Lifespan Emergencies - Week 4

Front 1

Pediatric Vital Signs - Rough Guide for BP and HR

Back 1

• HR = 150 – (5 x age in years)

• BP = < 70 mmHg + (child’s agein years X 2) mmHg (1-10 years)

Front 2

Pediatric Altered Mental State - GHOST

Back 2

· Glucose

· Headtrauma

· O2deficiency/overdose

· Shock/seizures

· Temperature

Front 3

Pediatric - Extra Hx Questions

Back 3

• Ask medication use in breast feeding mother

• Question parents/patient (asage appropriate) to:

– Signs and symptoms

– Prodromal illness, recentviral infections, abdominal pain

– Immunisation history

– General health

– Recent weight gain/loss

– Compliance with medications,if any.

– In infants – ask about nappiesin particular:

• Have they been normal inappearance

• Have they been as “wet” asnormal.

• Colour of urine.

Front 4

Syncope - More serious etiologies in Children - Investigate and be cautious w/

Back 4

o Evidence of injury especially head trauma. o Continuing altered mental state - especially if unconscious for > 5 minutes

o Recurrent episodes

o History of cardiac conditions/surgery - associated chest pain or palpations

o Significant persistent abnormalities in vital signs.

o Thesyncopal episode was exercise related or occurred in the recumbent position

o Afamily history of sudden death, deafnessor cardiac disease (QT syndrom)

Front 5

Febrile Convulsions

Back 5

o Usuallybetween 6 months to 6 years

§ Make sure no evidence of intracranialinfection, abnormality and toxins or endotoxins – if present, not febrileconvulsion

o Feverthought to lower seizure threshold

Front 6

Status Epilepticus - Standard Definition

Back 6

Seizures persisting or recurring without a return to consciousness for anextended period, usually 30 minutes

Front 7

Status Epilepticus - Issue with Standard Definition

Back 7

Most suggest that after 5 minutes the chance of the seizureself-resolving is limited and at .5 minutes neuronal injury can occur

Front 8

Status Epilepticus - Operational Definition

Back 8

Generalized, convulsive status epilepticus inadults and older children (>5 years old) refers to ≥ 5 minutes of either continuous seizures or 2 or more discrete seizures between which there is incomplete recovery of consciousness

Front 9

Prolonged Convulsion - Risks

Back 9

o Injury

o Acidosis& other electrolyte imbalanceso Hypoxia/hypercarbia

o Hypoglycaemia

o Hyperthermia

o Permanentneuronal injury

o Cardiovascularcollapse

o Longerit lasts the more difficult to control

o Increasesmorbidity and mortality

Front 10

DKA

Back 10

BGL11-15 mmol/L with ketonesusually seen in type 1 diabetics

Front 11

DKA Features

Back 11

o Dehydration(sometimes not apparent)

o Acidosis

o Electrolyteimbalances

o Kausmallsrespirations

Does not usually cause hypotension on its own

Front 12

DKA - Most common precipitating factors in children

Back 12

Ignorance and new onset diabetes followed byinfection – also six I’s

Front 13

DKA - 6 Is

Back 13

o Infection

o Infarction(brain)

o Ignorance

o Ischemia(AMI)

o Intoxication

o Implantation(conditions of pregnancy)

Front 14

DKA - Initial and Definitive Treatment

Back 14

- Fluid therapy if initiated first

- Definitive treatment is insulin therapy

Front 15

DKA - Insulin after Flfuis Justification

Back 15

o Insulincan lead to vascular collapse secondary to rapid shift of fluid intointracellular space. Should not be initiated until the blood pressure isstabilized.

o Hypokalemicpts should not receive insulin until K+ has been administered – could worsenhypokalemia

Front 16

DKA - Cerebral Edema

Back 16

- <1% patients - 40-90% mortality

- Poorly understood mechanism associated with

- Hypoxia

- Osmotically driven movement of water into CNS when plasma osmolality declines too rapidly during treatment of DKA with aggressive fluid therapy (careful)

- Usually 4-12 hours after treatment

Front 17

Inborn Errors of Metabolism (IEM)

Back 17

o Hereditarydisorders involves gene mutations, usually of a single enzyme or transportsystem, cause significant blocks in metabolic pathways and accumulation ordeficiency of a particular metabolite

o Permanentneurologic sequelae

o Previously normal neonate with acute clinicaldeterioration

o Vomiting,neurologic abnormalities, metabolic acidosis and hypoglycaemia

Front 18

Pediatric Chest Pain - Life Threatening

Back 18

Rarely unless serious physical findings are present or pt has significant problems in medical history

Front 19

Pediatric Chest Pain - Myocarditis

Back 19

Oftenpreceded by viral respiratory illness.

Presentswith:

§ Respiratory distress

§ Fever

§ Tachypnea

§ Tachycardia

§ Generalized malaise

§ ECG may show widespread ST segment changes

Front 20

PE - Adolescence - Risk Factors

Back 20

· Recent abortion

· Using birth control pill

· Recent long bone fractures, surgery orperiods of immobility

Front 21

Kawasaki Disease

Back 21

Inflammation of blood vessels (including coronary blood vessels and may cause saccular dilations - aneurysms)

Front 22

Kawasaki Disease - Main Risk

Back 22

Anuerysms can be come obstructer by a thrombas - risk of infart or embolisation

Front 23

Kawasaki Disease - Features

Back 23

· Conjunctivitis

· Mucousitis (Strawberry tongue and fissured lips)

· Persist fever exceeding 39.5°C not very responsive to normal treatment

· Rash

· Lymph node enlargement

· Spindle-shaped swelling of the digits followed by desquamation

Front 24

Marfan Syndrome

Back 24

Abnormality of connective tissue causing weakened blood vessels and dilation of the aorta

Front 25

Marfan Syndrome - Risks Factors

Back 25

Usually effects tall, thin childre with long arms and fingers - may have visual disturbances

Front 26

Marfan Syndrom - Risk

Back 26

- Aortic dissection

- Aortic rupture

Front 27

Pediatric ECG Intervals

Back 27

Front 28

Pediatric - Bradyarythmias - Cause and Indication

Back 28

o o Mostcauses associated with hypoxia and acidosis

o Indicatespre-arrest

Front 29

Primary Causes (rare) - Pediatric Bradyarthymias

Back 29

- Sick Sinus Syndrome

- AV block

Front 30

Secondary Cause - Pediatric Bradyarthmias

Back 30

Midline sternal scar indicates dysrythmia is secondary to congental heart disease - may have implanted pacemaker

Congenital heart defects may contribute to AV blocks (rare)

Front 31

Pediatric Tachycardias - Congenital Heart Disease - Most common rythm presentations

Back 31

o Atrialflutter

o Atrialfibrillation

Front 32

Pediatric Sinus Tachycardia

Back 32

o Childrenaugment cardiac output by increasing HR rather than SV

o HRincreases early, hypotension late

o Forevery 1 degree Celsius increase in body temperature, HR increases 9.6 BPM –consider underlying process rather than intrinsic cardiac issue

Front 33

SVT - Types

Back 33

- AV reentrant tachycardia – WPW

- AV nodal or junctional tachycardia,cyclical reentrant pattern

- Ectopic atrial tachycardia, is rare and ismanifested by rapid firing of a single ectopic focus in atrium

Front 34

SVT - Mx

Back 34

o Toleratedinitially – CHF and cardiogenic shock

o Valsalva

o Icetowel on faceICP cardioversion

Front 35

Assystole

Back 35

Most common arrest rythm - usually associated with hypoxia

Front 36

Vfib/VT - Arrest Considerations

Back 36

- Reversible causes

- A history of either congenital heartdisease or a precipitating event, such ashyperkalaemia (renal failure), hypomagnesaemia, or commotio cordis.

- Respiratory failure leading to severehypoxemia, particularly in older children or adolescents suffering anexacerbation of chronic pulmonary disease, such as asthma.

- Less commonly may occur with certain typesof drug overdose (tricyclic antidepressants; beta-agonists in asthmaticchildren),

- Electrocution

- Re-entry tachycardias includingWolff-Parkinson-White syndrome

Front 37

PEA - Arrest Considerations

Back 37

Tension pneumothorax, cardiac tamponade, severehypovolemia, severe acidosis, hypoxia, hypothermia or hypoglycemia

Front 38

Long QT Syndrome

Back 38

Long QT interval secondary to imaired ion channels in the myocardiuam

- Due to multiple genetic mutations leading to dysfunction of potassium, sodium and calcium channels

- Overabundance of cations within myocardium

- Risk of arrhythmias like torsades de pointes

Front 39

Long QT Syndrome - Common Presentation

Back 39

- Typically in late childhood and adolscence

- Syncope with exercise or stress

Front 40

Long QT Syndrome - Inherited (Congenital forms)

Back 40

o Anautosomal recessive trait (Jervell and Lange-Nielsen syndrome) that isassociated with deafness

o Asautosomal dominant (Romano-Ward syndrome).

Front 41

Long Q Syndrome - Aquired forms

Back 41

- Myocarditis

- Mitralvalve prolapse

- Electrolyte abnormalities

- Drug induced

Front 42

Commotio Cordis

Back 42

o Life threatening dysrhythmia caused by a direct non-penetrating injury

o VF typical but also heart block, VT, BBB, ST-T wave abnormalities andasystole can occur

Front 43

Pediatric - Heart Failure

Back 43

Rare and usually due to structual disease

Front 44

Pediatric Heart Failure- Structual heart disease

Back 44

Front 45

Pediatric Heart Failure - Features

Back 45

o Breathlessness

o Cyanosis

o Signs of cardiogenic shock

o Failure to thrive

o Refusal to feed

o Persistent irritability

o Poor toleration of respiratory illnesses

o Crackles/heart murmurs

Front 46

Duct-dependent Congenital Heart Diseases

Back 46

– Pulmonary atresia

– Critical pulmonary valvestenosis

– Tricuspid atresia

– Severe Tetralogy of Fallot

– Transposition of the GreatVessels

– Hypoplastic left heartsyndrome

– Critical aortic stenosis

Front 47

Tetralogy of Fallot

Back 47

o Most common cause of right-to-left shunt

o Pulmonary stenosis

o Overriding aorta (enlarged and appears to arise from both left and rightventricles instead of left ventricle, as occurs in normal hearts)

o Ventricular septal defect

o Right ventricle hypertrophy

Front 48

Tetralogy of Fallot - Diagram

Back 48

Front 49

Hypercyanotic Attacks (Tet Spells) - Definition and Immediate Tx

Back 49

– Patients with Tetralogy of Fallot havespells where they suddenly turn a blue color due to a low oxygen in theirbloodstream.

– When the patient has decreased blood flow throughthe lungs due to elevated resistance in the pulmonary blood vessels.

– This is due to much of the blood goesdirectly from the right heart (less oxygenated) to the left heart through thedefects such as the Ventricular Septal Defect and the overriding aorta.

– Immediate treatment includes puttingpatient in the lateral position with knees to chest or squatting.

Front 50

High Flow O2 in Neonatal Resucitation

Back 50

· High oxygen and lung-stretching lead to increased ROS (reactive oxygenspecies) production and expression of pro-inflammatory cytokines

· Vaginal flora in lungs also predisposes to inflammation - can lead to chronic lung disease

· Resuscitation of preterm neonates with 30% oxygen causes less oxidativestress, inflammation, need for oxygen, and risk of bronchopulmonary dysplasia.

· No optimal O2 found yet

Front 51

Barriers to Pain Releif - Pediatrics

Back 51

- Historical beleif infants don't feel pain

- No data existed on short and long-term effects of analgesics on children

- Age-appropriate pain assessment tools lef physicians unable to conceptualise and quantify subjective pain experienced by children (FLACC or Wrong Backer)

- Fear of adverse events persists

- Parents believe the role of the hospital

- Fear of inducing addiction

- Childs fear of receiving injections

Front 52

Neonatal Resuscitation - Other points

Back 52

· Placenta performs respiratory, excretory, andendocrine functions during fetal life. As the cord is clamped, the neonate hasto rapidly adapt and perform all of the above functions.

· Breathing inhibited during parturition - severe asphyxia can inducegasping movements, resulting in aspiration of meconium during delivery.

· Continuous breathing is triggered at birth by sensory stimulation suchas cooling, rising PCO2, removal of placental humoral inhibitory factors(possibly prostaglandins), catecholamine surge, and oxygen

· Expansion of the alveoli leads to release of surfactant with lowered surfacetension.

· During subsequent expiration, high positive pressures are createdpresumably by breathing against a closed glottis. This aids in clearing ofliquid in the lungs and a more uniform distribution of air throughout the lungand establishment of functional residual capacity

· Primary apnoea – don’t treat with assisted ventilations – secondaryapnoea – treat quickly with assisted ventilation and or oxygen

· Primary apnoea usually followed by 4-5 minutes of gasping

· PEEP useful in alveolar expansion

· Do APGAR at 1 and 5 minutes

- Assessment of colour and respiration every 30 seconds

· Auscultation more reliable than umbilicus palpation for pulse rate

· Umbilical venous catheter

· 10 ml/kg fluids in case of persistent hypotension – consider hypovolemia

· Naloxone in respiratory depression and maternal narcotic use in last 4hours

Front 53

Inconsolability

Back 53

In children 3-6 months generally distinguishes aggitation from serious pain