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Pediatrics Clerkship > Aquifer - Neuro (Part 1) > Flashcards

Aquifer - Neuro (Part 1) Flashcards

19, 23, 24

1
Q

DDx - unresponsiveness in children (7)

A
  1. Toxic ingestion
  2. Seizures
  3. Syncope
  4. Closed Head Injury
  5. Infection

Less common:
Intracranial process, intusussception

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2
Q

Most common age of presentation of toxic ingestion in children?

A

9 months-3 years

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3
Q

List some of the common medications that can lead to unresponsiveness. List some poisons that can lead to generalized seizures.

A

Opiates, benzodiazepines, and clonidine

Other medications that can cause a metabolic disturbance (e.g., oral diabetic agents causing hypoglycemia) should be considered

Acute alcohol poisoning and lead poisoning

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4
Q

Syncope due to ___ is common in children between what ages? What causes this phenomenon?

A

Breath-holding spells; 6 months to 6 years

Occurs during expiration and is reflexive in nature - child starts to cry, then suddenly falls silent in the expiratory phase of respiration, which can be followed by a color change

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5
Q

Two types of breath-holding spells?

A

Cyanotic (more common) or pallid (acyanotic) type

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6
Q

Key features of a cyanotic breath-holding spell? Key features of pallid spells?

A

Precipitating event that upsets the child resulting in vigorous crying and hyperventilation, followed by a prolonged expiratory apnea

Transient hypoxia results in the child turning pale or cyanotic followed by brief LOC and limpness

Quickly self-resolve, typically no associated post-ictal state

A child with a breath holding spell may have a brief generalized seizure, most likely due to hypoxia

Pallid: typically associated with injury

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7
Q

Prognosis of breath holding spells?

A

Parents should be reassured that these are a benign and self-limited condition. Very rarely, they have been reported to be associated with asystole.

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8
Q

Cardiac syncope is more unusual in an infant or toddler, but should be considered. It would most likely not be vasovagal type syncope - what can cause it?

A

Supraventricular arrhythmias (tachycardia) or ventricular arrhythmias (in the settling of prolonged QT syndrome) can decrease cerebral blood flow and cause syncope

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9
Q

Up to 30-40% of children with meningitis can present with seizure activity. What other signs may be seen?

A

Fever and irritability; post-seizure impairment

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10
Q

How do children with encephalitis present?

A

Waxing and waning mental status, as well as fever and seizure; post-seizure impairent

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11
Q

What 2 viruses should be considered as possible pathogens for encephalitis?

A

Enterviral infections and HSV

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12
Q

Medical history in a patient with a brain tumor?

A

Preceding history of headache, behavior change, vomiting, focal neurologic change, seizure from an intracranial mass lesion would most likely begin as a partial seizure

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13
Q

What are the most common solid tumors in children and where do they occur?

A

Brain tumors (1200 cases/year), usually in the posterior fossa

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14
Q

What is intussusception?

A

Telescoping or prolapsing of a portion of the intestine

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15
Q

Why can intussusception lead to a near unresponsive state or mental status changes?

A

As the condition becomes more long-standing, lethargy with a near unresponsive state can be seen between the episodes of colicky pain. In addition, children commonly have intravascular volume depletion due to vomiting and third spacing of fluids, leading to mental status changes similar to a child who is very dehydrated.

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16
Q

List the 5 types of seizures.

A
  1. Generalized tonic-clonic
  2. Simple partial
  3. Complex partial
  4. Petit mal (childhood absence epilepsy)
  5. Atonic (akinetic)
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17
Q

What is the most common type of seizure in children?

A

Generalized tonic-clonic

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18
Q

Describe a generalized tonic-clonic seizure.

A

Begins abruptly with tonic (rigid) stiffening of all extremities and upward deviation of the eyes. Clonic jerks of all extremities follow the tonic phases. Finally, the child becomes flaccid, and urinary incontinence may occur.

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19
Q

Describe a simple partial seizure.

A

Motor signs in a single extremity or on one side o the body; may spread to become generalized, making it difficult to distinguish from a generalized seizure

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20
Q

Describe a complex partial seizure.

A

Altered level of consciousness (hallmark), blank stare, lip-smacking, drooling, gurgling, N/V

Automatisms (quasi-purposeful motor or verbal behaviors that are repeated inappropriately) commonly accompany this type

Often last 30 seconds to 2 minutes and are associated with a post-ictal phase of confusion, sleep, or headache

Secondary generalization can occur in up to 1/3 of children

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21
Q

Age of onset of childhood absence epilepsy?

A

Around 3 years

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22
Q

Describe absence seizures.

A

Loss of environmental awareness (“staring off into space”) and automatisms (e.g., eye-fluttering or lip-smacking)

While these are generalized seizures, children usually regain their consciousness more quickly than in generalized tonic-clonic

No loss of tone or urinary continence

Can be precipitated by hyperventilation or photic stimulation

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23
Q

Describe an atonic (akinetic) seizure.

A

Loss of motor tone

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24
Q

True seizures result from ___. Many other conditions (e.g., motor tics, myoclonus, gastroesophageal reflux in Sandifer’s syndrome, and pseudoseizures, aka psychogenic non-epileptic seizures) can result in movements or behaviors mimicking a seizure.

A

Sudden and abnormal electrical activity in the brain

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25
Q

List evidence for a true seizure.

A

History of alteration or loss of consciousness
Incontinence
Deviation of the eyes
Rhythmic motor movements that cannot be stopped by touching or holding the child
Postictal state

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26
Q

List the steps in determining the etiology of a seizure.

A
  1. Detailed description of the event
  2. Detailed timeline of the events
  3. Any precipitating events such as fever
  4. Possibility of toxic ingestion
  5. Any history of injury
  6. Medical and family history - past history of seizures, developmental delay, premature birth, family history of seizure disorders or neurologic problems, family members with certain medical conditions which may require certain medications that could have been ingested by the patient.
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27
Q

List prenatal, perinatal, and neonatal events/complications that may be associated with neurologic abnormalities leading to a seizure.

A
  1. Intrauterine congenital infections can lead to microcephaly, developmental delay, and seizures
  2. Teratogens must be considered
  3. Perinatal complications such as asphyxia
  4. Premature infants are at risk for intracranial hemorrhages
  5. Neonatal meningitis, prolonged hypoglycemia, and kernicterus in the newborn period
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28
Q

What is the relationship between developmental maturation and seizures?

A

Abnormalities in neurodevelopmental maturation could suggest serious underlying disease in a child with seizures. Most children with febrile seizures are developmentally normal. Pre-existing developmental abnormalities are a risk factor for subsequent epilepsy.

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29
Q

DDx - seizure (8)

A
  1. CNS infection (meningitis/encephalitis)
  2. Febrile seizure
  3. Head injury/post-traumatic seizure
  4. Ingestion/poisoning
  5. Idiopathic seizure/epilepsy
  6. Hypoglycemia
  7. Brain tumor
  8. Breath-holding spell
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30
Q

A seizure related to head injury generally occurs ___ (time) after the incident.

A

1-2 hours

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31
Q

Discuss the presentation of epilepsy in children.

A

A fever often triggers the first seizure in children with epilepsy.

Although some children with epilepsy also have developmental delay due to genetic, congenital, or acquired disorders (symptomatic epilepsy), many other children with epilepsy are developmentally normal (idiopathic epilepsy).

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32
Q

In patients with very prolonged seizures, what can cause a fever?

A

Sustained motor activity and release of inflammatory mediators

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33
Q

Diagnosis of epilepsy?

A

2+ unprovoked seizures

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34
Q

Epilepsy in all forms has a prevalence of ___% throughout childhood

A

~1

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35
Q

One of the most common reasons for seizures in children is febrile seizures. They occur in ___% of children between ages ___. Discuss the general presentation.

A

2-5; 6 months-5 years; generalized

Usually occur on the first day of the febrile illness
Fever >38 degrees
Tend to be developmentally normal
Often have a +family history (other first-degree relatives with febrile seizures as children)
Most are generalized

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36
Q

Discuss febrile seizures vs. a CNS infection causing seizures in the setting of fever.

A

Febrile seizures - a fever, typically caused by a benign illness like a viral infection - triggers a seizure in a susceptible host (young child, positive family history, etc.)

CNS infection - infection itself causes both the fever and the seizure. Prolonged fever prior to the event, especially with irritability or inconsolability, is an indication of a more serious CNS condition

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37
Q

True or false - febrile seizures are hreditary.

A

True - the exact mode of inheritance is still unclear.

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38
Q

When should an LP be obtained in the setting of possible febrile seizure?

A

A child age 6-12 months with incomplete or unknown immunizations against Hib or S. pneumoniae, particularly if the child’s neurologic status is worrisome or difficult to obtain.

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39
Q

Evaluation of a first febrile seizure?

A

In general, if the child’s clinical history is consistent with the classic pattern of a simple febrile seizure and if his past medical history and physical exam are normal, then he likely has a febrile seizure and no further workup is necessary.

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40
Q

Evaluation of a first non-febrile seizure with EEG?

A

EEG - useful adjunct to H&P, but a routine interictal (between seizures) EEG will show an epileptiform abnormality in only ~60% of infants and children, and less in adolescents and adults.

May be useful to identify epilepsy syndromes based on both the patient’s history and EEG pattern

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41
Q

Evaluation of a first non-febrile seizure with MRI?

A

Frequently performed; brain MRI is much more likely to be abnormal in children with focal seizures than in generalized or febrile seizures

Can identify brain parenchymal malformations, vascular malformations, and temporal sclerosis

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42
Q

Evaluation of a first non-febrile seizure with CT?

A

Little use in the evaluation of a child with suspected epilepsy

Exceptions include trauma and the investigation of calcifications, such as in CMV infections or tuberous sclerosis

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43
Q

Compare the incidence, duration, frequency, and type of simple vs. complex febrile seizures.

A

Simple:
More common, <15 minutes, 1x in a 24-hour period, generalized

Complex:
Less common, >15 minutes, >1x in a 24-hour period, focal

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44
Q

Discuss the risk of recurrence in a child with a febrile seizure.

A

First febrile seizure before 12 months, recurrence risk is ~50%

First febrile seizure after 12 months, recurrence risk is ~30%

Parents should be reassured that recurrent, simple febrile seizures have no long-term effects in terms of child development

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45
Q

Discuss the risk of epilepsy in a child with a febrile seizure.

A

Risk of developing risk is slightly increased above the 0.5-1% baseline population risk

More common among children with early, recurrent febrile seizures, especially with a family history of epilepsy

Complex febrile seizures - increased risk

Abnormal development - increased risk

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46
Q

Guidance about febrile seizures for caregivers regarding treatment for fever

A

Give acetaminophen or ibuprofen if he is uncomfortable

Not helpful in preventing recurrence of febrile seizures

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47
Q

Guidance about febrile seizures for caregivers regarding what to do in the event of seizure?

A

Place child on his side so he won’t choke on stomach contents or saliva
Ensure a safe setting to prevent injury
Nothing should be placed in the child’s mouth to keep him from biting his tongue
Do not restrain the child’s movements during the seizure
Remain as calm as possible
Most seizures stop on their own within a few minutes
Call 911 if the seizure lasts >5 minutes

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48
Q

Guidance about febrile seizures for caregivers regarding medications?

A

While there are some medications that may prevent future seizures, the child would have to take them either all the time or intermittently when sick. Experts agree that such medications should not be used in children with simple febrile seizures because of the potential for serious AEs.

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49
Q

Which medications are effective in preventing recurrence of simple febrile seizures?

A

Phenobarbital (poor adherence, serious side effects in at least 20% of patients), primidone (high side effect profile), VPA (hepatotoxic)

Diazepam given at the start of the febrile illness can be effective in preventing recurrent febrile seizures - sedating side effects that may cloud the presentation of a serious CNS infection led to not recommending this

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50
Q

Which medications have not been shown to be effective in preventing febrile seizure recurrence?

A

Carbamazpeine, phenytoin

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51
Q

Primary ___ infection is associated with ~20-30% of first febrile seizures in children.

A

HHV-6 (roseola)

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52
Q

Describe the presentation of tension headaches.

A

Often occur in the setting of emotional stress, fatigue, lack of sleep, and other stressors

Most often episodic
Generally worsens throughout the day
Mild to moderate intensity
May feel like a band around the head or involve the occipital area with accompanying tenderness of the posterior muscles of the neck

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53
Q

What is the most common cause of recurrent headache in children?

A

Migraine headaches

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54
Q

Although uncommon, migraines can first manifest as what 3 periodic syndromes seen exclusively in the pediatric age group?

A
  1. Cyclical vomiting
  2. Abdominal migraines
  3. Benign paroxysmal vertigo
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55
Q

What are the symptoms of migraines?

A

More severe than tension headaches
Often throbbing in nature
Often accompanied by photophobia and/or phonophobia, abdominal pain, N/V

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56
Q

Common precipitating factors of migraines?

A

Stress, bright lights, odors (such as perfumes), foods

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57
Q

Alleviating factor of migraines?

A

Frequently relieved by sleep

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58
Q

Risk factor for migraines?

A

Family history in about 50% of those with migraine headaches

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59
Q

Describe a “classic” migraine (vs. common)

A

Accompanied by an “aura,” which can include visual symptoms (bright spots in the visual field), speech changes or sensory abnormalities (such as paresthesias

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60
Q

Describe a “common” migraine (vs. classic)

A

Migraine without an aura, typically unilateral, frontal or temporal in location, but may involve any part of the head

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61
Q

What is the most frequent type of migrainous headache seen in children?

A

Common migraine

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62
Q

List red flag symptoms for life-threatening causes of headaches.

A

Occurring with forceful vomiting after lying down (increased ICP)
Sudden onset (intracranial hemorrhage)
Awakens from sleep (increased ICP)
Accompanied by fever and photophobia (meningitis, encephalitis)
Worsens with cough or Valsalva (increased ICP)
Progressively worsening in frequency or severity

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63
Q

Discuss the relationship between development and migraines.

A

Normal development is reassuring, but does not exclude serious pathology. Abnormal development would cause the clinician to consider a potential relationship between the delay and headaches. If the child has always been delayed, a link may be unlikely. Loss of milestones, however, would be very concerning and would cause one to consider a neurologic process.

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64
Q

Genetic basis for migraine headaches?

A

Twin studies and the familial nature of migraines point to a genetic basis. However, no genes have clearly been linked to the common varieties of migraine. Studies of families with a rare form of migraines (Familial Hemiplegic Migraine - FMH) demonstrate evidence for the involvement of calcium channel gene mutations and alterations in the gene for a sodium/potassium ATPase.

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65
Q

Fever and tachycardia in a child with headache may indicate what?

A

Serious infectious process such as meningitis, encephalitis, intracranial abscess (such as from complications of sinusitis or otitis media), or even sepsis

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66
Q

What is Cushing’s triad and what does it suggest?

A

Elevations in BP, bradycardia, and irregular respirations

Increased ICP

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67
Q

What causes an abnormal Romberg test?

A

Diseases resulting in decreased position sense or abnormal vestibular function will lead to a + test only with eyes closed (vision helps compensate for the abnormality)

Patients with cerebellar pathology have a + test with eyes open and closed

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68
Q

What is Idiopathic Intracranial Hypertension (previously known as pseudotumor cerebra)?

A

Increased ICP in the absence of intracranial mass lesion or hydrocephalus, often mimics brain tumors in presentation. Thought to occur because of alterations in CSF absorption and/or production, or abnormalities in vasomotor control and cerebral blood flow

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69
Q

Symptoms of idiopathic intracranial hypertension?

A

Headache (most common presenting complaint), vomiting may occur, diplopia secondary to paralysis of the abducens nerve may be present

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70
Q

Causal/predisposing factors of idiopathic intracranial hypertension?

A

Obesity, medications (vitamin A derivatives, tetracycline, OCs, steroids, etc.), metabolic disorders (galactosemia, hypoparathyroidism, etc.), infections (sinusitis, chronic otitis media, etc.)

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71
Q

How is idiopathic intracranial hypertension diagnosed?

A

Increased ICP with associated symptoms such as headache and vomiting + normal brain anatomy + normal CSF

Brain imaging is usually normal; in some children ventricles may be small; no mass lesion is seen

Dx with an elevated CSF opening pressure during a lumbar puncture

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72
Q

Complications of idiopathic intracranial hypertension?

A

Blindness resulting from transmission of elevated CSF pressure to the optic nerve sheath.

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73
Q

What information should be included in a headache diary?

A

Character, duration, location, associated symptoms, activity at the time of the headache, potential triggers, alleviating factors

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74
Q

What is ataxia?

A

Lack of coordination of muscle movements; non-specific neurological sign which can result from dysfunction in various parts of the nervous system that coordinate movements, such as the cerebellum, the inner ear, and the dorsal columns. It can be congenital or acquired.

75
Q

DDx - acquired ataxia (10)

A
  1. Post-infectious cerebellitis (aka acute cerebellar ataxia)
  2. Infectious cerebellitis
  3. Medication or toxin
  4. Intracranial mass
  5. Opsoclonus-myoclonus syndrome
  6. Migraine headache
  7. Hydrocephalus
  8. Metabolic disease (MSUD, pyruvate decarboxylase deficiency, etc.)
  9. Neurodegenerative disease (ataxia-telangeictasis and Friedreich ataxia)
  10. Psychiatric illness (conversion disorder)
76
Q

What is the most common cause of acute ataxia in children?

A

Post-infectious cerebellitis

77
Q

Describe the presentation of post-infectious cerebellitis.

A

Primarily a diagnosis of exclusion in children 1-3 years
Occurs several weeks after a viral infection (e.g., varicella or coxsackie)
Sudden onset of ataxia, vomiting, nystagmus (in ~50%) and dysarthria (in some)
Not typically associated with fever or other systemic manifestations

78
Q

Possible pathogenesis of post-infectious cerebellitis?

A

Autoimmune response leading to cerebellar demyelination

79
Q

CSF in post-infectious cerebellitis?

A

May be normal or have a pleocytosis; eventually the CSF protein is elevated

80
Q

Prognosis of post-infectious cerebellitis?

A

Majority of children recover completely within a few months

81
Q

Etiology of infectious cerebellitis?

A

May be viral or bacterial
Viral pathogens include mumps, enterovirus, EBV
Bacterial pathogens include those that cause bacterial meningitis (S. pneumoniae, N. meningitidis, Hib)

82
Q

Presentation of infectious cerebellitis?

A

Ataxia, fever, mental status changes

83
Q

Examples of medications and toxins that can cause acute ataxia?

A

Anticonvulsant, alcohol, sedating antihistamines

84
Q

Presentation of ataxia in medication/toxin abuse?

A

May be accompanied by nystagmus and dysmetria, usually bilateral due to the diffuse involvement of the cerebellum including the vermis and hemispheres

85
Q

Ataxia due to an intracranial mass is most often associated with tumors in what parts of the brain?

A

Cerebellum or frontal lobe

86
Q

What is opsoclonus-myoclonus syndrome?

A

Paraneoplastic syndrome that occurs most often with neuroblastoma

87
Q

Presentation of opsoclonus-myoclonus syndrome?

A 
Younger child (6 months-3 years)
Ataxia accompanied by intermittent jerking movements (myoclonus) and erratic, jerky conjugate movements of the eyes (opsoclonus)
88
Q

What types of migraines can cause recurrent intermittent episodes of acute ataxia?

A

Basilar artery migraines or hemiplegic migraines

May be accompanied by intermittent loss of vision, change in speech, headache, and vomiting

89
Q

How does ataxia associated with hydrocephalus present?

A

Generally insidious in onset, quite chronic with increasing loss of coordination over weeks to months. Usually associated with headache and vomiting

90
Q

Type of ataxia seen in metabolic disease?

A

Intermittent or chronic with intermittent exacerbations

91
Q

Presentation of a neurodegenerative disease causing ataxia?

A

Most affected children are younger than 10, and their symptoms include a loss of developmental milestones, ataxia, and other neurologic symptoms

92
Q

What happens in conversion disorder?

A

Hysterical involuntary disturbance in gait (patient truly believes something is wrong but no physical pathology exists) known as astasia abasia

Unlike true ataxis, this gait is wildly erratic and involves lurching of the body which requires extraordinary balance

The child is generally able to sit without difficulty, but when put in a standing position, immediately begins to sway at the waist

These patients will rarely fall.

93
Q

Presentation of basilar migraine?

A

Often young women or children
First develop visual phenomena like those of a typical migraine except that they are bilateral
Transient cortical blindness may also occur
May have associated vertigo, ataxia, incoordination of the limbs, dysarthria, and bilateral limb and perioral paresthesias

Sometimes followed by a transient loss or impairment of consciousness or by a confusional state

This is followed by a throbbing headache (usually occpipital) often associated with N/V

94
Q

What is nystagmus?

A

Rhythmic oscillation of the eyes, analogous to tremor in other parts of the body; may occur in 1+ planes (horizontal, vertical, or rotary)

Usually quicker in one direction that in the other

Defined by its quicker phase

95
Q

What causes nystagmus?

A 
Cerebellar disease (when due to cerebellar disease, most prominent when looking toward the side of the lesion)
Tumor, toxins, cerebellitis, MS
96
Q

What causes periodic alternating nystagmus?

A

Diffuse cerebellar lesions and patients with midline cerebellar lesions arising from the vermis or the nodule, such as cerebellar medulloblastoma

97
Q

What is the role of the cerebellum?

A

Motor control, coordination, precision, and balance control

98
Q

Why do mass lesions in the cerebellum often lead to obstructive hydrocephalus?

A

Due to the close proximity of the cerebellum to the 4th ventricle

99
Q

Symptoms caused by cerebellar lesions within the vermis?

A

Dysarthria, truncal ataxia, and gait abnormalities

100
Q

Symptoms caused by cerebellar hemispheric lesions?

A

Ipsilateral limb abnormalities, nystagmus, tremor/dysmetria, sparing of speech

Patients fall toward the side of the lesion and have worse nystagmus when they look towards the side of the lesion

101
Q

Symptoms caused by lesions of the deep cerebellar nuclei?

A

Resting tremor, myoclonus, opsoclonus (seen in neuroblastoma)

102
Q

___ is contraindicated in a patient with increased ICP and focal findings on neurologic exam. Why?

A

LP; may lead to brain herniation

103
Q

Visualization of a suspected brain tumor?

A

MRI (excellent detail of the posterior fossa)

CT is not good in visualizing the posterior fossa as well. Would be used if intracranial hemorrhage needed to be ruled out

104
Q

How do infratentorial lesions usually present?

A

Cerebellar signs and signs of raised ICP

105
Q

How do cerebellar hemispheric lesions present?

A

Hypotonia and hyporeflexia

106
Q

How do supratentorial lesions usually present?

A

Focal motor and sensory abnormalities on the opposite side of the lesion

107
Q

How do brain stem tumors usually present?

A

CN and gaze palsies

108
Q

Incidence of brain tumors in children?

A

Most common solid tumor in children, second most common form of childhood cancer (#1 - leukemia)

Incidence has been increasing over the past several decades for unclear reasons

Incidence peaks in the first decade of life, with a second peak in the 8th decade of life

109
Q

Discuss survival of brain tumors in children.

A

Mortality rate has decreased by 20% in children since 1975, though this is disproportionately less than that seen with other childhood cancers

Deaths caused by childhood brain tumors are the highest among all childhood cancer deaths

Morbidity associated with brain tumors is significant

110
Q

Brain tumors are more common in the ___ age group.

A

Younger (<7 years)

111
Q

Incidence of childhood brain tumors in M vs. F

A

Males are slightly overrespresented, but this can be accounted for by the higher male incidence of 2 types of brain tumors (ependymomas and medulloblastomas)

112
Q

Which type of tumor (supra vs. infra) are more common in chidren?

A

Supratentorial - first 2 years of age

Infratentorial - dominate for the rest of the first decade

Supratentorial - more common in adolescence and adulthood

113
Q

Risk factors for childhood brain tumors?

A

Exposure to ionizing radiation

Certain genetic syndromes (tuberous sclerosis, neurofibromatosis, Li-Fraumeni syndrome - very rare)

114
Q

Histologic classification of the 4 most common brain tumors in children?

A

Medulloblastoma (20%)
Juvenile pilocytic astrocytoma (20%)
Low-grade astrocytoma (15%)
High-grade astrocytoma (7%)

115
Q

Most common pediatric brain tumor?

A

Medulloblastoma (aka infratentorial neuroectodermal tumor)

Malignant tumor that may spread through the CNS, capable of metastasizing to extracranial sites

116
Q

Prognosis and Rx of medulloblastoma?

A

Prognosis depends on size and dissemination

Rx - surgical resection, radiation, chemotherapy

117
Q

What tumor has the best prognosis of all infratentorial tumors in children?

A

Astrocytoma of the cerebellum

often have a cystic component

118
Q

Prognosis and treatment of astrocytoma of the cerebellum?

A

Prognosis - 5-year survival is ~90% with complete resection, 50-70% with partial resection

Rx - surgical resection; radiation reserved for patients with high-grade astrocytomas, partial resections, or those patients in whom postop tumor progression is evidence

119
Q

Prognosis and Rx of brain stem glioma?

A

Prognosis ranges from quite grave (aggressive, resulting in diffuse infiltration of the pons) or quite good (low-grade, resulting in a focal tumor in the midbrain or medulla)

Rx - surgical resection alone for low-grade

120
Q

Ependymomas arise from within the ___ and cause symptoms related to ___.

A

Fourth ventricle; hydrocephalus

121
Q

Prognosis and Rx of ependymoma?

A

5-year survival is ~50%

Rx - surgical resection followed by radiation

122
Q

General Rx for CNS tumors?

A

Except for unresectable tumors, therapy usually begins with surgery to establish the histologic diagnosis and to reduce tumor burden

Radiotherapy, chemotherapy, and other adjuvants such as BM transplantation may also be indicated based on histology

123
Q

Complications of brain tumor or treatment?

A

Obstructive hydrocephalus, seizures, hypothalamic-pituitary hormonal insufficiency

124
Q

Long-term sequelae of childhood brain tumors are most often from the effects of chemo and/or radiation. The most common are?

A 
Neurocognitive defects
ADD
Learning disabilities
Endocrine abnormalities
Stroke
Overall IQ deficits
125
Q

The rate of overall IQ deficits following childhood brain tumors are associated with what risk factors?

A 
Younger age at time of treatment
Longer time elapsed since treatment
Female gender
Hydrocephalus
Use of radiation therapy and its extent and dose
126
Q

What emergency conditions cause altered mental status due to a lack of cellular substrate and must be reversed quickly to prevent cellular damage?

A

Hypoxia
Shock
Hypoglycemia

127
Q

List specific CNS conditions that can lead to acute altered mental status (#).

A

Infection (sepsis, meningitis, encephalitis)
Poisoning/toxic ingestion
Increased ICP (CNS tumor, hemorrhage)
Trauma
Metabolic disturbance (e.g., diabetic ketoacidosis)

128
Q

What is the most sensitive measure of adequacy of circulation?

A

Heart rate - tachycardia is the first and most subtle sign of possible inadequate perfusion

Capillary refill time and strength of peripheral pulses are useful, but not as sensitive.

BP is not a sensitive measure of volume status or circulation because the body’s protective mechanisms maintain blood pressure, so hypotension is a late sign of shock. Pulse pressure may widen before systolic BP drops

129
Q

How are airway and breathing assessed?

A

Describing the effort and rate of breathing (look at the chest to count RR and describe WOB)
Listening to how the patient’s lungs sound (listening for wheezes, rales, rhonchi, diminished breath sounds)
Checking the patient’s oxygenation (pulse ox)

If the patient does not seem to be moving air when breathing, you should first check the airway to determine if there is an obstruction (position the neck and/or perform the jaw thrust)

130
Q

The best position to open the airway depends on the age of the patient. In general, the opening of the ___ should be aligned with the ___.

A

External ear canal; anterior aspect of the shoulder

131
Q

Airway positioning - infant

A

Place a blanket under the shoulders to tip the head into a “sniffing” position (nose tipped slightly upward)

132
Q

Airway positioning - 1-3 year old

A

Neutral position keeps the head slightly tipped back

133
Q

Airway positioning - 4-8 years old

A

Extend the neck (extend more with age)

134
Q

Airway positioning - child/adolescent

A

Hyperextend the neck

135
Q

When assessing breathing, always listen to the chest in the ___. Also, look at the alignment of the ___.

A

Axillae; trachea (if deviating from the midline significantly, check for distended neck veins - could be a sign of tension pneumothorax)

136
Q

In addition to the ABCs of emergency care, what are the D’s and E’s?

A

D - Disability (quick neurologic assessment for signs of increased ICP and clues for poisonings) - assess mental status, evaluate pupils (size and reaction to light) + Dextrose (check for hypoglycemia)

E - Exposure (expose and examine all parts of the patient) and Environment (keep the patient warm)

137
Q

Findings in adult patients with bacterial meningitis? Children? Infants?

A

Adults: nuchal rigidity (57-92%), fever (66-100%), altered mental status (44-96), Kernig’s or Brudzinski’s sign (61%)

Children: less reliable findings, present in only about 50%

Infants - presence of a bulging fontanelle and focal seizures are the only presenting signs or symptoms significantly associated

138
Q

Leading cause of bacterial meningitis in children?

A

N. meningitidis (since Hib and pneumococcal vaccines)

139
Q

Although outbreaks of bacterial meningitis can occur in institutions such as child care centers, schools, colleges, and military recruit camps, most cases are ___.

A

Sporadic (<5% associated with outbreaks)

140
Q

Peak incidence of meningococcal disease in chidlren?

A

<12 months of age, another peak at 16-21 years

141
Q

Which serogroups of N. meningitidis account for ~30% of total reported cases?

Among young adults, what serogroups cause most causes?

In infants?

A

B, C, Y

Young adults - C, Y, W-135 (vaccine)

Infants - B (no vaccine currently in the US)

142
Q

Risk factors for meningococcal disease?

A

Persons living in close accommodations (dorms, military boot camps), complement deficiency, anatomic or functional asplenia

143
Q

Transmission of meningococcal disease + incubation period?

A

Respiratory droplets, requires close person-to-person contact; 1-10 days

144
Q

Acute systemic meningococcal disease is most frequently manifested by what three syndromes?

A

Meningitis
Meningitis with accompanying meningococcemia
Meningococcemia without clinical evidence of meningitis

145
Q

Early signs of meningococcal disease?

A

Fever, chills, malaise, myalgia, prostration, rash (macular, maculopapular, petechial, purpuric)

146
Q

Signs of more fulminant meningococcal disease?

A

Purpura, limb ischemia, coagulopathy, pulmonary edema, shock

147
Q

Overall case-fatality rate of meningococcal disease?

A

10% (and is higher in adolescents)

148
Q

Sequelae of meningococcal disease?

A

Hearing loss, neurologic disability, loss of digits or limbs, scarring

149
Q

DDx - fever and petechiae (adolescent?) 4

A
  1. Meningococcal sepsis
  2. Toxic shock syndrome
  3. Rocky Mountain Spotted Fever
  4. Bacterial endocarditis
150
Q

Patients presenting to the ED with fever and a rash must be started on antibiotics as soon as possible. Most ED physicians will start a patient on…

A
  1. Ceftriaxone (GN such as N. meningitidis, GP such as S. aureus, GAS, and S. pneumoniae)
  2. Vancomycin (resistant S. pneumoniae, MRSA)
  3. Doxycycline (RMSF in endemic areas)
151
Q

Once a definitive diagnosis of meningococcal disease is made, how is treatment narrowed?

A

Switch to penicillin G to eradicate organism from blood and CSF, then treat with either rifampin (children/young adults) or ciprofloxacin (adults) to eliminate the carrier state, or 5-7 days of ceftriaxone

152
Q

Guidelines for meningococcal prophylaxis?

A

Close contacts warrant prophylaxis

  • Adults: ciprofloxacin
  • Children (<18 years): oral rifampin or IM ceftriaxone
  • Pregnant women: azithromycin
153
Q

DDx - acute onset altered mental status (2 year old) - 4

A 
Infection (sepsis, meningitis, encephalitis)
Toxic ingestion
Trauma
Seizure
Electrolyte/glucose abnormalities
154
Q

General DDx - Altered Mental Status (AEIOU and TIPS)

A 
Alcohol, ingested toxins
Epilepsy, encephalitis, endocrine, electrolyte
Infection (meningitis/sepsis)
Overdose, opiates, oxygen deprived
Uremia (renal failure)
Trauma, temperature
Insulin
Psychosis
Stroke, shock, space occupying lesions
155
Q

Initial treatment to address tachycardia, hypotension, hypoxia, and hypoglycemia?

A
  1. Bolus of 20 cc/kg normal saline (tachycardia and hypotension)
  2. Oxygen
  3. Bolus of 10% or 2% solution of dextrose (D10 or D25)
156
Q

Acute onset of altered mental status associated with hypoglycemia raises the suspicion of ___ or ___.

A

Toxic ingestion; serious infection

157
Q

List 5 common drug classes leading to classic toxidromes.

A
  1. Cholinergic (organophosphates)
  2. Anticholinergic (diphenhydramine, TCAs)
  3. Sedative-hypnotic (benzodiazepines, barbiturates)
  4. Opioids (codeine, morphine, heroin)
  5. Sympathomimetics (cocaine, amphetamines, pseudoephdrine)
158
Q

Toxidrome of cholinergics?

A

Miosis and blurred vision
Increased gastric motility (N/V, diarrhea)
Excessive tearing, salivation, sweating, and urination
Bronchorrea and bronchospasm
Muscle twitching and weakness
Bradycardia
Seizures and coma

SLUDGE (salivation, lacrimation, urination, defecation, GI motility, emesis)

159
Q

Toxidrome of anticholinergics?

A 
Mydriasis (dilated pupils) - blind as a bat
Dry skin - dry as a bone
Red skin (flushed) - red as a beet
Fever - hot as Hades
Delirium and seizures - mad as a hatter
Tachycardia
Urinary retention
Ileus
160
Q

Toxidrome of sedative-hypnotics?

A 
Blurred vision (miosis or mydriasis)
Hypotension
Apnea and bradycardia
Hypothermia
Sedation, confusion, delirium, coma
161
Q

Toxidrome of opioids?

A 
Miosis (constricted pupils)
Respiratory depression
Bradycardia and hypotension
Hypothermia
Depressed mental state (sedation, confusion, coma)
162
Q

Toxidrome of sympathomimemtics?

A

Mydriasis
Fever and diaphoresis
Tachycardia
Agitation and seizures

163
Q

What types of medications can cause mydriasis?

A

Anticholinergic
Sympathomimetic
Sedative/hypnotics (can cause either)

164
Q

What are two common medications seen in accidental ingestions in toddlers?

A

Iron

Acetaminophen (most common, commonly co-ingested)

165
Q

In the setting of a suspected ingestion, what lab studies should be ordered?

A
  1. Glucose
  2. Electrolytes and/or blood gas (metabolic acidosis/AG - aspirin or NSAID toxicity)
  3. EKG (TCAs, etc. can cause EKG changes and dysrhythmias)
  4. Calcium (affects cardiac function)
  5. Toxicology screen from the urine or blood (doesn’t include levels of all drug that might have been ingested)
  6. Acetaminophen
166
Q

List # decontamination treatment options.

A
  1. Activated charcoal (increases surface area for toxin absorption)
  2. Cathartic agent (induces defecation)
  3. Nasogastric lavage (removes pill fragments from stomach)
  4. Syrup of ipecac (induces vomiting)
167
Q

When is activated charcoal indicated? Contraindicated?

A

Indicated - strong acids, alkalis, heavy metals

Contraindicated - loss of protective airway reflexes (risk of aspiration)

168
Q

A single dose of a ___ may be given with the initial dose of charcoal.

A

Cathartic agent

169
Q

True or false - nasogastric lavage has not demonstrated consistent clinical benefit and is not recommended.

A

True

170
Q

Recommendations for syrup of ipecac? Contraindications?

A

Not first-line due to potential side effects

Contraindicated with a risk of aspiration with an altered mental status and the potential for serious cardiac side effects and seizures

171
Q

Mechanism of TCAs?

A

Inhibition of synaptic reuptake of NE and 5-HT
Antagonism of muscarinic ACh receptors and peripheral alpha receptors
Blockade of sodium channels and GABA receptors

172
Q

Presentation with TCA toxicity?

A 
Altered mental status
Anticholinergic signs and symptoms
Hypotension (hallmark)
Dysrhythmias
Seizures
173
Q

Cause of hypotension in TCA toxicity?

A

Direct myocardial depression from sodium channel blockade and peripheral vasodilation from alpha-1 adrenergic blockade

174
Q

Most common cause of death from TCA OD?

A

Refractory hypotension

175
Q

List management steps for a patient with a TCA ingestion.

A
  1. Continuous cardiac monitoring + serial EKGs for 6 hours (minimum)
  2. Serum alkalization
  3. Dose and frequency
  4. Target pH + close monitoring of blood gases
  5. Antiarrhythmics
  6. Rx hypotension
  7. Rx seizures
176
Q

What is the triad seen in cardiotoxicity?

A

Conduction delays
Dysrhythmias
Hypotension

177
Q

Mainstay treatment for cardiotoxicity?

A

Serum alkalization and sodium loading

178
Q

When is serum alkalization and sodium loading indicated?

A 
QRS > 100 msec
R wave in AVR > 3 mm
Wide-complex tachycardias
Fluid-refractory hypotension
Seizures
179
Q

How is serum alkalization done?

A

Hypertonic sodium bicarbonate (1 mEq/kg bolus initially and every 3-5 minutes until QRS narrows and hypotension improves)

Continue for 12-24 hours after the EKG normalizes because of the drug’s redistribution from the tissues

Target pH = 7.50-7.55

180
Q

How should life-threatening dysrhythmias be treated?

A

Lidocaine

Class IA (Na channel blockers) and Class III (can prolong QT interval) may also be contraindicated

181
Q

How should hypotension be treated?

A

Volume expansion and serum alkalization

NE in refractory situations

Beta-adrenergic agonists and dopamine are contraindicated

182
Q

How should seizures be treated?

A

Generally brief
Benzos, barbiturates, or propofol may be used
Phenytoin is controversial

183
Q

Ingestion of nortriptyline 2.5 mg/kg or higher in a 2-year-old will cause significant symptoms. Peak effect?

A

7-8 hours after ingestion

184
Q

One 10 mg tablet of glipizide can cause significant hypoglycemia in a 2-year-old. Peak effect?

A

2-3 hours after ingestion, but can last 24 hours

Pediatrics Clerkship (14 decks)

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