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