Exam 1 Flashcards

1
Q

Pressure related medical condition that compromised the tissue within a closed facial space

A

Compartment syndrome

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2
Q

Compartment syndrome causes

A

Injury
Infection
Surgery
Burns
Bleeding disorder
Venomous bites
IV/IO infiltrates
Thromboembolic event
Vascular reconstruction

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3
Q

Compartment syndrome is due to

A

Inadequate blood flow through the capillaries

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4
Q

Most common causes of compartment syndrome

A

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

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5
Q

Transient compartment syndrome cause

A

Heavy training
Due to muscle hypertrophy and increased intracompartmental pressure with exercise

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6
Q

Pain disproportionate to injury
Think…

A

Compartment syndrome

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7
Q

Early signs of compartment syndrome

A

Pain disproportionate to injury
Refusal to move affected area
Pain with a passive stretch

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8
Q

Late signs of compartment syndrome

A

Paralysis
Pallor
Paresthesia
Pain
Pulselessness

Ps in Lipincott
Pain with passive stretch
Pain out of proportion to clinical situation
Paresthesia
Paralyiss
Pulses absent

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9
Q

Compartment syndrome treat

A

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

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10
Q

Devices to measure intracompartmental pressure in compartment syndrome

A

Mercury manometer system
Arterial line system
Stryker intracompartmental pressure monitoring system

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11
Q

Compartment syndrome pressures that warrant surgical intervention

A

> 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

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12
Q

definitive treatment for compartment syndrome

A

incisional fasciotomy

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13
Q

preoperative antibiotic in compartment syndrome prior to incisional fasciotomy

A

cefazolin

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14
Q

post incisional fasciotomy, a full recovery can be expected in what time frame

A

with early identification and quick treatment, within 6 months

the open wound is closed within a few days or a skin graft is placed

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15
Q

Time period to surgical fasciotomy to regain normal function with compartment syndrome

A

6 hours

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16
Q

The 3 As of compartment syndrome

A

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

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17
Q

Ortolani maneuver identifies

A

a dislocated hip that can be reduced
A palpable clunk (not click) is felt as the hip reduces - positive Ortolani

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18
Q

Galleazzi sign

A

hip dislocation sign
difference in femur length when hips and knees are flexed to 90 degrees

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19
Q

Trendelenburg gait is seen when there is _____

A

weak abductor muscles of the hip seen when there is only one dysplastic hip

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20
Q

A hip click without hip instability in newborn is

A

common and benign finding

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21
Q

disorder that results from a temporary loss of blood supply to the proximal femoral epiphysis

A

Legg-Calve-Perthes disease

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22
Q

cause of Legg-Calve-Perthes disease

A

not well understood
it has been suggested:
trauma
infection
inflammation
acetabular retroversion

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23
Q

stages of Legg-Calve-Perthes disease

A

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

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24
Q

typical age range for Legg-Calve-Perthes disease

A

4-8 yrs old

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25
Q

gender more affected in Legg-Calve-Perthes disease

A

male

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26
Q

presentation of Legg-Calve-Perthes disease

A

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

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27
Q

what has better range of motion (typically)
septic hip
transient synovitis
Legg-Calve-Perthes disease

A

Legg-Calve-Perthes disease

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28
Q

a mild dysplasia of the proximal femoral epiphysis

A

Meyer Dysplasia - normal variation and is usually bilat

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29
Q

labs and imaging for Legg-Calve-Perthes disease

A

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

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30
Q

goal of treatment in Legg-Calve-Perthes disease

A

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

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31
Q

infection of the bone that may occur by hematogenous spread from bacteremia

A

Osteomyelitis

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32
Q

what causes osteomyelitis
and most common cause in pediatrics

A

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)

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33
Q

what happens if osteomyelitis goes untreated

A

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

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34
Q

most common pathogens in osteomyelitis
other common

A

S. Aureus

other common:
Streptococcus pyrogens
Streptococcus pneumoniae
K. kingae
HIB
MRSA

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35
Q

reporting of K.kingae in osteomyelitis primarily affects children of what age

A

6 mos - 4 yrs of age

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36
Q

Things to note on MRSA osteomyelitis

A

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

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37
Q

presentation of osteomyelitis

A

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

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38
Q

labs and imaging in osteomyelitis

A

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

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39
Q

Empiric antibiotics in osteomyelitis

A

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

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40
Q

when is surgical intervention warranted for osteomyelitis

A

presence of large subperiosteal, soft tissue or bone abscess
or concurrent septic arthritis
area of necrotic bone
direct invasion of growth plate

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41
Q

antibiotic route guidance in osteomyelitis

A

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

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42
Q

Treatment for children with MRSA osteomyelitis

A

4-6 weeks of abx with early oral abx acceptable if cultures show susceptibility to Clindamycin

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43
Q

MRSA infection is associated with increased _______ (complication)

A

DVT

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44
Q

risk factors for osteomyelitis associated with poor prognosis

A

MRSA
S. pneumoniae
pyomyositis
abscess
infection in hip
younger age
delayed treatment

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45
Q

long term complications of osteomyelitis

A

limb-length discrepancy
abnormal gait
recurrent infection

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46
Q

what happens in Chronic osteomyelitis

A

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

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47
Q

vaccination to help reduce risk of infection in osteomyelitis

A

HIB - prevents osteo by HIB

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48
Q

infection in the synovial space of a joint

A

septic arthritis

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49
Q

joints most often affected by septic arthritis

A

knee
hip
ankle
elbow

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50
Q

osteomyelitis can lead to septic arthritis esp in

A

hip
shoulder
elbow
ankle
(due to intra-articular location of metaphyseal bone in these joints)

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51
Q

Peak incidence of septic arthritis is

A

children younger than 3 yrs
males twice as often as females

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52
Q

risk factors for septic arthritis

A

prematurity
immune compromised

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53
Q

organisms associated with septic arthritis

A

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

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54
Q

presentation of septic arthritis

A

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.

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55
Q

what should be on your differential for a child with joint or bone pain

A

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)

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56
Q

Kocher criteria is for what and what does it include

A

septic arthritis
temp >38.5 C (101.3)
refusal to bear weight
elevation of ESR (>40) or CRP
and/or WBC > 12,000

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57
Q

key labs for septic arthritis

A

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

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58
Q

imaging in septic arthritis

A

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

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59
Q

surgical irrigation and drainage in septic arthritis

A

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

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60
Q

Abx for septic arthritis

A

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

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61
Q

a spinal fusion imitates

A

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

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62
Q

6 phases of bone remodeling

A

rest
activation
resorption
reversal
formation
mineralization

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63
Q

Bone remodeling is completely replaced in what time frame following mineralization of the bone

A

2-8 months

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64
Q

another name for spinal fusion

A

spinal arthrodesis

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65
Q

surgical procedure that joins one vertebra to an adjacent vertebra

A

spinal fusion

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66
Q

what warrants urgent intervention for spinal fustion

A

spinal deformity, trauma, degenerative conditions, tumors and infections that cause spinal instability exposing neural contents making risk for injury

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67
Q

what spinal deformities sometimes require spinal fusion

A

scoliosis
kyphosis
spondylolisthesis
for most cases this is elective

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68
Q

what degenerative spinal condition is seen during the adolescent period

A

lumbar disk degeneration most commonly related to strenuous physical activity, posttraumatic injury or congenital spinal deformity

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69
Q

what conditions can cause loss of bone integrity compromising the structural integrity of the spine

A

fracture
tumor invasion
infective process

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70
Q

the majority of spinal deformity procedures are performed through what type of approach

A

posterior

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71
Q

what type of surgical approach for spinal fusion
when fewer segments require fusion

A

anterior
so that leaving normal motion over more segments of the spine

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72
Q

what type of surgical approach for spinal fusion
in case of a spinal tumor located in the vertebral body

A

anterior
to remove the tumor and stabilize vertebra

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73
Q

what type of surgical approach for spinal fusion
in case of a spinal tumor located in the posterior elements of spinal column

A

posterior

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74
Q

in spinal fusion a bone graft taken from the Pt iliac crest is ______

A

autologous

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75
Q

in spinal fusion a bone graft taken from a cadaver donor is ______

A

autogenous

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76
Q

what protein can be used in bone graft to facilitate fusion healing

A

Bone morphogenic protein (BMP)

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77
Q

How often should a neuro assessment be performed following a spinal fusion surgery

A

every 2 hours for the first 24 hours to monitor for deficits

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78
Q

Narcotics and muscle relaxers are needed after a spinal fusion surgery for how long

A

typically needed for the first 2-4 weeks after surgery

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79
Q

what post op complications can occur following a spinal fusion

A

increased blood loss
resp changes due to thoracic rib cage changes
SIADH secondary to intraoperative volume replacement and spinal manipulation

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80
Q

immobilization after spinal fusion

A

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

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81
Q

postob mobility after spinal fusion

A

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

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82
Q

What technique for invasive device used to monitor compartment syndrome?
skin is opened and a catheter is placed into the compartment

A

Slit technique

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83
Q

What technique for invasive device used to monitor compartment syndrome?

a catheter with a wick is placed in the compartment

A

Wick technique

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84
Q

What technique for invasive device used to monitor compartment syndrome?

a straight or side-port needle is placed into the compartment

A

Needle technique

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85
Q

local inflammation of the muscle

A

myositis

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86
Q

symptoms of myositis

A

muscle pain, weakness, or difficulty performing tasks of daily living

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87
Q

what causes Myositis
who is it more common in

A

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;

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88
Q

presentation of myositis

A

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

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89
Q

Labs and diagnostics on myositis

A

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

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90
Q

treatment for Acute/viral myositis

A

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

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91
Q

Highlights on acute childhood myositis

what is it
symptoms
prognosis

A

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

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92
Q

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.

A

Legg-Calve-perthes disease

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93
Q

is osteomyelitis more common in adults or kids and why

A

more common in children bc of rich metaphyseal blood supply and thick periosteum

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94
Q

Approximately 50% of osteomyelitis occur in children < ____ years of age

A

5

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95
Q

Most common sites of osteomyelitis

A

femur
tibia

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96
Q

what disease processes increase risk of osteomyelitis

A

hemoglobinopathies such as sickle cell

chronic renal disease

type 1 DM

compromised immune system

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97
Q

________ 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.

A

Staph Aureus

Community acquired MRSA is becoming more prevalent

Other agents
Group A hemolytic strep
Strep pyogenes
Strep pneumoniae

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98
Q

what is the most common organism in neonates causing osteomyelitis

A

Group B strep

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99
Q

organism most common causing osteomyelitis associated with puncture wounds (esp of the foot)

A

Pseudomonas

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100
Q

in osteomyelitis, what imaging is helpful in identifying abscess and areas of destruction

A

CT

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101
Q

in osteomyelitis, what imaging is helpful in evaluating for abscess, though unable to image details of the bone

A

US

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102
Q

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.

A

Slipped Capital Femoral Epiphysis (SCFE)

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103
Q

what gender and age is more common in Slipped Capital Femoral Epiphysis (SCFE)

A

Males
ages 12-15

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104
Q

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.

A

SCFE

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105
Q

Etiology of SCFE

A

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.

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106
Q

Acute SCFE vs Chronic vs Acute on chronic SCFE

A

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.

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107
Q

symptoms for SCFE

A

•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.

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108
Q

Ice cream slipping off cone appearance on X ray

A

SCFE

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109
Q

SCFE management

A

•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.

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110
Q

Parkland formula Burn pt

A

> 15 % TBSA
4ml/kg
4ml x kg x % burn
divide by 2
divide by 8
LR

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111
Q

cafe au lait spots and lisch nodules are associated with what?

A

Neurofibromatosis type I

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112
Q

café au lait spots and lisch nodules are associated with what?

A

Neurofibromatosis type I

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113
Q

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.

A

Septic Arthritis

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114
Q

joints commonly affected in septic arthritis

A

hip
knee
elbow
ankle

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115
Q

age and gender for septic arthritis

A

less than 3 yrs
males

neonates and premature infants are at greatest risk due

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116
Q

what family of snake?
Rattlesnake

A

Crotalid

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117
Q

What family of snake
copperhead

A

Crotalid

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118
Q

What family of snake
Cottonmouth

A

Crotalid

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119
Q

What family of snake?
Coral snake

A

Elapid

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120
Q

what family of snake is venomous?
Crotalid
Elapid

A

Crotalid

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121
Q

characteristics of venomous snakes

A

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)

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122
Q

Characteristics of non-venomous snakes

A

round pupils
multiple small teeth instead of fangs
Oval-shaped head

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123
Q

what family of snake bites are most prevalent in US

A

95% in US are pit vipers (Crotalid)

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124
Q

Pit vipers are what family and what does that include

A

Crotalid
includes Rattlesnakes, copperheads and cottonmouths

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125
Q

whats the snake venom rhyme

A

“red on yellow, kill a fellow; red on black, venom lack”

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126
Q

what do coral snakes look like

A

black snout with alternating red, yellow, and black bands along the body

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127
Q

what family is a king snake?
Venomous?
what does it look like?

A

Colubridae

Non-venomous

Red band bordered by black on each side

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128
Q

black snout with alternating red, yellow, and black bands along the body

A

Coral snake

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129
Q

Red band bordered by black on each side

A

King snake

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130
Q

Crotalid venom contains 90% _____ by dry weight

A

protein

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131
Q

what problems come from Crotalid snake bites

A

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

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132
Q

what happens in Mojave rattlesnake envenomation (also Timber rattlesnake - rare)

A

neurotoxic effects -> cranial nerve paralysis (ptosis, ophthalmoplegia) and flaccid paralysis -> may require intubation

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133
Q

what happens in Elapids envenomation

A

Neurotoxin causes flaccid paralysis and myonecrosis

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134
Q

___% of all snake bites occur in the pedi population

A

25%

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135
Q

what time of year do snake bites happen more

A

warmer months of the year from April to October

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136
Q

Gender bitten more

A

males

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137
Q

what differentiates envenomation “DIC” from true DIC

A

the fibrin monomers are produced by the glycoproteins, rather than consumption or thrombin of activation of Factor XIII

True clinical bleeding is rare

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138
Q

Elapid venom exerts its effect through ___ and ___

A

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

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139
Q

Presentation of Crotalid envenomation

A

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

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140
Q

Presentation of Elapid envenomation

A

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

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141
Q

Plan of care for Crotaline envenomation

A

CBC, type and screen, UA, coags, CMP, BUN, Cr, CK, fibrinogen, fibrin split products: check Q6 to monitor for systemic effects and treatment

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142
Q

what labs do you need to draw for Elapid envenomation

A

None

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143
Q

what does dry envenomation mean

A

no venom injected

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144
Q

what category of envenomation

Local signs adjacent to bite without progression of proximal edema
Perioral paresthesia but will have normal lab studies

A

Mild

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145
Q

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

A

Moderate

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146
Q

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

A

Severe

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147
Q

Antidote for Crotaline venom

A

Crotaline Polyvalent Immune Fab (Crofab) – sheep derived

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148
Q

You may have a reaction to Crofab if your are allergic to

A

latex
papain
papaya
dust mites
sheep products

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149
Q

How is Crofab dosed?
when do you treat?

A

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)

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150
Q

After using Crofab for envenomation, how long do you need to monitor

A

24 hours after initial control is achieved. If they develop new or worsening symptoms, repeat appropriate bolus dose based on severity of new symptoms

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151
Q

What do you do if someone is allergic to crofab.

A

Call poison control. may use epi for anaphylaxis. May need to resume antivenom at slower rate

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152
Q

what treatment for elapid envenomation

A

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

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153
Q

wound care for envenomation

A

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

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154
Q

Action items on Crotaline envenomation

A

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

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155
Q

Latrodectus mactans

A

Black widow spider

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156
Q

what is the neurotoxin released in a Black widow spider envenomation

A

A-Latrotoxin

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157
Q

what happens with A-Latrotoxin

A

an excitatory neurotoxin that causes increased neurotransmitter release from presnyaptic neurons at the neuromuscular junction, sympathetic, and parasympathetic synapses.

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158
Q

what gender of black widow can envenomate humans

A

Female (larger than males)

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159
Q

true/false
black widow is very aggressive

A

false
not aggressive unless provoked or threatened

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160
Q

what sensation is felt in a black widow envenomation followed by what presentation

A

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

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161
Q

Positive tap test

A

Black widow envenomation
tapping at suspected bite site elicits pain

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162
Q

treatment for black widow envenomations

A

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

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163
Q

Loxosceles reclusa

A

Brown recluse

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164
Q

Venom toxin in a Brown recluse envenomation
what does it do?

A

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

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165
Q

where is the Brown recluse commonly found

A

Southern and midwestern USA

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166
Q

what does the brown recluse look like and when are they dangerous. Where do they like to be?

A

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).

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167
Q

Presentation of Brown recluse envenomations

A

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

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168
Q

Labs for Brown recluse envenomation

A

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

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169
Q

treatment for Brown recluse envenomation

A

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

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170
Q

Pts with suspected brown recluse bite with no symptoms can be discharged after __ hours of observation in the ED

A

6

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171
Q

most common places eczema dermatitis is seen

A

Cheeks
antecubital fossa
posterior knee folds

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172
Q

most common skin disease in children

A

Atopic dermatitis (20% of children)

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173
Q

who is at higher risk for atopic dermatitis

A

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%)

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174
Q

in eczema, what bugs cause secondary infections most often

A

Staph, strep pyro
HSV eczema herpeticum – life threatening
Varicella zoster virus
Coxsackievirus
Smallpox (eczema vaccinatum) – life threatening
Molluscum contagiosum
Fungal infections

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175
Q

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)

A

Seborrheic

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176
Q

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

A

Psoriasis

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177
Q

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)

A

Allergic contact dermatitis

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178
Q

contact sensitization to nickel in metals, occurs on areas of the body where nickel or other metal are

A

Nickel dermatitis

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179
Q

Mainstay treatment for dermatitis

A

Topical corticosteroids

Class I: highest potency (typically avoided in younger children or areas of thin skin)

Class VII: lowest potency

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180
Q

eczema care

A

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

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181
Q

How do you enhance penetration for topical corticosteroid application for dermatitis

A

use wet wraps with topical corticosteroid application

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182
Q

difference in ointment, creams, lotions and spray, foam and gels in dermatitis

A

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

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183
Q

How often do you apply corticosteroids in dermatitis

A

BID

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184
Q

systemic effects of topical corticosteroid applications

A

adrenal suppression or cushing -> can happen with application to large area or occluded area (diaper, bandages) at risk for enhanced penetration

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185
Q

immune modulators in Atopic dermatitis

A

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

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186
Q

atopic dermatitis
treatment

A

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

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187
Q

most common secondary skin infection found in atopic dermatitis

A

Impetigo with Staph

group A Strep also common

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188
Q

treatment for impetigo

A

Topical mupirocin for local lesions; widespread lesions require PO 1st gen ceph Cephalexin

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189
Q

Pustules, erythema, honey crusting, flare of disease, lack of response to adequate anti-inflam therapy

A

Impetigo

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190
Q

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

A

Eczema herpeticum after HSV infection – serious complication

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191
Q

Tzanck test

A

scraping of skin lesion and staining, can also send vesicle fluid

test for Eczema herpeticum after HSV infection

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192
Q

How to prevent atopic dermatitis

A

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

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193
Q

contact dermatitis is what type of hypersensitivity disorder

A

Type IV or delayed hypersensitivity

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194
Q

what type of contact dermatitis
ill-defined, scaly, pink or red patches and plaques

A

Irritant

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195
Q

what type of contact dermatitis
form of irritant derm

A

Diaper dermatitis

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196
Q

where is irritant contact dermatitis is usually seen

A

dorsal surface of hands, often from repeated hand washing or exposure to irritating chemicals

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197
Q

diaper dermatitis is a form of

A

irritant dermatitis

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198
Q

diaper dermatitis is caused by irritation to

A

urine/feces

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199
Q

what secondary infection can complicate diaper rash

A

Candida albicans or bacterial infection

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200
Q

what type of dermatitis is Poison ivy and poison oak

A

Acute allergic contact Rhus (or Urushiol induced) dermatitis

201
Q

describe the rash associated with Poison ivy/Poison oak

A

Bright pink, pruritic patches, linear or sharply marginated bizarre configurations
Inside the patches are clear vesicles and bullae

202
Q

Bright pink, pruritic patches, linear or sharply marginated bizarre configurations
Inside the patches are clear vesicles and bullae

A

Poison Ivy
Poison Oak

203
Q

timeline of exposure to rash for Poison ivy/poison oak

A

Sxs of disease may be delayed 7-14 days after first exposure, subsequent exposures will occur within hours and are more severe

204
Q

what type of dermatitis is nickel

A

Chronic Allergic nickel dermatitis

205
Q

what do the lesions look like for Chronic Allergic nickel dermatitis

A

Lesions are pink, scaly, pruritic plaques that mimic atopic derm

206
Q

Lesions are pink, scaly, pruritic plaques that mimic atopic derm

A

Chronic Allergic nickel dermatitis

207
Q

what is distribution of Rhus dermatitis

A

lower legs, distal arms + linear configuration of lesions

208
Q

what is distribution of Nickel dermatitis

A

derm of ears, wrists, periumbilical

209
Q

Treatment for contact dermatitis

A

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

210
Q

Seborrheic Dermatitis
in infant is what

A

cradle cap or dermatitis in the intertriginous areas of the axillae, groin, antecubital and popliteal fossae, umbilicus

211
Q

what does Seborrheic Dermatitis look like in adolescents

A

Dandruff

212
Q

what causes Seborrheic Dermatitis

A

Malassezia species in sebaceous rich areas such as Scalp, eyebrow, eyelid, nasolabial fold, external auditory canal

213
Q

How long does Cradle cap last

A

begins during first month and lasts through first year

214
Q

koplic spots

A

Measles

215
Q

Maculopapular rash with lymphadenopathy

A

Rubella

216
Q

Rash + koplik spots

A

Measles

217
Q

Rash + lymphadenopathy

A

Rubella

218
Q

Rash involving cheeks

A

Erythema infectiosum or Fifth disease

219
Q

Rash after the fever

A

Roseola

220
Q

Sandpaper like rash

A

Scarlet fever

221
Q

rash of different stages

A

chicken pox

222
Q

rash involves hand foot mouth

A

Hand foot mouth disease

223
Q

thick, greasy and waxy, yellow-white scaling and crusting of the scalp

A

cradle cap

224
Q

German measles is also called

A

Rubella

225
Q

Roseola is also called

A

Sixth disease

226
Q

How do you differentiate between cradle cap and tinea capitis

A

Fungal culture and potassium hydroxide

227
Q

Treatment for Seborrheic Dermatitis

A

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

228
Q

ordinary measles is called

A

Rubeola

229
Q

Roseola infantum is also called

A

Exanthum subitum

230
Q

symptoms of rubeola

A

conjunctivitis
cough
coryza
fever
koplik spots on buccal mucosa

rash starts at hairline and spreads cephalocaudally over 3 days

231
Q

Herald patch

A

Pityriasis Rosea

232
Q

when does Pityriasis Rosea occur (age)

A

adolescence

233
Q

Solitary 2-5cm pink oval patch with central clearing

A

Herald patch in Pityriasis Rosea

234
Q

Progression of Pityriasis Rosea

A

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

235
Q

treatment for Pityriasis Rosea

A

Self limiting
can use oral antihistamine or low potency topical corticosteroid for itching

236
Q

Christmas tree rash

A

Pityriasis Rosea

237
Q

Well-demarcated, erythematous scaling papules and plaques

· Occurs at all ages, chronic and relapsing

A

Psoriasis

238
Q

what things can exacerbate psoriasis

A

Infection (strep pyogenes)
stress
trauma
medications may exacerbate

239
Q

psoriasis vulgaris is also called

A

Plaque type psoriasis

240
Q

Auspitz sign

A

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,
241
Q

Lesions in psoriasis

A

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
·

242
Q

Treatment Psoriasis

A

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

243
Q

what type of psoriasis?
numerous small papules and plaques diffusely distributed on torso (teardrop-shaped)

A

Guttate

244
Q

what type of psoriasis?

red covering large body surface areas

A

Erythrodermic

245
Q

plaque psoriasis is symmetrical or assymmetrical

A

symmetrical

246
Q

most common psoriasis

A

Plaque psoriasis

247
Q

Plaque psoriasis is worse during what season

A

winter

248
Q

Guttate psoriasis classically preceded by what infection

A

psoriasis classically follows a preceding streptococcal infection, typically pharyngitis or perianal streptococcus.

249
Q

what type of psoriasis can be life threatening

A

Pustular psoriasis

250
Q

Psoriasis with sudden onset with leukocytosis, malaise, fever and hypocalcemia

A

Pustular psoriasis

251
Q

what electrolyte imbalance is associated with pustular psoriasis

A

hypocalcemia

252
Q

Triggers for pustular psoriasis

A

Pregnancy
withdrawal of oral glucocorticoids

253
Q

what type of psoriasis
Head to toe generalized erythema

A

erythrodermic

254
Q

Psoriasis that has issues with sepsis and fluid loss due to issues with barrier protection

A

Erythrodermic psoriasis

255
Q

symptoms for rubella

A

Headache
low grade fever
sore throat
coryza
Forchheimer spots on soft palate
Lymphadenopathy
Rash begins on face and spreads cephalocaudally

256
Q

Forchheimer Spots

A

Rubella

257
Q

Caused by Human Herpes virus 6

A

Roseola infantum

258
Q

Exanthem subitum

A

Roseola infantum

259
Q

S/S Roseola

A

Abrupt high fevers
After fever subsides, a rash develops, starting on neck and trunk and spreads to face and extremeties

260
Q

age for roseola

A

6-36 months old

261
Q

Pityriasis Rosea is caused by

A

HHV-6 and HHV-7

262
Q

How long before methotrexate reaches peak concentration

A

2-3 months

263
Q

How often do you give methotrexate vs Humira

A

Methotrexate is weekly
Humira is every 2 weeks

264
Q

Black box warning for Humira

A

Males with IBD have increased risk of Lymphoma

265
Q

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

A

Erythema Multiforme

266
Q

age/gender for Erythema Multiforme

A

Slight male predominance
Can occur at any age

267
Q

have been linked to the development of EM

A

infections, medications, malignancy, autoimmune disease, immunizations, radiation, poison ivy, and UV sunlight exposure

268
Q

Erythema Multiforme is what type of reaction

A

hypersensitivity reaction

269
Q

what is the most common infections trigger for Erythema Multiforme

other causes?

A

HSV

Other viral causes
Varicella
Parapoxvirus
EBV
CMV
Influenza
HIV

Mycoplasma Pneumoniae

Chlamydia
mycobacterium
TB
Histoplasmosis

270
Q

EM with high fever in infants can be a sign of

A

Kawasakis

271
Q

Rash in EM appears in crops over ___-___ days and resolves when?

A

3-7 days and resolve in over 1-2 weeks

272
Q

Rash in EM is found where, spread how and looks like what?

A

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

273
Q

Target lesions

A

EM

274
Q

Presentation of EM

A

Rash
mucosal involvement - usually border of lips

mild systemic - fever, malaise and myalgias

275
Q
A

Erythema Multiforme

276
Q
A

Erythema Multiforme

277
Q

skin lesions that are well circumscribed, red wheals, and plaques but lack the central dusky zones

A

Urticaria

278
Q

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….

A

Fixed drug eruption

279
Q

initially presents with mucosal erosions and atypical target lesions. distinct in that it’s widespread epidermal + mucosal membrane necrosis and sloughing of the skin.

A

SJS

280
Q

HX of eruption + target-like lesions with or without mucosal involvement is the most important infor to DXs

A

EM

281
Q

In severe cases of EM, what labs can you look like

A

Elevated
sed rate
CRP
WBC and liver enzymes

282
Q

treatment for EM

A

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

283
Q

What meds can cause EM

A

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

284
Q

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

A

SJS/TEN

285
Q

Nikolsky sign

A

(mild skin friction results in dermal exfoliation; basically skin falls off)

SJS/TEN

286
Q

whats worse SJS or TEN

A

TEN

287
Q

S/S SJS/TEN

A

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

288
Q

How do you dx TEN vs SJS

A

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

289
Q

treatment for SJS/TEN

A

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

290
Q

what are the 2 categories of vascular anomalies and treatment

A

Tumors
Malformations

291
Q

The most common pneumonia seen in school aged children

A

Mycoplasma pneumonia

292
Q

Breach in the corneal epithelium

A

Corneal abrasion

293
Q

s/s corneal abrasion

A

Pain, redness, tearing, photosensitive, blurred vision,
foreign body sensation

294
Q

most important risk factor for corneal abrasion

A

contact lens use

295
Q

if corneal abrasion is vertical……

A

foreign body may be imbedded under the upper eye lid

296
Q

corneal abrasion treatment

A

topical abx drops/ointment 4x/day
NEVER give STEROID (will increase risk of infection)
NEVER give TOPICAL ANESTHETIC (will impair healing)

297
Q

corneal abrasion takes how long to heal
when to follow up

A

1 week
f/u within 2 days to eval healing and presence of developing infection

Corneal whitening is a sign of infection

298
Q

corneal whitening is a sign of

A

infection….look for corneal ulcer (medical emergency)

299
Q

eye foreign body…..need to make sure of what?

A

that foreign body does not fully penetrate the cornea (open globe)

300
Q

Plan of care for foreign body in eye

A

CT scan if suspect globe penetration

document visual acuity and a seidel test (fluorescein and woods lamp)

301
Q

seidel test

A

Fluorescein and woods lamp

302
Q

signs of open globe

A

peaked pupil
flat anterior chamber

303
Q

what would an open globe look like on seidel test

A

fluid leaking from anterior chamber will appear green (aqueous humor leaking)

304
Q

treatment for foreign body removal

A

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)

305
Q

Inflammatory rxn causing chemotaxis of leukocytes and leakage of proteins into the anterior chamber called iritis

A

Traumatic iritis

306
Q

most common cause of traumatic iritis

A

being struck by or against an object
MVC
Falls

307
Q

Traumatic Iritis s/s

A

redness
photosensitive
tearing
blurred vision
positive history of blunt trauma withing 72 hours

308
Q

Physical findings in traumatic iritis

A

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

309
Q

treatment for traumatic iritis

A

Cycloplegic eye drops

If significant inflammation- use steroid eye drops

Healing within 1-2 weeks; ophtho follow up in 3-5 days

310
Q

Disruption of arterial vessels of the iris or ciliary body that causes hemorrhage

A

Hyphema

311
Q

most common cause of hyphema

A

being struck by or against an object, MVC, falls

312
Q

s/sx hyphema

A

Pain, redness, blurred vision, eccymosis, subconjunctival hemorrhage

313
Q

physical exam findings for hyphema

A

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

314
Q

plan of care for hyphema

A

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

315
Q

TX for hyphema

A

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)

316
Q

Orbital floor blow out fracture - what happens

A

Occurs when large object strikes the orbit, causing sudden increase in orbital pressure

Bones of orbital floor are weakest – most common site of fracture

317
Q

etiology of orbital floor blow out fx

A

struck by object
falls

318
Q

S/sx Orbital blow out fx

A

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

319
Q

Plan of care orbital blow out fx

A

CT through maxillary sinus with bone windows

Seidel test if concern for open globe (peaked pupils

320
Q

Tx orbital blow out fx

A

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

321
Q

open globe in younger than 9 is at risk for

A

amblyopia in injured eye

322
Q

signs of peritonitis

A

guarding
rebound tenderness
abd wall rigidity
abd wall discoloration in infants

323
Q

in the setting of abd trauma
what does a CBC evaluate?

A

Hemorrhage

324
Q

in the setting of abd trauma
what does ABG/VBG evaluate?

A

pH
base deficit
serum electrolytes
h/h

estimates degree of shock
acidosis
need for blood products

325
Q

in the setting of abd trauma
what does a CMP/AST/ALT evaluate?

A

elevated AST/ALT may suggest liver injury - CT image warranted

326
Q

in the setting of abd trauma
what does a amylase/lipase evaluate?

A

May be indicative of pancreatic injury if elevated 24 hours after trauma or upward trending values

Amylase high
-Pancreatic pseudocyst
-Parotid gland injury

327
Q

in the setting of abd trauma
what does a hematuria indicate?

A

> 5 RBCs indicates need for further abd eval

High sensitivity for injury but non-specific

gross hematuria - evaluate for renal injuries

328
Q

when should you obtain pregnancy test

A

all females above 10yo

329
Q

in the setting of abd trauma
what does a PT/PTT/INR evaluate?

A

Abnormal in hemorrhaging pt or pt who has been resuscitated with large volumes of crystalloid or RBCS alone

330
Q

in the setting of abd trauma
what does a chest or pelvic x ray evaluate?

A

Pneumo, hemothorax, mediastinal widening, traumatic diaphragmatic hernia and pneumoperitoneum
Pelvis fractures/ SI widening- cause of blood loss

331
Q

Preferred diagnostic modality for most intra-abdominal injuries in children

A

CT

332
Q

Contrast CT for abdominal injuries to see what

A

Must use IV contrast to determine bleeding

PO contrast is not to be used risk of aspiration, not tolerating

333
Q

free fluid on abdominal CT - think

A

Hollow viscus or mesenteric injury

334
Q

Abd CT is used in trauma to evaluate

A

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

335
Q

Abd trauma
CT
What is often not detected on initial scan

A

Diaphragmatic, bowel and pancreatic injuries

336
Q

What does FAST stand for

A

Focused abdominal sonography for trauma ultrasound

337
Q

what 4 areas are examined in a FAST exam

A

Hepatorenal fossa (Morrison pouch)
Splenorenal fossa
Pericardial sac
Pelvis (pouch of douglas)

338
Q

FAST exam can see fluid collections of what amount

A

100 ml and >

339
Q

Trauma
Exam findings for pelvic fx

A

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!

340
Q

In traumas, what diaphragm is more commonly injured

A

Left hemidiaphragm

341
Q

In diaphragm injury, what is the x ray finding

A

Blurring of hemidiaphragm, hemothorax or an abnormal gas shadow obscures the hemidiaphragm

confirmed with laparotomy, thoracoscopy or laparoscopy

342
Q

what abdominal organ is the most commonly injured in children

A

spleen

343
Q

what abdominal organ is the second most commonly injured in children

A

liver

344
Q

s/s spleen lac

A

Left UQ Pain
Left shoulder pain (Kehr’s Sign)
Abdominal pain/distention
Bruising/abrasions to LUQ
Abd pain with inspiration

possibly hypotension and tachycardia

345
Q

s/s liver lac

A

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

346
Q

what is located in the peritoneum

A

stomach
spleen
liver
1st and 4th parts of the duodenum, jejunum, ileum, transverse and sigmoid colon

347
Q

what is located in the retroperitoneal space

A

Aorta
kidneys
ureters
second and third parts of the duodenum, ascending and descending colon
adrenal glands

348
Q

eval for splenic lac

A

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

349
Q

non surgical treatment for splenic lac

A

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

350
Q

surgical treatment for splenic lac

A

In the unstable pt with splenic lac
-repair, partial splenectomy or total splenectomy

351
Q

splenectomy has what complication risk

A

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

352
Q

what grade splenic injury?

Laceration <1 cm
Subcapsular hematoma <10% of surface area

A

Grade I

353
Q

what grade splenic injury?

Laceration 1-3 cm
subcapsular hematoma 10% -50% of surface area

A

Grade II

354
Q

what grade splenic injury?

Laceration >3 cm
subcapsular hematoma >50% of surface area

A

Grade III

355
Q

what grade splenic injury?
Ruptured subcapsular or parenchymal herniation

A

Grade III

356
Q

what grade splenic injury?

Segmental or hilar vascular injury

Devascularization >25% of spleen

A

Grade IV

357
Q

Shattered spleen
Hilar injury

A

Grade V

358
Q

What grade liver injury?
Capsular tear < 1 cm deep

subcapsular hematoma <10% surface area

A

Grade I

359
Q

What grade liver injury?
Capsular tear 1-3 cm deep, <10 cm long

subcapsular hematoma 10-50% surface area
Intraparenchymal hematoma <10 cm

A

Grade II

360
Q

What grade liver injury?
Capsular more than 3 cm deep

subcapsular hematoma >50% surface area
parenchymal hematoma >10 cm or expanding

A

Grade III

361
Q

what liver lobe is injured more often

A

Right

362
Q

plan of care liver injury

A

CBC, CMP, transaminases, coagulation studies, amylase, lipase, and possible blood gas
FAST
US and CT- primary diagnostic modalities for stable pt.

363
Q

treatment liver lac

A

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

364
Q

what complications are associated with poor outcomes in liver lac

A

Recurrent bleeding
Haemobilia (upper GI bleeding from biliary tract)
Biliary fistula
intra abdominal abscess

365
Q

Pancreatic injury is associated with trauma to ___ and ___

A

duodenum and liver

366
Q

presentation of pacreatic injury

A

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

367
Q

labs in pancreatic injury

A

CBC, CMP, coag, amylase, lipase, blood gas
Repeat serum amylase >3 hours postinjury or trending higher over time, may not be high initially

368
Q

serum amylase may be elevated in what other type of trauma besides abd

A

facial trauma to parotid gland

369
Q

imaging in pancreatic injury

A

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

370
Q

treatment for pancreatic lac

A

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

371
Q

after discharging a pt with pancreatic injury. What should they watch out for and what can it indicate

A

Early satiety and colicky abd pain

pancreatitis or pseudocyst formation

372
Q

what grade pancreatic hematoma?
minor contusion without duct injury

A

Grade I

373
Q

what grade pancreatic hematoma?
Major contusion without duct injury or tissue loss

A

Grade II

374
Q

what grade pancreatic lac?

superficial laceration without duct injury

A

Grade I

375
Q

what grade pancreatic lac?

Major laceration without duct injury or tissue loss

A

Grade II

376
Q

what grade pancreatic lac?
distal transection or parenchymal injury with duct injury

A

Grade III

377
Q

what grade pancreatic lac?

Proximal (to right of superior mesenteric vein) transection or parenchymal injury

A

Grade IV

378
Q

what grade pancreatic lac?

massive disruption of pancreatic head

A

Grade V

379
Q

presentation of kidney/bladder injury

A

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

380
Q

Labs for kidney/bladder injury

A

CBC, CMP, coag, amylase, lipase, UA, blood gas

381
Q

is fast exam helpful in evaluating kidney/bladder injury

A

no

382
Q

imaging for kidney/bladder injury

A

CT with IV contrast

IVP (intravenous pyelogram intraoperatively to evaluate kidney fx

383
Q

Treatment for kidney/bladder injury

A

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

384
Q

what should be monitored in bladder/renal injury

A

HTN
UA for resolution of hematuria
F/U CT scans or US

385
Q

What grade?
Trauma renal injury scale
Contusion- Microscopic or gross hematuria
Urologic studies normal

Hematoma-Subcapsular, nonexpanding without parenchymal laceration

A

Grade I

386
Q

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

A

Grade II

387
Q

What Grade?
Trauma renal injury scale

Laceration: Greater than 1 cm parenchymal depth of renal cortex without collecting-system rupture or urinary extravasation

A

Grade III

388
Q

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

A

Grade IV

389
Q

What Grade?
Trauma renal injury scale

Laceration: Completely shattered kidney

Vascular - Avulsion of renal hylum that devascularizes the kidney

A

Grade V

390
Q

Hollow viscus injury involves

A

Bladder and intestines

391
Q

Presentation of Hollow viscus injury

A

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

392
Q

CT finding in Hollow viscus injury

A

Free fluid, thickened bowel, extraluminal air, mesenteric fat streaking, mesenteric hematoma, and vascular or luminal extravasation of contrast

393
Q

treatment in Hollow viscus injury

A

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

394
Q

presentation of abd compartment syndrome

A

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

395
Q

plan of care in abd compartment syndrome

A

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

396
Q

Post op complications in abd compartment syndrome

A

Prolonged ileus, small bowel obstruction, malabsorption from extensive small bowel resection (intestinal failure)

397
Q

diaphragm injury is a marker of severity of trauma and can lead to

A

obstruction of intestine
sepsis
death

398
Q

presentation of diaphragm injury

A

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%

399
Q

plan of care in diaphragm injury

A

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

400
Q

discharge in diaphragm injury

A

Prevent postoperative pneumonia- IS etc.
Follow up chest x-ray for several years
Complications- recurrent herniation

401
Q

presentation of pelvic fx

A

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

402
Q

plan of care pelvic fx

A

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

403
Q

complications in pelvic fx

A

DVT, limb discrepancy, neurologic deficits, acetabular growth disturbance, hip subluxation, urologic disorders, and sexual dysfx

404
Q

discharge info for pelvic fx

A

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

405
Q

spinal injury …look for what sign
increased risk for what?

A

seat belt sign
increased risk for lumbar spinal fx

406
Q

in pediatric pt facial trauma is unlikely why

A

large cranium and prominent forehead

407
Q

Causes of facial trauma in pediatric

A

MVC
falls
sports injury
physical abuse
animal bites

408
Q

What LeFort fx type?
transverse maxillary fracture, teeth are usually contained in detached portion of maxilla

A

Type I

409
Q

What LeFort fx type?
pyramidal fracture, results in a floating maxilla and nose with possible cribriform plate fracture

A

Type II

410
Q

what leFort fx type?
complete separation of facial bones from their cranial attachments, “dishface” deformity

A

Type III

411
Q

How to evaluate for facial trauma

A

Craniofacial CT

Plain x ray is unreliable in pedi population

412
Q

When should facial lacs be repaired (timeline)

A

within 8-12 hrs from injury
if the edges clean, can repair up to 24 hrs after

413
Q

facial trauma plan of care

A

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

414
Q

suture removal facial trauma

A

Sutures may remain in place for 5days – 2 weeks (some get reabsorbed and others have to be removed so follow up is necessary)

415
Q

diet for oral trauma

A

recommended soft food diet and avoidance of foods that can burn or sting, such as orange juice or hot, spicy foods.

416
Q

danger of dental trauma

A

can obstruct airway

417
Q

Category of dental trauma
treatment?

Tender to touch but has normal mobility

A

concussion

Least problematic
Close clinical observation

418
Q

Category of dental trauma?
Treatment?
Has not been displaced but has increased mobility

A

Subluxation
TX: observation, soft toothbrush and rinsing with chlorhexidine
May consider soft diet

419
Q

Category of dental trauma?
Treatment?

Removed from bone socket

A

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

420
Q

Tooth transport

A

cold storage solution, hanks balanced salt solution or cold milk or saliva, saline or water

421
Q

Tooth is broken but remains in the socket

A

Tooth fracture

422
Q

treatment for tooth fracture

A

depends on location

Fragment removal may be possible otherwise tooth is extracted

423
Q

fracture that Involves the alveolar bone and could extend into the adjacent mandible

A

Alveolar fx

424
Q

tx Alveolar fx

A

Soft tooth brush, liquid diet, chlorohexidine mouthwash

Consult oral surgery, dentistry, oral-maxillofacial surgery or plastic surgery.

425
Q

Prevention of dental injury

A

Mouth guards
face shields

426
Q

imaging of dental injury

A

Panorex or CT with 3D imaging

427
Q

Pediatric assessment triangle and ABCDE

A

Appearance
Work of breathing
circulation to skin

Airway
Breathing
Circulation
Disability/neurologic evaluation
Exposure

428
Q

categories of vascular anomalies

A

Tumors
Malformations

429
Q

most common soft tissue tumor of infancy

A

infantile hemangioma

430
Q

Color differences of superficial vs deeper infantile hemangiomas

A

When deeper they have blue discoloration

superficial red

can be both superficial and deep

431
Q

risk factors
infantile hemangiomas

A

female
low birth weight infant

432
Q

when does infantile hemangiomas present

A

55% present at birth, rest develop in first weeks of life

433
Q

superficial hemangioma reach max size by

A

6-8 months

434
Q

deep hemangioma grow for __ - __ months then spontaneous resolution by ___ -____

A

12-14 months
3-10 years

435
Q

complications of infantile hemangiomas

A

ulceration - painful, increased risk of infection, hemorrhage and scarring

436
Q

periorbital hemangioma has risk of

A

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

437
Q

subglottic hemangioma risk and symptoms

A

Hoarseness + stridor -> progression to resp failure may be rapid

438
Q

Symptomatic airway hemangioma develop in 50% of infants with _____________ on the chin and jaw (beard distribution)

What needs to happen?
·

A

extensive facial hemangiomas

Urgently refer for a laryngoscopy

439
Q

Cervicofacial hemangioma associated with: posterior fossa malformation, hemangiomas, arterial anomalies of the cerebrovasculature, coarctation of aorta/cardiac defects, eye abnormalities

A

PHACE Syndrome

440
Q

Occult spinal dysraphism with/without anorectal and urogenital anomalies

A

Lumbosacral hemangioma

441
Q

imaging for Lumbosacral hemangioma

A

MRI of spine: get if large midline cutaneous hemangioma in lumbosacral area

442
Q

Treatment for Lumbosacral hemangioma

A

Most resolve spontaneously
· If treatment is needed: PO propranolol or topical timolol = mainstay

443
Q

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

A

Pyogenic granuloma

444
Q

Most common location for pyogenic granuloma

A

Head neck and extremities

445
Q

what can happen when a pyogenic granuloma is traumatized

A

may bleed profusely -> requires emergency medical attention

446
Q

Treatment for Pyogenic granuloma

A

surgical excision is mainstay

Pulsed dye laser can be used for small lesions

447
Q

Small vessel vasculitis with a leukocytoclastic response

A

Urticarial Vasculitis

448
Q

what distinguishes urticarial vasculitis from normal urticaria

A

Lesions last longer than 24hr, may be tender, and leave behind skin pigmentation

skin biopsy needed to confirm

449
Q

what is it that causes purulent exudate or pus in abscess

A

Bacterial cause
Leukocyte accumulation and formation of the purulent exudate

450
Q

who is at highest risk for abscess

A

immunosuppressed

451
Q

Presentation difference of cutaneous abscess vs internal abscess

A

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

452
Q

recent flu infection with pain specific to calf….normal labs….what are you thinking

A

myositis - esp with calf pain.
workup should be done to r/o rhabdo

453
Q

complicated laceration in which the tissue is pulled away from the body, creating a flap-like appearance (foreign body can be hidden under flap)

A

Avulsion

454
Q

Puncture wounds are prone to what

A

deep wound infection

455
Q

Most common cause of puncture would

A

Dog Bite

456
Q

leading cause of lacerations
Population risk

A

cutting and piercing tools, falls, MVC,

4-7 yo males

457
Q

Most common method of foreign body induction into soft tissue:

A

metal
glass
ceramic

458
Q

Cleaning wounds - what should you use and what should you not use

A

Using antibacterial agents

hydrogen peroxide, or iodine is contraindicated -> can do damage to healthy tissue

459
Q

what happens in pressure injuries (short patho)

A

Hypoxia occurs at a pressure point that forms the epicenter of injury
Edema and ischemia occur, leading to progressive hypoxia -> necrosis

460
Q

Effects of pressure injury in kids:

A

compromised skin protection increasing risk of infection, altered thermoregulation, metabolic deficiency, compromised immunity, decreased sensation

461
Q

risk factors for pressure injury

A

terminal illness, sedation, hypotension, sepsis, spinal cord injury, impaired mobility, paralysis, cardiopulmonary bypass, vasopressors, young age, prolonged length of critical care stay, traction device

462
Q

risk assessment tools in pressure injury

A

Braden Q scale = best for critically ill patients (includes tissue oxygenation and perfusion)

Neonatal Skin Risk Assessment Scale

463
Q

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

A

stage 1

464
Q

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

A

Stage 2

465
Q

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

A

Stage 3

466
Q

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

A

Stage 4

467
Q

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

A

Unstageable

468
Q

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)

A

Deep tissue pressure injury:

469
Q

Wound care solution for pediatric and neonate

what other solution is safe

A

NS in Pedi
Sterile water neonate

Hypochlorous acid solution – safe

470
Q

whats wrong with using hydrogen peroxide to clean a wound

A

highly cytotoxic – do not use

471
Q

Wound care
Sodium hypochlorite (Dakin solution): caution with

A

use with caution at a concentration no greater than 0.025%

472
Q

In wound care, when is culture needed?

A

only when infection is present to get susceptibility testing

473
Q

Topicals for wound care

A

Mupirocin (nasal tx), polymyxin B, bacitracin

Silver sulfadiazine: contraindicated due to toxicity

If you need antimicrobial therapy, get wound nurse involved

474
Q

Wound care:
Silver sulfadiazine: contraindicated due to

A

toxicity

475
Q

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

A

Biofilm

476
Q

Benefits to Biofilm

A

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

477
Q

What factors do you need to consider when picking a dressing in wound care

A

condition of wound bed, amount of exudate, presence of infection, granulation tissue, slough or eschar, overall condition of patient, comorbidities

478
Q

Negative pressure wound therapy benefits

A

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

479
Q

contraindications to negative pressure wound therapy

A

presence of necrotic wound tissue, untreated osteomyelitis, malignancy of wound site, coagulopathy, nonenteric and unexplored fistulas, exposed blood vessels/organs/nerves

480
Q

Hydrocolloid dressing
description?
does what?
when should you not use?

A

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

481
Q

Sheet and amorphous hydrogels

description?
does what?

A

WAter based and non-adherent;
Maintains a moist environment

Nonadherent; no risk for skin irritation with removal; may require secondary dressing for reinforcement

482
Q

Transparent films

description?
does what?

A

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

483
Q

Hydrocolloid

description?
does what?

A

Hydrophilic polyurethane coated foam, nonadherent, absorptive

Nonadherent; trauma free removal; absorptive; not recommended for nondraining wounds

484
Q

when is gauze not recommended

A

for moist wound treatment

485
Q

Name that dressing
bound to foam, impermeable to bacteria; minimal to moderate absorption

A

Hydrocolloid dressing

486
Q

Name that dressing
WAter based and non-adherent;
Maintains a moist environment

A

Sheet and amorphous hydrogels

487
Q

Name that dressing
Polyurethane with porous adhesive layer; allows escape of moisture and exchange of oxygen

A

Transparent films

488
Q

Name that dressing

Hydrophilic polyurethane coated foam, nonadherent, absorptive

A

Polyurethane foam

489
Q

Tetraplegia is injury in

A

one of 8 cervical regions

490
Q

Paraplegia is injury in the

A

thoracic, lumbar, or sacral segments

491
Q

incomplete vs complete spinal injury ?

Residual motor or sensory function more than three segments below the level of injury

A

Incomplete

492
Q

incomplete vs complete spinal injury ?

sensation or voluntary movement in the lower extremities

A

incomplete

493
Q

Sensation around the anus/ voluntary rectal sphincter contractions/ or voluntary toe flexion

A

Sacral sparing in incomplete spinal injury

494
Q

Clonus, muscle spasticity or bladder involvement
-Typically a lesion in the middle or upper parts of the spinal cord or in the brain

A

Long tract signs in incomplete injury

495
Q

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

A

complete

496
Q

In spinal shock, flaccid paralysis and loss of rectal tone and reflexes leads to

A

Venous pooling and slight hypovolemia

497
Q

Triad in neurogenic shock

A

Vasodilation (hypotension)
Hypothermia
Bradycardia

less likely with injury below T6

498
Q

what happens in autonomic dysreflexia

A

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