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Pediatrics > Emergency Medicine > Flashcards

Emergency Medicine Flashcards

1
Q

What is the most common cause of cardiac arrest in a child? Uncommon cause? Survival?

A
  • Lack of oxygen supply to the heart secondary to a pulmonary problem, respiratory arrest, shock
    • Choking, suffocation, airway/lung disease, near drowning
  • Uncommon cause: heart disease
  • Chances for survival increase dramatically if CPR & advanced life support started quickly
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2
Q

What are the essentials of CPR?

A
  • Airway
  • Breathing
  • Circulation
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3
Q

How do you expose an airway?

A
  • First priority in resuscitation
  • Most common obstruction: tongue
  • Head-tilt method
  • Jaw-thrust method
    • Neck or cervical spine injury
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4
Q

How do you evalulate breathing?

A
  • Look. Listen. Feel.
    • Look for rise & fall in chest
    • Listen for exhaled air
    • Feel for exhaled airflow
  • Rescue breathing if spontaneous absent
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5
Q

How do you evaluate circulation?

A
  • Need for chest compressions determined after 2 rescue breaths
  • Pulse assessment
    • Infants: brachial artery
    • Children: carotid artery
  • Chest compressions: asystole, bradycardia
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6
Q

What is the definition of Shock?

A
  • Inadequate delivery of O2 & metabolic substrates to meet the metabolic demands of tissues
  • Normal or decreased BP
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7
Q

What are the 3 degrees of Shock?

A
  • Compensated
    • Normal BP & CO, adequate tissue perfusion
    • Maldistributed blood flow
  • Decompensated
    • Hypotension, low CO
    • Inadequate tissue perfusion
  • Irreversible
    • Cell death, refractory to medical treatment
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8
Q

What are the 3 categories of Shock?

A
  • Hypovolemic
  • Septic
  • Distributive
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9
Q

What is hypovolemic shock?

A
  • Most common cause of shock in children
  • Decreased circulating blood volume
    • Hemorrhage, dehydration
  • Amt volume determines compensation
    • Endogenous catecholamines
  • Volume loss >25% = decompensated shock
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10
Q

What is septic shock?

A
  • Secondary to inflammatory response to microorganisms & toxins, abnormal blood dist.
  • Hyperdynamic stage
    • Normal/high CO, bounding pulses, warm extremities, wide pulse pressure
  • Decompensated stage
    • Follows hyperdynamic stage
    • Impaired mental status, cool extremities, diminished pulses
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11
Q

What is distributive shock?

A
  • Distal pooling of blood or fluid extravasation
    • Anaphylactic or neurogenic shock
    • Medications/toxins
  • Types
    • Anaphylactic shock
    • Neurogenic shock
    • Cardiogenic shock
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12
Q

What is anaphylactic shock?

A

Extravasation of intracellular fluid from permeable capillaries

  • Acute angioedema of the upper airway
  • Bronchospasm
  • Pulmonary edema
  • Urticaria
  • Hypotension
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13
Q

What is neurogenic shock?

A
  • Secondary to spinal cord transection/injury
  • Characterized by:
    • Total loss of distal sympathetic CV tone
    • Hypotension from pooling of blood w/i the vascular bed
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14
Q

What is cardiogenic shock?

A
  • CO limited b/c of primary cardiac dysfunction
  • Causes
    • Dysrhythmias (supraventricular tachy)
    • Congenital heart disease
      • Impaired LV outflow
    • Cardiac dysfunction after cardiac surgery
  • Clinical features
    • Signs & symptoms of CHF
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15
Q

Recognition of shock may be difficult because…..

A
  • Presence of compensatory mechanisms
  • Prevent hypotension until 25% of intravascular volume lost
  • Index of suspicion for shock must be high
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16
Q

What are 6 historical features that may suggest the presence of shock?

A
  • Severe vomiting & diarrhea
  • Trauma w/ hemorrhage
  • Febrile illness (esp immunocompromised pt)
  • Symptoms of CHF
  • Exposure to known allergic antigen
  • Spinal cord injury
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17
Q

Physical exam of a patient in shock?

A
  • BP may be normal (initial hypovolemic/septic)
  • Tachycardia (before BP changes)
  • Tachypnea (compensation metabolic acidosis)
  • Mental status changes (poor cerebral perfusion)
  • Capillary refill prolonged (cool/mottled extrem)
  • Peripheral pulses bounding
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18
Q

Important laboratory studies for shock?

A
  • CBC - blood loss & infection
  • Electrolytes - metabolic acidosis, electrolyte ab
  • BUN & creatinine - renal function/perfusion
  • Ca & Glu - metabolic derangements
  • Coagulation factors - DIC
  • Toxicology screens - poisoning
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19
Q

How is shock managed?

Resuscitation? Medications?

A
  • Initial resuscitation (ABCs)
    • Supplemental O2
    • Early endotracheal intubation
    • Vascular access w/ fluid resuscitation
      • 20 mL/kg bolus of nl saline/LR
  • Restore intravascular volume
    • IV crystalloid/colloid
  • Inotropic & vasopressor meds
    • Dobutamine, dopamine, epinephrine
  • Metabolic derangements treated
    • Metabolic acidosos, hypocalcemia, hypoglycemia
  • Broad spectrum abx for septic shock
  • Blood products for hemorrhage
  • FFP for DIC
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20
Q

Trauma is the leading cause of death in children older than _____ year of age.

______ are the leading cause of trauma.

A

1 year of age

Motor vehicle accidents

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21
Q

How is a child’s response to trauma unique?

A
  • Head injuries common (larger % of body mass)
  • Neck shorter & supports greater weight
  • Rib cage more pliable, greater energy transmitted to spleen & liver
  • Growth plates = weak epiphyseal-metaphyseal junction, ligaments stronger than growth plate
  • Injury to the growth plate is highest risk
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22
Q

What is the primary survey in trauma?

A
  • w/i 5-10 min of arrival in the ER
  • ABCDEs
    • Airway
    • Breathing (100% O2)
    • Circulation (control hemorrhage)
    • Disability (Glasgow Coma Scale)
    • Exposure/Environmental control
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23
Q

Glascow Coma Scale in Verbal Patient

  • Eye opening
  • Best motor response
  • Best verbal response
A
  • Eye opening
    • Spontaneously (4)
    • Response to voice (3)
    • Response to pain (2)
    • No response (1)
  • Best motor response
    • Obeys commands (6)
    • Localizes pain (5)
    • Flexion withdrawal (4)
    • Decorticate posturing (3)
    • Decerebrate posturing (2)
    • No response (1)
  • Best verbal response
    • Oriented/appropriate (5)
    • Disoriented conversation (4)
    • Inappropriate words (3)
    • Incomprehensable words (2)
    • No response (1)
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24
Q

Glascow Coma Scale in Nonverbal Patient (Child)

  • Eye opening
  • Best motor response
  • Best verbal response
A
  • Eye opening
    • Spontaneously (4)
    • Response to voice (3)
    • Response to pain (2)
    • No response (1)
  • Best motor response
    • Normal movements (6)
    • Localizes pain (5)
    • Flexion withdrawal (4)
    • Flexion abnormal (3)
    • Extension abnormal (2)
    • No response (1)
  • Best verbal response
    • Cries normally, smiles, coos (5)
    • Cries (4)
    • Inappropriate crying & screaming (3)
    • Grunts (2)
    • No response (1)
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25
Q

What are 3 adjuncts to the primary survey?

A
  • ECG monitoring
    • Dysrhythmias (cardiac injury)
    • Pulseless electrical activity (cardiac tamponade, tension pneumo, hypovolemia)
  • Urinary catheter & NG tube
    • Monitor UOP, reduce abd distension
  • Diagnostic studies
    • Radiographs: cervical spine, chest, pelvis
    • CT scans: head, abdomen
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26
Q

What is the secondary survey?

A

Head-to-toe physical exam

Complete history

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27
Q

Head Trauma injuries & risk

A
  • Seizures common but self-limited
  • Infants at risk for bleeding in subgaleal & epidural spaces
    • Open fontanelles & cranial sutures
    • But more tolerant of expansion
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28
Q

What are the 3 different types if intracranial bleeds in children?

A
  • Epidural hematoma
  • Subdural hematoma
  • Intracerebral hematoma
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29
Q

Epidural hematoma

  • definition
  • clinical features
  • diagnosis
  • management
  • prognosis
A
  • Bleeding btwn the inner table of the skull/dura
  • Tearing of the middle meningeal artery
  • Signs & symptoms of intracranial pressure
  • Head CT: lenticular density
  • Immediate surgical drainage
  • Good prognosis w/ surgery
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30
Q

Subdural hematoma

  • definition
  • clinical features
  • diagnosis
  • management
  • prognosis
A
  • Blood beneath the dura
  • Tearing of bridging meningeal veins
    • Direct trauma or shaking
    • More common than epidural
  • Seizures, signs & symptoms of increased ICP
    • Bilateral (75%), slow development
  • Head CT: crescentic density
  • Neurosurgical consult, surgical drainage
  • Poor prognosis if underlying brain injured
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31
Q

Intracerebral hematoma

  • definition
  • management
A
  • Bleeding w/i the brain parenchyma
  • Frontal & temporal lobes
  • Opposite side of impact injury
    • Contrecoup injury
  • Surgical drainage
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32
Q

First sign & symptom of increased ICP

A
  • First symptoms
    • Headache
  • First signs
    • Pupillary changes
    • Altered mental status
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33
Q

What are the symptoms of increased ICP?

A
  • Headache
  • Vomiting
  • Stiff neck
  • Double vision
  • Transient loss of vision
  • Episodic severe headache
  • Gait disturbance
  • Dulled intelect
  • Irritability
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34
Q

What are the signs of increased ICP?

A
  • Papilledema
  • Cranial nerve palsies
  • Stiff neck
  • Head tilt
  • Retinal hemorrhage
  • Macewen’s sign
    • Hyperresonance of the skull on percussion
  • Obtundation
  • Unconsciousness
  • Progressive hemiparesis
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35
Q

Increased ICP may lead to ________.

A
  • Cerebral herniation
  • Transtentorial or uncal
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36
Q

What are the 5 clinical features of herniation?

A
  • Bradycardia
    • Early sign in children <4 YO
  • Fixed & dilated ipsilateral pupil
  • Contralateral hemiparesis
  • Pupils eventually bilaterally fixed & dilated
    • Bilateral hemiparesis
  • Cushing’s triad (late sign)
    • Bradycardia + HTN + irregular breathing
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37
Q

How is increased ICP managed?

A
  • Mild hyperventilation
    • 100% to lower PaCO2 to 30-35 mmHg
    • Vasoconstricts cerebral vessels
  • Elevation of head to 30-45o
    • Venous drainage
  • Diuretics
    • Mannitol
  • Neurosurgical consultation
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38
Q

Spinal cord injury in children

A
  • SCIWORA
    • Spinal cord injury w/o radiographic abnormality
  • More common in children than adults
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39
Q

Chest trauma

  • Children vs. adults
  • Complications
A
  • Child’s soft & pliable chest wall allows transmission of forces into lung parenchyma
  • Tension pneumothorax
    • Life-threatening
    • Distended neck veins, decreased breath sounds, hyperresonance to percussion, displaced trachea, pulseless electrical activity, shock
    • Emergent chest decompression by needle thoracotomy
    • Waiting for radiograph leads to death
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40
Q

Common sources of abdominal trauma in children

A
  • Duodenal hematoma
    • RUQ injury (bicycle handle bar)
    • Abd pain & vomiting
    • Bowel obstruction
  • Lap belt injuries
    • MVA, liver/spleen lacerations, bowel perf
    • Chance fracture: flexion disruption of the lumbar spine
  • Spleen, liver, kidney injury
    • Blunt trauma
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41
Q

_____ are the second most common cause of accidental death in children.

A

Burns

  • Scalding injuries from hot liquids most common
  • Always consider child abuse
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42
Q

What is a first degree burn?

A
  • Epidermis
  • Red, blanching, painful skin
  • Heals w/o scarring
  • Example: sunburn
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43
Q

What is a second degree burn?

A
  • Entire epidermis & part of the dermis
  • Superficial partial thickness burns
    • Entire epidermis & outer dermis
    • Moist, painful, red
    • Blister but don’t scar
  • Deep partial thickness burns
    • Entire epidermis & lower dermis
    • Pale white
    • Blister & heal w/ scarring
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44
Q

What is a third degree burn?

A
  • Full thickness burn
  • Epidermis, dermis, subq tissue
  • Dry, white, leathery
  • Skin grafts needed
  • Nerve endings burned (insensitivity to pain)
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45
Q

How do you calculate body surface area burned?

A
  • Lund-Browder classification
  • Adolescents & adults
    • each arm 9%
    • each leg 18%
    • anterior trunk 18%
    • posterior trunk 18%
    • head & neck 9%
  • Children: palm 1%
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46
Q

What is the initial resuscitation after a burn injury?

A
  • Endotracheal intubation
    • Inhalation of hot gas
    • Burn upper airway, edema, obstruction
  • Assess oxygenation
    • pulse ox, administer 100% O2
    • assess for CO inhalation
  • IV access
    • nonburned skin
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47
Q

_____ resuscitation after a burn injury is critical because _____.

A

Fluid

  • Large volumes of fluid may be lost from burned skin & leaky capillaries
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48
Q

What is the treatment for….

  • first degree burns
  • second degree burns
  • third degree burns
A
  • first degree burns
    • moisturizers, analgesics
  • second degree burns
    • analgesics (opiates)
    • debridement of skin to prevent infection
    • bullae (large blisters) left alone unless already ruptured
    • abx (topical 1% silver sulfadiazine)
  • third degree burns
    • skin grafting, hydrotherapy
    • escharotomy if restricts blood flow or chest expansion
    • abx (topical 1% silver sulfadiazine)
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49
Q

With a burn injury, when is hospitalization required?

A
  • Partial thickness burns >10% BSA
  • Full thickness burns >2% BSA
  • Burns specific to areas of the body
    • Face, perineum, hands, feet, burns overlying a joint, circumferential burns
  • Suspected inhalation injury
  • Suspected nonaccidental trauama (inflicted burn)
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50
Q

What is the definition of a near-drowning?

A

Victim who survives, sometimes only temporarily, after asphyxia while submerged in a liquid

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51
Q

Submersion-related injuries are the ___ leading cause of death in the US.

The age distribution in childhood is _____.

A
  • 5th leading cause, bimodal age distribution
  • Older infants & toddlers
    • Wander into unfenced pools or tip into water containers
  • Adolescents
    • M > F, submersion injury
    • Alcohol/drug ingestion
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52
Q

What is the pathophysiology of a near-drowning?

A
  • Asphyxia
    • aspirating liquid (wet drowner)
    • laryngospasm (dry drowner)
  • Fresh & salt water drowning
    • Denaturing of surfactant
    • Alveolar instability & collapse
    • Pulmonary edema
  • End result
    • Decreased pulmonary compliance
    • Increased airway resistance
    • Increased pulmonary artery pressures
    • Impaired gas exchange
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53
Q

What are the clinical features of a near-drowning?

A
  • Respirations absent/irregular
    • Coughing up pink/frothy material
    • Rales, rhonchi, wheezes
    • Pneumonia from fluid aspiration (>24 hrs)
    • Hypoxemia & hypercarbia (first 12-24 hrs)
  • Neurologic insult (hypoxic CNS injury)
    • Length & severity of hypoxia
    • Alert vs. agitated, combative, comatose
  • CV (dysrhythmias, myocardial ischemia)
  • Heme (hemolysis, DIC)
  • Renal failure
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54
Q

What is the management of a near-drowning?

A
  • Treatment same whether fresh or salt water
  • Initial resuscitation
    • ABCs, cervical spine immobilization, removal of wet clothing
  • Intubation & mechanical ventilation
    • High PEEP for respiratory failure
  • Rewarming of body temperature
    • Warm saline gastric lavage, bladder washings, peritoneal lavage
    • Severe hypothermia: until 32oC (89.6oF)
  • Attention to fluids/electrolytes
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55
Q

Prognosis after a near-drowning is poor for….

A
  • Children <3 YO
  • Submersion time >5 min
  • Resuscitation delay >10 min
  • Cardiopulmonary resuscitation required
  • Abnormal neuro exam or seizures
  • Arterial blood pH <7
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56
Q

What is the protocol for reporting child abuse?

What does child abuse include?

A
  • Health-care personnel have a legal obligation to report suspected child abuse or neglect
  • Index of suspicion of abuse should be high
  • Child abuse includes:
    • Physical abuse
    • Psychological abuse
    • Neglect
    • Sexual assault
57
Q

Which children are at high risk for abuse?

A
  • Any child is at risk for abuse
  • Greatest risk:
    • Age <4 YO (especially <1 YO)
    • Mental retardation, developmental delay, severe handicap, hyperactivity, challenging temperament (colic, tantrums)
    • Hx premature birth, low birth weight, neonatal separation from parents, multiple births
58
Q

What are the risk factors for an abusive caregiver?

A
  • Low self-esteem, social isolation, depression, hx of substance abuse
  • Hx of abuse as a child
  • Hx of mental illness
  • Hx of violent temperament
  • Family dynamics that include single parenthood, unemployment, poverty, marital conflicts, domestic violence, poor parent-child relationships, unrealistic expectations of the child
59
Q

What are the 6 clinical features of child abuse?

A
  • Bruises
  • Human bites
  • Burns
  • Fractures
  • Head injuries
  • Visceral injuries
60
Q

Age of bruise based on color pattern

  • Red-blue
  • Blue-purple
  • Green
  • Yellow-brown
A
  • Red-blue: 0-3 days
  • Blue-purple: 3-5 days
  • Green: 5-8 days
  • Yellow-brown: 8-14 days
61
Q

What types of bruises are indicative of child abuse?

A
  • Fleshy or protected areas
    • Inflicted injury: face, neck, back, chest, abdomen, buttocks, genitalia
    • Noninflicted injury: shins, knees, elbows, forehead (exposed areas)
  • Aged on basis of color
  • Patterns of bruising determine object
    • Belt loops, buckles, hangers, hands
62
Q

What types of burns are indicative of child abuse?

A
  • Accidental burns
    • Irregular, spashlike
  • Non-accidental burns
    • Clear line of demarcation
    • “stocking” or “glovelike” = submersion
  • Objects used to burn may be branded
    • Irons, cigarettes
63
Q

What types of fractures are indicative of child abuse?

A
  • Inconsistent w/ hx or child’s developmental ability
  • Metaphyseal fractures
    • “bucket handle” or corner fractures
    • Torsional force on the limb (pulling & twisting) or violent shaking
  • Fractures of the posterior or 1st ribs, sternum, scapula, vertebral spinous process
  • Multiple fractures in different stages of healing
64
Q

What types of head injuries are indicative of child abuse?

A
  • Trauma, asphyxiation, shaking
  • Leading cause of death & morbidity from child abuse
  • Shaken baby syndrome
    • Child <2 YO
    • Violently shaken
    • Retinal hemorrhages
    • Subdural hematomas
    • Metaphyseal fractures
    • Significant brain injury
65
Q

What types of visceral injury are indicative of child abuse?

A
  • Second leading cause of death from child abuse
  • Rupture & injury of the intestinal tract, liver, spleen
66
Q

How is child abuse diagnosed?

A
  • History is critical
    • Child development should correlated w/ nature of the injury
    • Delay in medical attention, implausable hx, inconsistency are suspicious
  • Physical exam
    • Acute injuries, old lesions
    • Dilated ophthalmoscopic evaluation for retinal hemorrhages
  • Accessory tests
    • Skeletal survey (old/healing fractures)
    • Head or abd CT scans (acute injuries)
67
Q

How is child abuse managed?

A
  • Child protective services or law enforcement agencies must be notified if there is a suspicion of abuse
  • Hospitalization may be required or until a safe location for the child is identified
68
Q

Are there physical signs of sexual abuse?

Who are the perpetrators?

Males vs. females?

A
  • Unlike physical abuse, there are typically no overt physical signs of trauma
  • Perpetrators are often known to the child
  • 80% occurs in females
69
Q

How do you use history to diagnose sexual abuse?

A
  • Hx of abuse from a young child is difficult
    • Open-ended questions
    • Interviewer trained in sexual abuse eval
  • Sexually abused children present w/ multiple non-specific complaints (abd & GU symptoms)
  • Sexual behavior in young children raises red flags for abuse
70
Q

How do you use physical exam to diagnose sexual abuse?

A
  • Signs of trauma should be noted
  • Genital & perianal examination
    • Females: hymen, vagina, perianal areas
    • Males: penis, scrotum, perianal area
    • Note discharge, injury, bleeding
  • Physical exam is normal in most victims
71
Q

What are some labs for evaluation of sexual abuse?

A
  • Labs to collect forensic evidence if abuse occurred w/i 72 hrs of presentation
  • Cultures or serologic testing for STIs (& HIV)
  • Test for pregnancy
  • Assess vaginal fluid for spermatozoa
72
Q

How do you manage sexual abuse?

A
  • Safety of the child should be the highest priority
  • Child protective services or social services must be notified & should arrage f/u & support
  • Pregnancy may be prevented w/ high-dose oral contraceptives (morning-after pills)
  • Antibiotics should be prescribed to empirically treat STDs
73
Q

What is Sudden Infant Death Syndrome (SIDS)?

A
  • Death of an infant younger than 1 YO
  • Death remains unexplained after a thorough case investigation
    • Autopsy
    • Death scene evaluation
    • Review of clinical hx
74
Q

What is the epidemiology of SIDS?

A
  • Most common cause of death in children <1 YO
  • 2 in 1,000 live births
  • Peak incidence at 2-4 mo
  • Typical victim found dead in the morning after being put to sleep at night
75
Q

How is SIDS managed?

A
  • Resuscitation
    • Difficult to ascertain period of time infant has been apneic & pulseless
  • If unsuccessful, autopsy
  • Postmortem exam
    • Intrathoracic petechaie (80%)
    • Pulmonary congestion or edema
    • Small airway inflammation
    • Evidence of hypoxia
76
Q

What is the epidemiology of child poisonings?

A
  • 60% in children <6 YO
  • 90% accidental
  • Majority at home when caregiver distracted
  • Most ingested
  • Some inhaled, spilled on skin or eyes, injected
  • Mortality <1%
77
Q

What are the 9 most common toxic exposures for children?

A
  • Cosmetics & personal-care products
    • Most common toxic exposure
  • Cleaning agents
  • Cough & cold preparations
  • Vitamins, including iron
  • Anagesics (acetaminophen, NSAIDs, aspirin)
  • Plants (6-7%)
  • Alcohols (ethanol) & hydrocarbons (gasoline, paint thinner, furniture polish)
  • Carbon monoxide
  • Prescription medications
78
Q

Consider poisoning in patients presenting with_____.

A

Nonspecific signs & symptoms

  • Seizures
  • Severe vomiting & diarrhea
  • Dysrhythmias
  • Altered mental status or abnormal behavior
  • Shock
  • Trauma
  • Unexplained metabolic acidosis
79
Q

How do you use history to diagnose poisoning?

A
  • Information about the toxin
    • Name, concentration, route
  • Potential poison dose calculated for worst-case scenario
    • Amount ingested per kg of body weight
  • Consider multiple agents in adolescents
  • Information about the environment
    • Location, meds, plants, vitamins, herbs, chemicals, timing
80
Q

Poisoning physical exam: odors

  • Bitter almond
  • Garlic
  • Acetone
  • Wintergreen
  • Moth balls
A
  • Bitter almond: cyanide
  • Garlic: arsenic, organophosphates
  • Acetone: salicylates, isopropyl alcohol
  • Wintergreen: methyl salicylate
  • Moth balls: camphor
81
Q

Poisoning physical exam: skin

  • Cherry red color
  • Sweaty
  • Dry skin
  • Urticaria
  • Gray cyanosis
A
  • Cherry red color: CO, cyanide
  • Sweaty: organophosphates, sympathomimetics
  • Dry skin: anticholinergics
  • Urticaria: allergic rxn
  • Gray cyanosis: methemoglobinemia
82
Q

Poisoning physical exam: eyes

  • Miosis
  • Mydriasis
  • Nystagmus
  • Retinal hemorrhages
A
  • Miosis: opiates, phencyclidine, organophosphates, phenothiazines
  • Mydriasis: amphetamines, cocaine, tricyclic antidepressants, atropine
  • Nystagmus: dilantin, phencyclidine
  • Retinal hemorrhages: CO, methanol
83
Q

Poisoning physical exam: fever

A
  • Cocaine
  • TCAs
  • Phencyclidine
  • Salicylates
  • Thyroxine
  • Anticholinergics
  • Amphetamines
  • Theophylline
84
Q

What are some lab studies to do after poisoning?

A
  • Screening lab tests
    • Serum glucose, serum & urine toxicology screens, electrolytes
  • Anion gap should be calculated
    • Na+ - (Cl- + HCO3-)
    • Increased anion gap (>16): AMUDPILES
      • Alcohol
      • Methanol
      • Uremia
      • DKA
      • Paraldehyde
      • Iron/isoniazid
      • Lactic acidosis
      • Ethylene glycol
      • Salicylates
85
Q

What imaging should be done after poisoning?

A
  • Radiographic imaging of the abdomen
  • Radiopaque substances (CHIPE)
    • Chloral hydrate & calcium
    • Heavy metals
    • Iodine & iron
    • Phenothiazines
    • Enteric-coated tablets
86
Q

What should be managed initially after poisoning?

A
  • ABCs
  • Altered mental status
    • Dextrose for hypoglycemia
    • Naloxone for opiate overdose
  • Poison control center consult for assitance
87
Q

What are the steps of gastric decontamination?

A
  • Syrup of ipecac
  • Gastric lavage
  • Activated charcoal
  • Whole-bowel irrigation
  • Antidotes
88
Q

How is syrup of ipecac used for gastric decontamination?

A
  • Induces emesis
    • direct gastric irritation
    • CNS chemoreceptor stimulation
  • Only effective w/i first 30 min after ingestion
  • Contraindicated in victims w/ decreased level of consciousness, caustic or hydrocarbon ingestions & children <6 mo
  • Doesn’t improve clinical outcome
    • Use out of favor
89
Q

How is gastric lavage used for gastric decontamination?

A
  • Large bore orogastric tube
  • Indications
    • Life-threatening ingestions
    • w/i 1 hr after ingestion
    • Toxins that delay gastric emptying (salicylates)
  • Contraindications
    • Caustic
    • Hydrocarbon
    • Non-toxic ingestions
    • Delayed presentation
  • Lack of evidence of clinical improvement
90
Q

How is activated charcoal used for gastric decontamination?

A
  • Very large absorptive surface area
  • Binds toxins & minimizes absorption
  • Should be considered for all poisonings
  • Disadvantages
    • Ineffective for: iron, lithium, alcohols, ethylene glycol, iodine, potassium, arsenic
    • Interferes w/ visualization during endoscopy
    • Don’t use for caustic ingestions
  • Improves clinical outcome (esp w/i 1 hr)
91
Q

How is whole-bowel irrigation used for gastric decontamination?

A
  • Rapid, complete emptying of the intestinal tract w/ polytheylene glycol (osmotic agent) + electrolyte solution (prevents electrolyte imbalance)
  • Helpful for ingestion of iron, heavy metals, sustained release medications
92
Q

What is the pathophysiology of acetaminophen poisoning?

A
  • Hepatic damage
    • Major sequelae of toxicity
    • Depletion of glutathione (cofactor for metabolism by CYP450 system)
  • Toxic intermediates
    • Produced when glutathione depeleted
    • Bind to hepatocytes
    • Hepatocellular necrosis
93
Q

Stages of Acetaminophen Toxicity (timing)

  • Stage 1
  • Stage 2
  • Stage 3
  • Stage 4
A
  • Stage 1
    • 30 min - 2 hrs
  • Stage 2
    • 24-72 hrs
  • Stage 3
    • 72-96 hrs
  • Stage 4
    • 4 days - 2 wks
94
Q

What are the signs/symptoms of stage 1 of acetaminophen toxicity?

A
  • Asymptomatic
  • Vomiting & diarrhea
95
Q

What are the signs/symptoms of stage 2 of acetaminophen toxicity?

A
  • GI symptoms resolve
  • 36 hrs: hepatic transaminases begin to increase
96
Q

What are the signs/symptoms of stage 3 of acetaminophen toxicity?

A
  • Hepatic necrosis
  • Jaundice
  • Hypoglycemia
  • Lactic acidosis
  • Hepatic encephalopathy
  • Coagulopathy
  • Renal failure
97
Q

What are the signs/symptoms of stage 4 of acetaminophen toxicity?

A
  • Resolution of symptoms
  • Progressive liver damage requiring liver transplantation
  • Death
98
Q

How is acetaminophen toxicity managed?

A
  • Gastric lavage (life-threatening ingestion)
  • Activated charcoal
  • Obtain serum acetaminophen level 2-4 hrs after
    • Matthew-Rumack nomogram
    • Determines hepatitis potential
  • Hepatitis –> antidote is N-acetylcysteine
    • Glutathione precursor
    • Oral 140 mg/kg loading dose
    • 70 mg/kg every 4 hrs for 17 doses
    • Hepatoprotective w/i 8 hrs of ingestion
    • Helpful up to 72 hrs post ingestion
99
Q

What are some examples of salicylates?

What is the pathophysiology of salicylate poisoning?

A
  • Pepto-Bismol, Ben-Gay, oil of wintergreen
  • Salicylates directly stimulate respiratory centers
    • Hyperventilation
    • Overcompensation of metabolic acidosis
    • Respiratory alkalosis
  • Salicylates uncouple oxidative phosphorylation
    • Lactic acidosis, enhances ketosis
100
Q

What are the clinical features of salicylate poisoning?

A
  • Fever, diaphoresis, flushed appearance
  • Tinnitus
  • Vomiting
  • Headache
  • Lethargy, restlessness, coma, seizures
  • Hyperpnea
  • Dehydration
101
Q

What are the laboratory features of salicylate poisoning?

A
  • Respiratory alkalosis + anion gap metabolic acidosis
  • Hyperglycemia followed by hypoglycemia
  • Hypokalemia
102
Q

How is salicylate poisoning managed?

A
  • Gastric lavage
  • Activate charcoal every 4 hrs
  • Obtain serum salicylate level at least 6 hrs after
    • Done nomogram to assess toxicity
  • Alkalinization of urine w/ NaHCO3 (urine pH >7) & large volume IVF enhance renal excretion
  • Dialysis (life-threatening)
103
Q

_____ is one of the most common & potentially fatal childhood poisonings. As little as ____ is toxic.

A

Iron

20 mg/kg

104
Q

What are the most common sources of accidental iron ingestion?

A
  • Adult-strength ferrous sulfate tablets
  • Iron in prenatal vitamins
105
Q

What is the pathophysiology of iron poisoning?

A
  • Direct damage to the GI tract (hemorrhage)
  • Hepatic injury & necrosis
  • Third spacing & pooling of fluid in the vasculature (hypotension)
  • Interference w/ oxidative phosphorylation
106
Q

Iron Toxicity

  • Stage 1
  • Stage 2
  • Stage 3
  • Stage 4
A
  • Stage 1 (1-6 hrs)
    • Abd pain, vomiting, diarrhea, GI bleeding
    • Shock from bleeding & vasodilation
    • Fever & leukocytosis
  • Stage 2 (6-12 hrs)
    • Resolution of stage 1 symptoms
  • Stage 3 (12-36 hrs)
    • Metabolic acidosis
    • Circulatory collapse
    • Hepatic & renal failure
    • DIC
    • Neurologic deterioration
  • Stage 4 (2-6 wks)
    • Late sequelae: pyloric or intestinal scarring w/ stenosis
107
Q

How should iron poisoning be managed?

A
  • Gastric lavage
  • Activated charcoal does NOT bind to iron
  • Hypovolemia, blood loss, shock treatment
  • WBI considered for life-threatening indigestion
  • Serum iron level 2-6 hrs post-ingestion
  • IV deferoxamine (iron-binding ligand)
    • Serum iron >500 ug/dL [OR]
    • >300 ug/dL & acidosis, hyperglycemia, leukocytosis present
    • Severe GI symptoms
    • >100 mg/kg iron ingested
  • Test dose of deferoxamine
    • Urine red/pink (vin rose) = +++ challenge
    • Clinically significant iron ingestion
108
Q

What are some sources of lead?

A
  • Lead based paint chips
  • Water carried by outdated lead pipes
  • Improperly glazed or foreign-made ceramic food or water containers
  • Pica: compulsive eating of non-nutrient substances such as dirt, paint, clay
109
Q

What are the 4 clinical features of lead poisoning?

(can be chronic ingestion or acute)

A
  • Abdominal complaints
    • Colicky pain, constipation, anorexia, vomiting
  • CNS complaints
    • Listlessness, irritability, seizures, decreased consciousness w/ encephalopathy
  • Peripheral blood smear
    • Microcytic anemia, basophilic stippling, RBC precursors
  • Abd radiographs: radioopacities
  • Radiographs of knees/wrists
    • Dense metaphyseal bands (lead lines)
110
Q

Lead poisoning

diagnosis

management

A
  • Elevated lead level
  • Elevated erythrocyte protoporphyrin
  • Treatment
    • Dimercaprol
    • British anti-lewisite (BAL)
    • EDTA
111
Q

What are caustic agents?

A

acids or alkalis w/ corrosive potential

112
Q

What kind of injury does acid poisoning cause?

A
  • ex: toilet bowl cleaner
  • Coagulation necrosis
  • Superficial damage to the mouth, esophagus, stomach
  • More severe damage if pH < 2
113
Q

What kind of injury does alkalis poisoning cause?

A
  • ex: oven & drain cleaners, bleach, laundry detergent
  • Liquefaction necrosis
  • Deep & penetrating damage to the mouth & esophagus
  • More severe if pH > 12
114
Q

What are the 4 clinical features of poisoning w/ caustic agents?

A
  • Immediate burning sensation
    • Intense dysphagia, salivation, restrosternal chest pain, vomiting
  • Obstructive airway edema (acid > alkalis)
  • Gastric perforation & peritonitis (acid)
  • Esophageal perforation w/ mediastinitis (alkali)
115
Q

How should poisoning w/ caustic agents be managed?

A
  • No attempt should be made to neutralize
    • Combination of acid + alkali will generate an exothermic rxn & worsen any burn
  • Ipecac, gastric lavage, activated charcoal are all CONTRAINDICATED
    • Charcoal interferes w/ endoscopy
  • Endoscopy to assess damage
  • Household bleach has less corrosive potential
    • No treatment
116
Q

How are people exposed to excessive CO?

A
  • Byproduct of incomplete combustion of carbon-containing material
  • Fires, tobacco, faulty home heaters, car exhaust, industrial pollution
  • CO is odorless, tasteless, colorless
117
Q

What is the pathophysiology of CO poisoning?

A
  • CO interferes w/ O2 delivery & utilization
  • CO displaces O2 from the Hgb molecule
    • Forms CO-Hgb, can’t carry O2
    • Bond 200X stronger w/ CO than O2
  • O2-Hgb dissociation curve shifted to the left
    • Tighter binding of remaining O2
    • Impaired release of O2 to tissues
  • CO interferes w/ cellular oxidative metabolism
118
Q

Clinical features of CO poisoning

  • Low levels
  • High levels
A
  • Low levels
    • Nonspecific symptoms
    • HA, flulike illness, dyspnea w/ exertion, dizziness
  • High levels
    • Visual & auditory changes, vomiting, confusion, syncope, slurred speech, cyanosis, myocardial ischemia, coma, death
119
Q

What are the clinical findings of CO poisoning?

  • classic
  • young children
  • neuro
A
  • Cherry red skin
  • Retinal hemorrhages
  • Tachycardia, tachypnea
  • Young children (<8 YO)
    • More symptoms at lower CO-Hb levels
    • GI symptoms (vomiting, diarrhea)
  • Delayed permanent neuropsychiatric syndrome
    • Memory loss, personality changes, deafness, seizures
    • Up to 4 wks after exposure
120
Q

How is CO poisoning diagnosed?

A
  • Measuring CO-Hb level
    • Not always indicative of CO exposure
    • May be low in victims w/ significant intoxication
  • Anion-gap metabolic acidosis
  • Low O2 saturation (PaO2 may be normal)
  • Evidence of myocardial ischemia on ECG
  • Elevated cardiac enzymes
121
Q

How is CO poisoning managed?

A
  • 100% O2
    • Displace CO from Hgb
  • Hyperbaric O2
    • More rapidly displaces CO from Hgb
    • Improves O2 delivery to tissues
  • Hospitalization
    • CO-Hb >25%
    • CO-Hb >10% during pregnancy, hx or presence of neuro symptoms, metabolic acidosis or ECG changes
122
Q

What is the epidemiology of mammalian bites?

A
  • Dogs (80%)
  • Cats, rodents, other wild/domestic animals
  • Humans (2-3%)
  • Boys during spring/summer months
123
Q

What are the clinical features of dog bites?

A
  • Bites range in severity
    • Scratches, punctures, lacerations, severe tissue injury
    • Jaw pressure >200-450 lb/in2
  • Young children bitten on head & neck
  • Older children bitten on extremities
  • Secondary infections
    • Anaerobic & aerobic organisms
    • Staph aureus, Pasteurella multocida, Strep
124
Q

How are dog bites managed?

A
  • Copious wound irrigation
  • Wounds on the face, large wounds, wounds <12 hrs old should be sutured
    • Facial wounds <24 hrs old can be sutured
    • Face has increased vascularity
  • Wounds at high risk for infection
    • Hand, wrist, foot, small puncture wounds
  • Antibiotics: amoxicillin-clavulanic acid
  • Tetanus prophylaxis
125
Q

What are the clinical features of cat bites?

What is the treatment?

A
  • Puncture wounds to the UE most common
  • Victims have higher risk of infection
    • Pasteurella multocida
  • Cat scratch disease (regional lymphadenitis)
  • Treatment
    • Similar to dog bites
    • Adequate irrigation difficult
126
Q

What are the common types of wounds w/ human bites?

A
  • Trunk or face in young children
  • Fist fight: metacarpophalangeal joint
    • Wounds extremely serious
    • Infection may penetrate the avascular fascial layers –> deep infection & tendonitis
127
Q

What types of infections in human bites?

A
  • Infection rate is high
  • Mixed bacterial infection
    • Streptococcus viridans, Staph aureus
    • Bacteroides, Peptostreptococcus, Eikenella corrodens
  • Other systemic infections
    • Hepatitis B, HIV, syphilis
128
Q

How are human bites managed?

A
  • Copious wound irrigation
  • Closure of large lacerations
  • Antibiotics: amoxicillin-clavulanic acid
129
Q

What are the types of poisonous spiders?

A
  • Black Widow Spider (Lactrodectus species)
  • Brown Recluse Spider (Loxosceles species)
130
Q

The black widow spider is characterized by….

A
  • Red/orange hourglass marking on ventral surface
  • Only the female spider is dangerous
  • Bites only if provoked
  • Web located in dark recesses
    • Closets, woodpiles, attics
131
Q

What are the clinical features of a Black Widow Spider bite?

A
  • Venom is a potent neurotoxin
  • Few local symptoms (burning, sharp pinprick)
  • Pathognomonic signs/symptoms
    • Severe HTN, muscle cramps
  • Nonspecific symptoms
    • HA, dizziness, nausea, vomiting, anxiety, sweating
132
Q

What is the management of a Black Widow Spider bite?

A
  • Local wound care
    • Wound irrigation, tetanus prophylaxis
  • Benzodiazepines & narcotics
    • Muscle cramps
  • Lactrodectus antivenin
    • Signs/symptoms of severe envenomation
133
Q

The Brown Recluse Spider is characterized by…

A
  • “Fiddle-back spider”
  • Brown violin-shaped marking on dorsum of thorax
  • Bites only if provoked
  • Web located in dark recesses
134
Q

What are the clinical features of a brown recluse spider bite?

A
  • Venom: cytotoxic compound containing tissue-destructive enzymes
  • Bite
    • Little initial pain
    • 1-8 hrs: painfully itchy papule
    • 3-4 days: increases in size, discolors
  • Necrotic & ulcerated deep lesion
  • Systemic rxns (24-48 hrs)
    • Fever, chills, weakness, vomiting, joint pain, DIC, hemolysis, renal failure from myoglobinuria
135
Q

How is a brown recluse spider bite treated?

A
  • Local wound care
  • Tetanus prophylaxis
  • Treatment of necrotic ulcer
    • Steroids, skin grafting, dapsone, hyperbaric oxygen
  • No antivenin
136
Q

What are the characteristics & pathophysiology of

pit viper snake bites?

A
  • Family Crotalidae, >95% snake bites
  • Rattlesnake, cottonmouth, copperhead snakes
  • Bite location & amt of venom injected determine the severity of envenomation
  • Head & trunk bites most severe
  • Venom: complex mixture of proteolytic enzymes
137
Q

What are the clinical features of a pit viper snake bite?

A
  • Local findings
    • Puncture marks, progressive severe swelling, ecchymosis
  • Systemic effects
    • Paresthesias of the scalp
    • Periorbital fasciculations
    • Weakness, diaphoresis, dizziness, nausea
    • Metallic taste in the mouth
  • Coagulopathy, thrombocytopenia, hypotension, shock
138
Q

How are pit viper snake bites treated?

A
  • Local wound care, tetanus prophylaxis, immobilization, immediate transport to ER
  • Incision & suction NOT recommended
  • More injury: tourniquets, ice, direct pressure
  • Crotalidae polyvalent antivenin (all bites)
    • Children: more antivenin
    • Most effective w/i 4-6 hrs
    • Complications: serum sickness, anaphylaxis
  • Crotalidae polyvalent immune Fab
    • Safe, more potent, very effective
139
Q

Coral snake bites

  • characteristics
  • clinical features
  • management
A
  • Family Elapidae, 1-2% all snakebites
  • “red next to yellow, kill a fellow”
  • “red next to black, venom lack”
  • Clinical (neurotoxic venom)
    • Local swelling & tenderness
    • Severe systemic symptoms
      • Paresthesias, vomiting, weakness, diplopia, fasciculations, confusion, respiratory depression
  • Treatment
    • Antivenin, local wound care, supportive

Pediatrics (24 decks)

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