
intermittent attacks of colicky pain
characterized by screaming, drawing
knees to the chest.
Parents
report vomitus containing bile or
fecal material
Jelly
like stools
Most Common
Most
common forms
include ileocolic (at the
ileocecal valve), ileoileal
(the ileus into itself), and
colocolic (the colon into
itself)
Intussusception (cont.)
Diagnostic
evaluation- Spontaneous
reduction occurs in up to 10% of patients
Therapeutic management- IV fluids, NG
decompression- Radiologist guided
pneumoenema (air enema)
Prognosis – nonoperative reduction is
successful in 80% of cases
Intussusception (cont.)
Nursing
considerations- Consent,
NPO status, routine labs
Why
is this problematic?
Intestinal perforation/intestinal
infarction
Intussusception (cont.)
Symptoms include acute abdominal pain (manifested in infants by
crying and knee chest position, vomiting, and red currant jelly
stools.
Physical examination may reveal a sausage shaped mass in the
right upper quadrant while the lower right quadrant feels empty
(dance sign)
A barium enema, although often not required, is the test of choice
in diagnosing intussusception. The barium enema alone may
reduce the intussusception……
Omphalocele
herniation
of abdominal contents through umbilical ring, usually
with an intact peritoneal sac
Gastroschisis
herniation
is lateral to the umbilical ring, and peritoneal sac not present
HEPATIC FAILURE
Liver Functions
Protein synthesis
Excretion of
metabolic wastes
Oxidative
phosphorylation
Breakdown of
glycogen
Fatty acid oxidation
Synthesis of
cholesterol & bile
acids
Enzymes
NADPH
Cytochrome P-450
Cytochrome
reductase systems
Necessities for Normal Liver Function
Adequate blood flow
Majority of blood flow comes from the portal venous system
Oxygen
20 – 40% of cardiac output with only ~25% of blood entering through the Hepatic
Artery
Hepatocyte damage from hypoxia/hypotension
Low-pressure biliary system
Biliary Atresia
The Biliary organs and
duct system that creates,
transports, stores, and
releases bile into the
duodenum for digestion
includes the liver,
gallbladder, and bile
ducts
Jaundice, manifesting
with yellow discoloration
of the kin is the most
common early symptom
Biliary Atresia—Kasai Procedure
MANAGEMENT CONSIDERATIONS
Nutrition Gi
EN vs. PN
Bleed
Common
Neuro
Infection
Medications
Renal
Review of Anatomy/Physiology
A- Renal Vein
B- Renal Artery
C- Ureter
D- Medulla
E – Pelvis
F – Cortex
1 – Ascending limb loop of Henle
2 - Descending limb loop of Henle
3 – Peritubular Capillaries
4 – Proximal Tubule
5 – Glomerulus (Bowman’s capsule +
glomerular capillaries)
6 – Distal tubule
Clinical Conditions
Congenital anomalies of ureter, bladder,
urethra
Infectious, immunologic, circulatory
UTI, Glomerulonephritis, nephrotic syndrome, hemolytic uremic
syndrome, CHF
Tumors
Duplicating systems, strictures, ureterocele, exstrophy of
bladder, reflux, hypospadias,
Wilm’s tumor
Enuresis
CCRN FOCUS
Acute Renal Failure
Chronic Renal Failure
Electrolyte Imbalances
PHYSIOLOGY: Pediatric Considerations
Greater % of total body weight that is
water in neonates and infants
Immaturity of physiological processes
Higher basal metabolic rate and
respiratory rate
Higher body surface area to weight ratio
Health conditions that make children more
vulnerable
CHLA 2005
PHYSIOLOGY: Metabolic Rate
Infant’s
adult
rate is three times that of an
Increased
need requires a much higher
caloric intake and water requirement.
Metabolic
turnover of water
Infants
have 5 times greater turnover of
water than adults.
Results
in increased need for H2O as well
as vulnerability to illnesses with
dehydration.
PHYSIOLOGY: Immature Systems
Renal
system
Matures
by 24 months old
Decreased
Inability
GFR
to concentrate urine
Greater
loss daily under normal
circumstances
Limited
renal capabilities until
maturity of system is reached
FLUID AND ELECTROLYTES
Precise regulation is necessary for life
Volume and composition remain relatively constant in
the presence of wide changes in intake and output
Stress and disease increase losses
Fluid balance is maintained when excretion and losses
are balanced by proper volume and type of fluid intake
What is make up of body
fluids ??
How do we lose fluid??
PHYSIOLOGY: Total Body Water
Premature: 75–80% TBW
Newborn: 65-75% TBW
One year: 65% TBW
Older children: 60% TBW
Adolescents: 55-60% TBW
PHYSIOLOGY
ECF
ICF
Premature
50%
30%
Newborn
50%
30%
1 year
25%
45%
Child
20%
45%
Adolescent
20%
45%
DEHYDRATION:
Clinical Management
Children’s water requirements in 24
hours
100
ml/kg for first 10 kg
50
ml/kg for next 10 kg
20
ml/kg for each kg above 20
Commercial solutions contain
Water,
sugar, NA+, K+, CL-, and
lactate
PEDIALYTE
for >12 months old
DEHYDRATION:
Clinical Management
IV fluids when the child is severely dehydrated,
usually hospitalized
Ringers lactate
Isotonic (same osmolarity as blood)
Has multiple electrolytes
.9 or .45 NS
Use after LR to replenish ECF volume
Acute Renal Failure
Causes:
Prerenal:
Hypoxia & ischemia due to low blood flow and
oxygen delivery
Intrarenal:
Inflammatory, nephrotoxic, unresolved ischemic flow
Postrenal:
Obstructive- bladder, ureter, urethra
S/S:
Electrolyte
imbalances, progressive metabolic acidosis
Multisystem
GI,
effects:
CNS, dermatologic, CV, respiratory
images.MD 2005
Acute Renal Failure
Diagnostic
Studies:
Electrolytes, BUN,
creatinine
Urinalysis
ECG
Renal Ultrasound
VCUG, etc.
Treatment:
Prevention
is key
Diet
– high CHO, fats, low protein,
sodium, potassium
Fluid
restriction
Careful
status,
monitoring – electrolytes, fluid
Diuretics,
antihypertensives,
kayexalate, blood products,
hemodialysis/peritoneal dialysis
Case Scenario
Baby Huey
4 mo old
Vomiting & Diarrhea x 2 days
Wt. 5.6 kg
Birth wt: 3.4 kg
What information do you want???
History
4 days ago began vomiting and a few loose stools
Went to pediatrician – wt in office was 6 kg.
Placed on oral rehydration
Had fever last night – vomiting continued, brought
to ER
What other questions would you ask?
Physical Assessment
Lethargic, dry mucus membranes, dark urine
VS: HR 160, RR 48, BP 78/56
Skin turgor – dry
Fontanel – sunken
What is going on???
What other info do you want???
ENDOCRINE
Endocrine system
Hypothalamus
Pituitary – Anterior, Posterior
Thyroid
Parathyroid
Adrenals – Cortex, Medulla
Endocrine Pancreas
Testes/ovaries
Pineal
Hormones
Chemical messengers released by endocrine glands
Classified by structure, gland of origin or chemical
composition
Each hormone stimulates a particular receptor in a
designated (target) organ or gland
The Endocrine System Consists Of Three
Components:
1. The cell, which sends a chemical message by
means of a hormone
2. The target cells, or end organs, which received
the chemical message
3. The environment through which the chemical is
transported (blood, lymph, extracellular fluids)
from the site of synthesis to the sites of cellular
action
CCRN ENDOCRINE FOCUS:
Acute
Hypoglycemia
Diabetes insipidus
DKA
Inborn Errors of Metabolism
SIADH
Diabetes Mellitus
Diabetes (to siphon) Mellitus (honey)
Diabetes is a group of metabolic diseases characterized by
hyperglycemia resulting
from defects in insulin secretion, insulin
action, or both.
(American Diabetes Association Diabetes Care Volume 37, Supplement 1, January 2014)
Type 1 Diabetes
Autoimmune process-destruction of the pancreatic
beta cells.
There are multiple genetic markers for
predisposition. It is also related to environmental
factors. Certain viruses have also been associated
with ß-cell destruction.
Accounts for only 5-10% of all diabetics but 90-95%
of children with diabetes.
Presentation
Hyperglycemia (high blood sugar)
Polyuria (increased urination)
Polydipsia (increased thirst)
Polyphagia (increased eating)
Severity of S/S depends on degree of hyperglycemia
and acidosis
May appear thin and malnourished
May be nauseous or vomiting
May be confused or obtunded
Intervention
Treatment of type 1 diabetes is always insulin and…
Blood glucose control
Healthy food choices:
Avoiding concentrated sweets
Carbohydrate counting or consistent carbohydrates
Healthy lifestyle:
Physical activity
Maintain normal weight
Hypoglycemia
By
definition - Blood glucose < 70 mg/dl
Symptoms
vary. Typically; sweaty, shakiness,
tachycardia, and pallor if dropping quickly
Behavior
change; confusion, irritability, and
lack of coordination if lasts longer
Can
progress to unconsciousness and
seizures if untreated
Intervention
15 grams of fast acting carbohydrate:
4 oz juice
6 oz regular soda
3-4 tsp honey, sugar, 3-4 candies - should always have
something on hand- like glucose tablets, glucose gel
Recheck BG in 15 minutes, re-treat till > 70 mg/dl.
Follow with snack of protein and carbohydrate if meal not
due for 30 minutes.
Glucagon IM or SQ - If unconscious or seizing
Diabetic Ketoacidosis - DKA
Occurs when fat is broken down for energy,
due to lack of insulin
Fats break down into fatty acids, and glycerol
in the fat cells is converted by the liver to
Ketones.
Eliminated in the urine (ketonuria) or the lungs
(acetone breath)
Leads to dehydration, acidosis, electrolyte
imbalance, coma, and death if untreated
Diabetic Ketoacidosis
Clinical Manifestations:
Hyperglycemia,
dehydration, cv collapse
Acidosis
Hyponatremic
Potassium
shift ICF to ECF and will eventually
decrease
Arrhythmia
Ketonuria
Hyperpnea
Mental status changes
SIADH
Syndrome of Inappropriate Antidiuretic Hormone
Low
serum osmolality (,275 mOsm/L)
Hyponatremic
(Na <130mEq/L)
Hypervolemic
There is increased water reabsorption and vascular
volume and decreased urine volume (<0.5ml/kg/hr)
SIADH
Management includes prevention of complications
related to decreased Na+ levels
Frequent
neuro assessments
Hypertonic
Loop
saline (2-4mL/kg of 3% NSS)
diuretics
Restrict
free water (1/2 to 2/3 of fluid maintenance
requirements)
DIABETES INSIPIDUS
DI is a deficiency of ADH secretion or an insensitivity of
renal receptors for uptake of ADH
Etiologies include:
CNS
lesions
Lesion
or tumor resection
Complication
Medication
of TBI
such as Amphotericin B, loop diuretics, some
anesthetics (these are reversible)
DIABETES INSIPIDUS
What to look for:
Polyuria,
Severe
hypernatremia and increased thirst
cases lead to hypovolemic shock
Management will include:
Vasopressin
Fluid
(SubQ, IV, intranasally DDAVP)
replacement 5% dextrose and H2O alternating with D5%
with 0.2 NSS) along with maintenance fluids
Clinical Manifestations
DI
SIADH
Serum Na+
Increased
Decreased
Serum osmolality
increased
Decreased
Urine output
Increased
Decreased
Urine Osmolality
Decreased
Increased
Body Weight
Stable or decreased
Stable or increased
BUN
Normal or increased
Normal or decreased
ECF volume
Decreased
Increased
Management
Vasopressin, DDAVP, fluid
replacement
Fluid restriction, Na+ administration
for neurologic complications,
possibly diuretics
Renal Replacement Therapy
Peritoneal Dialysis
Used for infants and children with
ARF or chronic RF
Can be ambulatory, manual, or
cont. cycling using a device.
Dialysate is instilled via catheter.
Volume between 15-50 mL/kg
K, heparin, and antimicrobials can
be added to solution
Hemodialysis
Used in children with
electrolyte imbalance,
hypervolemia, pulm. Edema,
severe acidosis, anuria, severly
elevated BUN & create, CV
failure, hepatic failure,
hyperammonemia, drug intox.
CRRT
Used in children with ARF w/
hemodynamic instability,
azotemia, sever electrolyte
imbalance, hyervolemia,
symptomatic metabolic
abnormalities. Who are not
candidates for PD or HD
Renal Replacement Therapy:
complications
Peritoneal Dialysis
Hemodialysis
Peritonitis
Hypovolemia
Catheter issues-leakage,
obstruction
Hypervolemia
Impaired pulm. Function r/t
abd. Distention.
Filter rupture
Systemic bleeding
Fluid overload
Circuit disconnection
Dec. cv output
Infection
Hypoproteinemia
Transfusion rxn.
Hyperglycemia r/t
absorption of dextrose from
solution
CRRT
Same as HD
Dialysis
https://youtu.be/fKlY2SKi_dk
A 5 year-old female was admitted to ICU
following a craniotomy for excision of a
tumor. 12 hours post admission the following
were noted:
Decreased LOC
Tacycardia
Hypotension
Urine output of 15 mL/kg per hour & a SG of
1.003
Na+ 160
Serum osmolality 340
Urine Na+ 20 mmol/d
The diagnosis of DI was made. The initial
treatment consisted of urine replacement
with half NS. 24 hours later her LOC improved,
urine output remained at 10-15 mL/kg per hr.
with a low SG, serum Na+ 150mmol/L, serum
osmolality was 305 mOsm/kg.
DDAVP 5mcg/kg intranasally
was begun. Within 2 hrs. her
urine output had dropped to
3mL/kg hr. with a SG of 1.010. IV
replacement of urinary losses
was d/c’d and maintenance
fluids were continued. Another
dose of DDAVP was given for
an SG below 1.010 and urine
output that exceeded 2mL/kg.
2 days later the IV was d/c’d
and DI was managed with BID
desmopressin.
QUESTION
This child would require
fluid and electrolyte
correction over a period
of 48 hours to prevent
which of the following?
a. Cerebral
dehydration &
hemorrhage
b. Cerebral
edema and
herniation
c. Cerebral
hemorrhage
and edema
d. Cerebral
dehydration
and herniation
QUESTION
The cardiovascular signs
and symptoms of DI are
primarily due to:
a. Decreased
preload
b. Decreased
afterload
c. Decreased
contractility
d. Decreased
conduction
QUESTION
Desmopressin is the
synthetic form of which
of the following?
a. ADH
b. Renin
c. Aldosterone
d. Insulin
A 6 month old girl has been
admitted to the ED with a
tempurature of 38.9 and history
of cold and flu symptoms for
the last 24 hours. She is
lethargic, Tachy at 190 bpm, rr is
50/min, bp is 80/45 along with a
sunken fontanelle. No wet
diapers have been made in the
last 18 hours.
Which signs and symptoms
would indicate dehydration?
a. Urine output of less than
0.5mL/kg per hour,
decreased urine sodium
content, urine osmolality less
than 300
b. Urine output < 0.5mL/kg per
hour, decreased urine sodium
content, urine osmolality >
500
c. Urine output > 1mL/kg per
hour, increased urine sodium
content, urine osmolality >
500
d. Urine output >1mL/kg per
hour, decreased urine sodium
content, urine osmolality <300
A child presents to the PICU with
lethargy, polyuria, a serum
glucose of 550, a blood pH of 7.25,
glycosuria, and ketonuria
Hyperglycemia is present in the
child with uncontrolled DKA due
to:
A. Decreased tissue utilization of
glucose and increased
counterregulatory hormones
B. Increased counterregulatory
hormones and increased
tissue utilization of glucose
C.Increase tissue utilization of
glucose and decreased
counterregulatory hormones
D. Decreased counterregulatory
hormones and decreased
tissue use of oxygen
Match the laboratory data with
symptoms of either SIADH or DI
a.
Inappropriate secretion of ADH
b.
hypernatremia
c.
Low serum sodium and low serum osmolality
d.
Deficiency of ADH
e.
Serum hyperosmolality
f.
Treatment: fluid restriction
g.
polydipsia
h.
Treatment: vasopressin or DDAVP
i.
j.
Low urine output in the absence of hypovolemia
Dehydration is a complication
SIADH: A,C,F,I
DI:
B,D,E,G,H,J