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Final topics Flashcards

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1
Q

What are the risk factors for meningitis?

paediatrics

A
  • Maternal GBS colonisation in infants <3 months
  • Not immunised
  • Immunocompromised
  • History of neurosurgery or penetrating head injury
  • VP shunt
  • Cochlear implant
  • Younger age <5yo

GBS stands for Group B Streptococcus, a common bacterium that can cause serious infections in newborns.

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2
Q

What initial investigations (Ix) should be conducted for suspected meningitis?

A
  • Urgent LP for CSF microscopy, biochem and glucose
  • Blood cultures
  • FBE
  • BSL
  • Lactate
  • UEC – hyponatraemia
  • Coags if suspected coagulopathy or shocked
  • LFTs, metabolic, toxicology
  • Serum bacterial and viral PCR

LP stands for lumbar puncture, a procedure to collect cerebrospinal fluid.

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3
Q

When should neuroimaging be performed in suspected meningitis cases?

A
  • Focal neurology
  • Raised ICP
  • Encephalopathy
  • Diagnostic uncertainty e.g. to look for mass

ICP stands for intracranial pressure.

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4
Q

What is the recommended treatment for meningitis?

A
  • Antibiotics within 30 minutes of decision to treat
  • Consider steroids with first dose
  • IV fluids – saline bolus 10mL/kg
  • 2/3 maintenance fluids due to SIADH

SIADH stands for Syndrome of Inappropriate Antidiuretic Hormone secretion.

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5
Q

What are some complications of meningitis?

A
  • Septic shock
  • Multi-organ failure
  • Venous sinus thrombosis
  • Hydrocephalus
  • Seizures, subsequent epilepsy
  • Hearing impairment
  • Neurodevelopmental impairment
  • Permanent focal neurological deficit

Hearing impairment is particularly associated with S. pneumoniae meningitis.

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6
Q

What criteria should be used to determine the need for a CT head scan in paediatric head trauma?

A
  • PECARN rule out criteria: none present means no CT
  • CHALICE rule in criteria: any present means CT is warranted

PECARN stands for Paediatric Emergency Care Applied Research Network.

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7
Q

Criteria for PECARN rule

What exclusion criteria?

A

Patients with NONE of the criteria DO NOT require CT head
Patients with ONE criteria MAY require CT head – apply clinical judgement; usu more prolonged observation.

Exclusion criteria
- GCS <14
- Trivial mechanism e.g. ground level fall, walking/running into stationary object, no features of head trauma except scalp abrasions/lacerations
- Penetrating trauma
- Known brain tumour
- Pre-existing neuro disorder complicating assessment
- Presence of VP shunt
- Presence of bleeding disorder

Age 2-18
- Abnormal mental status (agitation, somnolence, repetitive questioning, slow response to verbal communication)
- LOC
- Vomiting
- Severe headache
- Severe injury mechanism
o MVA ejection, death of another passenger, rollover, pedestrian/cyclist without helmet struck by vehicle
o Fall >1.5m for 2+
o High impact object vs head
- Signs of basal skull fracture

Age <2
- Abnormal mental status (GCS <14, agitation, somnolence, repetitive questioning, slow response to verbal communication, not acting normal according to parent)
- Severe injury mechanism
o MVA as above
o Fall >3 feet for children <2years (0.9m)
o Head vs high impact object
- Palpable skull fracture
- Occipital/parietal/temporal scalp haematoma

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8
Q

What does the CHALICE criteria include for CT head scans?

A

Criteria: presence of any warrants CT

History
- Witnessed LOC >5 mins
- Amnesia (antegrade or retrograde) > 5 mins
- Drowsiness in excess of that expected by examining doctor
- ≥ 3 episodes of vomiting after head injury
- Suspicion of NAI
- Seizure after head injury in patient with no epilepsy

Exam
- GCS <14 or <15 if <1yo
- Suspicion of penetrating/depressed skull injury
- Tense fontanelle
- Features of basal skull fracture
- Focal neurological defects
- Bruise, swelling or lac >5cm if <1yo

Mechanism
- >40km/hr collision as pedestrian, cyclist or occupant
- Fall >3m height
- High speed injury from projectile or object

NAI stands for non-accidental injury.

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9
Q

What are the diagnostic criteria for Kawasaki disease?

A
  • Fever for 5 days plus 4 of:
    • Conjunctival injection
    • Rash
    • Oral changes
    • Extremity changes
    • Cervical lymphadenopathy

Kawasaki disease is a significant cause of acquired heart disease in children.

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10
Q

What is the treatment for Kawasaki disease?

A
  • IVIG 2g/kg IV single infusion
  • Aspirin 3-5mg/kg daily until normal echo
  • Steroids in some cases

IVIG stands for intravenous immunoglobulin.

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11
Q

historical indicators of non-accidental injury (NAI) in children?

A
  • Detached, depressed, hostile behavior
  • Poor eye contact
  • Delayed developmental milestones
  • Changing history of events
  • Patterns of injuries in high-risk areas

History
- Developmental
- Mental health of child/parent
- Previous presentations/injuries
- Personal/FHx of bleeding disorders, developmental disorders
- Previous contact with CPS/police
- Other children in household

FACES refers to high-risk injury areas: Frenulum, Angle of jaw, Cheeks, Eyelids, Sclera.

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12
Q

Patterns of NAI

A

FACES (these areas of injuries are high risk for NAI)
- Frenulum
- Angle of jaw
- Cheeks
- Eyelids
- Sclera

Patterned bruising
- Grab marks
- Pinch
- Slap
- Hair brush
- Loop impression
- Restraining marks; circumferential
- Bites

Location
- Torso, ear, neck in under 4yo (TEN4)
- Head
- Cheeks, ear = slap to face
- Perineum
- Upper arms

Any bruising in <6 months
Multiple sites and ages

Burns
- Immersion in hot water – feet and buttocks
- Branding
- Cigarette on palms/soles

Fractures
- Multiple sites and ages
- Inconsistent history
- Metaphyseal long bone fractures (bucket handle) – from violent torsion/traction injury; almost always NAI in <18 months
- Epiphyseal Salter Harris I & II from jerking
- Spiral long bone esp femur, tibia, radius
- Scapula
- Spinous processes
- Sternal/rib fractures
- Multiple, complex, occipital, depressed skull fractures

Shaken baby syndrome – NA head Injury
- Altered GCS, seizures
- Acute SDH
- Retinal haemorrhages

Other injuries
- Abdo – blunt trauma e.g. intramural duodenal haematoma
- Pancreatic injuries
- Neglect – poor hygiene
- Sexual abuse

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13
Q

What are the symptoms of hyperemesis gravidarum?

A
  • Persistent, severe nausea/vomiting
  • Dehydration
  • Electrolyte imbalance
  • Ketosis
  • Weight loss of at least 5% of pre-pregnant weight

It affects 1-2% of pregnancies.

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14
Q

What are the risk factors for ectopic pregnancy?

A
  • IVF
  • IUD
  • Previous ectopic
  • Previous PID/tubal infection
  • Increased maternal age
  • Endometriosis
  • Abnormal anatomy
  • Previous tubal ligation

PID stands for pelvic inflammatory disease.

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15
Q

History and exam for ectopic pregnancy?

Ix and results

A

Assessment
- PV bleeding
- Abdo pain
- Irregular bleeding
- Shoulder tip pain (rupture, diaphragmatic irritation)
- Syncope

Exam
- Adnexal tenderness
- Adnexal mass
- Uterine enlargement
- Cervical motion tenderness
- Shock

Ix
- FBE
- Blood group & cross match
- Coagulation if severe bleeding
- BHCG
- US
o TVUS - visible gestational sac if BHCG >1500
o Haemosalpinx
o Extra-uterine empty gestational sac
o Empty uterine cavity
o Pelvic fluid
o Abnormal gestational sac

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16
Q

What are the clinical signs of pre-eclampsia?

A
  • Headache
  • Visual disturbance
  • Hyperreflexia
  • Vomiting
  • Epigastric pain
  • Generalised oedema
  • Seizures (eclampsia)

Pre-eclampsia occurs after 20 weeks of gestation.

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17
Q

What is the management for pre-eclampsia?

A
  • Nifedipine
  • Labetalol
  • Hydralazine
  • MgSO4 for seizure prevention
  • Betamethasone for fetal lung maturation

MgSO4 stands for magnesium sulfate.

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18
Q

Risk factors for pre-eclampsia?

A

Obstetric risk factors
- Primigravida
- Prior pre-eclampsia
- Multiple pregnancies
- Hydatidiform mole
- Family history

Others
- Obesity
- CKD
- HTN
- DM
- Autoimmune diseases
- Thrombophilia

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19
Q

Sodium valproate poisoning
List S&S, Ix, Mx

A

Symptoms within 4 hours of SR and 12 hours of MR

Risk assessment
- Dose
- Formulation – syrup, IR or enteric coated
- <200mg/kg – mild sedation
- 200-400mg/kg – moderate toxicity with CNS depression
- >400mg/kg – risk of multi-organ system toxicity
- >1000mg/kg – coma, multi-organ failure, cerebral oedema, life-threatening

Examination
- CNS – drowsy, ataxia, seizures, coma
- GI – N/V/Abdo pain, liver failure
- CV – hypotension, QT prolongation, arrhythmias, tachycardia
- Metabolic – hypernatraemia, elevated lactate, metabolic acidosis, hypocalcaemia, hypoglycaemia, hyperammonaemia, deranged LFTs
- Myelosuppression (late)

Ix
- ECG (QTc, tachycardia)
- Sodium valproate level every 6 hours; >6000micromol/L = severe poisoning
- BSL (hypoglycaemia)
- UECs
- LFTs
- VBG (HAGMA)
- Ammonia
- CMP (hypocalcaemia)
- Paracetamol level
- FBE (bone marrow suppression)
- CK (rhabdo with coma)
- CTB (cerebral oedema)

Mx
- Resus – fluids 20mL/kg for hypotension +/- pressors
- ABCs
- K/BSL replacement
- Decontamination – AC if >200mg/kg and within 4 hours
- MDAC if >500mg/kg or rising sodium valproate levels
- Haemodialysis if >1g/kg or >6000 micromol/L
- Antidote
o Carnitine – limited evidence but low risk of harm and inexpensive
o Give if severe metabolic acidosis, cerebral oedema, hyperammonia, hepatotoxicity

Symptoms can vary based on the dose and formulation of sodium valproate.

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20
Q

What is the management for torsades in sotalol overdose?

A

MgSO4 10mmol IV over 15 mins

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21
Q

What are the clinical features of calcium channel blocker toxicity?

A
  • Hypotension
  • 1st degree HB
  • Pulmonary oedema
  • Refractory shock/death
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22
Q

What is the recommended decontamination for CCB overdose?

A

AC 50g in alert patients <2h post exposure IR and <12h MR

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23
Q

What are the effects of neurotoxins from snake bites?

A
  • Paralysis of voluntary and respiratory muscles
  • Delayed onset 2-4h
  • Ptosis
  • EOM ophthalmoplegia
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24
Q

What are the indications for antivenom administration?

A
  • Confirmed/suspected snake bite with clinical or lab evidence of envenomation
  • Regional lymphadenopathy after bite from highly venomous snake
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25
What are common clinical features of Type 1 hypersensitivity?
* Nausea/Vomiting * Bronchospasm * Collapse * Severe anaphylaxis in 5%
26
What should be done in suspected bite cases that are not clinically envenomed?
* Leave PIB in place * Await investigations * Remove PIB if results NAD * Administer antivenom if developing envenomation
27
What is tumour lysis syndrome?
Mass destruction of rapidly proliferating neoplastic cells - Usu. 1-5 days after chemo - Rarely due to spontaneous necrosis of malignancies Metabolic features - Hyperuricaemia - Hyperkalaemia - Hyperphosphataemia - Lactic acidosis - Hypocalcaemia Complications - AKI - Tetany - Arrhythmias Mx - Allopurinol - IV saline - Alkalinise urine – sodium bicarb to urinary pH >7 - Rasburicase - Correct electrolytes
28
What are the metabolic features of tumour lysis syndrome?
* Hyperuricaemia * Hyperkalaemia * Hyperphosphataemia * Lactic acidosis * Hypocalcaemia
29
What are common complications of tumour lysis syndrome?
* Acute Kidney Injury (AKI) * Tetany * Arrhythmias
30
What is the management for tumour lysis syndrome?
* Allopurinol * IV saline * Alkalinise urine with sodium bicarbonate * Rasburicase * Correct electrolytes
31
What are checkpoint inhibitors commonly used to treat?
* Melanoma * RCC * Lung cancer * Other solid tumours * Some lymphomas
32
What are the clinical features of checkpoint inhibitor toxicity?
* Iritis * Myocarditis * Aseptic meningitis * Myositis * Pneumonitis * Arthritis * Colitis * Thyroiditis * Dermatitis * Hepatitis * Adrenal insufficiency
33
What are common causes of febrile neutropenia?
* Post chemotherapy * Overwhelming bacterial sepsis * Post viral * Aplastic anaemia * HIV * Congenital/cyclic
34
What are the most common organisms associated with febrile neutropenia?
* Gram positives: coag negative staph, S. aureus, Streptococci, Enterococci * Gram negatives: Pseudomonas, E. Coli, Klebsiella * Fungi: Aspergillosis * Viruses
35
What antibiotics for febrile neutropenia?
* Piptaz * Gentamicin 7mg/kg if systemically unwell * Vancomycin 1.5g if shocked or suspecting vascular line infection/known MRSA * Metronidazole if abdominal/perineal infection
36
What is graft vs host disease?
Activation of donor T cells in transplanted marrow that cause tissue damage
37
When does acute graft vs host disease occur?
<100 days post transplant
38
What is the incidence of acute graft vs host disease in marrow transplant recipients?
40%
39
When does chronic graft vs host disease typically onset?
>100 days, usually within 2 years
40
What are common features of graft vs host disease?
* Increased risk of infection * Mucositis * Lichenoid lesions * Pruritic skin lesions * Vitiligo * Peri-orbital hyperpigmentation * Keratoconjunctivitis sicca * Scleroderma
41
What is the management for graft vs host disease?
* Glucocorticoids * Tacrolimus * Ciclosporin * Irradiate blood products if required
42
What factors can affect the accuracy of pulse oximetry monitoring?
* Patient movement * Sensor displacement * Poor perfusion * Dark skin * Anaemia * Carboxy-, Met- and sulphaemoglobin * Methylene blue * False nails * Nail polish
43
What are the indications for capnography?
* Confirm intubation * Monitor ventilation * Effectiveness of CPR * Detect ventilator circuit disconnection * Detect air embolisation
44
What are limitations of RCTs?
* Limited generalisability * Specific questions may not apply to unique patients * Ethical concerns * High cost and time-consuming * Strict inclusion/exclusion criteria * Potential for noncompliance & dropouts
45
What is power in the analysis of a study?
Ability to detect a difference in measurement between the two groups
46
What are some determinants for calculating sample size in a study?
* Effect size * Degree of variation * Degree of certainty * Desired power * Distribution of data
47
What does sensitivity measure in a test?
Ability to detect a true positive result
48
What does specificity measure in a test?
Ability to detect a true negative result
49
What is the formula for the positive likelihood ratio?
SN/(1-SP)
50
What is the formula for the negative likelihood ratio?
(1-SN)/SP
51
What is the formula for Positive Predictive Value (PPV)?
True positives/(true positives + false positives)
52
What is the formula for Negative Predictive Value (NPV)?
True negatives/(true negatives + false negatives)
53
What is the formula for Odds Ratio (OR)?
ad/bc
54
What is the formula for Relative Risk (RR)?
a(b+d)/b(a+c)
55
How is Relative Risk Reduction calculated?
Difference in outcome rates between control and study groups / outcome in control group
56
What is Absolute Risk Reduction (ARR)?
Risk of condition in control group – risk in study group
57
What does NNT stand for and what does it indicate?
Number Needed to Treat; how many patients need treatment for one to benefit
58
What is the relationship between treatment effect and NNT?
Larger treatment effect results in smaller NNT
59
What is the formula for NNT?
1/ARR
60
DDx for Kawasaki disease
- Group A Strep – scarlet fever, rheumatic fever, tonsilitis - Viral – EBV, CMV, adenovirus, COVID - Systemic JIA - Sepsis - Toxic shock syndrome (staph/strep) - SJS - Drug reaction - Malignancy
61
Screening questions for domestic violence?
- Has your partner threatened to harm or kill you? - Previous physical violence against you? - Ever choked, strangled you - Threatened/assaulted with weapon? - Harmed/killed family pet? - Partner previously breached apprehended violence order? - Partner jealous or controlling? - Violence becoming more frequent? - Stalking behaviour? - Control your money? - Recent separation or imminent? - Does partner have financial difficulties? - Partner unemployed? - Mental health problems? - Substance abuse problems? - On bail/parole? - Access to firearms? - Are you pregnant? - Any children? - Previous harm to children? - Conflicts regarding custody issues? - Sexual assault?
62
Beta blocker overdose
Most are benign except - Elderly & those with decreased cardio-respiratory reserve - Co-ingestions esp with other negative inotropes - Severe overdoses Propranolol also causes sodium channel blockade  widening of QRS, ventricular dysrhythmias and direct CNS toxicity - Very lipophilic Sotalol also causes potassium efflux blockade  QT prolongation & Torsades Risk assessment - Onset of effects 1-2h - Delayed in MR formulation Clinical Features CVS - Hypotension, negative dromotropy (AV block, PR prolongation may be first sign) - Bradycardia - Heart failure incl. APO - Cardiogenic shock Resp - Bronchospasm - E.g. if coexisting asthma Metabolic - Hypoglycaemia - Hyperkalaemia Neuro - Altered GCS/coma usu secondary to hypotension Propranolol – QRS prolongation, ventricular arrhythmias, cardiac arrest Delirium, coma, seizures Sotalol – QT & Torsades Resuscitation Bradycardia - Atropine as temporising measure - Adrenaline 10-20mcg boluses (child 0.1mcg/kg) Q2-3mins until adequate perfusion then consider infusion - Isoprenaline 1-10mcg/min - Electrical pacing – often ineffective Hypotension (poor contractility or vasodilation) - 20mL/kg IV bolus – beware APO with repeated boluses - Adrenaline first line if brady & hypotensive - If refractory to adrenaline  HIET - Vasodilation – treat with noradrenaline - ECMO if refractory Torsades (sotalol) - MgSO4 10mmol IV over 15 mins - Correct hypoxia, hypoK, hypoCa - Isoprenaline infusion 1-10mcg/min if HR <100 or overdrive pacing to maintain HR 100-120 QRS widening/ventricular arrhythmias (propranolol) - Suspect impending VT/VF if QRS >120 - Sodium bicarb 2mmol/kg IV repeated every 1-2 mins o Titrate to effect of QRS narrowing - Defib – attempt but may not be effective - Intubate/hyperventilation to target pH 7.5-7.55 to decrease sodium channel - blockade - Lignocaine 1.5mg/kg IV as third line if pH >7.5 CNS effects - Early intubation if progressive obtundation (GCS <12), seizures - Hyperventilation to target pH 7.5 to 7.55 Ix - ECG for QT interval - Paracetamol level - UEC - TTE
63
CCB overdose
Dihydropyridine - More vasodilation, but less myocardial depression/conduction delays than verapamil/diltiazem - Non-Dihydropyridine CCBs Toxicity/risk assessment - Negative inotropy/chronotropy - Vasodilation - Dose: 2-3x usual dose = serious toxicity - >10 tablets – life threatening - Standard release – sx after 1-2h - Modified release – may be delayed up to 12h Clinical features CVS - Hypotension - 1st degree HB - Pulmonary oedema - Refractory shock/death Metabolic - Hyperglycaemia - Lactic acidosis GIT - Nausea/vomiting - Ileus CNS - Agitation - Confusion secondary to inadequate perfusion - Seizures/coma – rare Renal failure Ix - ECG – bradycardia, heart block, sinus arrest, asystole - Hyperglycaemia – marker of severity - VBG: hyperlactataemia, metabolic acidosis, impaired O2 delivery - UECs: AKI due to shock - CXR – APO - TTE – impaired contractility Management Resuscitation - Early intubation/ventilation if life threatening toxicity anticipated - Early invasive BP monitoring if evolving hypotension/shock Decontamination - AC 50g in alert patients <2h post exposure IR and <12h MR o Intubated pts – give regardless of time post ingestion - WBI in some cases Bradycardia - Atropine 600mcg boluses Q5mins up to 3 doses - Cardiac pacing to bypass AV block, set rates >60/min. Capture may be difficult Hypotension (due to myocardial depression, vasodilation & heart block) - Fluids – 10-20mL/kg crystalloid bolus; further IVT may cause APO - Calcium – 30mL Ca gluconate (6.6mmol, 3g) bolus IV over 5 mins o Repeat boluses x3 in 1st 60 mins o Infusion to maintain ionised Ca 1.5-2mmol/L o Monitor Ca Q2hourly - Adrenaline – reasonable first line agent if bradycardia - Noradrenaline +/- vasopressin for vasoplegia High-dose Insulin Euglycaemia Therapy (HIET) effective if commenced early Refractory shock +/- arrest - Early VA ECMO - Methylene blue/lipid emulsion Sodium bicarb – if severe metabolic acidosis
64
HIET
- To manage cardiovascular toxicity in verapamil/diltiazem OD - Is an inotrope & can be used alone or with standard catecholamine inotropes - HIET is NOT a pressor or chronotrope o Bradycardia & peripheral vasodilation with CVS compromise requires standard inotropes - HIET may worsen peripheral vasodilation in amlodipine/non-dihydro toxicity But may be useful in some beta blocker toxicities resistant to fluid & adrenaline Adverse effects - Hypoglycaemia - Hypokalaemia - Vasodilation Dose - 500 units short acting insulin in 50mL NS in syringe driver - 50mL of 50% glucose as slow IV bolus followed by 100mL 10% glucose/hr - (children: 2.5mL/kg 10% glucose bolus then3-5ml/kg/hr 10%) o If BSL >15mmol, no bolus required - 1 unit/kg IV short acting insulin then 1 unit/kg/hr infusion - Titrate to effect every 15 mins up to 5units/kg/hr over 1st hour then up to 10units/kg/hr Maintain BSL 5.5-11mmol/L Maintain K 2.8-3.3mmol Check K and glucose every 15 mins initially Endpoints: - Cease after CVS toxicity resolved - Increasing glucose requirements may be early sign of resolution
65
What are the neurovascular complications of supracondylar fractures?
- Brachial artery compression – pulseless, white hand - Radial nerve injury – sensory loss 1st dorsal web space; motor – wrist/digit extension loss - Median nerve – commonly entrapped o Sensory: lateral 3.5 fingers palmar o Motor: LOAF (lateral 2 lumbricals, opponens pollicus, abductor pollicus brevis, flexor policus brevis) - Ant osseous nerve (branch of median) – unable to flex IPJ of thumb and DIPJ of fingers - Ulnar nerve o Sensory – medial 1.5 fingers o Motor – intrinsic muscles of hand – interosseai, spread/cross fingers against resistaqnce o Medial 2 lumbricals
66
Monteggia fracture Discuss neurovascular complications? Management?
Monteggia frature - Fracture proximal 1/3 ulna - Radial head dislocation NV exam: posterior interosseous nerve (branch of radial nerve) injury – most likely nerve injury due to radial head dislocation - Weakness of thumb extension - Weakness of MCP extension Tx - Closed reduction & immobilisation - Cast in supination - Or ORIF if open/unstable/comminuted
67
Galeazzi fracture
- Fracture distal 1/3 radial shaft - Distal radio-ulnar joint (DRUJ) injury DRUJ instability - If radial fracture is <7.5cm from articular surface – unstable in 55% - If >7.5cm, unstable in 6% Tx - Anatomical reduction - ORIF Complications - Compartment syndrome - Neurovascular – uncommon - Refracture post plate removal - Nonunion - Malunion - DRUJ subluxation
68
Escalating drugs for paediatric asthma
Salbutamol Atrovent Steroids e.g. hydrocortisone IV MgSO2 0.2mmol/kg (max 8 mmol) Aminophylline 10mg/kg IV salbutamol 10mcg/kg IM adrenaline 10mcg/kg (max 500mcg) IV adrenaline 0.5-1mcg/kg or infusion 0.1mcg/kg/min IV ketamine 0.5mg/kg for tolerance of bipap and bronchodilation
69
MOA of drugs used in thyroid storm
Iodine - inhibits thyroid hormone release and blocks hormone synthesis Propranolol - beta blocker controls adrenergic symptoms and inhibits T4 to T3 conversion PTU - inhibits T4 to T3 conversion Hydrocortisone - inhibits T4 to T3 conversion Carbimazole - no effect on T4/T3 conversion, but inhibits thyroid peroxidase to reduce synthesis of thyroid hormones (T3 and T4)
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