Exam 1 Flashcards
Pressure related medical condition that compromised the tissue within a closed facial space
Compartment syndrome
Compartment syndrome causes
Injury
Infection
Surgery
Burns
Bleeding disorder
Venomous bites
IV/IO infiltrates
Thromboembolic event
Vascular reconstruction
Compartment syndrome is due to
Inadequate blood flow through the capillaries
Most common causes of compartment syndrome
Acute high impact trauma
Long bone fractures (distal humerus and proximal tibia
Pediatric most common-
displaced supracondylar humerus fracture
Proximal/mid shaft tibia fracture
IV infiltrates
Transient compartment syndrome cause
Heavy training
Due to muscle hypertrophy and increased intracompartmental pressure with exercise
Pain disproportionate to injury
Think…
Compartment syndrome
Early signs of compartment syndrome
Pain disproportionate to injury
Refusal to move affected area
Pain with a passive stretch
Late signs of compartment syndrome
Paralysis
Pallor
Paresthesia
Pain
Pulselessness
Ps in Lipincott
Pain with passive stretch
Pain out of proportion to clinical situation
Paresthesia
Paralyiss
Pulses absent
Compartment syndrome treat
Remove casts
Keep extremity at level of heart
Do not elevate or dangle (further restrict blood flow)
Administer oxygen
Pain meds
Use isotonic fluids for hypotension
Devices to measure intracompartmental pressure in compartment syndrome
Mercury manometer system
Arterial line system
Stryker intracompartmental pressure monitoring system
Compartment syndrome pressures that warrant surgical intervention
> 35 mmHg (slit or wick catheter)
40 (needle technique)
Another technique is measure the diff between diastolic BP and intracompartmental pressure - if diff is less than 30 - suggestive of compartmental syndrome
definitive treatment for compartment syndrome
incisional fasciotomy
preoperative antibiotic in compartment syndrome prior to incisional fasciotomy
cefazolin
post incisional fasciotomy, a full recovery can be expected in what time frame
with early identification and quick treatment, within 6 months
the open wound is closed within a few days or a skin graft is placed
Time period to surgical fasciotomy to regain normal function with compartment syndrome
6 hours
The 3 As of compartment syndrome
Anxiety (increasing)
Agitation
Analgesic requirement
have been shown to precede the classic 5 Ps signs in children by several hours
5 ps
Paralysis
pallor
paresthesia
pain
pulselessness
Ortolani maneuver identifies
a dislocated hip that can be reduced
A palpable clunk (not click) is felt as the hip reduces - positive Ortolani
Galleazzi sign
hip dislocation sign
difference in femur length when hips and knees are flexed to 90 degrees
Trendelenburg gait is seen when there is _____
weak abductor muscles of the hip seen when there is only one dysplastic hip
A hip click without hip instability in newborn is
common and benign finding
disorder that results from a temporary loss of blood supply to the proximal femoral epiphysis
Legg-Calve-Perthes disease
cause of Legg-Calve-Perthes disease
not well understood
it has been suggested:
trauma
infection
inflammation
acetabular retroversion
stages of Legg-Calve-Perthes disease
initial stage - begins with ischemic event
ossification is arrested
bone becomes sclerotic
second stage
“fragmentation stage”
bone is deformed and even fractured
third stage
healing stage or reossification stage where old necrotic bone is reabsorbed and new bone is formed
last stage
remodeling stage
residual deformity may be observed
typical age range for Legg-Calve-Perthes disease
4-8 yrs old
gender more affected in Legg-Calve-Perthes disease
male
presentation of Legg-Calve-Perthes disease
pain on affected side
persistent
can start in hip and radiate to thigh or knee and not usually severe
can even be chronic
many patients have delayed skeletal maturation and are often shorter than normal
what has better range of motion (typically)
septic hip
transient synovitis
Legg-Calve-Perthes disease
Legg-Calve-Perthes disease
a mild dysplasia of the proximal femoral epiphysis
Meyer Dysplasia - normal variation and is usually bilat
labs and imaging for Legg-Calve-Perthes disease
CBC
CRP
ESR
blood cultures
Which are all typically WNL
In some kids
abnormal thyroid hormone levels and insulin-like growth factors have been noted
X rays
-Hip
-Pelvis
Anterior/posterior and frog leg views help in tracking the progression
Bone scan or MRI can be useful in the early stages of the disease when x ray changes are difficult to detect
goal of treatment in Legg-Calve-Perthes disease
keep the femoral head seated in the acetabulum
promote good range of motion
Mild cases
-observe with normal activity
Severe cases
-need activity restriction
-physical therapy
-bracing to hold the head of the femur in proper position to optimize its functional shape
infection of the bone that may occur by hematogenous spread from bacteremia
Osteomyelitis
what causes osteomyelitis
and most common cause in pediatrics
local invasion from contiguous infection
or from direct inoculation from sustained trauma or surgical procedure
most common:
hematogenous - when blood borne organisms seed the metaphysis of the bone (can happen in transient bacteremia from ear infection or URI)
what happens if osteomyelitis goes untreated
purulent material may extend through the cortex into the subperiosteal space. Once in the periosteal space, accumulation of purulent material increases and results in bone necrosis
most common pathogens in osteomyelitis
other common
S. Aureus
other common:
Streptococcus pyrogens
Streptococcus pneumoniae
K. kingae
HIB
MRSA
reporting of K.kingae in osteomyelitis primarily affects children of what age
6 mos - 4 yrs of age
Things to note on MRSA osteomyelitis
more virulent
higher and prolonged fevers
increased inflammatory markers
more local tissue destruction
longer hospital stays
higher risk of complications such as DVT, septic pulmonary emboli and Septic thrombophlebitis
presentation of osteomyelitis
localized pain - constant and increasing in severity
may stop using upper extremity
may walk with limp or refuse to walk
Neonates, infants and nonverbal patients can present with
-new onset irritability
-poor feeding
-change in sleep habits
discrete tenderness at site of infection
edematous
erythema
warm to touch
labs and imaging in osteomyelitis
CBC with diff
ESR
CRP
Blood cultures
WBC elevated in 35% of children with osteomyelitis
CRP and ESR more sensitive to infection
ESR rises slowly and typically elevated (>20 mm/hr) within 48-72 hrs
CRP >10 mg/L more quickly within 6 hours of infection. This number falls more quickly in response to effective management
Plain x-rays to evaluate for other causes of limb pain such as fracture or tumor
MRI is imaging of choice for strong suspicion of osteomyelitis
Empiric antibiotics in osteomyelitis
cover for S. aureus
- flucloxacillin and 1st gen cephalosporins
k.kingae - good sensitivity to PCN and cephalosporins such as cefotaxime bc it also covers for GBS and enteric gram neg bacilli
MRSA - vancomycin, clindamycin, daptomycin, linezolid
when is surgical intervention warranted for osteomyelitis
presence of large subperiosteal, soft tissue or bone abscess
or concurrent septic arthritis
area of necrotic bone
direct invasion of growth plate
antibiotic route guidance in osteomyelitis
2-4 days of IV antibiotics before transitioning to oral antibiotics for 3 weeks
criteria to transition to oral
-clinical improvement as evidence by
–lack of bony tenderness
–normal temps
–reduction of inflammatory markers - primarily CRP
Treatment for children with MRSA osteomyelitis
4-6 weeks of abx with early oral abx acceptable if cultures show susceptibility to Clindamycin
MRSA infection is associated with increased _______ (complication)
DVT
risk factors for osteomyelitis associated with poor prognosis
MRSA
S. pneumoniae
pyomyositis
abscess
infection in hip
younger age
delayed treatment
long term complications of osteomyelitis
limb-length discrepancy
abnormal gait
recurrent infection
what happens in Chronic osteomyelitis
a segment of the cortex becomes devascularized to form a sequestrum or dead bone. An involucrum, which is new bone with a limited vascular supply may form. Treatment involves several surgical procedures and long term (4-6 months) antibiotic treatment
vaccination to help reduce risk of infection in osteomyelitis
HIB - prevents osteo by HIB
infection in the synovial space of a joint
septic arthritis
joints most often affected by septic arthritis
knee
hip
ankle
elbow
osteomyelitis can lead to septic arthritis esp in
hip
shoulder
elbow
ankle
(due to intra-articular location of metaphyseal bone in these joints)
Peak incidence of septic arthritis is
children younger than 3 yrs
males twice as often as females
risk factors for septic arthritis
prematurity
immune compromised
organisms associated with septic arthritis
S. aureus
MRSA
K. kingae (Moraxella)- more popular in children younger than 4
GBS occasionally in neonates
other organisms
-A. Streptococcus
-S. pneumoniae
-Salmonella
-Neisseria gonorrhoeae
-HIB not as common due to vaccinations
-S pneumoniae rates are also on the decline
presentation of septic arthritis
pain in affected joint
may not use the affected extremity
If the hip, knee or ankle is involved: child will limp or refuse to bear weight
Neonates - irritable, can refuse to eat, might not spontaneously move the affected limb (pseudoparalysis)
can have history of URI or skin/soft tissue infection
joint painful to palpation
likely red, warm and swollen
range of motion is painful and limited
If hip is affected - pt may prefer to lay with hip in external rotation, abduction and mild flexion bc it creates more space in the joint capsule
Lipincott
-Ill appearing
-Fever >38
-Joint pain
-•History of recent viral illness, soft tissue or upper respiratory tract infection. • Insidious joint pain. •Affected joint: painful to palpation, erythematous, warm, edematous; limited range of motion. •If the hip, knee, or ankle are affected, refusal to bear weight. •If hip, external rotation, adduction and mild flexion.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1407). Wolters Kluwer Health. Kindle Edition.
what should be on your differential for a child with joint or bone pain
osteomyelitis
poststreptococcal arthritis
juvenile idiopathic arthritis
leukemia
Lyme disease
accidental or inflicted trauma
tuberculosis
osteomyelitis and septic arthritis often occur together
if hip is involved:
SCFE
LCPD
myositis of obturator or psoas muscle
transient synovitis of the hip (self limiting)
Kocher criteria is for what and what does it include
septic arthritis
temp >38.5 C (101.3)
refusal to bear weight
elevation of ESR (>40) or CRP
and/or WBC > 12,000
key labs for septic arthritis
CBC with diff
ESR
CRP
Blood cultures
WBC is usually elevated >12,000 but not invariably
ESR and CRP will rise
ESR (rises within 48-72 hrs)
CRP (rises in 6 hours)
purulent aspiration - culture
imaging in septic arthritis
X rays - to look for trauma and noninfectious conditions
finding of joint space widening suggests an effusion
US to evaluate irritable joints (esp hip joints)- can detect distention of the joint capsule and effusion
If fluid is found in joint, diagnostic aspiration should be done with US guidance
MRI can also identify a joint effusion but most helpful in identifying concomitant osteomyelitis in an adjacent bone or myositis in the adjacent musculature.
Technetium bone scans are indicated when infections are located in difficult to assess areas such as ankle and shoulder. Bone scans are esp beneficials for evaluating neonate because there may be more than one site of infection
surgical irrigation and drainage in septic arthritis
smaller joints such as wrist are controversial bc they usually resolve with abx
larger joints (esp hip and shoulder) irrigation and drainage should be performed emergently in the OR bc of potential for cartilage damage and compromised blood supply
Abx for septic arthritis
parenteral abx begin as soon as blood and joint aspiration cultures are obtained
Empirics should cover
-S. aureus (MSSA and MRSA)
-group A strep
-K. kingae
and if not immunized
-HIB
-S pneumoniae
Combo of Vanc and 3rd or 4th gen cephalosporin (Cefotaxime, ceftriaxone, cefepime)
infants younger than 2 months should get abx that cover for GBS, S aureus and Gram neg bacteria such as Vancomycin and Cefepime or Gentamicin
Nafcillin or Oxacillin and cephalosporin (cefazolin) are preferred for MSSA
Clindamycin or newer agents (Ceftaroline, linezolid) can be considered for susceptible MRSA (also Vancomycin)
Group A Strep- Amp/Amox
Strep pneumoniae - amp/amox, ceftriaxone/cefotaxime, vanc
Kingella kingae - amp/amox, cefotaxime
neonates - 3rd gen cephalosporins (Cefotaxime)
3-5 days of IV abx followed by 2-3 weeks of oral for uncomplicated cases of septic arthritis (no concomitant septic shock, osteomyelitis, abscess or marginal abx susceptibility
switching to oral abx - needs to have clinical improvement - fever, pain, declining CRP to <10 and ability to tolerate oral abx
a spinal fusion imitates
a fracture of a bone by decorticating (removing the outer layer of the bone) to mimic the need for bone healing
The bone graft then acts as a scaffold for bone remodeling
6 phases of bone remodeling
rest
activation
resorption
reversal
formation
mineralization
Bone remodeling is completely replaced in what time frame following mineralization of the bone
2-8 months
another name for spinal fusion
spinal arthrodesis
surgical procedure that joins one vertebra to an adjacent vertebra
spinal fusion
what warrants urgent intervention for spinal fustion
spinal deformity, trauma, degenerative conditions, tumors and infections that cause spinal instability exposing neural contents making risk for injury
what spinal deformities sometimes require spinal fusion
scoliosis
kyphosis
spondylolisthesis
for most cases this is elective
what degenerative spinal condition is seen during the adolescent period
lumbar disk degeneration most commonly related to strenuous physical activity, posttraumatic injury or congenital spinal deformity
what conditions can cause loss of bone integrity compromising the structural integrity of the spine
fracture
tumor invasion
infective process
the majority of spinal deformity procedures are performed through what type of approach
posterior
what type of surgical approach for spinal fusion
when fewer segments require fusion
anterior
so that leaving normal motion over more segments of the spine
what type of surgical approach for spinal fusion
in case of a spinal tumor located in the vertebral body
anterior
to remove the tumor and stabilize vertebra
what type of surgical approach for spinal fusion
in case of a spinal tumor located in the posterior elements of spinal column
posterior
in spinal fusion a bone graft taken from the Pt iliac crest is ______
autologous
in spinal fusion a bone graft taken from a cadaver donor is ______
autogenous
what protein can be used in bone graft to facilitate fusion healing
Bone morphogenic protein (BMP)
How often should a neuro assessment be performed following a spinal fusion surgery
every 2 hours for the first 24 hours to monitor for deficits
Narcotics and muscle relaxers are needed after a spinal fusion surgery for how long
typically needed for the first 2-4 weeks after surgery
what post op complications can occur following a spinal fusion
increased blood loss
resp changes due to thoracic rib cage changes
SIADH secondary to intraoperative volume replacement and spinal manipulation
immobilization after spinal fusion
Sometimes Lumbosacral orthosis (LSO) or a thoracolumbar orthosis (TSO) will be required if it is determined that the spinal column requires additional support until the spinal fusion solidifies - approx 6 months
postob mobility after spinal fusion
sitting within the first 24 hours
walking within 48-72 hours
prior to discharge they should be ambulatory with minimal assistance
for the first month after - progressive walking program, mild upper and lower extremity strengthening and participation in activities of daily living
No flexion, extension or rotation of the spine until fusion has healed
What technique for invasive device used to monitor compartment syndrome?
skin is opened and a catheter is placed into the compartment
Slit technique
What technique for invasive device used to monitor compartment syndrome?
a catheter with a wick is placed in the compartment
Wick technique
What technique for invasive device used to monitor compartment syndrome?
a straight or side-port needle is placed into the compartment
Needle technique
local inflammation of the muscle
myositis
symptoms of myositis
muscle pain, weakness, or difficulty performing tasks of daily living
what causes Myositis
who is it more common in
Viral
Acute
self-limited illness occurs during epidemics of flu A/B; also more predominant in males
Suspected to be caused by invasion of the muscle tissue by inflammatory cells;
presentation of myositis
viral symptoms such as
fever
anorexia
muscle pains
Myalgias: mild to moderate and muscle tenderness with calves most affected during the
early phase of many acute viral infection
Weakness: mild to severe
Dark urine in those who develop rhabdo
Benign self limiting conditon
Bilateral muscle pain, tenderness, and something swelling during first week of flu illness
with calf muscles most severely affected
Child may refuse to walk or toe walk
On exam, calves are tender
Serum creatinine phosphokinase may be elevated
Myoglobinuria with AKI rare→ when rhabdo develops it occurs
Labs and diagnostics on myositis
CK may/ will be mildly elevated but no myoglobinuria or acute renal failure
Muscle imaging and biopsy reserved for cases of weakness unrelated to acute pain,
markedly elevated CK, or EMG abnormalities
treatment for Acute/viral myositis
Most are self-limited and management is directed at relief of symptoms
Analgesic agents such as tylenol or NSAIDs
Usually resolve in 3-10 days
Highlights on acute childhood myositis
what is it
symptoms
prognosis
Accompany acute viral infections seen during flu epidemics
Symptoms include marked pain and tenderness, localized to calves
Occurs as acute illness is subsiding, usually 24-48 hours after resolution of presenting symptoms
Child will refused to walk or will have difficulty walking due to pain or true muscle weakness
Ankles held in plantar-flexion with resistance to dorsiflex
Muscle enzymes elevated 20-30x normal, rhabdo is rar
Muscle biopsy reveals muscle necrosis and muscle fiber regeneration
Full recovery in 3-10 days with decrease in muscle enzymes within 3 weeks
Childhood condition in which the proximal femoral epiphysis has a temporary interruption in blood supply, leading to bone necrosis and subsequent repair.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1395-1396). Wolters Kluwer Health. Kindle Edition.
Legg-Calve-perthes disease
is osteomyelitis more common in adults or kids and why
more common in children bc of rich metaphyseal blood supply and thick periosteum
Approximately 50% of osteomyelitis occur in children < ____ years of age
5
Most common sites of osteomyelitis
femur
tibia
what disease processes increase risk of osteomyelitis
hemoglobinopathies such as sickle cell
chronic renal disease
type 1 DM
compromised immune system
________ is the most common organism in children (except neonates), 70% to 90% of Osteomyelitis infections.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1399). Wolters Kluwer Health. Kindle Edition.
Staph Aureus
Community acquired MRSA is becoming more prevalent
Other agents
Group A hemolytic strep
Strep pyogenes
Strep pneumoniae
what is the most common organism in neonates causing osteomyelitis
Group B strep
organism most common causing osteomyelitis associated with puncture wounds (esp of the foot)
Pseudomonas
in osteomyelitis, what imaging is helpful in identifying abscess and areas of destruction
CT
in osteomyelitis, what imaging is helpful in evaluating for abscess, though unable to image details of the bone
US
Most common hip disorder in adolescence, typically associated with obese African American or Latino adolescents.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1403). Wolters Kluwer Health. Kindle Edition.
Slipped Capital Femoral Epiphysis (SCFE)
what gender and age is more common in Slipped Capital Femoral Epiphysis (SCFE)
Males
ages 12-15
Characterized by the separation of the growth plate in the proximal femoral head with the epiphysis slipping posteriorly with potential for complete dislocation.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1403). Wolters Kluwer Health. Kindle Edition.
SCFE
Etiology of SCFE
Unknown, but may be related to rapid growth, obesity, hypothyroidism, family history, trauma, or genetic conditions such as Trisomy 21.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1403). Wolters Kluwer Health. Kindle Edition.
Acute SCFE vs Chronic vs Acute on chronic SCFE
Acute: is a sudden exacerbation of < 3 weeks; a radiological shift in the epiphysis without a callus formation.
Chronic: has a gradual onset of symptoms over 3 weeks with some remodeling of the bone.
Acute on Chronic: involves symptoms for months, but exacerbated with injury.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1403). Wolters Kluwer Health. Kindle Edition.
symptoms for SCFE
•Acute or chronic hip, thigh, or knee pain. •Limited rotation and obligated external rotation of the hip.
Pain can be severe with shortened stance of affected leg and Trendelenburg gait.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1403-1404). Wolters Kluwer Health. Kindle Edition.
Ice cream slipping off cone appearance on X ray
SCFE
SCFE management
•Strict non–weight-bearing status until percutaneous pinning or in situ screw fixation of the femoral head through the growth plate has been placed.
•More severe dysfunction may require open osteotomy and internal fixation to secure the bones.
•Crutches are issued for 2 to 3 weeks postoperation for stable SCFE; 6 to 8 weeks for unstable SCFE.
•Team approach requires PT for gait training, hip precautions, and range of motion exercises.
•Sports and vigorous activity should be avoided until growth plates close.
•Overall care is provided by the primary care provider.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1404). Wolters Kluwer Health. Kindle Edition.
Parkland formula Burn pt
> 15 % TBSA
4ml/kg
4ml x kg x % burn
divide by 2
divide by 8
LR
cafe au lait spots and lisch nodules are associated with what?
Neurofibromatosis type I
café au lait spots and lisch nodules are associated with what?
Neurofibromatosis type I
a purulent bacterial infection in the synovial fluid joint spaces; causes rapid destruction of the articulate cartilage. Considered a medical emergency
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1405). Wolters Kluwer Health. Kindle Edition.
Septic Arthritis
joints commonly affected in septic arthritis
hip
knee
elbow
ankle
age and gender for septic arthritis
less than 3 yrs
males
neonates and premature infants are at greatest risk due
what family of snake?
Rattlesnake
Crotalid
What family of snake
copperhead
Crotalid
What family of snake
Cottonmouth
Crotalid
What family of snake?
Coral snake
Elapid
what family of snake is venomous?
Crotalid
Elapid
Crotalid
characteristics of venomous snakes
elliptical pupil
presence of retractable fang
Triangular head
Will have heat-sensing pit located between the nostril and eye (differentiates between bite of coral snake)
Characteristics of non-venomous snakes
round pupils
multiple small teeth instead of fangs
Oval-shaped head
what family of snake bites are most prevalent in US
95% in US are pit vipers (Crotalid)
Pit vipers are what family and what does that include
Crotalid
includes Rattlesnakes, copperheads and cottonmouths
whats the snake venom rhyme
“red on yellow, kill a fellow; red on black, venom lack”
what do coral snakes look like
black snout with alternating red, yellow, and black bands along the body
what family is a king snake?
Venomous?
what does it look like?
Colubridae
Non-venomous
Red band bordered by black on each side
black snout with alternating red, yellow, and black bands along the body
Coral snake
Red band bordered by black on each side
King snake
Crotalid venom contains 90% _____ by dry weight
protein
what problems come from Crotalid snake bites
Local tissue destruction, edema, red cell extravasation -> platelet aggregation -> thrombocytopenia
May also lead to shock
Glycoprotein can cause reaction similar to DIC
Intravascular fluid leaks through damaged membrane causing more edema and shock
what happens in Mojave rattlesnake envenomation (also Timber rattlesnake - rare)
neurotoxic effects -> cranial nerve paralysis (ptosis, ophthalmoplegia) and flaccid paralysis -> may require intubation
what happens in Elapids envenomation
Neurotoxin causes flaccid paralysis and myonecrosis
___% of all snake bites occur in the pedi population
25%
what time of year do snake bites happen more
warmer months of the year from April to October
Gender bitten more
males
what differentiates envenomation “DIC” from true DIC
the fibrin monomers are produced by the glycoproteins, rather than consumption or thrombin of activation of Factor XIII
True clinical bleeding is rare
Elapid venom exerts its effect through ___ and ___
neurotoxins
Phospholipase A2
Direct neurotoxins bind the postsynaptic membrane of the neuromuscular junction, causing a flaccid paralysis, which can be long lasting.
Phospholipase A2 causes myonecrosis
Presentation of Crotalid envenomation
1st: immediate burning pain at the bite site
2nd: edema, erythema that will increase over next 8-10hr
Ecchymosis or bullae (serous or hemorrhagic) may form at the site within hours and can lead to lymphadenopathy or lymphangitis
Necrosis of extremity
Compartment syndrome rare (bite directly into compartment)
Local edema can cause airway compromise if bite is near neck/face
Systemic signs
Perioral paresthesia or metallic taste within minutes
Weakness,
N/V,
diaphoresis,
dizziness,
syncope, tachycardia
Rhabdo,
pulm edema with resp failure,
hypotension,
shock,
CV collapse,
kidney failure
Anaphylactic reactions
Presentation of Elapid envenomation
Bites are unimpressive -> minimal pain and swelling and no puncture marks
Systemic sxs take hours to develop
Malaise and nausea,
muscle fasciculation,
ptosis,
diplopia -> can progress to difficulty swallowing or talking with diaphragmatic paralysis -> resp failure
Plan of care for Crotaline envenomation
CBC, type and screen, UA, coags, CMP, BUN, Cr, CK, fibrinogen, fibrin split products: check Q6 to monitor for systemic effects and treatment
what labs do you need to draw for Elapid envenomation
None
what does dry envenomation mean
no venom injected
what category of envenomation
Local signs adjacent to bite without progression of proximal edema
Perioral paresthesia but will have normal lab studies
Mild
what category of envenomation?
Edema extending proximally from bite
Systemic: N/V, diarrhea, dizzy, weak, diaphoresis
Neurotoxicity: fasciculation
Any coag abnormality is considered moderate -> incr PTT and PT, decr plt or fibrinogen, presence of fibrin split products
Moderate
what category of envenomation?
Edema extending proximally from bite
Systemic: N/V, diarrhea, dizzy, weak, diaphoresis
Neurotoxicity: fasciculation
Any coag abnormality is considered moderate -> incr PTT and PT, decr plt or fibrinogen, presence of fibrin split products
Impending resp failure or shock
Significant (beyond gingival or mild epistaxis) bleeding
Altered mental status
Severely deranged labs
Severe
Antidote for Crotaline venom
Crotaline Polyvalent Immune Fab (Crofab) – sheep derived
You may have a reaction to Crofab if your are allergic to
latex
papain
papaya
dust mites
sheep products
How is Crofab dosed?
when do you treat?
in vials, not by weight - dosed by severity of the envenomation
Pediatric dose is equivalent to pediatric dose
Moderate to severe envenomation: Give 4-6 vials asap
If hemodynamic instability or life-threatening toxicity -> initial bolus is 8-12 vials
If after 1hr there is no improvement, repeat bolus dose
Can give more boluses, but contact specialist if patient needs more than 2 rounds
Sxs improvement: halt to edema progression, normal lab values (hemodynamic parameters), clear improvement in any neurotoxicity
Maintenance dosing of antivenom once symptoms are controlled
After 6hr of sxs control: 2 vials of antivenom are given Q6hr for a total of 3 doses (6 vials total)
After using Crofab for envenomation, how long do you need to monitor
24 hours after initial control is achieved. If they develop new or worsening symptoms, repeat appropriate bolus dose based on severity of new symptoms
What do you do if someone is allergic to crofab.
Call poison control. may use epi for anaphylaxis. May need to resume antivenom at slower rate
what treatment for elapid envenomation
Might not be able to reverse symptoms with antivenom
Antivenom to coral snakes has not been produced in US for decades
Supportive care is the MAINSTAY – may need to intubation
wound care for envenomation
Do not use tourniquets or compression bands -> may cause release of toxin once released
Always search patient for multiple bites
Wash with soap and water and search for remaining teeth/fangs
Tissue necrosis -> debridement
Tetanus prophy
Action items on Crotaline envenomation
Immobilize extremity in comfortable position at or slightly below heart level
Mark bite, measure circumference to follow progression of edema (take hourly until no more edema); leading border of edema should be marked and timed with each measurement
Check distal pulses hourly -> if none are found, check compartment pressures to see if it is above 30 (fasciotomy is not recommended, give more antivenom)
Leave bullae intact unless on the digits and they interfere with distal perfusion
Pain control with narcotics if CV stable
Skin grafting for large areas of tissue breakdown
Latrodectus mactans
Black widow spider
what is the neurotoxin released in a Black widow spider envenomation
A-Latrotoxin
what happens with A-Latrotoxin
an excitatory neurotoxin that causes increased neurotransmitter release from presnyaptic neurons at the neuromuscular junction, sympathetic, and parasympathetic synapses.
what gender of black widow can envenomate humans
Female (larger than males)
true/false
black widow is very aggressive
false
not aggressive unless provoked or threatened
what sensation is felt in a black widow envenomation followed by what presentation
small pinprick
Severe cramping pain at the site of the bite begins within 15-60 minutes. Pain spreads from bite to rest of body.
Chest and abdominal pain are prominent, but all muscles may be involved
Abdominal pain may be accompanied with abd rigidity
Diaphoresis, N/V, dizziness, ptosis, headache, irritability, dyspnea, dysarthria, facial swelling, and conjunctivitis
HTN, increased ICP, or resp failure
may see one or two fang marks
Positive tap test
Black widow envenomation
tapping at suspected bite site elicits pain
treatment for black widow envenomations
1st responders should apply a cold pack to bite site and elevate site if possible
In ED, perform wound care cleansing with soap and water and tetanus prophylaxis as indicated. CBC, coag studies, ECG, and urinalysis should be obtained and shoudnt come back abnormal. Start IVF
Symptom control→ oral analgesic if mild and IV opoids/benzos for sereve cases
Latrodectus antivenom used for high-risk pts or those with uncontrolled symptoms despite therapy. Symptoms may improve within 45 minutes of antivenom administration
Asymptomatic pts or those with mild/local symptoms should be observed in the ED for 6 hours
Loxosceles reclusa
Brown recluse
Venom toxin in a Brown recluse envenomation
what does it do?
Venom includes Sphingomyelinase D that damages cell membranes of RBCs, endothelial cells, and PLTs→ hemolysis, PLT aggregation, coagulation→ local tissue damage and occasional systemic toxicity
where is the Brown recluse commonly found
Southern and midwestern USA
what does the brown recluse look like and when are they dangerous. Where do they like to be?
They are brown and will only attack if provoked. They are usually found outdoors under rocks or woodpiles, but can be found indoors inside dark areas (closets).
Presentation of Brown recluse envenomations
Local symptoms: pain at site of bite, usually within 3-4 hours. A white ring of tissue ischemia secondary to vasoconstriction can develop, followed by a pustule or blister. This pustule and ring of erythema gives a bull’s-eye appearance to the lesion. Over the next few days, the pustule will darken, become necrotic, and expand uo to 10-15 cm in diameter. The pustule then drains, leaving a dark/necrotic/ulcerated crater. Necrosis is usually worse in areas with increased subcutaneous fat
Systemic symptoms: appear 24-48 hours after bite; hemolysis, thrombocytopenia, shock, jaundice, kidney failure, bleeding, or pulm edema
Labs for Brown recluse envenomation
No definitive lab test. If the spider cannot be brought to ED and history is atypical, diagnosis can be challenging
CBC, metabolic panel, coag studies, and urinalysis if showing systemic s/s
treatment for Brown recluse envenomation
Systemic: Supportive since there is no available antivenom in the US
Local: area should be washed with soap and water. The wounded extremity should be splinted and elevated with a cold compress at the site.
As necrosis develops, surgical debridement may be beneficial. Large areas of necrosis may require skin grafting
Tetanus prophylaxis given if indicated.
Pts with suspected brown recluse bite with no symptoms can be discharged after 6 hours of observation in the ED
Pts with suspected brown recluse bite with no symptoms can be discharged after __ hours of observation in the ED
6
most common places eczema dermatitis is seen
Cheeks
antecubital fossa
posterior knee folds
most common skin disease in children
Atopic dermatitis (20% of children)
who is at higher risk for atopic dermatitis
Most common skin disease in children, 20% of children have it
Urban areas, higher socioeconomic classes
Lower risks: area where industrial pollution is less, eosinophil-mediated infections (helminth) are endemic
Atopic march: will get atopic dermatitis with allergic rhinitis and allergy (asthma occurs in 50%)
in eczema, what bugs cause secondary infections most often
Staph, strep pyro
HSV eczema herpeticum – life threatening
Varicella zoster virus
Coxsackievirus
Smallpox (eczema vaccinatum) – life threatening
Molluscum contagiosum
Fungal infections
circumscribed and well defined borders, scale or hyperkeratosis is thicker/greasy/yellowish, located on scalp/eyebrow/perinasal region/upper chest/back (dandruff and cradle cap)
Seborrheic
localize on elbow/knee/lower back/scalp, lesions are salmon colored at the base with an overlying hyperkeratosis that is thick with silver coloration, well demarcated/oval or round/thick plaques
Psoriasis
distribution limited to one area of the body corresponding to contact with the allergen, lesion is well demarcated, bizarre, linear, square, or angulated (poison ivy, diaper rash)
Allergic contact dermatitis
contact sensitization to nickel in metals, occurs on areas of the body where nickel or other metal are
Nickel dermatitis
Mainstay treatment for dermatitis
Topical corticosteroids
Class I: highest potency (typically avoided in younger children or areas of thin skin)
Class VII: lowest potency
eczema care
KEY: Frequent liberal use of bland moisturizers to restore skin barrier, avoidance of triggers of inflammation, use of topical anti-inflammatory medication
Control of pruritus and infection
If topical is not working, systemic therapy with immunosuppressive agents or UV light therapy can be used
Daily short bath with warm (not hot) water
Moisturizing cream/ointment to entire body immediately after to trap moisture, apply topical medications immediately after bath as well
Avoid common triggers of inflammation: rubbing/scratching, contact with saliva or acidic foods, soaps/detergents, wool or other harsh material, fragrances, sweat, chlorinated pools, low humidity, tobacco smoke, dust mite, animal dander, environmental pollen, mold
How do you enhance penetration for topical corticosteroid application for dermatitis
use wet wraps with topical corticosteroid application
difference in ointment, creams, lotions and spray, foam and gels in dermatitis
OINTMENT PREFERRED: increased efficacy, occlusive nature, tolerability
Creams: better for older patients for cosmetic reason and in warmer climates
Lotion: cause irritation
Spray, foam, gel: good for hair-bearing areas
Everything but ointment will be irritating to open skin and should be avoided
How often do you apply corticosteroids in dermatitis
BID
systemic effects of topical corticosteroid applications
adrenal suppression or cushing -> can happen with application to large area or occluded area (diaper, bandages) at risk for enhanced penetration
immune modulators in Atopic dermatitis
Topical calcinerurin inhibitors (immune modulators): Tacrolimus, pimecrolimus
No potential for skin atrophy -> good for face or genital lesions
Approved as second line for mild to moderate dermatitis
atopic dermatitis
treatment
Topical Corticosteroids
Topical calcinerurin inhibitors (immune modulators): Tacrolimus, pimecrolimus
-No potential for skin atrophy -> good for face or genital lesions
-Approved as second line for mild to moderate dermatitis
Sedating antihistamines (Benadryl): mild effect on pruritus but can improve sleeplessness due to scratching (non-sedating are of little benefit during day)
Systemic corticosteroids is rarely used and should be tapered when given and be aware of rebound dermatitis
UV light: moderate to severe cases in older children
2-3 times weekly
Potential for skin CA
Systemic immunosuppressives: cyclosporin methotrexate, azathioprine, mycophenolate – severe cases
most common secondary skin infection found in atopic dermatitis
Impetigo with Staph
group A Strep also common
treatment for impetigo
Topical mupirocin for local lesions; widespread lesions require PO 1st gen ceph Cephalexin
Pustules, erythema, honey crusting, flare of disease, lack of response to adequate anti-inflam therapy
Impetigo
Multiple, pruritic, vesiculopustular lesions occur in disseminated pattern ( on normal skin and areas of dermatitis)
Rupture and form crusted umbilicated papules and punched out hemorrhagic erosions
Irritability, anorexia, fever
Eczema herpeticum after HSV infection – serious complication
Tzanck test
scraping of skin lesion and staining, can also send vesicle fluid
test for Eczema herpeticum after HSV infection
How to prevent atopic dermatitis
Avoid triggers of inflammation and apply moisturizer
Breast feeding for at least 4 months can decrease risk
Extensively hydrolyzed casein based formula
Early intro of peanuts in children at high risk for allergy (have severe eczema, egg allergy, or both) may decr risk of getting the peanut allergy
contact dermatitis is what type of hypersensitivity disorder
Type IV or delayed hypersensitivity
what type of contact dermatitis
ill-defined, scaly, pink or red patches and plaques
Irritant
what type of contact dermatitis
form of irritant derm
Diaper dermatitis
where is irritant contact dermatitis is usually seen
dorsal surface of hands, often from repeated hand washing or exposure to irritating chemicals
diaper dermatitis is a form of
irritant dermatitis
diaper dermatitis is caused by irritation to
urine/feces
what secondary infection can complicate diaper rash
Candida albicans or bacterial infection
what type of dermatitis is Poison ivy and poison oak
Acute allergic contact Rhus (or Urushiol induced) dermatitis
describe the rash associated with Poison ivy/Poison oak
Bright pink, pruritic patches, linear or sharply marginated bizarre configurations
Inside the patches are clear vesicles and bullae
Bright pink, pruritic patches, linear or sharply marginated bizarre configurations
Inside the patches are clear vesicles and bullae
Poison Ivy
Poison Oak
timeline of exposure to rash for Poison ivy/poison oak
Sxs of disease may be delayed 7-14 days after first exposure, subsequent exposures will occur within hours and are more severe
what type of dermatitis is nickel
Chronic Allergic nickel dermatitis
what do the lesions look like for Chronic Allergic nickel dermatitis
Lesions are pink, scaly, pruritic plaques that mimic atopic derm
Lesions are pink, scaly, pruritic plaques that mimic atopic derm
Chronic Allergic nickel dermatitis
what is distribution of Rhus dermatitis
lower legs, distal arms + linear configuration of lesions
what is distribution of Nickel dermatitis
derm of ears, wrists, periumbilical
Treatment for contact dermatitis
Topical corticosteroids for allergic and irritant
High potency and short course of PO may be necessary for severe reaction to allergic contact derm
Oral antihistamine to control itching
Candia diaper rash: topical nystatin or topical azole antifungal + low potency topical corticosteroid
Seborrheic Dermatitis
in infant is what
cradle cap or dermatitis in the intertriginous areas of the axillae, groin, antecubital and popliteal fossae, umbilicus
what does Seborrheic Dermatitis look like in adolescents
Dandruff
what causes Seborrheic Dermatitis
Malassezia species in sebaceous rich areas such as Scalp, eyebrow, eyelid, nasolabial fold, external auditory canal
How long does Cradle cap last
begins during first month and lasts through first year
koplic spots
Measles
Maculopapular rash with lymphadenopathy
Rubella
Rash + koplik spots
Measles
Rash + lymphadenopathy
Rubella
Rash involving cheeks
Erythema infectiosum or Fifth disease
Rash after the fever
Roseola
Sandpaper like rash
Scarlet fever
rash of different stages
chicken pox
rash involves hand foot mouth
Hand foot mouth disease
thick, greasy and waxy, yellow-white scaling and crusting of the scalp
cradle cap
German measles is also called
Rubella
Roseola is also called
Sixth disease
How do you differentiate between cradle cap and tinea capitis
Fungal culture and potassium hydroxide
Treatment for Seborrheic Dermatitis
Asymptomatic and does not require any treatment
Cradle cap: oil may be gently massaged into scalp and left on for few minutes before brushing out the scale and shampooing
Daily shampoo with ketoconazole, zinc pyrithione, selenium sulfide, salicylic acid shampoo
Seborrheic derm with inflamed lesions -> low potency steroids 2x/day
ordinary measles is called
Rubeola
Roseola infantum is also called
Exanthum subitum
symptoms of rubeola
conjunctivitis
cough
coryza
fever
koplik spots on buccal mucosa
rash starts at hairline and spreads cephalocaudally over 3 days
Herald patch
Pityriasis Rosea
when does Pityriasis Rosea occur (age)
adolescence
Solitary 2-5cm pink oval patch with central clearing
Herald patch in Pityriasis Rosea
Progression of Pityriasis Rosea
Solitary 2-5cm pink oval patch with central clearing = herald patch = 1ST MANIFESTATION, found on trunk or thigh
· 1-2 weeks later a general eruption occurs on torso and proximal extremities
· 0.5-2cm oval red or tan macules with fine, bran like scale arranged parallel to skin tension lines = Christmas tree pattern
· Pruritus present in 25% of cases
· Lasts 4-14 weeks
· Residual hypopigmentation or hypopigmentation can take months to clear
treatment for Pityriasis Rosea
Self limiting
can use oral antihistamine or low potency topical corticosteroid for itching
Christmas tree rash
Pityriasis Rosea
Well-demarcated, erythematous scaling papules and plaques
· Occurs at all ages, chronic and relapsing
Psoriasis
what things can exacerbate psoriasis
Infection (strep pyogenes)
stress
trauma
medications may exacerbate
psoriasis vulgaris is also called
Plaque type psoriasis
Auspitz sign
Plaque-type psoriasis (psoriasis vulgaris)
Lesions are localized or general
o Round, well demarcated red plaques measuring 1-7cm with micaceous scale = thick, silvery appearance with pinpoint bleeding points revealed on removal of scales (Auspitz sign)
Lesions in psoriasis have distinct distribution involving extensor aspect of elbow/knee,
Lesions in psoriasis
Lesions are localized or general
o Round, well demarcated red plaques measuring 1-7cm with micaceous scale = thick, silvery appearance with pinpoint bleeding points revealed on removal of scales (Auspitz sign)
Lesions in psoriasis have distinct distribution involving extensor aspect of elbow/knee,
Lesions in psoriasis have distinct distribution involving extensor aspect of elbow/knee, posterior occipital scalp, periumbilical region, lumbosacral, intergluteal cleft
· Children will have facial lesions
· Nail plate: pitting, onycholysis, subungual hyperkeratosis, oil staining (reddish, brown color)
· Guttate = numerous small papules and plaques diffusely distributed on torso
· Erythrodermic = covering large body surface areas
· Inverse = moist red patches affecting body folds
· Pustular
·
Treatment Psoriasis
Topical corticosteroid – least potent as possible to avoid AE
o Do not use oral -> can induce pustular psoriasis
o Phototherapy, vit D analog, salicylic acid
o Immune suppressive meds may be needed for severe cases
what type of psoriasis?
numerous small papules and plaques diffusely distributed on torso (teardrop-shaped)
Guttate
what type of psoriasis?
red covering large body surface areas
Erythrodermic
plaque psoriasis is symmetrical or assymmetrical
symmetrical
most common psoriasis
Plaque psoriasis
Plaque psoriasis is worse during what season
winter
Guttate psoriasis classically preceded by what infection
psoriasis classically follows a preceding streptococcal infection, typically pharyngitis or perianal streptococcus.
what type of psoriasis can be life threatening
Pustular psoriasis
Psoriasis with sudden onset with leukocytosis, malaise, fever and hypocalcemia
Pustular psoriasis
what electrolyte imbalance is associated with pustular psoriasis
hypocalcemia
Triggers for pustular psoriasis
Pregnancy
withdrawal of oral glucocorticoids
what type of psoriasis
Head to toe generalized erythema
erythrodermic
Psoriasis that has issues with sepsis and fluid loss due to issues with barrier protection
Erythrodermic psoriasis
symptoms for rubella
Headache
low grade fever
sore throat
coryza
Forchheimer spots on soft palate
Lymphadenopathy
Rash begins on face and spreads cephalocaudally
Forchheimer Spots
Rubella
Caused by Human Herpes virus 6
Roseola infantum
Exanthem subitum
Roseola infantum
S/S Roseola
Abrupt high fevers
After fever subsides, a rash develops, starting on neck and trunk and spreads to face and extremeties
age for roseola
6-36 months old
Pityriasis Rosea is caused by
HHV-6 and HHV-7
How long before methotrexate reaches peak concentration
2-3 months
How often do you give methotrexate vs Humira
Methotrexate is weekly
Humira is every 2 weeks
Black box warning for Humira
Males with IBD have increased risk of Lymphoma
An acute immune-immediated mucocutaneous disorder characterized by distinctive target-like lesions on the skin.
Typically accompanied by oral, genital, and/or ocular mucosal erosions
Erythema Multiforme
age/gender for Erythema Multiforme
Slight male predominance
Can occur at any age
have been linked to the development of EM
infections, medications, malignancy, autoimmune disease, immunizations, radiation, poison ivy, and UV sunlight exposure
Erythema Multiforme is what type of reaction
hypersensitivity reaction
what is the most common infections trigger for Erythema Multiforme
other causes?
HSV
Other viral causes
Varicella
Parapoxvirus
EBV
CMV
Influenza
HIV
Mycoplasma Pneumoniae
Chlamydia
mycobacterium
TB
Histoplasmosis
EM with high fever in infants can be a sign of
Kawasakis
Rash in EM appears in crops over ___-___ days and resolves when?
3-7 days and resolve in over 1-2 weeks
Rash in EM is found where, spread how and looks like what?
Symmetric
Any part of the body→ palms, soles of feet, and exterior surfaces of arms/legs are most commonly affected
Spread in a centripetal fashion, but the trunk is usually less affected
Lesions start as dusky red macules or red wheals that evolve into target lesions (hallmark sign). Compared to SJS/TEN, bullae develop less than 2% of the time
May be asymptomatic or may have burning/itching
Target lesions
EM
Presentation of EM
Rash
mucosal involvement - usually border of lips
mild systemic - fever, malaise and myalgias
Erythema Multiforme
Erythema Multiforme
skin lesions that are well circumscribed, red wheals, and plaques but lack the central dusky zones
Urticaria
dusky, red plaques with or without central necrosis. Compared to EM, there are fewer lesions and the lesions recur in the same spot within hours of ingestion of offending agent. Clinical findings are hard to differentiate from EM….
Fixed drug eruption
initially presents with mucosal erosions and atypical target lesions. distinct in that it’s widespread epidermal + mucosal membrane necrosis and sloughing of the skin.
SJS
HX of eruption + target-like lesions with or without mucosal involvement is the most important infor to DXs
EM
In severe cases of EM, what labs can you look like
Elevated
sed rate
CRP
WBC and liver enzymes
treatment for EM
self limiting, resolves in 4 weeks
if caused by Medication -> stop that med
If caused by HSV - give PO acyclovir - 25mg/kg/day divided BID for 10 days. For recurrent HSV-associated EM 5-10mg/kg/day for 6-12 months
Mostly supportive
Topical emolient, systemics antihistamines, and NSAIDs for burning or itching
Oral antiseptic washes or local anesthetic solutions for painful oral lesions
EM with severe functional impairment→ prednisolone 0.5-2 mg/kg/day divide BID for 3-5 days should be considered despite controversy of increase risk of infection
What meds can cause EM
Barbiturates
Hydantoins
Nonsteroidal anti-inflammatory drugs
Penicillins
Phenothiazines
Sulfonamides
seizure meds such as lamictal
NSAID, sulfonamide, anticonvulsants (lamotrigine, pheno), antibiotics,
Can also be d/t viral/bacterial, syphilis, fungal
Mycoplasma pneumoniae may have new distinct disease form (mycoplasma pnemonia is seen in school age children- previous test question)
cmv
Acute hypersensitivity reactions characterized by cutaneous and mucosal necrosis
Inflamatory infiltration of the epidermis that leads to skin cell death as well as keratinocyte apoptosis
SJS/TEN
Nikolsky sign
(mild skin friction results in dermal exfoliation; basically skin falls off)
SJS/TEN
whats worse SJS or TEN
TEN
S/S SJS/TEN
Proceed HIGH fever, malaise, URI 1-14days before onset of cutaneous lesions
Vomitting, diarrhea
Target lesions on face and trunk→ bullae and vesicles with central necrosis
Erythema, edema, and pain typically precede development of ulcers
Red macules appear suddenly -> coalesce into large patches -> occur over face and trunk
Nikolsky sign (mild skin friction results in dermal exfoliation; basically skin falls off)
2 mucosal surface involvement
-Genitalia,
-respiratory tract and -eyes
-urinary tract,
-gastrointestinal tract)
Atypical targets may be present at first -> can cause confusion with EM but this target does not have the 3 zones
SJS: epidermal detachment of <10% of BSA
SJS/TEN overlap: 10-30% BSA
TEN: >30% BSA and 1 severe mucosal erosion progressing to diffuse, generalized detachment of the epidermis
How do you dx TEN vs SJS
SJS: epidermal detachment of <10% of BSA
SJS/TEN overlap: 10-30% BSA
TEN: >30% BSA and 1 severe mucosal erosion progressing to diffuse, generalized detachment of the epidermis
treatment for SJS/TEN
supportive therapy
1)Fluid and electrolyte imbalances occur due to water loss from the affected dermis and decrease oral intake in patients with mucositis → strict I/Os and fluid replacement initiated to prevent shock. In the first 24 hours, fluid replacement should be 2 mL/kg/BSA percent affected and then titrated to achieve urine output goal of 0.5 to 1 mL/kg/hr.
2) Wound Care:
Surgical: the detached epidermis is removed by manual scrubbing, debridement, or whirlpools and an allograft subsequently applied
Non-surgical approach: the detached epidermis is left in place and cleansed with sterile water or diluted chlorhexidine prior to the application of a non-adhesive dressing. The wound should be cleaned and redressed every 7 days to promote healing and prevent infection.
3) Infection prevention and management: At a higher risk for infection
Monitoring for signs and symptoms of infection → altered mental status, hypothermia, hypotension, tachycardia, and decreased urine output
Repeat wound and blood cultures every 48 hours
Broad-spectrum antibiotics should be initiated if have s/s of infection of (+) BC
4)Nutritional support:
Caloric requirement of 20 to 25 kcal/kg/day during the catabolic phase
25 to 30 kcal/kg/day during the anabolic phase
Mucosal involvement→ NGT
5)Temperature control: Room temperature should be kept at 82 to 90 degrees and a bear hugger utilized to prevent excessive caloric expenditures.
6)Pain Control
Early involvement of eye doctor due to ocular complications
Management of TEN
-Burn unit for wound care
-Resp support because of tracheal sloughing
-Fluid management due to insensible losses
what are the 2 categories of vascular anomalies and treatment
Tumors
Malformations
The most common pneumonia seen in school aged children
Mycoplasma pneumonia
Breach in the corneal epithelium
Corneal abrasion
s/s corneal abrasion
Pain, redness, tearing, photosensitive, blurred vision,
foreign body sensation
most important risk factor for corneal abrasion
contact lens use
if corneal abrasion is vertical……
foreign body may be imbedded under the upper eye lid
corneal abrasion treatment
topical abx drops/ointment 4x/day
NEVER give STEROID (will increase risk of infection)
NEVER give TOPICAL ANESTHETIC (will impair healing)
corneal abrasion takes how long to heal
when to follow up
1 week
f/u within 2 days to eval healing and presence of developing infection
Corneal whitening is a sign of infection
corneal whitening is a sign of
infection….look for corneal ulcer (medical emergency)
eye foreign body…..need to make sure of what?
that foreign body does not fully penetrate the cornea (open globe)
Plan of care for foreign body in eye
CT scan if suspect globe penetration
document visual acuity and a seidel test (fluorescein and woods lamp)
seidel test
Fluorescein and woods lamp
signs of open globe
peaked pupil
flat anterior chamber
what would an open globe look like on seidel test
fluid leaking from anterior chamber will appear green (aqueous humor leaking)
treatment for foreign body removal
Topical anesthetic applied, foreign body removed with irrigation or cotton-tipped applicator
4th gen fluoroquinolone or cipro 4x/day to affected eye until healed
NEVER USE STEROIDS, NEVER USE TOPICAL ANESTHETIC
Pain medication will not be helpful
Can have sxs before and after foreign body is removed until the cornea heals (1 week)
Inflammatory rxn causing chemotaxis of leukocytes and leakage of proteins into the anterior chamber called iritis
Traumatic iritis
most common cause of traumatic iritis
being struck by or against an object
MVC
Falls
Traumatic Iritis s/s
redness
photosensitive
tearing
blurred vision
positive history of blunt trauma withing 72 hours
Physical findings in traumatic iritis
conjunctival hyperemia with constricted and poorly reactive pupil
Pain in affected eye when light is shown in the unaffected eye = consensual photophobia – pain is originating from iris contraction (uveitis)
Slit lamp exam: anterior chamber cellular reaction will be present
treatment for traumatic iritis
Cycloplegic eye drops
If significant inflammation- use steroid eye drops
Healing within 1-2 weeks; ophtho follow up in 3-5 days
Disruption of arterial vessels of the iris or ciliary body that causes hemorrhage
Hyphema
most common cause of hyphema
being struck by or against an object, MVC, falls
s/sx hyphema
Pain, redness, blurred vision, eccymosis, subconjunctival hemorrhage
physical exam findings for hyphema
PE: layered blood in the anterior chamber when sitting up (area between cornea and iris)
Blood that fills entire chamber and is black = “eight ball hyphema” = see ophtho asap with high suspicion of ruptured globe
plan of care for hyphema
Sickle cell prep test on all African Americans if status unknown
CT scan if MOI unknown – looking for foreign body or orbital fracture
Seidel Test if suspicion of open globe (peaked pupil)
Visual acuity test
TX for hyphema
Cycloplegic and intraocular pressure-lowering drops should be started (may need IV intra-ocular pressure lowering meds)
AVOID CARBONIC ANHYDRASE INHIBITORS in sickle cell (will increase sickling of RBC)
Shield eye with metal shield
24 strict bed rest – do not want another bleed, very important to educate on this and admit if they cannot do bedrest at home
HOB at 30
Ophthal consult asap
Biggest risk: secondary hemorrhage within 1 week (greatest risk in first 4 days)
Wash out surgery if pressure lowering meds don’t work
Poor outcomes: vision of 20/200, have a greater than 1/3 anterior chamber hyphema, delayed presentation to eye doctor (may have glaucoma later in life)
Orbital floor blow out fracture - what happens
Occurs when large object strikes the orbit, causing sudden increase in orbital pressure
Bones of orbital floor are weakest – most common site of fracture
etiology of orbital floor blow out fx
struck by object
falls
S/sx Orbital blow out fx
Pain with diplopia, blurred vision
PE: eyelid edema, ecchymosis, subcutaneous/conjunctival emphysema, enophthalmos (sunken globe)
Bradycardia occurs with eye movement secondary to oculocardiac reflex in setting of muscle entrapment = immediate surgical intervention
Plan of care orbital blow out fx
CT through maxillary sinus with bone windows
Seidel test if concern for open globe (peaked pupils
Tx orbital blow out fx
Cephalexin (or broad spec) PO abx
PO prednisone (multidose pack)
Avoid nose blowing
If muscle entrapment – surgical emergency
Cold packs in first 48hr can decrease swelling, bruising, and pain
open globe in younger than 9 is at risk for
amblyopia in injured eye
signs of peritonitis
guarding
rebound tenderness
abd wall rigidity
abd wall discoloration in infants
in the setting of abd trauma
what does a CBC evaluate?
Hemorrhage
in the setting of abd trauma
what does ABG/VBG evaluate?
pH
base deficit
serum electrolytes
h/h
estimates degree of shock
acidosis
need for blood products
in the setting of abd trauma
what does a CMP/AST/ALT evaluate?
elevated AST/ALT may suggest liver injury - CT image warranted
in the setting of abd trauma
what does a amylase/lipase evaluate?
May be indicative of pancreatic injury if elevated 24 hours after trauma or upward trending values
Amylase high
-Pancreatic pseudocyst
-Parotid gland injury
in the setting of abd trauma
what does a hematuria indicate?
> 5 RBCs indicates need for further abd eval
High sensitivity for injury but non-specific
gross hematuria - evaluate for renal injuries
when should you obtain pregnancy test
all females above 10yo
in the setting of abd trauma
what does a PT/PTT/INR evaluate?
Abnormal in hemorrhaging pt or pt who has been resuscitated with large volumes of crystalloid or RBCS alone
in the setting of abd trauma
what does a chest or pelvic x ray evaluate?
Pneumo, hemothorax, mediastinal widening, traumatic diaphragmatic hernia and pneumoperitoneum
Pelvis fractures/ SI widening- cause of blood loss
Preferred diagnostic modality for most intra-abdominal injuries in children
CT
Contrast CT for abdominal injuries to see what
Must use IV contrast to determine bleeding
PO contrast is not to be used risk of aspiration, not tolerating
free fluid on abdominal CT - think
Hollow viscus or mesenteric injury
Abd CT is used in trauma to evaluate
Hematomas, free fluid or air and retroperitoneal, pelvic, or solid organ injury
Grade solid organ injuries
Pelvis and spine
Must use IV contrast to determine bleeding
Diaphragmatic, bowel and pancreatic injuries often not detected via initial CT scan
If free fluid= hollow viscus or mesenteric injury
Abd trauma
CT
What is often not detected on initial scan
Diaphragmatic, bowel and pancreatic injuries
What does FAST stand for
Focused abdominal sonography for trauma ultrasound
what 4 areas are examined in a FAST exam
Hepatorenal fossa (Morrison pouch)
Splenorenal fossa
Pericardial sac
Pelvis (pouch of douglas)
FAST exam can see fluid collections of what amount
100 ml and >
Trauma
Exam findings for pelvic fx
Blood at the urethra and or bruising/swelling/open lacerations to the perineum/vagina/rectum
High-Riding Prostate Gland
Avoid manual manipulation of the pelvis!
In traumas, what diaphragm is more commonly injured
Left hemidiaphragm
In diaphragm injury, what is the x ray finding
Blurring of hemidiaphragm, hemothorax or an abnormal gas shadow obscures the hemidiaphragm
confirmed with laparotomy, thoracoscopy or laparoscopy
what abdominal organ is the most commonly injured in children
spleen
what abdominal organ is the second most commonly injured in children
liver
s/s spleen lac
Left UQ Pain
Left shoulder pain (Kehr’s Sign)
Abdominal pain/distention
Bruising/abrasions to LUQ
Abd pain with inspiration
possibly hypotension and tachycardia
s/s liver lac
Right lobe injured > left
RUQ Abdominal pain
Right shoulder pain
Elevated Transaminases
ecchymosis or abrasions to R torso
R sided rib pain or tenderness
possibly hypotension and tachycardia
what is located in the peritoneum
stomach
spleen
liver
1st and 4th parts of the duodenum, jejunum, ileum, transverse and sigmoid colon
what is located in the retroperitoneal space
Aorta
kidneys
ureters
second and third parts of the duodenum, ascending and descending colon
adrenal glands
eval for splenic lac
CBC, CMP, coag, amylase, lipase, and possible blood gas.
FAST- not always conclusive in pedi
CT abdomen with IV contrast
blush/ extravasation of contrast can represent ongoing bleeding or arterial bleed
May need serial CT scanning, angiography, or surgery
non surgical treatment for splenic lac
NOM (splenic salvage)- for hemo stable pt
to Prevent emergent operation and preserve immune fx
-Bed rest
-NPO
-Heme monitoring
-serial abdominal examinations
-Serial H/H
-Blood products prn
-IVF
-Incentive spirometry
-Judicious pain control to -avoid atelectasis
-Diet titrated dependent on hemostability
surgical treatment for splenic lac
In the unstable pt with splenic lac
-repair, partial splenectomy or total splenectomy
splenectomy has what complication risk
Removal has large risk of infection, 50% mortality rate
Strep pneumoniae, Haemophilus influenza, meningococcus, E. Coli, staph aureus
Postsplenectomy vaccinations
-Pneumococcal, H. influenzae, and meningococcal vaccines consider at 14 days
Prophylaxis ABX
-Before age 5 daily
-Prior to any future surgical or dental procedures
what grade splenic injury?
Laceration <1 cm
Subcapsular hematoma <10% of surface area
Grade I
what grade splenic injury?
Laceration 1-3 cm
subcapsular hematoma 10% -50% of surface area
Grade II
what grade splenic injury?
Laceration >3 cm
subcapsular hematoma >50% of surface area
Grade III
what grade splenic injury?
Ruptured subcapsular or parenchymal herniation
Grade III
what grade splenic injury?
Segmental or hilar vascular injury
Devascularization >25% of spleen
Grade IV
Shattered spleen
Hilar injury
Grade V
What grade liver injury?
Capsular tear < 1 cm deep
subcapsular hematoma <10% surface area
Grade I
What grade liver injury?
Capsular tear 1-3 cm deep, <10 cm long
subcapsular hematoma 10-50% surface area
Intraparenchymal hematoma <10 cm
Grade II
What grade liver injury?
Capsular more than 3 cm deep
subcapsular hematoma >50% surface area
parenchymal hematoma >10 cm or expanding
Grade III
what liver lobe is injured more often
Right
plan of care liver injury
CBC, CMP, transaminases, coagulation studies, amylase, lipase, and possible blood gas
FAST
US and CT- primary diagnostic modalities for stable pt.
treatment liver lac
NOM is the most common approach to liver injury
Adjunctive hepatic artery embolization in pt with blush increase success rate of NOM
Hemodynamically unstable pt.
-Emergency surgical consultation and possible exploratory laparotomy
-Hemorrhage due to Surgical manipulation of venous injuries often results in death
what complications are associated with poor outcomes in liver lac
Recurrent bleeding
Haemobilia (upper GI bleeding from biliary tract)
Biliary fistula
intra abdominal abscess
Pancreatic injury is associated with trauma to ___ and ___
duodenum and liver
presentation of pacreatic injury
soft tissue contusion in upper abd
handlebar marking in epigastric region
Tenderness to the lower ribs and costal cartilage
Epigastric tenderness out of proportion to finding of the abd exam
concomitant lower thoracic spine fx
signs of peritonitis (rebound tenderness, guarding or abd wall rigidity)
Hypotension and tachycardia
vomiting
Late findings:
-abd pain
-palpable abd mass
-persistently elevated amylase levels
labs in pancreatic injury
CBC, CMP, coag, amylase, lipase, blood gas
Repeat serum amylase >3 hours postinjury or trending higher over time, may not be high initially
serum amylase may be elevated in what other type of trauma besides abd
facial trauma to parotid gland
imaging in pancreatic injury
Fast exam not reliable
CT scan is not helpful to determine pancreatic trauma after injury, CT should be repeated in pt with persistent abdominal pain, fever, and elevated amylase levels.
Repeat CT with IV and oral contrast
treatment for pancreatic lac
Nom is approriate for grades I, II, sometimes III injuries
Bed rest, bowel ret, nasogastric decompression, PN, enteral feedings distal to the duodenum or octreotide therapy
May need surgery or drainage if duct is disrupted
Surgical intervention for high grade injury to reduce risk of pseudocyst
after discharging a pt with pancreatic injury. What should they watch out for and what can it indicate
Early satiety and colicky abd pain
pancreatitis or pseudocyst formation
what grade pancreatic hematoma?
minor contusion without duct injury
Grade I
what grade pancreatic hematoma?
Major contusion without duct injury or tissue loss
Grade II
what grade pancreatic lac?
superficial laceration without duct injury
Grade I
what grade pancreatic lac?
Major laceration without duct injury or tissue loss
Grade II
what grade pancreatic lac?
distal transection or parenchymal injury with duct injury
Grade III
what grade pancreatic lac?
Proximal (to right of superior mesenteric vein) transection or parenchymal injury
Grade IV
what grade pancreatic lac?
massive disruption of pancreatic head
Grade V
presentation of kidney/bladder injury
Contusion, hematoma, ecchymosis to the back, flank or lower abdomen
Abdominal or flank tenderness
Hematuria
Palpable flank mass
Tenderness in the flank, costovertebral angel or back
Stab wounds posterior to the anterior axillary line
Difficulty or inability to urinate
Urine leaking from vagina
Blood at the urethral meatus
Labs for kidney/bladder injury
CBC, CMP, coag, amylase, lipase, UA, blood gas
is fast exam helpful in evaluating kidney/bladder injury
no
imaging for kidney/bladder injury
CT with IV contrast
IVP (intravenous pyelogram intraoperatively to evaluate kidney fx
Treatment for kidney/bladder injury
NOM for lower grade injury
Bed rest until gross hematuria resolves, H/H, IV hydration, blood press monitoring
Higher grade injuries- within 24 to 48 hours to evaluate kidney perfusion, hematoma size, and urinoma formation
High grade injuries can be managed with nonsurgical interventions- stenting, percutaneous drainage, and angiographic embolization
Surgical intervention
-Hemodynamic instability and penetrating injuries rather than injury grading
Intraperitoneal bladder ruptures
-Surgical repair with urethral or suprapubic catheter for two weeks
-Usually be removed within 2 weeks
Extraperitoneal ruptures
-Urethral catheter kept in place until follow up shows no further leak
what should be monitored in bladder/renal injury
HTN
UA for resolution of hematuria
F/U CT scans or US
What grade?
Trauma renal injury scale
Contusion- Microscopic or gross hematuria
Urologic studies normal
Hematoma-Subcapsular, nonexpanding without parenchymal laceration
Grade I
What Grade?
Trauma renal injury scale
Hematoma- Nonexpanding perirenal hematoma confined to renal retroperitoneum
Laceration: Less than 1 cm parenchymal depth of renal cortex without urinary extravasion
Grade II
What Grade?
Trauma renal injury scale
Laceration: Greater than 1 cm parenchymal depth of renal cortex without collecting-system rupture or urinary extravasation
Grade III
What Grade?
Trauma renal injury scale
Laceration: Parenchymal lac extending through the renal cortex, medulla and collecting system
Vascular: main renal artery or vein injury with contained hemorrhage
Grade IV
What Grade?
Trauma renal injury scale
Laceration: Completely shattered kidney
Vascular - Avulsion of renal hylum that devascularizes the kidney
Grade V
Hollow viscus injury involves
Bladder and intestines
Presentation of Hollow viscus injury
Abd wall ecchymoses or abrasion
Abd tenderness
Seat belt sign
Associated injuries such as presence of lumbar distraction fracture (Chance fracture T12-L2) and solid organ injury
Signs of peritonitis (rebound tenderness, guarding or abd wall rigidity)
handlebar marks
CT finding in Hollow viscus injury
Free fluid, thickened bowel, extraluminal air, mesenteric fat streaking, mesenteric hematoma, and vascular or luminal extravasation of contrast
treatment in Hollow viscus injury
NOM- nasogastric decompression, PN, enteral feeding beyond hematoma
Exploratory laparotomy with focus on higher risk injuries and controlling bleeding
Repeated abdominal explorations be be required in days following injury
presentation of abd compartment syndrome
Life Threatening complication
Contents of confined body space begin to exceed the space available within that compartment
Bowel swelling
Ascites
Blood
Bowel distension
May develop after laparotomy- third spacing, hemoperitoneum and bowel edema develop
Worsening abdominal distension,
decreased urine output,
poor lower extremity perfusion with edema, increased peak pressures in ventilated patients
plan of care in abd compartment syndrome
Intra abdominal pressure is monitored indirectly by monitoring urinary bladder pressure
ACS pressure: 15-35mmHG
Intubation, sedation, chemical paralysis, diuresis
Immediate decompression of abdomen needed
Post op complications in abd compartment syndrome
Prolonged ileus, small bowel obstruction, malabsorption from extensive small bowel resection (intestinal failure)
diaphragm injury is a marker of severity of trauma and can lead to
obstruction of intestine
sepsis
death
presentation of diaphragm injury
May be asymptomatic,
delaying diagnosis
dyspnea/ orthopnea
Chest pain
Referred scapular pain
Decreased breath sounds
Flail chest
Localized or diffuse severe abdominal tenderness
Guarding
Rebound tenderness
Progressive abdominal distention
Anxiety
Increased oxygen demand
Tachycardia
Bilious emesis
initial x ray is normal in 50%
plan of care in diaphragm injury
Need for a chest tube has to be carefully assessed prior to placement to prevent injury to herniated organs
Upper GI study and barium enema- herniated colon within the thoracic cavity
Definitive diagnosis- laparoscopy, laparotomy, thoracoscopy
Isolated asymptomatic diaphragm injuries should be repaired prior to discharge
Typically repaired in hemo unstable patients when repairing other injuries
NG tube inserted with care and not forced
discharge in diaphragm injury
Prevent postoperative pneumonia- IS etc.
Follow up chest x-ray for several years
Complications- recurrent herniation
presentation of pelvic fx
Ecchymosis over iliac wings, pubis, labia, or scrotum
Deformity
Abnormal movement
Pain on palpation of pelvic ring
Hematoma to scrotum or vulva
Lacerations or palpation of bone fragments on rectal or vaginal exam
High riding prostate or blood at the urinary meatus
Abnormal peripheral pulses
Leg length discrepancy
Asymmetry in rotation of the hips
plan of care pelvic fx
Anteroposterior AP pelvic xray
CT
Orthopedics consult
Can produce significant hemorrhage- control and fluid replacement- bedsheet or pelvic binder to control bleeding
Angiography can be needed to diagnose and control bleeding when hemo unstable
Immature pelvis is less likely to require surgical intervention
Unstable fractures in pedi patient or adolescents with mature pelvis should follow adult surgical guidelines
Surgical benefits- hemorrhage control, wound therapy, deformity prevention, improved mobility and decreased risk of growth disruption
complications in pelvic fx
DVT, limb discrepancy, neurologic deficits, acetabular growth disturbance, hip subluxation, urologic disorders, and sexual dysfx
discharge info for pelvic fx
Early PT, xray one week post
Weight bearing status and gradual return to activity
4-6 weeks healing
About 6 months to return to normal
spinal injury …look for what sign
increased risk for what?
seat belt sign
increased risk for lumbar spinal fx
in pediatric pt facial trauma is unlikely why
large cranium and prominent forehead
Causes of facial trauma in pediatric
MVC
falls
sports injury
physical abuse
animal bites
What LeFort fx type?
transverse maxillary fracture, teeth are usually contained in detached portion of maxilla
Type I
What LeFort fx type?
pyramidal fracture, results in a floating maxilla and nose with possible cribriform plate fracture
Type II
what leFort fx type?
complete separation of facial bones from their cranial attachments, “dishface” deformity
Type III
How to evaluate for facial trauma
Craniofacial CT
Plain x ray is unreliable in pedi population
When should facial lacs be repaired (timeline)
within 8-12 hrs from injury
if the edges clean, can repair up to 24 hrs after
facial trauma plan of care
Pedi is handled more conservatively: observation, full liquid diet, bedrest, analgesics
Peds have an accelerated rate of healing -> fracture reduction becomes difficult if care is delayed because of early bone healing
Fracture reduction and fixation should be performed as soon as possible
suture removal facial trauma
Sutures may remain in place for 5days – 2 weeks (some get reabsorbed and others have to be removed so follow up is necessary)
diet for oral trauma
recommended soft food diet and avoidance of foods that can burn or sting, such as orange juice or hot, spicy foods.
danger of dental trauma
can obstruct airway
Category of dental trauma
treatment?
Tender to touch but has normal mobility
concussion
Least problematic
Close clinical observation
Category of dental trauma?
Treatment?
Has not been displaced but has increased mobility
Subluxation
TX: observation, soft toothbrush and rinsing with chlorhexidine
May consider soft diet
Category of dental trauma?
Treatment?
Removed from bone socket
Avulsion
Primary vs. permanent for treatment
Primary: not replanted
Area cleansed and evaluated for foreign bodies or fractured roots
Permanent
Considered emergency
Cleansed and replanted with splinting, being careful not to disrupt the cementum
15 minutes have an excellent prognosis
If out of the mouth for 60 minutes in dry storage it will most likely not survive long term.
Transport: cold storage solution, hanks balanced salt solution or cold milk or saliva, saline or water
Consider tetanus prophy and antibiotics
Tooth transport
cold storage solution, hanks balanced salt solution or cold milk or saliva, saline or water
Tooth is broken but remains in the socket
Tooth fracture
treatment for tooth fracture
depends on location
Fragment removal may be possible otherwise tooth is extracted
fracture that Involves the alveolar bone and could extend into the adjacent mandible
Alveolar fx
tx Alveolar fx
Soft tooth brush, liquid diet, chlorohexidine mouthwash
Consult oral surgery, dentistry, oral-maxillofacial surgery or plastic surgery.
Prevention of dental injury
Mouth guards
face shields
imaging of dental injury
Panorex or CT with 3D imaging
Pediatric assessment triangle and ABCDE
Appearance
Work of breathing
circulation to skin
Airway
Breathing
Circulation
Disability/neurologic evaluation
Exposure
categories of vascular anomalies
Tumors
Malformations
most common soft tissue tumor of infancy
infantile hemangioma
Color differences of superficial vs deeper infantile hemangiomas
When deeper they have blue discoloration
superficial red
can be both superficial and deep
risk factors
infantile hemangiomas
female
low birth weight infant
when does infantile hemangiomas present
55% present at birth, rest develop in first weeks of life
superficial hemangioma reach max size by
6-8 months
deep hemangioma grow for __ - __ months then spontaneous resolution by ___ -____
12-14 months
3-10 years
complications of infantile hemangiomas
ulceration - painful, increased risk of infection, hemorrhage and scarring
periorbital hemangioma has risk of
vision disruption
Amblyopia ->will cause obstruction of the visual axis or pressure on the globe, resulting in astigmatism
· Get eye doctor involved to prevent vision loss
subglottic hemangioma risk and symptoms
Hoarseness + stridor -> progression to resp failure may be rapid
Symptomatic airway hemangioma develop in 50% of infants with _____________ on the chin and jaw (beard distribution)
What needs to happen?
·
extensive facial hemangiomas
Urgently refer for a laryngoscopy
Cervicofacial hemangioma associated with: posterior fossa malformation, hemangiomas, arterial anomalies of the cerebrovasculature, coarctation of aorta/cardiac defects, eye abnormalities
PHACE Syndrome
Occult spinal dysraphism with/without anorectal and urogenital anomalies
Lumbosacral hemangioma
imaging for Lumbosacral hemangioma
MRI of spine: get if large midline cutaneous hemangioma in lumbosacral area
Treatment for Lumbosacral hemangioma
Most resolve spontaneously
· If treatment is needed: PO propranolol or topical timolol = mainstay
Acquired, benign vascular tumor
· Initially, the lesions appear as pink-red papules that arise after minor trauma, growing rapidly over a period of weeks into a bright red, vascular, often predunculated papule measuring 2-10mm
Lesion has appearance of granulation tissue and very friable
Pyogenic granuloma
Most common location for pyogenic granuloma
Head neck and extremities
what can happen when a pyogenic granuloma is traumatized
may bleed profusely -> requires emergency medical attention
Treatment for Pyogenic granuloma
surgical excision is mainstay
Pulsed dye laser can be used for small lesions
Small vessel vasculitis with a leukocytoclastic response
Urticarial Vasculitis
what distinguishes urticarial vasculitis from normal urticaria
Lesions last longer than 24hr, may be tender, and leave behind skin pigmentation
skin biopsy needed to confirm
what is it that causes purulent exudate or pus in abscess
Bacterial cause
Leukocyte accumulation and formation of the purulent exudate
who is at highest risk for abscess
immunosuppressed
Presentation difference of cutaneous abscess vs internal abscess
Cutaneous abscess:
erythema, tenderness, pain, warmth, induration, fluctuance, drainage
Internal abscess:
fever, malaise, fatigue -> sxs become more specific to the area as the abscess progresses (fever, elevated WBC, pain
recent flu infection with pain specific to calf….normal labs….what are you thinking
myositis - esp with calf pain.
workup should be done to r/o rhabdo
complicated laceration in which the tissue is pulled away from the body, creating a flap-like appearance (foreign body can be hidden under flap)
Avulsion
Puncture wounds are prone to what
deep wound infection
Most common cause of puncture would
Dog Bite
leading cause of lacerations
Population risk
cutting and piercing tools, falls, MVC,
4-7 yo males
Most common method of foreign body induction into soft tissue:
metal
glass
ceramic
Cleaning wounds - what should you use and what should you not use
Using antibacterial agents
hydrogen peroxide, or iodine is contraindicated -> can do damage to healthy tissue
what happens in pressure injuries (short patho)
Hypoxia occurs at a pressure point that forms the epicenter of injury
Edema and ischemia occur, leading to progressive hypoxia -> necrosis
Effects of pressure injury in kids:
compromised skin protection increasing risk of infection, altered thermoregulation, metabolic deficiency, compromised immunity, decreased sensation
risk factors for pressure injury
terminal illness, sedation, hypotension, sepsis, spinal cord injury, impaired mobility, paralysis, cardiopulmonary bypass, vasopressors, young age, prolonged length of critical care stay, traction device
risk assessment tools in pressure injury
Braden Q scale = best for critically ill patients (includes tissue oxygenation and perfusion)
Neonatal Skin Risk Assessment Scale
Pressure injury wound staging
what stage?
non-blanchable erythema of intact skin
Color changes do not include purple or maroon discoloration -> deep tissue pressure injury
stage 1
Pressure injury wound staging
what stage?
partial-thickness skin loss with exposed dermis
Wound bed viable, pink or red, moist
Can have intact or ruptured serum-filled blister
Adipose and deeper tissue not visible
Granulation tissue, slough, eschar are not present
Stage 2
Pressure injury wound staging
what stage?
full-thickness skin loss
Adipose is visible in the ulcer
Granulation tissue and epibole (rolled wound edges)
Slough and eschar may be present
If slough or eschar obscures the extent of tissue loss = UNSTAGABLE
Depth of tissue damage varies by location
Undermining and tunneling occur
Fascia, muscle, tendon, ligament, cartilage and bone NOT EXPOSED
Stage 3
Pressure injury wound staging
what stage?
full-thickness skin and tissue loss
Exposed fascia, muscle, tendon, ligament, cartilage, bone in the wound
Slough/eschar visible
If slough or eschar obscures the extent of tissue loss = UNSTAGABLE
Stage 4
Pressure injury wound staging
what stage?
obscured full-thickness skin and tissue loss
Extent of tissue damage cannot be confirmed because it is obscured by slough or eschar
If slough removed, stage 3 or 4 will be revelaed
Stable eschar (dry, adherent, intact without erythema or fluctuance) on the heel or ischemic limb should not be softened or removed
Unstageable
Pressure injury wound staging
what stage?
persistent non-blanchable deep red, maroon, or purple discoloration
Intact or non-intact skin with localized area of persistent non-blanchable deep red/maroon/purple discoloration or epidermal separation revealing a dark wound bed or blood-filled blister
Pain and temperature change often proceed skin color changes
Results from intense/prolonged pressure and shear forces at the bone-muscle interface
If necrotic tissue, subq tissue, granulation tissue, fascia, muscle, are visible = full thickness pressure injury (3, 4, unstageable)
Deep tissue pressure injury:
Wound care solution for pediatric and neonate
what other solution is safe
NS in Pedi
Sterile water neonate
Hypochlorous acid solution – safe
whats wrong with using hydrogen peroxide to clean a wound
highly cytotoxic – do not use
Wound care
Sodium hypochlorite (Dakin solution): caution with
use with caution at a concentration no greater than 0.025%
In wound care, when is culture needed?
only when infection is present to get susceptibility testing
Topicals for wound care
Mupirocin (nasal tx), polymyxin B, bacitracin
Silver sulfadiazine: contraindicated due to toxicity
If you need antimicrobial therapy, get wound nurse involved
Wound care:
Silver sulfadiazine: contraindicated due to
toxicity
aggregation of microbial cells enclosed in a polysaccharide matric material that forms thin film or patchy layer of varying thickness that is not removed by gentle rinsing and traditional wound cleansing techniques
Biofilm
Benefits to Biofilm
Gives bacteria protection
Adheres to wound surface, prolongs inflammation, erodes tissue, disables skin barrier function
Recalcitrant to topical or systemic antibiotics
Will cause complicated wound healing and increased risk of infection
Studies being done now to figure out how to get rid of this
What factors do you need to consider when picking a dressing in wound care
condition of wound bed, amount of exudate, presence of infection, granulation tissue, slough or eschar, overall condition of patient, comorbidities
Negative pressure wound therapy benefits
Increased granulation formation, improved tissue perfusion, exudate management, reduced tissue edema
Controlled suction through custom cut sponge -> evacuates excess wound fluid, provides moist healing environment, prevents maceration, decreases bacterial count
Only changed 3x/week
contraindications to negative pressure wound therapy
presence of necrotic wound tissue, untreated osteomyelitis, malignancy of wound site, coagulopathy, nonenteric and unexplored fistulas, exposed blood vessels/organs/nerves
Hydrocolloid dressing
description?
does what?
when should you not use?
bound to foam, impermeable to bacteria; minimal to moderate absorption
Facilitates autolytic debridement
not to be used in wounds with significant drainage
difficult removal; use caution with delicate skin
Sheet and amorphous hydrogels
description?
does what?
WAter based and non-adherent;
Maintains a moist environment
Nonadherent; no risk for skin irritation with removal; may require secondary dressing for reinforcement
Transparent films
description?
does what?
Polyurethane with porous adhesive layer; allows escape of moisture and exchange of oxygen
Allows for easy wound inspection; impermeable to external fluids; nonabsorbent; may adhere to wound
Hydrocolloid
description?
does what?
Hydrophilic polyurethane coated foam, nonadherent, absorptive
Nonadherent; trauma free removal; absorptive; not recommended for nondraining wounds
when is gauze not recommended
for moist wound treatment
Name that dressing
bound to foam, impermeable to bacteria; minimal to moderate absorption
Hydrocolloid dressing
Name that dressing
WAter based and non-adherent;
Maintains a moist environment
Sheet and amorphous hydrogels
Name that dressing
Polyurethane with porous adhesive layer; allows escape of moisture and exchange of oxygen
Transparent films
Name that dressing
Hydrophilic polyurethane coated foam, nonadherent, absorptive
Polyurethane foam
Tetraplegia is injury in
one of 8 cervical regions
Paraplegia is injury in the
thoracic, lumbar, or sacral segments
incomplete vs complete spinal injury ?
Residual motor or sensory function more than three segments below the level of injury
Incomplete
incomplete vs complete spinal injury ?
sensation or voluntary movement in the lower extremities
incomplete
Sensation around the anus/ voluntary rectal sphincter contractions/ or voluntary toe flexion
Sacral sparing in incomplete spinal injury
Clonus, muscle spasticity or bladder involvement
-Typically a lesion in the middle or upper parts of the spinal cord or in the brain
Long tract signs in incomplete injury
complete or incomplete spinal injury
No preservation of motor/ and or sensory function more than three levels below the level of injury…the persistence of a complete lesion beyond 24 hours can be prognostic that function is unlikely to recover
complete
In spinal shock, flaccid paralysis and loss of rectal tone and reflexes leads to
Venous pooling and slight hypovolemia
Triad in neurogenic shock
Vasodilation (hypotension)
Hypothermia
Bradycardia
less likely with injury below T6
what happens in autonomic dysreflexia
Reflexes return after neurogenic shock, now more sympathetic below injury than parasympathetic
Massive arterial vasoconstriction and reflex HTN
Severe HA from the vasodilation above the level of injury
Parasympathetic responses
Sweating and skin flushing, bradycardia develops to control the HTN
