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DTM&H 2024 > Misc > Flashcards

Misc Flashcards

1
Q

Encephalitis Seizures

A

Neurocysticercosis is the most common preventable cause of epilepsy

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2
Q

Misc Social innovation

A

Community-engaged process that sees the wisdom of communities and impacts social and health outcomes eg pay-it-forward

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3
Q

STI Screening What

A

Importance of condition, high prevalence

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4
Q

STI Screening Why

A

Curable, treatable, preventable, effective

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5
Q

STI Screening How

A

Tests available, sens/spec, simple, feasible, cost effective

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6
Q

STI Screening Who

A

Acceptability

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7
Q

STI Screening When

A

Accessibility

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8
Q

STI Screening Where

A

At high risk of infection or complications

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9
Q

STI Screening Pregnancy

A

CT/NG, TV, TP, HIV, HBV

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10
Q

STI POCT Environment

A

Power supply, Space, Security, Temperature/humidity

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11
Q

STI POCT Device limitations

A

Analytic capacity, maintenance, reliance on technology

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12
Q

STI POCT Provider buy-in

A

Impact on workload/services, staffing

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13
Q

STI POCT Patients

A

Competing priorities - willingness to wait for results (?true POCT)

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14
Q

STI Incidence 2020

A

TP 7.1m GC 82m CT 129m TV 156m

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15
Q

STI Prevalence 2020

A

HBV 296m HPV 300m HSV 490m

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16
Q

STI High frequency transmitters

A

Sex workers, others with high numbers of sexual partners

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17
Q

STI Bridging population

A

male clients of female sex workers (this becomes less relevant if general population has high background risk)

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18
Q

STI Partner notification

A

Little evidence of effectiveness in LMIC and potential harm (violence, abuse)

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19
Q

STI Male circumcision

A

60% reduction in HIV incidence, 25-45 reduction in GUD, HSV, TV, HPV, little effect GC/CT from voluntary medical male circumcision (VMMC)

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20
Q

STI Management

A

Syndromic mx recommended where diagnostic tests aren’t available - urethral/cervical discharge, vaginal discharge, genital ulcer

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21
Q

STI Urethritis cause

A

GC, CT, TV, MG

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22
Q

STI Urethritis/cervicitis treatment

A

GC CRO+Azith, CT Doxy or Azith, TV Metro, MG Azith

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23
Q

STI Vaginal discharge cause

A

TV, Calb, BV, CT, GC

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24
Q

STI Vaginal discharge treatment

A

TV Metro, Calb Clotri pessary, BV Metro

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25
Q

STI Genital ulcer cause

A

HSV, TP, Hducreyi (Chancroid), K granulomatis (Donavanosis), CT LGV

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26
Q

STI Genital ulcer treatment

A

HIV aciclovir, TP Benzathine pen, Hducreyi Azith, Kgranu Azith, CT LGV Azith or Doxy - treatment of GC/CT has wiped out Hd & Kg

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27
Q

STI WHO screening recommendation

A

HIV and Syphilis should both be tested

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28
Q

Snakebite Annual mortality

A

> 130,000

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29
Q

Snakebite Annual morbidity

A

400,000 (physical or psychological)

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30
Q

Snakebite Recognised as NTD

A

2016

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31
Q

Snakebite Epidemiology

A

Depends on human-snake interaction (agriculture, building projects, travel, sleeping on ground, intentional handling, nocturnal hunting, mating season), weather, and children

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32
Q

Snakebite Viperidae

A

Viper, adder, moccasins, rattlesnakes > short thick body, distinctive dorsal pattern, long fully erectable fangs which penetrate deep into tissues > shock, coagulopathy etc

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33
Q

Snakebite Elapidae

A

Cobra, krait, mambas, all Oceanian/Aus, and sea snakes > long thin body and tail, uniformly coloured, fast, short permanently erect front fangs > descending flaccid paralysis, bilateral ptosis -> bulbar (+coagulopathy etc)

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34
Q

Snakebite Snake venom

A

Complex - 100 protein/polypeptide toxins including phospholipases, metalloproteases, serine proteases, three-finger toxins (neuro- cyto-toxins) which clip over acetylcholine receptor > paralysis

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35
Q

Snakebite Clinical effects

A

Cytotoxicity (swelling, bruising, necrosis)l Haemo (coagulopathy), Neuro (descending flaccid paralysis), Cardio (arrhythmia, myocardial damage, leak, shock, orthostatic hypotension), Myo (rhabdo, hyperkalaemia), Nephro (AKI)

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36
Q

Snakebite Clotting 20min test

A

Clean dry glass vessel, tip once, positive (no clotting), negative (clotting)

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37
Q

Snakebite Prevention

A

Education, Protect feet, legs and hands, use light and prodding stick, sleep off the ground

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38
Q

Snakebite First aid

A

Remove from danger, reassure, immobilise, remove any potential tourniquets, pressure-pad-immobilisation, transport rapidly in recovery position and admit for 24h

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39
Q

Snakebite Pressure pad immobilisation

A

compress veins and lymphatics in immediate vicinity of bite

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40
Q

Snakebite Antivenom

A

Refined IgG from hyperimmune horse/sheep plasma, scare and expensive to produce, only neutralises venom used in manufacture - cover medically-most-important snakes in geographical region

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41
Q

Snakebite Antivenom indications

A

Shock, Systemic envenoming - incoagulable blood, neurotoxicity (ptosis), black urine, rapidly progressive local swelling (bites over digits)

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42
Q

Snakebite Antivenom administration

A

Check species covered, infuse IV 10-60min, same dose for adults & children, prophylactic adrenaline SC may reduce reactions

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43
Q

Snakebite Antivenom reactions

A

IM adrenaline, early pyrogenic and/or anaphylactic reactions, late serum sickness

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44
Q

Snakebite Adjunctive care

A

Tetanus, drain abscess & remove necrotic tissue, early rehabilitation. No evidence for other Rx including fasciotomy

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45
Q

Arthropod bite Prevention

A

Wear boots, repellents, search clothing & footwear/backpack, sleeping environment etc, sleep under insecticide impregnated bed net

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46
Q

Arthropod bite Scorpion epidemiology

A

> 3250 fatalities, in Mexico, Sth America, Africa, Middle East, India, esp children, prevention is excluding from home and awareness, UV light useful

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47
Q

Arthropod bite Scorpion mechanism

A

Ion channel stimulate/block cation Na K Ca channels > parasympathetic (cholinergic) and sympathetic (adrenergic)

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48
Q

Arthropod bite Scorpion symptoms

A

Severe local pain, Systemic ‘autonomic’ storm from massive release of acetylcholine and catecholamines -> shock, arrhythmias, erratic eye movements, muscle spasms

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49
Q

Arthropod bite Scorpion treatment

A

Lignocaine infiltration, antivenom in some countries, and/or prazosin/vasodilators in ICU

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50
Q

Arthropod bite Spiderbite Epidemiology

A

Very few bites, common in Americas, mediterranean, South Africa, Australia

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51
Q

Arthropod bite Spiderbite Necrotic arachnidism

A

Brown recluse spiders - local pain, swelling, followed by classic red-white-blue sign, generalised rash, malaise, eventually eschar, necrotic slough, systemic sx 4-10%

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52
Q

Arthropod bite Spiderbite Neurotoxic arachnidism

A

Black/brown cosmopolitan spiders & funnel well - local immediate pain, sweating, systemic rapidly evolving headache, NV, priapism, muscle spasms,

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53
Q

Arthropod bite Hymenoptera anaphylaxis

A

History, mast cell tryptase, venom-specific IgE (skin or RAST), treat with adrenaline

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54
Q

Marine injury Water organisms

A

Salty V vulnificus, Brackish A hydrophila

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55
Q

Marine injury Treatment

A

Remove from water to prevent drowning, immerse hot water 45C, box JF wash/shave tentacles with sea water, topical lignocaine, antivenom for seawasp and scorpion fish

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56
Q

Marine injury Jelly fish prevention

A

Obey warning, don’t swim alone in tropical seas, protective clothing, stings may hypersensitise with anaphylaxis on reexposure

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57
Q

Marine injury Other marine sting prevention

A

Beware of handing fish, avoid touching coral, anemones, sea snakes etc, beware wading barefoot

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58
Q

Marine injury Poisoning

A

Scombroid 1-120min, Puffer 10-180min, Shellfish 30-180min, Ciguatera 1-12h

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59
Q

Marine injury Ciguatera

A

1-12h, GI sx plus paraesthesias (esp hot-cold reversed sensation), rash, bradycardia, hypotension, can be confirmed by toxin detection in fish remnant (but not in patients) treat supportive +/- mannitol (controversial), amitriptyline

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60
Q

Marine injury Scombroid

A

1-120min immediate perioral tingling, progressing to anaphylactic response, treat with histamine inhibitors +/- adrenaline

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61
Q

Marine injury Poisoning prevention

A

Don’t rely on cooking - seafood toxins are heat/acid stable, avoid large fish (>10kg), eat only fresh fish and never eat puffer fish, avoid shellfish in red algae, don’t swallow seafood that makes your lips tingle

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62
Q

Global Surgery Epidemiology

A

5bil lack access to surgical care, 18 mil deaths could be avoided, 33mil face catastrophic expense after surgical care, 30% of Global Health Burden require surgery

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63
Q

Global Surgery Definition

A

Multidisciplinary field concerning the improved and equitable access to surgical care across international healthcare systems with focus on LMICs

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64
Q

Global Surgery Minimum procedures required

A

Laparotomy, C-section, Open fracture management and wound debridement, D&C, closed fracture reduction

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65
Q

Global Surgery Burn depth

A

1 superficial 2A sup partial (red, painful, weeping), 2B deep partial (red, painful, dry), 3 full thickness (black/white, no feeling)

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66
Q

Global Surgery Burn assess BSA

A

1% BSA is size of child’s hand

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67
Q

Global Surgery Burn management

A

Fluid (Modified Parkland), Pain (affects catabolism), Nutrition, Infection control, Tetanus vax

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68
Q

Global Surgery Aim

A

Early referral and advice, transport

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69
Q

NTD Definition

A

Disproportionately affects populations living in poverty; and causes important morbidity and mortality – including stigma and discrimination - in such populations, justifying a global response

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70
Q

NTD Epidemiology

A

Primarily affects populations living in tropical and sub-tropical areas

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71
Q

NTD Schistosoma strategy

A

MDA (praziquantel), sanitation, snail control

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72
Q

NTD Onchocerca strategy

A

MDA (ivermectin), (vector control) - does not kill adult worm, need to treat for long time, and barrier to ivermectin use in loa loa endemic regions -> cerebral inflammation

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73
Q

NTD Lymphatic filariasis strategy

A

MDA (ivermectin, albendazole), vector control - does not kill adult worm, need to treat for long time. Transmission targets - W bancrofti regions antigen prevalence by ICT rapid test <1% in children aged 6-7y. B malayi regions seroprevalence by BrugiaRapid <2% in children aged 6-7y

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74
Q

NTD Trachoma strategy

A

MDA (azithromycin), water, sanitation, education “SAFE” = Surgery, Antibiotics, clean Faces, Environment

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75
Q

NTD Yaws strategy

A

MDA (azithromycin) - issue is latent infection is common, and serological test needed (VDRL/RPR)

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76
Q

NTD Soil transmitted helminth strategy

A

MDA (albendazole)

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77
Q

NTD Guinea worm strategy

A

Safe water, health education

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78
Q

NTD HAT strategy

A

Case finding and treatment (vector control). Challenge accessing to remote rural communities in areas of conflict

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79
Q

NTD Visceral leishmaniasis strategy

A

Case finding and treatment

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80
Q

NTD Leprosy strategy

A

Case finding and treatment

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81
Q

NTD Taeniasis/cysticercosis strategy

A

Sanitation, meat inspection, vaccination of pigs

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82
Q

NTD Echinococcosis strategy

A

Abattoir control, treatment of dogs, education

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83
Q

NTD Foodborne trematodes strategy

A

Treatment of sheep, health education

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84
Q

NTD Chagas disease strategy

A

Vector control, blood screening

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85
Q

NTD Buruli ulcer strategy

A

Case finding and treatment

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86
Q

NTD Rabies strategy

A

Vaccination of dogs, health education

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87
Q

NTD Dengue and Chikungunya strategy

A

Vector control

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88
Q

NTD Mycetoma strategy

A

Case finding and treatment

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89
Q

NTD Scabies strategy

A

?MDA (ivermectin)

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90
Q

NTD Snakebite strategy

A

?Case finding, education - not yet established

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91
Q

NTD Noma strategy

A

?Case finding and treatment - not established

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92
Q

NTD Elimination

A

Reduction to zero of the incidence of a disease in a defined geographical area. Continued interventions required to prevent re-introduction

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93
Q

NTD Eradication

A

Permanent reduction to zero of the worldwide incidence of infection caused by a specific agent. Intervention measures no longer needed

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94
Q

NTD Biological req for elimination/eradication

A

Intervention effective, Surveillance (good diagnostic), No animal reservoir

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95
Q

NTD Social req for elimination/eradication

A

Recognised as public health importance, technically feasible intervention, political commitment, advocacy plan

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96
Q

NTD Negatives of elimination strategies

A

Lead to underreporting, lack of ongoing surveillance may lead to resurgence

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97
Q

NTD Elimination challenges

A

New animal reservoir, or reduced surveillance once country certified as having met targets = resurgence. Attempts to meet the target may lead to under-reporting

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98
Q

Biomarker Definition

A

a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathological processes, or pharmacological response to a therapeutic intervention

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99
Q

Medicine Quality WHO estimate SF

A

WHO estimated in 2017 that 10.5% of medicines in LMIC are SF (substandard or falsified)

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100
Q

Medicine Quality Substandard

A

Degraded - leave factory in good quality but degrade due to improper storage (frozen/heated/light exposure etc), substandard - fail to meet quality standards or their specifications or both - result from factory error

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101
Q

Medicine Quality Falsified

A

Medical products that deliberately/fraudulently misrepresent their identity, composition or source

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102
Q

Medicine Quality Measures

A

Medicine Quality Scientific Literature surveyor, early warning systems, ‘Globe’ monitoring system,

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103
Q

Medicine Quality Vaccine incidents

A

Plague vaccine 1902 contaminated with tetanus, Cutter incident 1955 Salk inactivated polio vaccine - failure of formaldehyde treatment resulting in live polio - many infections and deaths

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104
Q

Medicine Quality Monitoring devices

A

Minilab thin layer chromatography, Rama spectroscopy ‘see through bottles’, Paper analytical devices 12 lines colorimetry

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105
Q

Medicine Quality Diethylene & ethylene glycol

A

Used instead of propylene glycol -> renal toxins, consider if unexplained children with AKI

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106
Q

Medicine Quality Resolution

A

Functional regulatory authorities and monitoring, greater international political will, timely data sharing, targeted research

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107
Q

Medicine Quality Summary

A

Always consider SF if you encounter AE, therapeutic or diagnostic failure, surprisingly inexpensive medical products, typos and packaging defects, report to NMRA and WHOrapidalert. Medicine falsification is world’s 3rd oldest profession - not going to go away, key to minimising occurrence and impact, screening devices hold hope, multidisciplinary approach needed with increased research

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108
Q

NCD Diabetes

A

Increased risk of common and health-care associated infection, association with 3.6 times higher TB risk

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109
Q

Obstetrics Strategies that have improved maternal mortality

A

Handwashing, RCOG, antisepsis, antibiotics, midwives, universal healthcare, oxytocin, training, contraception, MgSO4, abortion laws, living standards, safer anaesthesia

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110
Q

Obstetrics Maternal mortality

A

Every day in 2020, almost 800 women died from preventable causes related to pregnancy and childbirth, 95% in LMIC, reflects inequalities in access to quality health services, humanitarian, conflict and post-conflict hinder progress in reducing burden,

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111
Q

Obstetrics Lifetime maternal mortality risk

A

HIC 1 in 5300, LMIC 1 in 49. For every woman who dies, another 20-30 suffer considerable morbidity

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112
Q

Obstetrics Maternal mortality causes 75%

A

Severe bleeding (PPH), infections (usually after childbirth), high blood pressure during pregnancy, delivery complications, unsafe abortion

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113
Q

Obstetrics Maternal death direct causes

A

As a consequence of a disorder specific to pregnancy: haemorrhage, preeclampsia, genital tract sepsis

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114
Q

Obstetrics Maternal death indirect causes

A

As a consequence of previous existing disease or diseases that developed during pregnancy and which were not due to direct obstetric causes but aggravated by pregnancy: eg cardiac disease, other infections (sepsis)

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115
Q

Obstetrics Maternal death other

A

Coincidental: incidental/accidental deaths not due to pregnancy or aggravated by pregnancy eg MVA, late: deaths >42d but less than 1y after end of pregnancy

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116
Q

Obstetrics Model questions: Maternal health

A

Most maternal deaths are preventable. Maternal health services are vulnerable to external factors such as conflict and humanitarian crises. Family planning is the most cost-effective intervention to reduce maternal mortality as part of an essential package for maternal health. WHO recommends a minimum of eight antenatal visits during pregnancy

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117
Q

Obstetrics Model questions: Antenatal care

A

Handheld notes are recommended by the WHO to improve quality of antenatal care. 90% of anaemia in pregnancy is due to nutritional deficiency. Tocolysis should be given in preterm labour as long as no infection or abruption is present, to allow time for steroids. Preterm birth is the single leading cause of perinatal mortality

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118
Q

Obstetrics Model questions: Obstetric emergencies

A

There is evidence to show that clearly stating what the emergency is improves the outcome. Verbal consent may be taken for emergency Caesarean section. Delivery of the baby by perimortem Caesarean section (resuscitative hysterotomy) is part of resuscitating the woman, and the baby does not need to be alive. Maternal morbidity and mortality is higher in women who have poor access to antenatal care

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119
Q

Obstetrics Model questions: Maternal seizures

A

Eclamptic seizures usually resolve initially prior to MgSO4 administration, but can be prolonged in severe disease. Causes of seizures in pregnancy include TB, malaria and eclampsia. It is essential to restrict intravenous fluids and monitor fluid balance with pre-eclampsia and eclampsia as women can develop pulmonary oedema due to capillary leakage. If a woman has an eclamptic fit she can have another pregnancy with prenatal counselling, consideration of aspirin, and monitoring. Pre-eclampsia generally develops a few weeks later in a subsequent pregnancy

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120
Q

Obstetrics Model questions: Maternal haemorrhage

A

Women with blood loss do not have tachycardia and hypovolaemia until very late. Risk factors for uterine rupture include previous Caesarean section, grandmultiparity and twin pregnancy. Signs of placental abruption may include a tender uterus and fetal distress. Haemorrhage is more common after a long labour

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121
Q

Obstetrics Determinants of maternal mortality

A

Most maternal deaths are preventable. Strategies to avoid unintended pregnancies (contraception, safe abortion), healthcare access to prevent or manage common pregnancy complications, UK mortality rate is lower, black women have 4x risk of dying in childbirth, and socially deprived (poor) 2x risk

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122
Q

Obstetrics Why do women globally not get the care they need?

A

Health system failures (poor quality care, insufficient numbers or training of healthcare staff, lack of essential resources/medical supplies, poor accountability), Social determinants (income, nutrition, education, race/ethnicity), Harmful gender norms (structural and individual), External factors (instability of health systems in conflict, climate, humanitarian crises)

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123
Q

Obstetrics 3 delays model

A

1 Delay in decision to seek care (family/community level perceptions, education and awareness) 2 Delay in reaching appropriate care (accessibility: distance, time to travel, transportation cost/availability, distribution and location of health facilities) 3 Delay in receiving adequate care (quality of care: facilities, supplies, equipment, staff training, adequate & timely referral systems)

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124
Q

Obstetrics WHO: Ending preventable maternal mortality

A

1 Address inequities in access to and quality of sexual, reproductive, maternal and newborn healthcare, 2 Ensure universal health coverage for comprehensive sexual, reproductive, maternal and newborn healthcare 3 Address all causes of maternal mortality, reproductive and maternal morbidities and related disabilities 4 Strengthen health systems to respond to the needs and priorities of women and girls 5 Ensure accountability in order to improve quality of care and equity

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125
Q

Obstetrics Cost effective components of maternal health

A

Family planning and preventing/managing unplanned pregnancy, Skilled assistance for delivery and management of complications including pre-eclampsia, sepsis, hypertensive disorders in pregnancy. Comprehensive antenatal care (including syphilis, tetanus vax and IPTp (intermittent preventive treatment) malaria. Iron and folic acid supplementation, antibiotics for PPROM and management of eclampsia with MgSO4

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126
Q

Obstetrics Antenatal care

A

MultiD care to ensure best pregnancy outcomes, risk identification for preexisting conditions and those that develop during pregnancy, prevention and management of complications, prevent and manage concurrent diseases

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127
Q

Obstetrics Antenatal nutrition

A

Counsel on healthy eating & keeping physically active, daily oral iron and folic acid, and if appropriate calcium can reduce PET, Vitamin A in high deficiency states

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128
Q

Obstetrics Antenatal maternal and fetal assessment

A

Hb and urine culture, ask about intimate partner violence, routinely screen for gestational diabetes, tobacco/substance misuse, HIV and syphilis, plus TB in high prevalence settings (>100/100,000 incidence), Ax fetal growth with SFH & US <24/40

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129
Q

Obstetrics Antenatal preventive measures

A

Treat asymptomatic bacteriuria, antihelminthic treatment in endemic areas (>20% incidence), tetanus vax, intermittent preventive treatment and insecticide treated nets in malaria endemic areas

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130
Q

Obstetrics Antenatal symptomatic management

A

N&V, reflux, cramps, low back/pelvic pain, constipation, varicose veins & oedema

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131
Q

Obstetrics Antenatal health system interventions

A

Woman-held case notes, midwifery-led continuity of care, task shifting, support to recruit and retain healthworkers in rural/remote areas

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132
Q

Obstetrics Antenatal community interventions

A

Participatory learning and action cycles: increase communication and support, birth preparedness, increased use of antenatal services and skilled care, increase male involvement, build partnership with traditional birth attendants

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133
Q

Obstetrics Maternal anaemia

A

T1 <110, T2/3 <105, PP <100, prevalence 40% globally higher SE Asia & Africa. Causes: pregnancy physiology (haemodilution), nutritional deficiency (90% due to iron def), parasitic helminth infections, other infections (TB, HIV, Malaria), Chronic diseases, acute/chronic blood loss, haemoglobinopathies. Complications: Fatigue/SOB, Immune dysfunction, placental abruption, PPH (reduced uterine contraction), increased maternal mortality. Fetal complications: preterm birth, low birth weight, increased infant mortality. Management oral iron, folic acid +/-B12

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134
Q

Obstetrics Preterm birth

A

Extreme <28, Very 28-32, Mod/late preterm 32-37w. 5-18% of births globally, increased burden in Asia and sub-Saharan Africa, 13.4 million babies in 2020. Causes: idiopathic, iatrogenic (early delivery by healthcare to treat PET, growth restriction), preterm prelabour ROM, infection (intra and extrauterine), bleeding (APH), multiple pregnancy. Preterm birth is a leading global cause of perinatal mortality (30%)

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135
Q

Obstetrics Preterm birth risk factors

A

Maternal: demographic (low BMI, age<18 >35yo, black), lifestyle (smoking, drugs, stress, DV), psychological stress, low SES, history of spontaneous preterm, LLETZ, uterine anomaly. Pregnancy: uterine overdistension (multiple pregnancies, polyhydramnios), interpregnancy interval <6m, fetal anomaly, antepartum haemorrhage, PPROM in current pregnancy, Infections UTI/BV

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136
Q

Obstetrics Preterm birth prevention

A

Optimal antenatal care: nutrition and lifestyle, identify and treat anaemia, asymptomatic bacteriuria, US to determine GA and multiple pregnancy, cervical length monitoring, progesterone and cervical cerclage

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137
Q

Obstetrics Management of threatened preterm labour

A

Tocolysis (Nifedipine) to allow antenatal corticosteroids or transfer to a facility for care, 24-34/40, contraindicated with PV bleeding, placental abruption and intrauterine infection. Antenatal steroids 24-34/40 if high chance of labour within 7d, antibiotics for PPROM <37/40, MgSO4 30% reduction in CP<32/40, delayed cord clamping, thermal care (plastic bag/wraps for stabilisation and transfer)

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138
Q

Obstetrics Hypertensive disorders of pregnancy

A

Can be pre-existing, pregnancy-induced, or PET (HTN & proteinuria) - BP and urine should be checked at every point of contact in pregnancy

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139
Q

Obstetrics PET

A

Reduced by low-dose aspirin if one high or two moderate risks. PET/HELLP can affect any organ system, seizure in pregnancy is eclampsia until proven otherwise, needs prompt and careful control of HTN, meticulous fluid balance, seizure prophylaxis with MgSO4 Have an eclampsia box wherever you work. Use the post-partum period for pre-pregnancy planning. Pre-eclampsia has a recurrence rate of 10-40% but usually occurs 2-3 weeks later

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140
Q

Obstetrics Antenatal summary

A

Good quality ANC can reduce maternal morbidity and mortality from both direct and indirect causes. ‘Simple’ conditions like anaemia in pregnancy can have a big impact on maternal and neonatal outcomes. Preterm birth is the leading cause of perinatal mortality globally.

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141
Q

Obstetrics Obstetric emergencies key concepts

A

Stating the nature of the emergency improves outcomes, look after primips and the multips will look after themselves, deliver only when the intrauterine environment is more hostile than the neonatal cot, the sun should not rise and set twice on a woman in labour. Antepartum haemorrhage APH - get ready for the PPH. PPH - a contracted empty uterus does not bleed. Young fit women will decompensate late. Can be difficult to identify in labour and postnatally. Breech delivery - hands off the breech. Shoulder dystocia - don’t just pull. Cord prolapse - elevate the presenting part

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142
Q

Obstetrics Obstetric emergencies maternal collapse

A

Manual uterine displacement. If cardiac arrest, think about perimortem C-section - it will create 30-40% return of blood flow

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143
Q

Obstetrics Placenta praevia

A

Placenta implanted totally or partially in the lower segment of the uterus, more common in multiple pregnancy and previous Caesarean, recurrent bright red bleeding without pain, fetus is not usually compromised unless major bleed, do not do a vaginal examination, think through C-section delivery - entry and haemorrhage control

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144
Q

Obstetrics Placental abruption

A

Separation from the placental bed of a normally sited placenta, unknown cause, usually pain, bleeding may or may not be present, fetus may be compromised, may lead to maternal shock and DIC. NVD not contraindicated - labour may happen quickly and successfully

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145
Q

Obstetrics Uterine rupture

A

Occurs in labour, with pain, bleeding, fetal distress, maternal collapse. RF: VBAC, grandmultiparity, obstructed labour, trauma. Transfer to theatre for Caesarean +/- hysterectomy

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146
Q

Obstetrics Postpartum haemorrhage

A

Causes: retained placenta, uterine rupture, uterine inversion or atony, genital tract trauma (cervix or vagina), coagulopathy. Management: ABC, call for help, state nature of emergency, uterotonic medications (oxytocin, ergometrine, carboprost, misoprostol PR, tranexamic acid), theatre for manual removal of placenta, urgent suturing, intrauterine pressure with balloon, laparotomy and compression of uterus. Decision for hysterectomy saves lives if all other measures have failed

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147
Q

Obstetrics Sepsis Six

A

Give O2 for SaO2>94%, BC, IVAbx, fluid challenge, lactate, measure urine output

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148
Q

Obstetrics Shoulder dystocia

A

Obstetric emergency, bony impaction on pubic symphysis, hard to predict, early recognition with failure to turn as expected, knees to chest to maximise size of pelvic outlet, suprapubic pressure, internal rotational manoeuvres or delivery of posterior arm, prepare for PPH

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149
Q

Obstetrics Cord prolapse

A

Loop of cord descends below presenting part, mechanical compression and spasm of cord -> fetal distress/death. RF: Malpresentation (ie head not plugging the pelvis), multiparity, polyhydramnios, prematurity. Management manually elevate the presenting part to allow blood flow, all fours, 500ml in bladder (helps to stop presenting part to come down), turn off any oxytocin, consider tocolysis to transfer to theatre,

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150
Q

Neonates Introductory summary

A

Neonatal conditions are amongst the leading causes of child mortality, and are responsible for almost half of all deaths under 5 years. The highest risk of death is the day of birth, 75% in the first 7 days. Prematurity, birth complications and neonatal infections are the leading causes of neonatal deaths. ‘Every Newborn Action Plan’ lays out strategic objectives and ambitious targets to reduce neonatal mortality NMR or <12 per 1000 births. Neonatal conditions are associated with an increased risk of developmental delay and disability. Important to think ‘Beyond Survival’ … to survive AND THRIVE including early intervention for young children with developmental disability

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151
Q

Neonates Preterm birth definitions

A

Extreme <28, Very 28-32, Moderate 32-34, Late 34-37

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152
Q

Neonates Inequalities in preterm mortality

A

LMIC 32/40 50% mortality, HIC 24/40 50% mortality

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153
Q

Neonates Challenges in LMIC neonatal care

A

Assessing gestational age, providing warmth, feeding and fluids, infection prevention, recognition and treatment, respiratory support, prevention of apnoea, high patient to nurse ratio

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154
Q

Neonates Risk of hypothermia in preterm

A

Greatest risk for mortality. Stop producing surfactant, increased respiratory distress. Use more energy, increased glucose requirements, become hypoglycaemic and have increased risk for apnoea

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155
Q

Neonates Preventing hypothermia from birth

A

Dry and cover, avoid bathing, put on a hat and a nappy, skin to skin

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156
Q

Neonates Kangaroo care outcomes

A

Reduces mortality up to 25% in trial, risk of sepsis (if occurs is less severe), improves weight gain, higher success in establishing breast feeding, maternal bonding, and reduced time to discharge

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157
Q

Neonates Benefits of breastmilk

A

Reduces risk of sepsis, NEC, retinopathy of prematurity, feeding intolerance, neurodevelopmental delay

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158
Q

Neonates Neonatal care summary

A

Implementation of a low-cost hospital based neonatal care within the existing healthcare system can have a significant impact on neonatal mortality in a resource- limited setting. Focusing on simple, affordable and sustainable care can have a HUGE impact on neonatal survival. We must FOCUS on educating and training the nursing staff. Education is key

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159
Q

Neonates Top five causes of newborn deaths

A

Preterm birth, intrapartum-related birth complications, neonatal infections, birth detects, neonatal jaundice

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160
Q

Neonates Neonatal sepsis

A

Potential severe bacterial infection - meningitis, sepsis, pneumonia, tetanus with increased risk for those born at pre-term with complex outcomes of neurological, neurodevelopmental and hearing deficits - these may or may not have effects upon physical and mental health, some of these effects may predispose to early death

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161
Q

Neonates Early onset neonatal sepsis

A

First 72h of life, pathogens exposed to before or during birth, may originate from maternal genital tract, unhygienic delivery practices and unclean birth area

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162
Q

Neonates Late onset neonatal sepsis risk factors

A

NICU admission, invasive procedures (IVC, mechanical ventilation), administration of stock solutions, contaminated equipment, IV or enteral solutions, prolonged hospitalisation

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163
Q

Neonates Community acquired neonatal sepsis risk factors

A

Poor hygiene practices in the home setting, inadequate cord card, bottle feeding instead of breastfeeding, lack of exclusive breastfeeding. Preventive measures exclusive breastfeeding and proper handwashing

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164
Q

Neonates Management and prevention of neonatal sepsis

A

Detection: improved lab support, rapid response, POCT. Antimicrobials: treatment protocols, current local/regional epi. AMS. AMR: vectors of transmission, surveillance. IPC: environmental and hand hygiene, context-specific guidelines. Investment: resources and research

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165
Q

Neonates Prevention of maternally acquired infections

A

Intrapartum Abx: Pen, Azith, Vaccines: RSV, Pneumococcus, GBS. Other: Handwashing, umbi and eye care, breastfeeding, removing lines as soon as not required, strict asepsis for all procedures

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166
Q

Neonates Early onset GBS

A

First week of life, leading cause of sepsis in neonates, can also cause pneumonia, meningitis, generally acquired by fetus inutero or during birth

167
Q

Neonates Late onset GBS

A

1-4 weeks of life, wider clinical spectrum, may cause meningitis, sepsis, septic arthritis, osteomyelitis, pneumonia

168
Q

Neonates Causes of neonatal sepsis

A

South Asia: RSV, Ureaplasma, K pneumoniae, E coli. Sub-Saharan Africa: S aureus, Klebsiella sp, E coli

169
Q

Neonates Definitions

A

Birth asphyxia: Failure to initiate breathing at birth. Intrapartum-related death (& stillbirth) ‘Death as a result of damage to the brain and other vital organs from oxygen deprivation around the time of delivery’, Neonatal encephalopathy: A disturbance of neurological function: newborn brain dysfunction, Hypoxic ischaemic encephalopathy: implies causality and is out of vogue

170
Q

Neonates Top five causes of child mortality

A

Prematurity 16%, Pneumonia 13%, intrapartum related 11%, diarrhoea 8%, neonatal infection 7%

171
Q

Neonates Maternity and neonatal care challenges

A

Different exposures context and care settings, care largely supportive, minimal capacity for investigations, low nursing ratios with minimal monitoring, risk of compounding brain injury (cooling not universally implemented), limited access to fit-for-context equipment (pumps), supply chain challenges and drug shortages, inconsistent electricity and water supplies

172
Q

Neonates Severity grading of neonatal encephalopathy

A

Mild: hypertonic, hyperalert (staring), partial primitive reflexes, irritable, hand clenching, voracious or poor feeders. Moderate: hypotonic, lethargic, don’t feed, absent primitive reflexes, strong distal flexion, apnoeas, seizures. Severe: completely floppy, comatose, apnoeic, decerebrate, absent reflexes, full fontanelle

173
Q

Neonates Neonatal seizures treatment

A

Phenobarbitone, followed by phenytoin

174
Q

Neonates Neonatal encephalopathy cooling

A

Controversial - not universally implemented in LMIC due to limited resources and evidence. Passive cooling common. Challenges: lack of data from SSA with no NICU facilities, comorbidity with perinatal infection/inflammation may impact effectiveness, likely higher prevalence of chronic partial hypoxic ischaemia due to quality of intrapartum care and lack of fetal monitoring

175
Q

Neonates Neonatal encephalopathy outcomes

A

Neurodevelopmental impairment in 29.3%, Cerebral palsy in 19%, most commonly four-limb spasticity. Among those with disability malnutrition common - 44.1% had undernutrition, 32.4% with microcephaly. Clinical risk factors for impairment included: Neonatal clinical seizures, feeding difficulty at discharge, Small head circumference at one year and Abnormality on cUS

176
Q

Neonates Neonatal summary

A

Neonatal conditions substantially contribute to death and disability globally. Highest burden is in sub-Saharan Africa ‘where there is no NICU’. Neonatal target populations differ in perinatal exposures and care context meaning HIC interventions can’t be universally applied. Predictors of adverse outcome useful to inform targeted follow-up, and future trials, however more locally implementable tools are needed. Few comprehensive neurodevelopmental assessment tools have been validated in LIC populations. Early care and support programmes are crucial and will need to be integrated with routine government services for sustainability at scale

177
Q

SDGs SDGs

A

1 No Poverty, 2 Zero Hunger, 3 Good health and wellbeing, 4 quality education, 5 gender equality, 6 clean water and sanitation, 7 affordable and clean energy, 8 decent work and economic growth, 9 industry, innovation and infrastructure, 10 reduced inequalities, 11 sustainable cities and communities, 12 responsible consumption and production, 13 climate action, 14 life below water (aquatic), 15 life on land, 16 peace, justice and strong institutions, 17 partnerships for the goals,

178
Q

WASH The F Diagram

A

Faeces -> fluids, fingers, flies, fields -> food -> new host. Sanitation, safe water and hygiene/handwashing can break the onward transmission

179
Q

WASH Sanitary revolution

A

Started in western Europe in 19th century, resulted in sanitary policies and actions across western Europe and North America. Significant decline in diarrhoea deaths, particularly among infants and young children. 1866 The Great Sanitary Act

180
Q

WASH Cholera in Soho

A

1854 John Snow

181
Q

WASH Sanitation Definition

A

“the safe disposal of excreta and human faeces to protect the health and contamination of the environment”. (UN Water 2008)

182
Q

WASH Sanitation chain definition

A

“the safe containment, transport, treatment and disposal/re-use of human excreta”. (UNICEF definition)

183
Q

WASH Sanitation ladder

A

Safely managed: use of improved facilities which are not shared with other households and where excreta are safely disposed in situ or transported and treated off-site. Basic: use of improved facilities which are not shared with other households. Limited: Use of improved facilities shared between two or more households. Unimproved: use of pit latrines without a slab or platform, hanging latrines or bucket latrines. Open defaecation: disposal of human faeces in fields, forests, bushes, open bodies of water, beaches and other open spaces or with solid waste

184
Q

WASH Pit latrine

A

Advantages: Easy to build, Low cost (capital and operating). Disadvantages: Flies and odours, Needs emptying, Difficult to clean, Excreta is visible, Requires treatment of sludge, Pits are susceptible to overflowing during floods and can collapse, Stagnant water in pits may promote mosquito breeding, Leachate can contaminate groundwater

185
Q

WASH Improved dry pit latrine (lined with slab)

A

Advantages: Easy to clean, More structurally stable, Easy to build, No need for constant source of water, Low capital and operating costs. Disadvantages: Flies and odours, Needs emptying (cost), Requires treatment of sludge, Leachate can contaminate groundwater

186
Q

WASH Epidemiology

A

46% of the world do not have safely managed services, and 20% (1.7 billion people) lack basic sanitation services

187
Q

WASH Sanitation value chain

A

Containment > Emptying > Transport > Treatment > Reuse/disposal

188
Q

WASH What to do when the pit fills?

A

Consumer concerns: cost of dealing with it, visible excreta, flies and smells, social embarrassment, access to emptying services

189
Q

WASH Sanitation and diarrhoea

A

Improved vs unimproved - 16% reduction in diarrhoea, however effect of sewered vs unimproved 40% reduction in diarrhoea

190
Q

WASH Sanitation non-health benefits

A

Provides privacy, More convenient, Save time, Cleanliness and smell, Increases school-attendance, Don’t have to withhold food/drinks, Prevent imprisonment by daylight, Protection from harassment & rape, Avoid dangers at night, Avoid snakes, Increase value of property/tenant’s rent

191
Q

WASH Sanitation disability and inclusion

A

Issues: pain and discomfort, stigma, lack of privacy, decreased self-esteem and social participation. Accessing sanitation was among the top challenges of daily living among people with disabilities in Malawi

192
Q

WASH Water Sources

A

Surface water: Drinking water from a river, dam, lake, pond, stream, canal or irrigation canal. Unimproved: drinking water from an unprotected dug well or unprotected spring. Limited: drinking water from an improved source for which collection time exceeds 30 minutes for a round trip, including queuing. Basic: drinking water from an improved source, provided collection time is not more than 30 minutes for a round trip, including queuing. Safely managed: drinking water from an improved water source that is located on premises, available when needed and free from faecal and priority chemical contamination

193
Q

WASH Improved water source definition

A

A source that by nature of its construction or through active intervention, is protected from outside contamination, in particular from contamination with fecal matter

194
Q

WASH Improved water source example

A

Piped water into dwelling, piped water into yard/plot, public tap/public standpost, tubewell/borehole/hand pump, protected dug well/spring, protected spring, rainwater

195
Q

WASH Unimproved water source example

A

Collected surface water, unprotected dug well, unprotected spring, tanker truck/cart with tank

196
Q

WASH Safely managed water service

A

Free from contamination, accessible on premises, available when needed

197
Q

WASH Water plateau

A

> 30 minutes - water consumption drops and therefore decreased hygiene practices. A 15 min decrease in roundtrip water collection time is associated with 41% reduction in diarrhoea and 11% reduction in under-5 child mortality

198
Q

WASH Point of use water treatment

A

Chlorination (not effective Giardia or Crypto), Boiling, Filtration (slow sand filters), UV disinfection

199
Q

WASH Water-borne transmission

A

Description: you drink it. Example: Cholera. Interventions: Improve drinking water quality, improve sanitation

200
Q

WASH Water-washed transmission

A

Description: Person-to-person transmission due to inadequate personal and domestic hygiene. Example: trachoma, conjunctivitis, louse-borne typhus. Interventions; Increase quantity of water. Improved hygiene by increasing access and availability of water

201
Q

WASH Water-based transmission

A

Description: Transmission of infections via an obligatory aquatic host (eg snail). Example: Schistosomiasis, guinea worm. Interventions: decrease contact with contaminated water. Control aquatic animals. Reduce excreta entering environment

202
Q

WASH Water-related insect vector

A

Description: Transmission by insects which breed in (or bite near) water. Example: Malaria, dengue, yellow fever, sleeping sickness, filariasis. Interventions: Eliminate breeding sites, netting, repellent, keeping people away from breeding sites

203
Q

WASH Water summary

A

Water ladder for service level: from surface water to safely managed. Minimum for ‘basic’ access according to WHO: improved source and available within 30 minutes (round trip. Safe water can prevent waterborne and water-washed diseases (water quality and quantity), non-health benefits mainly for women and children

204
Q

WASH Handwashing with soap

A

Diarrhoeal disease reductions of 30%, acute respiratory infection reduction of 11%. Averted 607,000 deaths of children under 5 annually

205
Q

WASH WHO Five moments of hand hygiene

A

1 Before touching a patient, 2 before clean/aseptic procedure, 3 after body fluid exposure risk, 4 after touching a patient, 5 after touching patient surroundings

206
Q

WASH Healthcare settings

A

39% of healthcare professionals globally manage to wash their hands at WHO 5 key times. 35% of health facilities in LMIC do not even have water and soap available for handwashing

207
Q

WASH SDG6 WASH targets

A

Need significant acceleration to achieve targets of drinking water, sanitation, and hygiene

208
Q

Definition Mortality

A

Death due to illness

209
Q

Definition Morbidity

A

Consequences and complications (other than death) that result from a disease

210
Q

WASH Causes of moderate-to-severe diarrhoea in children

A

Rotavirus, Cryptosporidium, enterotoxigenic E coli, Shigella. Diarrhoeal mortality has decreased, but morbidity is still very high. Repeated diarrhoea has impact on growth curve

211
Q

WASH Diarrhoea morbidity in children

A

Inhibits nutrient absorption -> malnutrition, even if sufficient nutrition is consumed. Reduces resistance to infections. Early childhood development including stunting and wasting. Cognitive development (eg language and memory), lifelong consequences, such as productivity or ability to learn

212
Q

WASH Environmental Enteric Dysfunction (EED)

A

Inflammation of small intestine, marked by alterations in gut lining - as a result of diarrhoea disease. Also reduces absorption of oral vaccines

213
Q

WASH Impact of WASH interventions on diarrhoea

A

Drinking water: 33% RR (75% RR if treated water is piped to premises), Sanitation: 25% RR (45% RR if >75% sanitation coverage), Hygiene: 30%

214
Q

WASH WASH Improvements

A

Consult with the communities - what do they want/need, and what can they afford? Onsite sanitation is probably a better/cheaper solution and will reach more people. Addressing child faeces disposal with child-friendly latrines and education. Health education not likely to work - improving sanitation coverage will need promotion of sanitation as part of the approach. Provide water vendors with means to treat water, build more boreholes in the rural areas. Think about where the waste from latrines goes - can it be treated or reused? Poor household would likely not connect to an expensive system, particularly if there is abundant free water and sanitation is rarely a priority.

215
Q

Malnutrition Social/Economic model of malnutrition

A

Production based (reduced harvest), Trade based (import bottlenecks), Labour based (poverty, unemployment), Transfer-based (late delivery of food aid, profiteering)

216
Q

Malnutrition Integrated models

A

Consider not just maternal and child nutrition, diets/care, food, feeding and environments, but also consider resources, and governance. Resources: sufficient resources include environmental, financial, social and human resources to enable children and women’s right to nutrition. Norms: positive social and cultural norms and actions to advance children’s and women’s right to nutrition. Governance: includes political, financial, social and public and private sector actions - to enable children’s and women’s right to nutrition

217
Q

Malnutrition Vitamin A deficiency

A

Xerophthalmia is the clinical spectrum of ocular manifestations of vitamin A deficiency; these range from the milder stages of night blindness and Bitot spots to the potentially blinding stages of corneal xerosis, ulceration and necrosis (keratomalacia). An estimated 250 000–500 000 children who are vitamin A-deficient become blind every year, and half of them die within 12 months of losing their sight. Deficiency of vitamin A is associated with significant morbidity and mortality from common childhood infections, and is the world’s leading preventable cause of childhood blindness. Vitamin A deficiency also contributes to maternal mortality and other poor outcomes of pregnancy and lactation. It also diminishes the ability to fight infections. Even mild, subclinical deficiency can be a problem, because it may increase children’s risk for respiratory and diarrhoeal infections, decrease growth rates, slow bone development and decrease the likelihood of survival from serious illness.

218
Q

Malnutrition Marasmus (wasting)

A

Generally wasted, thin arms (mid upper arm circumference), thin face, ribs visible, sunken eyes, lack of skin turgor (difficult to assess hydration)

219
Q

Malnutrition Kwashiorkor malnutrition

A

Bilateral pitting oedema, apathetic, sparse/discoloured hair, dermatosis, enlarged liver, angular cheilitis

220
Q

Malnutrition Definition of severe acute malnutrition (SAM)

A

Normal = +/- 2SD median. Moderate (MAM) = -2-3 z-scores or MUAC<125mm without oedema; Severe (SAM) <-3 z-scores or MUAC <115mm -> marasmus (severe wasting) with oedema -> Kwashiorkor

221
Q

Malnutrition Inadequate caloric intake causes

A

GORD, inadequate breast milk supply or ineffective latching, incorrect formula preparation, mechanical feeding difficulties (cleft lip or palate), neglect or abuse, poor feeding habits, poor oral neuromotor coordination, toxin-induced gastrointestinal upset (eg lead levels leading to anorexia, constipation or abdominal pain)

222
Q

Malnutrition Inadequate nutrient absorption

A

Anaemia (iron deficiency), biliary atresia, celiac disease, chronic gastrointestinal conditions (irritable bowel syndrome, infections), cystic fibrosis, inborn errors of metabolism, milk protein allergy, pancreatic cholestatic conditions

223
Q

Malnutrition Increased metabolism

A

Chronic infection (HIV/AIDS, TB), chronic lung disease of prematurity, congenital heart disease, hyperthyroidism, inflammatory conditions (eg asthma, inflammatory bowel disease), malignancy, renal failure

224
Q

Malnutrition Reductive adaptation

A

METABOLISM: Metabolic rate -24% and Protein synthesis -37%. VITAL ORGANS & SYSTEMS: Heart / Cardiovascular: Output -31%, Anaemia (decreased production /increased loss RBC), Kidneys: Glomerular. Filtration rate -41%, Sodium excretion -54% Liver: Fatty liver (+++ in kwashiorkor; (+) in marasmus), decreased endogenous glucose production. Pancreas: decreased Beta cell function, decreased enzyme production (NB. amylase trial). Hormonal: decreased Thyroid function, decreased Cortisol, growth hormone responses. Gut: Atrophy, decreased Nutrient absorption (even though increasing the feeding), Chronic Inflammation, Microbiome changes (?interventions). Skin: decreased barrier role, decreased subcutaneous fat (decreased insulation), decreased collagen / protein ‘reserve’. Immune function: Greater vulnerability to infection, Atypical (decreased) response to infection, Atypical manifestations of infection, Poorer outcomes from infection. Brain / Central Nervous System: Relatively protected but…Lethargy, irritability, Decreased appetite, Decreased interaction with environment

225
Q

Malnutrition Assessment of dehydration

A

Usual signs do not apply - skin turgor can represent loss of subcut fat, sunken eyes can represent loss of retroorbital fat and dry mouth/eyes may represent atrophied glands. Better to assess for recent changes in turgor, eyes, dry stat, in addition to input/output (charts) urine/stool, weight changes, thirst, conscious level

226
Q

Malnutrition Treatment of dehydration

A

Treatment with great care: risk of heart failure/worsening, oral/NGT whenever possible, specially formulated solutions, monitor response clearly (weight, vitals, fluid in/output, alert) - pause/slow fluids if worsening. Prevention is better (early feeds, ORS, breastfeeding)

227
Q

Malnutrition Treatment of malnutrition

A

Infection - assume infection and give Abx. Phase 1 (Stabilisation) small volumes (total and per feed), frequent feeds, light/easy to digest and metabolise (oral whenever possible), may need nasogastric tube if not tolerating -> Transition phase -> Phase 2 (Rehabilitation) larger volumes (total and per feed), less frequent, nutrient dense

228
Q

Malnutrition Key concept CMAM

A

Community Management of Acute Malnutrition - provides improved access, higher coverage, less opportunity cost for parents in attending, and earlier intervention for affected children. Made possible by ready-to-use therapeutic foods that are locally made, acceptable, accordable with no preparation needed - can be given at home. Assisted by patient-held card with improved records, improved clinical care, and therefore information on previous treatment - includes weight, height, MUAC, target weight (85 & 90%), oedema, assessment of marasmus/kwashiorkor/moderate, treatment with vitamin A (x2), albendazole, and discharge weight

229
Q

Malnutrition Benefits of CMAM

A

Children: good for patients, prefer home treatment, decreased nosocomial infection, decreased AMR, decreased hospital costs, Carers: Prefer home treatment, time for other children, time for other home duties, earlier presentation, less absconders. Community: empower communities, improves impact, begins to address the root causes

230
Q

Paediatrics Top 5 causes of mortality in <5

A

Neonatal disorders, Pneumonia, Diarrhoeal diseases, Congenital defects, Malaria (next 5 = meningitis, malnutrition, STDs, whooping cough, measles)

231
Q

Paediatrics Issues in treating children

A

Major issue is resource allocation, O2 concentration, access to oxygen

232
Q

Paediatrics Oxygen delivery

A

Cylinder: produced in manufacturing plants, needs regular refilling, often means intermittent supply. Concentrators: extract nitrogen from air in the atmosphere to leave O2, done at the bedside, can supply up to 5 patients with flow splitters, need constant electricity, need cylinders as backup in case of power-cuts. Central piped O2 pied from large O2 source, but high cost, usually only in central hospitals

233
Q

Paediatrics Prioritisation of O2

A

Very high: central cyanosis, decreased conscious (PU), grunting with every breath, nasal flaring, severe palmer or conjunctival pallor, acute coma or convulsions >15 min. High: inability to drink or feed. Priority: severe chest indrawing, RR>=70, head nodding

234
Q

Paediatrics Parental mistrust of oxygen

A

In areas where oxygen supply is limited it is only given to the sickest children. These children tend to die at a higher rate than children not on oxygen. This leads to a common belief amongst parents that it is the oxygen that caused the death. This can be difficult to overcome. Strategies include: gentle discussion with a trusted healthcare professional from the same community, demonstrate O2 use on yourself, use of sats probe if available to show increase in oxygen levels in the blood

235
Q

Paediatrics TB Sx in children

A

Cough 2w, Night sweats 2w, loss of weight/failure to gain as expected

236
Q

Paediatrics TB Ix in children

A

CXR +/- other imaging if clinically indicated. Molecular WHO-recommended rapid diagnostic eg Xpert MTB/Rif, Xpert Ultra, LAMP, Trunat on sputum/induced sputum, early morning GA, Stool, NPA, Biopsy samples eg of LN, CSF if LP

237
Q

Paediatrics TB Rx in children

A

Non-severe: non-cavitatory, non-miliary PTB in one lung lobe, or peripheral LN TB or intrathoracic LN TB without airway obstruction, or simple TB pleural effusion. Rx 2HRZ[E]>2HR (SHINE Trial NEJM 2022)

238
Q

Paediatrics Contact tracing for children

A

All asymptomatic household contacts should be offered TPT. Children <5 and LMHIV particularly high risk are target populations for TPT - options are 6H, 3HR

239
Q

Paediatrics MDR Rx in children

A

Bedaquiline, delamonid, linezolid, levofloxacin, clofazimine BDLLfxC regimen (Need MDT discussion to treat MDR)

240
Q

Paediatrics MDR TPT in children

A

Levofloxacin

241
Q

Paediatrics Seizures in neonates

A

Sucking movements, moving hands (neonates have no purposeful movements),

242
Q

Paediatrics WHO Serious Bacterial infection in neonate

A

Fast breathing (RR>60), severe chest in-drawing, fever >38, hypothermia <35.5, no movement at all or movement only on stimulation, feeding poorly or not feeding at all, convulsions

243
Q

Paediatrics Ix and Mx of unwell neonates

A

Ix: BC, LP if safe, malaria RDT, BM if available. A: support if needed (neutral head position, chin lift), B: O2 (0.5-1L/min) via NP if seizing/resp distress and available, C: NG feeding EBM if not breastfeeding, D treat low BM (2-5ml/kg 10% dextrose IV or NG) phenobarbitone for seizures (then phenytoin or benzos if needed - benzos not first line as tendency for apnoea), E: keep warm - hat KMC. Phototherapy for jaundice if available - if not then transfer, if not possible, sunlight. IV Abx - go on local resistance pattern/local guidelines if available. If unknown Amp and gent, if meningitis concerns add 3rd gen cephalosporin

244
Q

Paediatrics Watery diarrhoea - three questions

A

Is the child severely malnourished? Is the child shocked? How dehydrated is the child?

245
Q

Paediatrics Diarrhoea, no dehydration

A

Signs not meeting some/severe dehydration: WHO treatment plan A ORS <1yo 50-100ml/loose stool >1yo 100-20ml/loose stool, zinc

246
Q

Paediatrics Diarrhoea, some dehydration

A

2 or more of: restless/irritable, sunken eyes, thirsty/drinks eagerly, skin pinch goes back slowly. WHO Treatment plan B: ORS in hospital over 4h, home if tolerates, zinc po, treat as 7.5% fluid deficit

247
Q

Paediatrics Diarrhoea, severe dehydration

A

2 or more of lethargy or unconsciousness, sunken eyes, unable to drink or drinks poorly, skin pinch goes back very slowly (>2sec). WHO Treatment Plan C: IV or NG rehydration (30ml/kg over 30-60min, then 70ml/kg over 2.5-5h + 5ml/kg/h ORS when tolerates oral). hospital admission, zinc po, treated as 10% fluid deficit

248
Q

Paediatrics Top 5 pathogens for acute watery diarrhoea

A

Rotavirus, Shigella, ST-ETEC, cryptosporidium and enteropathogenic E coli

249
Q

Paediatrics Fluid administration

A

Challenging in resource-limited settings: options: in-line burettes (not commonly found, cheap but single use). Drop rates: most common method ~20 drops/ml clear fluids, ~15 drops/ml blood. Issues: high risk of over/under hydration due to incorrect drip rates and lack of availability of paediatric size fluid bags. Alternatives: NG administration. Issues: placement checking (lack of pH strips/CXR availability), persistent vomiting, lack of absorption, aspiration risk, tolerability issues

250
Q

Paediatrics 4 general principles of diarrhoea and vomiting management

A

1 replace lost fluid and give extra for ongoing losses. 2 feed early and extra (only withhold food in initial fluid replacement phase), 3 zinc po 14d (though limited evidence, no evidence <6m) 4 advise when to return (worsening/fever/blood in stool/persistent diarrhoea)

251
Q

Paediatrics SAM management

A

Initial: hypoglycaemia, hypothermia, dehydration, stabilisation: electrolytes, infection, micronutrients (without iron), initiate feeding, sensory stimulation. Rehabilitation: Continue electrolytes, micronutrients (with iron), catch-up feeding, continue sensory stimulation, prepare for follow up

252
Q

Paediatrics Breast feeding in HIV

A

U does not equal U (promise study)

253
Q

Paediatrics HIV testing in infancy

A

<18m look for virus (DNA, p24 Ag) >18m EIA

254
Q

Paediatrics Starting ART in a young child

A

Screen for TB and other opportunistic infections and test/treat if present - delay ARVs for as short a time as possible (<2-8w) following TB/OI treatment commencement. Start ARVs according to national guidelines. Daily cotrimoxazole prophylaxis for all children <1y (older children if CD4 <25%/200 or WHO stage 2, 3, 4), TPT if TB contact and not concerned about active TB disease. Baseline bloods and CD4 count for monitoring purposes. Support parents and family.

255
Q

Paediatrics Diagnostic criteria for severe malaria

A

Clinical: prostration, confusion/agitation GCS<11, Coma (GCS<3 or Blantyre <3), respiratory distress (acidotic breathing), convulsions, shock (prolonged cap refill or sBP<80 in adults <70 in children, pulmonary oedema, abnormal bleeding, jaundice, anuria, repeated vomiting. Laboratory Hb <7 adults <5 children. Haemoglobuinuria, hypoglycaemia (BSL<2.2), acidosis, AKI, asexual parasitaemia >10% of infected RBCs)

256
Q

Paediatrics Sepsis red flags

A

Responds only to voice or pain/unresponsive, acute confusional state, sBP<90 (or drop >40), HR >130, RR>25, Need oxygen to keep SaO2>92%, non-blanching rash, mottled/ashen/cyanotic. Not passed urine in last 18h, UO<0.5ml/kg/h. Lactate >2, Recent chemotherapy

257
Q

Paediatrics Malaria RDT with recent treatment

A

Key point: RDTs can remain positive with recent malaria treatment. Fever and positive RDT within a few weeks of recent treatment (?reinfection ?treatment failure ?persistent antigen but no malaria (if using PfHRP2)). Need microscopy or LDH-based RDT. If current infection confirmed WHO suggests: <4w from previous infection - assume treatment failure, give 2nd line antimalarials. If >4w from previous infection - treat as new infection but consider different oral agent if available). If severely unwell and delay in getting microscopy/LDH RDT treat as severe malaria and other causes eg sepsis until results known

258
Q

Paediatrics Severe malaria

A

Malaria parasites in blood should be treated for malaria, but this doesn’t necessarily mean that the child has cerebral malaria (though you can also have cerebral malaria with low parasitaemias)

259
Q

Paediatrics Clinical test for cerebral malaria

A

Retinal fundoscopy: patchy retinal whitening, focal changes of vessel colour, retinal haemorrhages often white centred +/- papilloedema

260
Q

Paediatrics Malaria key point

A

Parasitaemia in endemic areas is common and not always causative. Post-mortem studies - up to 1/3 of children dying with presumed cerebral/severe malaria actually died from something else: most often bacterial infections. Malaria also increases the risk of serious bacterial infections, esp NTS. As it is mainly impossible to tell at the outset whether a seriously unwell child with positive RDT/film has severe/cerebral malaria or a serious bacterial infection you mostly need to treat for both. We desperately need point of care diagnostics that can accurately distinguish malaria vs bacteria vs viral causes of pathology

261
Q

Paediatrics Emergency management of septic child

A

A: Recovery position, airway adjuncts. B: O2 if available (coma/shock), C: IV access - RDT/film, BC, FBC (at minimum if available then BM, UE, LFT, Gas, G&S) - IV artesunate (if malaria), IV broad spectrum abx, maintenance fluids. D: treat for hypoglycaemia if BM unknown. E: antipyretics, LP when stable. Consider nutrition if prolonged coma

262
Q

Paediatrics Fluid boluses in children

A

Feast trial - 3.3% greater risk of 48h mortality with any bolus given

263
Q

Paediatrics Key messages

A

O2 use and prioritisation can be challenging. Fluids can be dangerous and need to be prescribed and administered carefully. Malaria parasitaemia is common in endemic areas and may not be why the child is unwell: treat it, but also investigate/treat other causes. Even healthcare that is free at point of access can have catastrophic indirect costs for families. Much of what we thin we know to be correct in medicine (particularly in paediatrics) has never been properly tested. Be curious, engage in research and advocate for the best possible evidence base for every patient you see!

264
Q

Paediatrics URTI not pneumonia

A

Cough. No Ix (consider malaria RDT if febrile in endemic area +/- opportunistic HIV test). Management: home, conservative, check weight, immunisations and deworming. Advise when to return, follow up in 5 days if not improving

265
Q

Paediatrics Some pneumonia

A

Cough & tachypnoea, some mild chest indrawing allowed. No Ix (consider malaria RDT if febrile in endemic area +/- opportunistic HIV test). Management: home, oral abx, check weight, immunisations, deworming, advise when to return, follow up in 3 days

266
Q

Paediatrics Severe pneumonia

A

Cough & tachypnoea + danger sign (severe resp distress, grunting, severe chest indrawing, SaO2<90 on air or central cyanosis, inability to feed/drink, reduced consciousness/lethargy/convulsions). Ix Consider CXR, BSL if reduced conscious/convulsions, SaO2 if available. Management: admit, O2 therapy if known low sats, central cyanosis or severe resp distress, IV Abx, Care with fluid balance. Antipyretics if child distressed, bronchodilators if wheeze.

267
Q

Paediatrics Global

A

Brandt line, best term is ‘low-resource settings’ (do not use third world. Terms out of vogue include global south, developing, low-income countries). Consider equity

268
Q

Paediatrics Equity in Child and adolescent health

A

Repercussions of early childhood inequities are far reaching and long lasting. Focus on equity in policy formulation and programme implementation. Use data to target interventions towards undeserved groups. Remove access barriers (cost, availability, distance) through targeted outreach, mobile services, removing user fees, support for child health workers. Address socioeconomic determinants through multisectoral action (eg female education), cash transfers

269
Q

Paediatrics Interventions in child health: what has worked in 1-59 months

A

Multiple disease-specific and integrated interventions: HIV/malaria prevention and treatment, expanded vaccination IMCI (integrated management of childhood illness) (ETAT is used for inpatients). Investment in health systems: free/subsidised healthcare for mothers and young children, training CHW for prevention and basic care, infrastructure, equipment, supply chains, quality standards, data availability and use. Cross-sectoral collaboration addressing malnutrition, water and sanitation, income. Governance: Sustained, high-level political commitment, stakeholder involvement, partner coordination.

270
Q

Paediatrics Children 5-9: a neglected population

A

Focus on prevention: this age group is ideal for health interventions due to increased independence and lifestyle habit development, Scheduled well child visits: ensuring scheduled health contacts for older children is key, as they are less likely to seek care when critically ill. Interventions with potential: priority interventions for children aged 5-9 include school feeding, micronutrient supplementation, health education, vision screening, deworming, mass drug administration for trachoma, vaccine catch-up and mental health support, Delivery platforms: primary care services and outreach, schools and childcare centres, home and community platforms, child and social protection services, digital platforms

271
Q

Paediatrics Adolescent strategies

A

Integrated approach: NCDs, mental health, injuries, sexual and reproductive health, nutrition, communicable disease and wider determinants. Strengthening health systems and multisectoral work (horizontal rather than vertical approaches)

272
Q

Paediatrics Early childhood development

A

Nourished, stimulated, safe, secure and loved

273
Q

Paediatrics The global strategy for women’s, children’s and adolescent’s health

A

Survive (end preventable deaths), thrive (ensure health and wellbeing), transform (expand enabling environments)

274
Q

Paediatrics Vaccines save lives

A

Polio vaccines and eradication. DTP vaccines (83% coverage), MMR vaccines and ongoing measles outbreaks. MenAfriVac and African Meningitis Belt, HPV vaccines and cancer prevention. Money vs disease burden (rotavirus), Political commitment to invest in vaccines. War and Civil unrest. International commitment: GATES and PATH

275
Q

Paediatrics Vaccination during pregnancy

A

90% protection against pertussis disease and 97% protection against death from pertussis in the first 2 months of life. The acellular pertussis however does not stop infection, it just minimises the illness

276
Q

Child Sexual Violence Epidemiology

A

1 in 3 women will experience physical and/or sexual violence by a partner or sexual violence by a non-partner. Child sexual abuse 20% of girls (5% raped), female genital mutilation ‘FGM’ 125 million, forced early marriage 60 million

277
Q

Child Sexual Violence Reporting of childhood sexual abuse

A

2/3 of those who experienced sexual abuse before 18y told someone in authority about it…fewer than 10% received professional services

278
Q

Child Sexual Violence One-stop centre services

A

Clinical officers/doctors trained in diagnosis of CSA, services for women and children, 24/7 access to PEP/VCT/EC, social worker/community child protection worker - ensure place of safety, police victim support, volunteer led child trauma counselling

279
Q

Child Sexual Violence Cultural and societal norms that perpetuate sexual abuse

A

Patriarchal systems, initiation ceremonies, victim blaming, limited education, normalisation of violence, corruption and impunity, silence and stigma, societal hierarchies

280
Q

Child Sexual Violence Support and Challenges

A

Support: comfort, listen, letting them know they are believed, helping them make informed decisions, exploring coping mechanisms, building family and community supports - these enhance ability of survivor to cope and prevent the distress from developing into serious mental illness. Challenges: limited staffing resources, insufficient education on trauma-informed care and survivor-centred approach, difficulty establishing trust, long process for survivors to get help, societal attitudes (personal biases) affecting support, empathy fatigue, perpetrator and survivor close relationships

281
Q

Prescribing Pregnancy key considerations

A

Which trimester, duration of therapy, is treatment necessary, is the drug orally absorbed, can another route be used, what is the likely duration of exposure, is anticipated effect known and measurable, can effects of the drug be safely monitored?

282
Q

Prescribing Altered pharmacokinetics in pregnancy

A

Absorption: reduced gut motility, increased lung function, increased skin blood circulation. Distribution: increased plasma volume, body water, and fat deposition affecting volume of distribution. Protein binding - decreased plasma proteins. Metabolism: hepatic enzyme activity could be increased (maternal hormones). Excretion: increased glomerular filtration rate, gastric motility reduced.

283
Q

Prescribing Breastfeeding key considerations

A

Distinct from medicines use in pregnancy, most medicines are unlicensed for use in breastfeeding, information is sparse on the effects so often prefer older medicines that have more data (observational), ensure you know how to give the information and whoever receives it to repeat what you said. The benefits of breastfeeding and maternal bonding. Drugs licensed for use in children unlikely to be a problem, avoid breastfeeding only if there is no suitable alternative drug. Where possible use drugs and dosing regimens that will minimise infant exposure. Monitor infant - especially if premature

284
Q

Prescribing Breastfeeding how to minimise exposure

A

Withhold or delay therapy if possible, use a drug with poor penetration into milk, use an alternative route of administration, avoid nursing at peak drug concentrations, give drug before infant’s longest sleep, as a last resort - ‘pump and dump’ milk if short courses or discontinue breastfeeding - needs to be individualised

285
Q

Prescribing Pregnancy and breastfeeding

A

Before initiating anything ensure patient is aware of risks. Mitigate where possible - delay/withhold if therapy known to cause problems. Do not suggest patient stops taking regular medication before checking first. Vitamin D supplementation is currently recommended within the first weeks after birth and during breastfeeding - but incurred cost does not support its use for all breastfed term infants.

286
Q

Prescribing TB treatment in pregnancy

A

Risk of TB to mother and child outweighs risk to treatment. First line anti TB drugs cross the placenta but do not appear to be harmful. Second-line anti TB drugs more risky, avoid streptomycin (ototoxic to fetus). Continue breastfeeding (low concentrations of anti-TB drugs present)

287
Q

Prescribing Malaria in pregnancy

A

Risk to mother: severe malaria, maternal anaemia. Risk to infant: spontaneous abortion, stillbirth, prematurity, low birthweight - important risk factor for infant mortality, stunting and later life course impacts

288
Q

Prescribing Intermittent preventive treatment of malaria in pregnancy

A

In malaria-endemic areas, pregnant women of all gravidities should be given antimalarial medicine at predetermined intervals to reduce disease burden in pregnancy and adverse pregnancy and birth outcomes. Sulfadoxine-pyrimethamine (SP) has been widely used for malaria chemoprevention during pregnancy. Start in second trimester and give three doses at least one month apart

289
Q

Prescribing Malaria treatment in the first trimester of pregnancy

A

Pregnant women with uncomplicated P falciparum malaria should be treated with artemether-lumefantrine during the first trimester

290
Q

Prescribing Severe Malaria treatment in pregnancy

A

Artesunate in all trimesters. Once a patient has received at least 24h of parenteral therapy and can tolerate oral therapy, treatment should be completed with 3 days of an ACT. Same as in non-pregnant population

291
Q

Prescribing Pregnancy and breastfeeding

A

1 Weigh up risks and benefits to mother and fetus - try to keep duration short, ensure good adherence. 2 For pregnant women with active TB, same treatment as in non-pregnant population except avoid streptomycin and the safety of pyrazinamide in fetus unknown. 3 For pregnant women with malaria same treatment as in non-pregnant population except avoid primaquine and doxycycline

292
Q

Prescribing Paediatric definitions

A

Neonate 0-28d, Infant 1-12m, Toddler 1-3y, Child 4-12y, Adolescent 13-19y

293
Q

Prescribing Pharmacokinetics

A

Body water and fat content change, gastric pH is high at birth with reduced peristalsis in first 6m and reduced bile production. Neonates have immature skin barrier - large surface area relative to body weight and well hydrated skin = increased systemic absorption more likely (NB excipients eg alcohol content - can cause burns - steroid creams - systemic absorption). Rectal absorption is highly vascular and most of the dose will bypass first pass metabolism but may not be acceptable. Muscle mass low in neonates and infants IM administration may have unpredictable absorption due to reduced/variable blood flow. Use the Schwartz formula in children and young people to calculate renal function - renal excretion is dependent on gestational age, reduced in babies compared to adults, clearance of renally excreted medicines is prolonged in infants.

294
Q

Prescribing Paediatric key considerations

A

Are antimicrobials essential, likely organism, local sensitivities, where do they need to act, how quickly, side effects, allergies, interactions, vaccines

295
Q

Prescribing Paediatric creative administration

A

Crushing dispersing tablets (this renders them unlicensed, but is common practice), alternate routes, administration with/in food-check pharmacokinetics, pill swallowing techniques, play, ownership, don’t assume liquids are always the best option - taste/volume/excipients/preference, dose rounding (+/- ~10%). Counselling - individualised approach, concrete vs abstract thinking with teenagers - do not use ultimatums, understand barriers - timing/school - understanding/reluctance to give, pill size, volume, measurable doses

296
Q

Prescribing Paediatric licensing and drug trials

A

Difficult to complete trials on children (recruitment/retention), older drugs may not have originally done trials in children, but some have since extended licensing, new drugs must have clinical trials in paeds. >12y and >40kg physiologically ~adult

297
Q

Prescribing Paediatric difference in LMIC settings

A

Different spectrum of infections and drug resistance, different comorbidities, different treatment seeking and other cultural differences, fewer resources (access to medicines, tests, staff and experience), different use of drugs, intermittent/seasonal prophylaxis

298
Q

Migrant Children Why?

A

Country of origin: poverty, war, conflict, genocide, drought, famine, disrupted healthcare. Journey: exposure, risk, poor sanitation, crowding, poor nutrition, sexual violence. Destination: language barrier, cultural barriers, fear of authority, overcrowding

299
Q

Migrant Children Asymptomatic screening

A

Stool: OCP microscopy, Giardia PCR. Bloods: FBC (anaemia, eosinophilia), LFTs (in case needs TB Rx), Vit D, IGRA, Serology HBV/HCV/HIV/Syph, Schisto & Strongy. Urine NAAT NG/CT. Recommendation: panel-based approach with additional tailoring based on significant population determinants - there are issues with unpicking exposures due to stigma and people may not tell you everything. If in a setting without ability to test, may be safer and quicker to give empiric albendazole & praziquantel. Often good model of care is to see family groups

300
Q

Migrant Children Asymptomatic rate

A

TB 18%, Parasites 7-10%, BBV 3% (mostly HBV), Schisto 12% Does it matter? Yes - there is a lifetime risk unless you do something about it (plus the public health implications)

301
Q

Migrant Children Holistic models of care

A

Mental health, hearing and vision health, physical health, oral health, social, safeguarding, sexual and reproductive health, preventive medicine

302
Q

Migrant Children Maslow’s hierarchy of needs

A

Physiological needs: air, water, food, shelter, sleep, clothing, reproduction. Safety needs: personal security, employment, resources, health, property. Love and belonging: friendship, intimacy, family, sense of connection. Esteem: respect, self-esteem, status, recognition, strength, freedom. Self-actualisation: desire to become the most that one can be

303
Q

Paediatrics TB meningitis Rx

A

Control seizures, train to take pills. Manage ICP, steroids (high dose then wean). TB Rx: 2HRZ + fourth agent (streptomycin or levofloxacin) > 7-10HR. Note WHO 2021 allowed for 6m regimen of HRZ + ethionamide in children (Sth Africa have adopted this, UK cannot access ethionamide)

304
Q

Paediatrics Neurocysticercosis Rx

A

Control seizures, train to take pills. Manage ICP, steroids (high dose then wean). Albendazole 15mg/kg for 10-14d + praziquantel 50mg/kg if >2 viable cysts. No antihelminthics if lots of oedema/raised ICP. MUST have ophthalmological assessment for eye involvement BEFORE starting treatment (risk of blindness with degenerating active cysts)

305
Q

Paediatrics Multiple neurological lesions

A

The differentials for cerebral ring enhancing lesions are broad and diagnosis can be challenging particularly in kids: make friends with a neuroradiologist. Tuberculomas and neurocysticercomas are often classically silent until seizures. Sometimes treatment needs to be presumptive or brain biopsies are required. IGRA/Mantoux can be negative in active TB: IGRAs perform poorly in young children. Care with ethambutol in kids with TBM as difficult to monitor optic neuritis. Treatment duration for TBM in kids is debated - SURE trial ongoing! Poor evidence for treatments (duration, steroids etc) in tuberculomas specifically. Serology in children with single/calcified neurocysticerci has low sensitivity

306
Q

Paediatrics Dengue in children

A

Often mild/asymptomatic. Febrile phase (fever, rash, retroorbital pain, arthralgia, positive torniquet test). Critical phase (plasma leak, risk of bleeding, shock, commoner in children and more common with second infection or infants 6-12m). Recovery phase: can get prolonged fatigue. Complications: liver failure, CNS involvement, myocardial dysfunction, retinal vasculitis, HLH. Management supportive, WHO stepwise criteria, careful fluid management. Prevention: bite reduction, vaccine

307
Q

Paediatrics Dengue warning signs

A

Abdominal pain or tenderness, persisting vomiting, clinical fluid accumulation, mucosal bleed, lethargy/restlessness, liver enlargement >2cm, increased HCT with rapidly decreased Plt

308
Q

Paediatrics Bartonella

A

Intracellular, Transmission through bite of scratch from infected cat, exposure to cat fleas of infected cats. Global distribution. Incubation 3-10d, 7-60d for lymphadenopathy. Most commonly localised cutaneous/LN infection (85-90%), PUO, disseminated disease (liver, spleen, eye, CNS), complications: neuroretinitis, encephalopathy, transverse myelitis, osteomyelitis, endocarditis. Diagnosis: IgG most useful with convalescent serology, PCR, culture, histopathology. IgM unreliable. Treatment: localised disease mostly self-resolving, or 5d azithro. Disseminated: Rif/azithro 2-3w, Neuroretinitis - doxy plus azithro (risk benefit conversation about doxy use in childhood - <3 weeks is generally ok)

309
Q

Paediatrics Management approach

A

Always consider ABCDE and isolation in parallel to clinical management and public health notification. Always consider the need to cover for multiple pathogens concurrently

310
Q

Paediatrics Mpox in children

A

Orthopox, Transmission: contact with lesions, resp droplets (prolonged face to face) and fomites. Sexual. Incubation 5-21d, infectious 4d prior to symptoms and until all lesions epithelialised. Clinical manifestations: fever, flu-like sx, lymphadenopathy, centrifugal maculopapular rash after 3d - spreads all over body including palms, soles, vesicles, pustules. Complications: encephalitis, pneumonitis, conjunctivitis, secondary bacterial infections. CFR 0-11% (endemic areas). Pregnant women - fetal loss. Diagnosis: PCR from vesicle fluid/respiratory samples/blood. Treatment options: supportive, tecovirimat, brincidofovir, cidofovir. Vaccine: 3rd gen MVB-BA not currently licensed for pregnant women or children - though data from UK in children reported good safety and tolerability.

311
Q

Paediatrics Mpox epidemiology

A

First identified DRC 1970, first reported outside Africa in US in 2003 with sporadic travel associated clusters in countries outside Africa. May 2022 multicountry outbreak of Mpox declared - majority of cases in MSM community (Clade Iib >100,000 >500 children (<1%). September 2023 outbreak of new subclade (Ib) in DRC - sustained human to human transmission. Upsurge in reported cases in DRC, plus transmission to neighbouring countries for the first time - August 2024 WHO declared PHEIC. Clade I Mpox reported to have higher case fatality than Clade II and remains a high consequence infectious disease in the UK. Currently only a few sporadic case of Clade I Mpox outside Africa

312
Q

Paediatrics HCID

A

High consequence infectious disease - always need to think about it! Remember travel history - including close contacts. Evolving situation - check up to date government websites. Isolate - side room, minimise contacts, log on door, family group etc. PPE, sampling, know who to call - local infection team/microbiology, paediatric ID team, Imported Fever Service

313
Q

Paediatrics Congenital syphilis

A

Clinical features <2y present by 3m of life, majority asymptomatic at birth, hepatosplenomegaly and cholestatic jaundice, nasal discharge, rash (palms and soles), condylomata lata, lymphadenopathy, skeletal abnormalities. >2y facial features: frontal bossing, saddle nose, eyes: interstitial keratitis, optic atrophy, keratitis, sensorineural hearing loss, dental abnormalities, palatal perforation, skin: gummas, perioral fissures, CNS: hydrocephalus, CN palsy, learning difficulties, skeletal: saber shins, painless arthritis, paroxysmal cold haemoglobinuria. Key investigations: LP including VDRL and PCR, neuroimaging, imaging of other bones, audiology, ophthalmology review, HIV/HBV/HCV, STI screening and treatment for parents. Treatment procaine penicillin or benzylpenicillin 10d course if symptoms or abnormal Ix

314
Q

Paediatrics HEEADSSS assessment

A

Home, Education, Employment, Eating, Activities, Drugs/Alcohol, Sexuality, Self-harm, Suicide, Safety

315
Q

Paediatrics SSHADES

A

Strengths, School, Home, Activities, Drugs/Substance Use, Emotions/Eating/Depression, Sexuality, Safety

316
Q

Adolescent Jaundice

A

Unconjugated: haemolytic anaemias, Gilberts, Crigler-Najjar. Conjugated: Viral (HAV HBV HCV HDV HEV EBV CMV EBV) Metabolic (Wilsons, alpha1 antitrypsin, CF) Biliary (stones, cholecystitis, choledochal cyst, sclerosing cholangitis) Autoimmune liver disease (type 1 antiSM Ab, type 2 anti-LKM Ab) Hepatotoxins (drugs eg COCP, antiTB, paracetamol, alcohol, organophosphates) Vascular (Budd-Chiari, Venoocclusive disease)

317
Q

Adolescent Prevention

A

1 Vaccination HAV HBV HPV Mpox MenB 2 PrEP PEPSE 3 Condoms 4 DoxyPEP. PEPSE = post-exposure prophylaxis after sexual encounter

318
Q

Adolescent Impact of HIV on the developing brain

A

Infantile HIV encephalopathy, speech and language delay, behavioural difficulties, learning difficulties, mental health. Perinatally acquired HIV: neurotropic virus, chronic inflammation, previous CNS infections, complex psychosocial/family circumstances, antiretrovirals, in utero drug exposure, prematurity, malnutrition

319
Q

Adolescent Morbidity of PaHIV (even with viral suppression)

A

Emerging PaHIV data in adult life (even with viral suppression) - increased risk of CVS, metabolic syndrome, DM2, chronic lung disease, malignancy (lymphoma, cervical, HCC, KS)

320
Q

Adolescent Supporting adherence in young adults

A

Non-judgmental MDT adherence support, ART. Stigma (in healthcare, in families, in relationships) -> 25% MH diagnosis, 50% parental loss, 33% learning difficulties -> poor adherence, LTFU -> HIV associated morbidity onward transmission

321
Q

Paediatrics Cutaneous Leishmania

A

LL infantum, transmission Sandfly (dusk-dawn biters), Incubation weeks-months. Clinical manifestations: papule>nodule>plaque>ulcer (painless, indurated). Single or multiple +/- regional lymphadenopathy. Typically on exposed skin. Often in normal hosts. Diagnosis: Punch biopsy or skin scapings. Histology, PCR +/- culture. Treatment options: Nothing, intralesional cryotherapy, intralesional stibogluconate (painful), topical paromomycin systemic ambisome or antimonials, especially if multiple, risk of dissemination or risk of mucosal leishmaniasis. Follow up: can reactivate or relapse (usually within 1 year but also with future immunosuppression eg chemotherapy, chronic steroids, when it can disseminate). Having CL doesn’t imply VL esp if immunocompetent

322
Q

Paediatrics Typhoid

A

Epi: Most UK cases acquired overseas esp Pakistan, India, Bangladesh. Children 30%, XDR Pakistan, Incubation 7-21d. Clinical: fever +/- rigors (often prolonged), GI symptoms (pain, diarrhoea, constipation), myalgia, arthralgia, cough, headache, delirium/drowsiness, rose spots, hepatosplenomegaly (up to 37% in non-endemic, 90% in endemic). Ix: Serial BC, routine susceptibilities and WGS, stool cultures, full infection screen (eg malaria), FBC, EUC< LFT, CRP, Treatment: non-XDR endemic, uncomplicated oral Azith 7d, complicated CRO 7-10d.. XDR endemic, uncomplicated oral Azith 7d, complicated Mero 10d + azith. Public Health Notification

323
Q

Paediatrics Histoplasmosis

A

Clinical: subacute pulmonary infection, incubation 3-21d, mild symptoms: fever, headache, myalgia, anorexia, cough and chest pain, disseminated in immunocompromised. Treatment: prolonged antifungal therapy - itraconazole, if disseminated/unwell/immunocompromised - amphotericin B

324
Q

Paediatrics Congenital malaria

A

RF: Pf>Pv>others. First pregnancy (high transmission areas), placenta or cord blood film+, Clinical: presents at 2-8w, fever, poor feeding, D&V, irritability, splenomegaly, thrombocytopaenia, anaemia, raised bilirubin. Ix: Cord blood film & RDT, Placenta; histo for parasites, at birth and weekly for 4 weeks: film, RDT, FBC, clinical review. Treatment: admit, artemisinin combination therapy (ACT) if severe IV artesunate

325
Q

Paediatrics Adolescent HIV key points

A

Up to 10% of HIV vertically infected infants who are undiagnosed and untreated will reach adolescence - slow progressors. Appearances can be deceptive - always test for HIV. Close follow up and monitoring for side effects/OI/IRIS essential in early stages. Differences in HIV management between high and low income and HIV endemic and non-endemic centres. Resources for paediatric HIV: CHIVA, Penta, PVC

326
Q

Paediatrics Melioidosis

A

Burkholderia pseudomallei, Transmission: percutaneous from soil and haematogenous spread, inhalation during severe storms, ingestion of contaminated water in some areas. Distribution: endemic in SE Asia, South Asia, China and Northern Australia. Most cases from Thailand, Malaysia, Singapore and Northern Australia. Sporadic elsewhere. Reports of environmental transmission outside endemic areas from aromatherapy spray and tropical fish. Incubation: usually 1-21d but can establish latency analogous to TB, longest documented time from travel to endemic area and disease is 29y. Clinical manifestations: pneumonia, bacteraemia, skin infections, parotitis, GU infections, less often BJI and neurological. Diagnosis: microscopy and culture of fluid (blood, sputum, BAL, pus, urine etc), cultures on standard media, Ashdown’s is selective for it +/- MALDI-ToF/PCR). Treatment IV Ceftazidime (or a carbapenem) for 14d, then high dose cotrimoxazole for 3-6 months. Follow up: monitor for relapses, low threshold for ceftazidime if future severe pneumonia/sepsis. Melioidosis occurs much less commonly in children than adults (5% of all cases <15y), less often associated with underlying immunodeficiencies and comorbidities (diabetes, CKD, EtOH). More likely to be localised/cutaneous presentation (46% of cases), less likely to be bacteraemic. Lower mortality rate (outside the neonatal period). Guidelines for an oral-only approach (3/12 high dose cotrimoxazole with folic acid) without an IV intensification phase for cutaneous disease if systemic spread has been ruled out (US abdomen, CXR and baseline bloos). Non-evidence based. Need to ensure adherence and follow up

327
Q

Paediatrics Melioid lab exposure

A

B pseudomallei is a hazard group 3 pathogen, ideally should be handled in biosafety level 3 facility in a biosafety cabinet. Some case reports of laboratory acquisition, though appears rare in practice. Risk assessment: prophylaxis for high-risk lab exposure (aerosol, needlestick, splash to mucus membrane) or high risk person (comorbidities) - 3 weeks of SXT or Amox/Clav, take serology on D1 and repeat at 2, 4, 5 weeks. If seroconverts then 3/12 PEP

328
Q

NTD Onchocerciasis (River blindness)

A

Transmitted by biting insect, live in nodule, microfilaria live in skin and eyes. Ivermectin kill microfilaria but ton the adult worm - have to treat for 15y to eradicate from human. Diagnosis by skin snip in saline, review 1h later to see microfilaria. Elimination target = prevalence <0.1% in children, with absence of infective larvae in vector population (<1 infected blackfly per 2000 - need to test 6000). In Loa loa endemic areas - use LoaScope mobile-phone based video microscope to count L loa microfilariae in peripheral blood collected in capillary tube

329
Q

NTD Leprosy campaign pros and cons

A

Target <1 case per 10,000 at global level - with new target of zero grade 2 disability among paediatric leprosy patients, reduction of new leprosy cases with G2D to <1 per million population, confirmed absence of children with leprosy for 5 consecutive years, and zero countries with legislation allowing discrimination on basis of leprosy. Positive outcomes: commitment by governments/donors, simplified diagnosis. Negative outcomes: attempts to meet targets led to underreporting, case definition changed, shortage of drugs, funding and trained staff once target achieved, and transmission continues (esp in India)

330
Q

NTD WHO 2030 roadmap targets

A

90% reduction in the number of people requiring interventions against NTDs. Global eradication aim: Guinea worm, Yaws. Elimination: HAT T gambiense from 15 countries, Leprosy from 120 countries, Onchocerciasis from 12 countries. Elimination as a public health problem: Trachoma (already met), Lymphatic filariasis (80% have met), VL (64 countries have met target <1% CFR), Others: STH, Chagas, Rabies (zero human deaths), HAT T rhodesiense, Schisto

331
Q

NTD Integrated models

A

Move away from siloed care - put all skin diseases together -

332
Q

NTD Skin NTDs

A

Yaws, Leprosy, Onchocerciasis, Lymphatic filariasis, Buruli ulcer, Cutaneous leishmaniasis, Mycetoma/chromoblastomycosis, Post kala-azar dermal leishmaniasis, Scabies, Tungiasis

333
Q

Podoconiosis Key messages

A

Podoconiosis is not infectious - no organism is responsible. Diagnosis uses a panel approach rather than single POCT, it is treatable using simple lymphoedema management package, for which patients can take responsibility. Treatment brings radical improvement in quality of life for stigmatised and marginalised people. Preventable by avoiding contact with irritant soil, primarily by wearing shoes - but needs to be with a package of education and sustainable shoe sources. Elimination is possible through behaviour change and accessible treatment

334
Q

Podoconiosis Epidemiology

A

Subsistence farming communities, prolonged exposure of barefeet to soil. 17 countries, 12 in Africa, others include India, Sth America, Indonesia. Triggered by combination of factors: exposure to irritant soil, genetic susceptibility and foot vulnerability (lack of shoes, hygiene). Tend to be >1500m above sea level (LF <1000m)

335
Q

Podoconiosis Clinical

A

Commonly confused with lymphatic filariasis. Bilateral in 87%. Early signs: itching, burning, splaying of forefeet, reversible plantar oedema, hyperkeratosis. Late signs: persistent oedema, interdigital maceration, nodules, waterbag or fibrotic swelling. Differential diagnoses: LF, onchocerciasis, leprosy and protein-energy malnutrition in children. Clinical staging 1 reversible overnight, 2 below knee not completely reversible overnight (below ankle), 3 as for 2 but present above ankle, 4 Above knee, 5 joint fixation, swelling at any place in the foot or leg (different from Dreyer staging for LF)

336
Q

Podoconiosis Complications

A

Acute episodes characterised by malaise, fever, chills, diffuse inflammation and swelling of the limb, lymphangitis, adenitis and skin peeling - requires analgesia, fluids, antibiotics, rest and elevation - during acute episodes do not exercise, put anything warm or hot on skin, open or cut blister, bandage leg, rub anything into the skin or use scarification - these will exacerbate the attack

337
Q

Podoconiosis Management

A

Hygiene, Skin care, bandaging, elevation and exercise, footwear

338
Q

Noma Epidemiology

A

Burden not well understood or described. Disease known for over 1000 years, 1994 declared PH problem, 140,000 estimated new cases per annum. No proven risk factors, but likely to be a combination of chronic malnutrition, comorbidities (recent measles, probably malaria), lack of access to quality health care including childhood vaccines, not being breastfed, poor oral hygiene practices, low SES, high number of previous pregnancies in the mother. Noma Children’s Hospital run by Nigerian MoH - care for noma sequela - blocks of 30-35pt have surgery and then rehabilitation, occurs 3-4 times per year

339
Q

Noma Clinical

A

Rapidly acting orofacial gangrene, reportedly 90% mortality if untreated - rapid progression within 2-3 weeks. Mostly affects children aged 2-5y, very occasionally adults with advanced HIV or lymphoma. Minimal research available Reversible stages: 0 Simple gingivitis (warning sign, Rx high protein diet, good oral hygiene, chlorhex mouth wash) 1 Acute necrotising gingivitis (admit, amox/clav and metro plus malnutrition management) 2 Oedema (IV Amox/Clav, Metro, Gent, Vitamin A (helps mucosa), improve nutrition), Irreversible stages: 3 Gangrene (Debridement, IV Amox/Clav Metro, Gent) 4 Scarring (if survive gangrene - only 10% survive to this point) 5 Sequela (stigma, poor oral opening, loss of teeth, inability to eat or talk easily, lots shunned within community - surgical intervention is the only way of improving quality of life)

340
Q

Noma Differential diagnosis

A

Tooth abscess, cellulitis, animal bites, burn injuries, syphilis, yaws, buruli ulcer, leprosy, oral cancer, chemical burns and burns in general. Distinguishing factors of noma: face, age (2-5), fetid odour, short time frame, well demarcated perimeter, comorbidity. Rapid destruction of tissue is typical of noma

341
Q

Noma Treatment

A

Antibiotics, wound debridement, nutritional support, reconstructive surgery, physiotherapy (backbone of care and not available in most settings), psychosocial support

342
Q

Paediatrics ETAT

A

Emergency Triage Assessment and Treat. SSSS-ABCD Safe, Stimulate, Shout for help, Setting (what is available). Airway Breathing Circulation Disability

343
Q

Paediatrics ETAT Airway

A

Suction, Airway opening manoeuvres, Airway adjuncts

344
Q

Paediatrics ETAT Breathing

A

Look, listen, feel, if absent/inadequate give 5 breaths with bag-valve mask

345
Q

Paediatrics ETAT Circulation

A

Feel large artery, Dehydration (cap refill, skin turgor) Malnutrition (MUAC, buttock wasting, oedema), Anaemia (compare parent and child palmar pallor). FEAST Trial demonstrated worse outcome in fluid bolus. Dehydration 30ml/kg over 30-60min then 70ml/kg over 2-4h. Malnutrition 10ml/kg/hr 5%D, Anaemia 10ml/kg/h PRBC

346
Q

Paediatrics ETAT Disability

A

BSL, AVPU, Seizure Mx (Benzo in paeds - although in reality, whatever you have…)

347
Q

Decolonising Colonial remnants

A

Practice that reinforces an imbalanced power structure, institutional rules that further concentrate power among the wealthy and influential. Assumption that resource-limited sector lacks the capacity to solve its own health problems. Manifests as power imbalance, top-down priority setting, verticalisation of intervention (disrupting an existing structure) with disregard for local culture and staff

348
Q

Decolonising Local solutions to local problems

A

Task shifting - limited doctors, pharmacists, use community to dispense medications. Integrated approach - HIV and NCD, context-based approaches. Simplification of treatment - difficult to manage at primary health centre - started concept of simplified treatment in terms of monitoring and follow up

349
Q

Travel Medicine Definition

A

Multidisciplinary subspecialty committed to the prevention and management of health problems and risk associated with international travel and travellers. People, diseases, wildlife and other threats cross borders

350
Q

Travel Medicine Epidemiology

A

Diverse group - older, younger, comorbidities, immunosuppressed, PSAR. Changing disease patterns in over 220 countries. Preventive/therapeutic interventions change. Limited evidence base. National and international guidelines differ. Understanding and communicating risk. May find cost of interventions prohibitive. Those that travel go to more remote/exotic locales, do more ‘risky things’ while abroad, may not seek advice, don’t do what they say they will and have their own perception and tolerance of risk. >95% of travel associated illness is not preventable

351
Q

Travel Medicine Approach - person

A

Who is this person? Risk thresholds are important. Causes of severe morbidity in travellers: associated with pre-existing medical condition, identifiable pre-travel, the added risk of pre-existing conditions is difficult to quantify, particularly affects the older traveller. Risk assessment reflects the health risks and not the interventions available, is it common, treatable/avoidable and/or potentially fatal, individual risk threshold, evidence not perception or intuition

352
Q

Travel Medicine Approach - place

A

What do they plan to do, where and with whom? Visiting friends and relatives, travellers/expats, business/migration etc. Where in the country? Spectrum of disease vs place of exposure is important and not everywhere in one country will have the same exposure risks

353
Q

Travel Medicine Approach - time

A

How long are they going for, what is the season

354
Q

Travel Medicine Interventions

A

Malaria prevention, vaccines, non-vaccine preventable infections. Other: sexual health/altitude/DVT/trauma/security/insurance, patient education

355
Q

Travel Medicine Consultation

A

Patient’s agenda, Clinician’s agenda, Negotiate agenda and clarify boundaries. Ask before advise - ask permission to discuss, ask what the patient thinks about their health, ask questions to find out what they already know, tell patient information in a way that is easy to understand, gauge the patient’s understanding. People like numbers for risk assessment - MedRA can assist in risk ratio.

356
Q

Travel Medicine Pregnancy

A

T1 concern for mother: miscarriage, ectopic, bleeding, retained products, N&V, DVT, infection. T2 concern for mother: congenital abnormalities, anaemia, DVT, gestational diabetes, hypertension, infection T3 concern for mother and baby: premature labour, stillbirth, post partum haemorrhage, DVT, hypertension, pre-eclampsia, infection. Mitigation of risks of above (include early USS - heart beat reduces miscarriage to <5%), and consider malaria, vaccines, travel specific infections, insurance, other

357
Q

Travel Medicine DVT risks

A

Pregnancy (conception to 6w pp). Flights/journeys >4h, older age, previous clot, family history, additional clotting disorder, obesity, severe oedema, immobility, other medical conditions. Risk reduction: compression stockings, hydration, mobilisation, aisle seat, no EtOH or sleeping medication. Low molecular weight heparin safe in pregnancy

358
Q

Travel Medicine Vaccines during pregnancy

A

Pertussis, RSV, flu and COVID. No evidence of harm from inactivated vaccines. Live - balance risk vs theoretical fetal harm. Inadvertent vaccine administration is never an indication for termination.

359
Q

Travel Medicine Pregnancy infections and travel

A

UTI, GI, Resp, Listeria, Malaria, Arboviral, Hep A/E, Toxo, AMR

360
Q

Travel Medicine Travel key points

A

Risk assessment and risk benefit are unique to each traveller and should be evidence based where possible. Shared decision making is essential, especially where evidence is lacking. Exacerbation/complications of chronic illness and motor vehicle accidents are the leading causes of death and severe disability. Promoting/changing behaviour requires effective communication and skill, but has not been proven effective.

361
Q

Travel Vaccinations Inactivated vaccines

A

Safe, less robust immune response, multiple doses often needed. Waning immunity. Include: pneumococcus, IPV, hepatitis, DTP, typhoid

362
Q

Travel Vaccinations Live-attenuated vaccines

A

Robust immune response, often lifelong immunity but potential vaccine-derived infections. Include: MMR, YF, OPV, Zoster

363
Q

Travel Vaccinations Immunology of vaccine

A

1 Antigen presentation (dendritic cell) or LN 2 Activation of cell cycle and clonal expansion of T cells 3 Activation and clonal expansion of B cells. Vaccines provide long term protection through Ab persistence above threshold +/- memory cells –> rapid clonal expansion on exposure to pathogen (second immune response is robust and swift

364
Q

Travel Vaccinations Immunodeficiency

A

Primary: SCID, CVID, DiGeorge, IgA deficiency. Secondary/acquired: physiological state, illness or treatment for a condition that reduces immune function (HIV, extreme of age, pregnancy, malignancy, post BMT, medication

365
Q

Travel Vaccinations Immunosenesence

A

Reduced number of antigen presenting cells. Reduced proinflammatory toll-like receptor response to antigen presenting cells, increased inflammation, specific adjuvants, revaccination before old age is ideal. Might need vaccines with specific adjuvants to stimulate the immune system

366
Q

Travel Vaccinations Consider

A

Individualised risk profile (person, place, time), country regulations/requirements, future travel, individual preference, vaccine availability, cost, time, safety, epidemiology, population level risk/public health benefit, cost effectiveness, safety, acceptability

367
Q

Travel Vaccinations India

A

Measles, Hepatitis A, Typhoid, Dengue, Rabies

368
Q

Travel Vaccinations Animal bite

A

Wash wound for 15 min with soap and water seek medical attention ASAP, DTP booster if required, Simian Herpes B virus: Macaque monkeys in SEA - aciclovir within 5d for 14d. Rabies PEP +/- HRIG

369
Q

Travel Vaccinations Splenectomy

A

Vaccinate: Hib, Nmen ACWY & B, Pneumococcus, Influenza. Prophylax abx: penV +/- standby abx. Other infection risks: Malaria, Babesiosis

370
Q

Travel Vaccinations Hajj pilgrimage

A

Men ACWY at least 10d before travel, polio if travelling from country with wild-type polio, YF if travelling from ‘at risk country’, COVID-19, influenza, hepatitis B, Rabies, and consider risks for MERS-CoV, diarrhoea

371
Q

Travel Vaccinations Summary

A

Update routine vaccinations (MMR), check certification requirements (YF, polio, Men ACWY, COVID), check additional person specific risks (immunocompromised, pregnant), consider levels of sanitation (Hep A, typhoid, cholera), estimate additional risks (animal bites, HBV, JE, TBE, flu etc)

372
Q

Genitourinary fistula Definition

A

Abnormal opening between the vagina and other nearby organs in the pelvis, including the bladder or rectum. A fistula can cause many complications, such as urinary and faecal leakage, abnormal vaginal discharge, tissue damage, kidney infections and other irritative type symptoms. It often, but not always, leads to infertility. There are several types of fistulae defined by the location vesicovaginal (bladder), rectovaginal (rectum), colovaginal (large intestine), enterovaginal (small intestine), uretovaginal (ureter), urethrovaginal (urethra)

373
Q

Genitourinary fistula Risk factors

A

Prolonged or obstructed labour, distended bladder, use of oxytocin, failed instrumental delivery, rupture or pre-rupture of uterus. Most prevalent in marginalised members of population: teenagers, child brides, poor SES, low education, rural or remote regions.

374
Q

Genitourinary fistula Iatrogenic fistula

A

Rising cause, often by unsafe surgery eg hysterectomy, caesarean hysterectomy and caesarean delivery. Root causes include gaps in healthcare worker density, skill sets and infrastructure. Gynaecological and obstetric operations should be restricted to authorised, registered and trained surgeons.

375
Q

Genitourinary fistula Iatrogenic fistula prevention

A

1 Advocate for and ensure safer surgery practices at health facilities/institutions. 2 Advocate for/ensure safer surgery at the national level. 3 Advocate for/ensure safer surgery at the international level. 4 Reduce non-indicated Caesarean section rates

376
Q

Genitourinary fistula Epidemiology

A

Estimated 2 million women affected, incidence 50-100,000 new cases per year. Decreased in HIC, remains a major public health challenge in LMIC

377
Q

Genitourinary fistula Socioeconomic impact

A

Loss of job and income, stigma, loss of community and family (often childless), constant leaking of urine leads to smell, fear, economic consequences of other obstetric injuries such as wounds or foot drop, homelessness, begging, loss of financial security when husbands divorce/leave them, infertility and inability to engage in sex, costs of buying soap, pads, hygiene, unable to afford nutritious food or education for children. Concerns about cost of treatment are a significant barrier to care - despite care being ‘free’ in many countries, the costs of food, clothing, travel and medications can be prohibitive, costs associated with traditional healers, difficulty in accessing money if household finances controlled by men, loss of income whilst receiving care

378
Q

Genitourinary fistula Prevention

A

Primary (health promotion, planned pregnancies, birth spacing, contraception, community awareness). Secondary (antenatal care, skilled health personnel at birth, partograph use, identification of signs and symptoms of obstructed labour, immediate referral, bladder care and/or catheterisation during labour if needed). Tertiary (access to emergency obstetric and neonatal care, use of indwelling catheter)

379
Q

Genitourinary fistula Bandt’s ring

A

Ummer myometrium becomes tense, lower becomes oedematous and peri-rupture

380
Q

Genitourinary fistula Fistula dye test

A

Diagnosis of GU fistula, after 2 weeks continuous catheterisation, pack vagina with gauze, inject methylene blue into catheter, observe gauze for blue discolouration. If positive, continue catheter and recheck again in 4 weeks, if remains positive again (6w) refer for surgery

381
Q

Genitourinary fistula Surgery

A

Surgical access is key to quality repair and prevention of both obstetric and iatrogenic fistula. Repair is a complicated procedure and should be performed by subspecialist. Coordination should liaise with national and international facility to provide care

382
Q

Genitourinary fistula Summary

A

Genitourinary fistula is important, preventable and treatable. It has devastating consequences for individuals, families, communities and countries. It is possible to eradicate them entirely and good work is being done to do so. The pathophysiology of obstetric fistulas is simple but the prevention and treatment is complex. The root cause of the significant rise in iatrogenic fistula is access to specialised surgical input. There is a role for the non-specialist in diagnosis, data-collection and referral pathways, prevention of new cases, advocacy work in promoting training for healthcare professionals (esp midwives), advocacy for access to comprehensive healthcare, advocacy and healthcare design for access to contraception and abortion services, and the promotion of safe surgery across the board.

383
Q

Gynaecology Epidemiology

A

810 women die daily from preventable causes related to pregnancy and childbirth. 94% of maternal deaths occur in LMIC, maternal mortality is higher in women living in rural areas and among poorer communities. Young adolescents (10-14y) face a higher risk of complications and death as a result of pregnancy than other women. Skilled care saves lives. No woman should die in pregnancy or child health.

384
Q

Gynaecology Early pregnancy emergencies

A

Maternal collapse, septic abortion/termination of pregnancy (TOP), management of miscarriage, ectopic pregnancy

385
Q

Gynaecology Antenatal emergencies

A

Maternal collapse, VTE (DVT/PE), HTN (PET/ET), Sepsis, Antepartum haemorrhage (APH)

386
Q

Gynaecology Intrapartum emergencies

A

Umbilical cord prolapse, shoulder dystocia, breech delivery, hypertension (PET/ET), sepsis

387
Q

Gynaecology Postpartum emergencies

A

PPH -> massive obstetric haemorrhage (MOH), VTE (DVT/PE), HTN (PET/ET), Sepsis

388
Q

Gynaecology Prepare

A

15% of pregnant women will have a potentially life threatening complication, the majority of which are unpredictable. Know what equipment is available and where it is. Organise emergency boxes/bags with clearly labelled drugs, equipment and protocols, and run simulation. Always come back to ABC

389
Q

Gynaecology Violence against women and girls

A

Affects all societies, all ages, all genders, all socioeconomic groups. There is an overlap with other types of abuse. It has a significant impact and consequences on the individual, secondary survivors, society, impact on GDP and local economy.

390
Q

Gynaecology Medical care following sexual assault

A

1 Assessment of injuries 2 Risk of pregnancy 3 Emergency contraception 4 Sexually transmitted infections 5 Mental health assessment - remember will not have a positive urinary pregnancy test until 3 weeks post event

391
Q

Gynaecology Miscarriage (abortion)

A

Threatened: light bleeding, abdominal pain, cervix closed. Incomplete: more or less bleeding, abdominal pain, uterine contractions, open cervix. Trauma to vagina or cervix or presence of a foreign body are strongly suggestive of unsafe abortion. US is Ix of choice. If threatened - advise to reduce activity, look for a possible cause and treat pain. If missed - no urgency for uterine evacuation (use misoprostol or manual vacuum). Ongoing or incomplete: general measures, ABC, treat pain, remove POC from vagina and cervix, look for cause (malaria, STI). Septic abortion: (fever, abdo pain, tender uterus, foul-smelling discharge) do as above, plus remove foreign bodies from vagina and cervix, uterine evacuation ASAP and administer Abx

392
Q

Gynaecology Treatment of heavy menstrual bleeding

A

NSAID, Tranexamic acid on bleeding days, COCP, oral progesterone, refer for gynae input. Consider CaCx

393
Q

Gynaecology Pelvic inflammatory disease

A

Symptoms (lower abdo/pelvic pain, mucopurulent discharge, fever, loss of appetite/vomiting, intermenstrual bleeding, heavy menstrual bleeding, deep dyspareunia, later subfertility/ectopic), Examination (cervical motion tenderness, mucopurulent discharge, friable cervix) Admission if (febrile, tachycardic, rebound tenderness, pelvic mass) Antibiotics (CRO plus Doxy plus Metro for 14d), treat partner,

394
Q

Gynaecology Summary

A

Maternal mortality does not just happen at delivery. Medical leadership in organisation, planning, preparedness and training could be initiated by a non-specialist. Always come back to ABC, always do a urine pregnancy test. Young women don’t decompensate until the very end - don’t rely on hypotension and tachycardia. Safeguarding and contraception are the forgotten heroes of gynaecology. Women need good healthcare to thrive. It is a human right, not just when they are pregnant. Without addressing this significant burden, global goals and targets such as the sustainable development goals cannot be met.

395
Q

History Key messages

A

Individuals, communities, nations and organisations all have a complex past, and their histories (what has happened, and also what stories are told about the past) will affect how they behave today and tomorrow. Today’s inequalities in health have deep historical roots. Power imbalances in terms of whose knowledge matters, and whose health matters, were established through colonialism and persist today. Tropical medicine (and hygiene) was entangled with empires, economics, exploitation, politics, and racism: it went on to become entangled with global health - which retains many of these entanglements. Healthcare past and present is a lot to do with human decisions concerning resources, priorities, expertise, and evidence, in society: it’s affected by power relationships and its always political. BUT that doesn’t mean we give up and go home. What can we do with this? Listen for the histories (of nations, communities, individuals, and organisations) that you encounter: they will help you understand what’s happening now. Reflect on your own history; how it shapes your experiences and views of the world; and how other histories will differ. Ask questions about the past, in relation to people and places as well as problems. Be alert to the risks of falling too easily into the well-trodden pathways set by the past. Think about how you, in your future work, might want to confront negative legacies from the past (and build on past strengths)

396
Q

History Why historical perspectives matter

A

One third of income inequality today can be explained by the impact of European colonialism. Colonialism led to an increase in the national income of colonising nations of between 14-79%. $45 trillion was taken from India by Britain between 1765 and 1938.

397
Q

History Empire

A

A large, composite, multi-ethnic, or multinational political unit, usually created by conquest, and divided between a dominant centre and subordinate, sometimes far distant, peripheries.

398
Q

History Imperialism

A

The actions and attitudes which create or uphold such big political units. This is about exercising power and influence: it can be economic and/or cultural; and can be enacted at a distance

399
Q

History Colonialism

A

Direct or indirect political rule by a foreign state: particularly European practices from the 1600s onwards (Spain, Portugal, France, Britain, Belgium, Netherlands) involving the movement of people and/or control of economic resources

400
Q

History Emergence of tropical medicine

A

Tropical’ regions near the equator. But the interest of tropical medicine were not uniquely problems of the ‘tropical’ regions. Late 19th century: dengue, malaria, yellow fever, cholera, leprosy, plague, smallpox. 20th century: TB, syphilis, mal/nutrition, HIV and AIDS. Early features of tropical medicine: attention to climate and environment as they might affect health; attention to racial difference as explanation for health outcomes; confidence that knowledge and expertise lie in Europe (and later, the USA/’global north’)

401
Q

History Alma Ata Declaration 1978

A

Health ‘is a fundamental human right and the existing gross inequality…between developed and developing countries is politically, socially, and economically unacceptable…primary health care is essential health care based on practical scientifically sound and socially acceptable methods and technology made universally accessible…bringing health care as close as possible to where people live and work’ BUT: Global financial problems of the 1970s, the involvement of the World Bank, and political shifts (post-Cold War, neoliberalism) led to a renewed focus on selective (vertical) interventions.

402
Q

Rheumatic heart disease Definitions

A

ARF (acute rheumatic fever): acute multisystem inflammatory process occurring 2-3 after GAS pharyngitis. RHD (Rheumatic heart disease): chronic process due to scarring of valves during ARF associated with complications such as heart failure and death. GAS: S pyogenes, Gram positive beta-haemolytic cocci in chains

403
Q

Rheumatic heart disease Epidemiology

A

Not straightforward to diagnose, significant underestimates. Global prevalence estimate ~33m

404
Q

Rheumatic heart disease Recognition

A

ARF: 5-15yo in high risk population, dominant features are joint pain, carditis (and chorea), classically 10-14d following GAS pharyngitis. Diagnosis based on Jones Criteria

405
Q

Rheumatic heart disease Jones Criteria

A

GAS plus 2 Major or 1 Major and 2 Minor (Major: Carditis, Arthritis, Chorea, Subcut nodules, EM) (Minor: Polyarthralgia, Fever>38.5C, ESR>60 or CRP>30, Prolonged PR) - in high risk areas polyarthralgia upgraded to Major, and monoarthralgia to minor, and fever limit dropped to 38

406
Q

Rheumatic heart disease Clinical features - major

A

Carditis (50-65%, MV first, echocardiographic criteria, rarely peri/myocarditis). Arthritis (migratory, large joint arthritis, very responsive to NSAIDs, self-limiting and not deforming). Chorea (movement disorder, relief with sleep, facial grimacing/tongue, spooning/milkmaid’s grip) Subcutaneous nodules. Erythema marginatum

407
Q

Rheumatic heart disease Clinical features - minor

A

Fever, acute phase reactants, heart block

408
Q

Rheumatic heart disease ARF management

A

Diagnostics -> Echo +/- antecedent GAS. Patient/family education, analgesia/NSAIDs, diuresis, ACEi +/- steroids. Longer-term prevent recurrence

409
Q

Rheumatic heart disease RHD management

A

Prophylaxis: IM penicillin. Anticoagulation: Warfarin (not DOAC)

410
Q

Rheumatic heart disease Disease control

A

Case detection, register, prophylaxis, family planning, education & advocacy. Ideally: primary prevention, echo screening, diagnostics, chronic disease, access to surgery

411
Q

Rheumatic heart disease Key messages

A

Infection triggered disease of depravity and poverty. Leading cause of cardiac death & disability in young. Challenging diagnosis in challenging settings. Emerging evidence for prevention and therapeutics. Vaccine development is the key longterm goal

412
Q

Geography Why is this important

A

Why did this person from this place, develop these symptoms at this time? It is not just as simple as the region, but also the time of year, and the area within the region, and need to have an understanding of the diversity within one country on how to advise.

413
Q

Geography High consequence infections

A

Lassa (West Africa due to distribution of Multimammate), Ebola (Western/Central Africa linked with distribution of territodidiae fruit bat) Endemic mycoses, Blastomycosis (Northern America), Paracocci (South America), Coccidiodomycosis (Lower North/Central/South America), Talaromycosis (SE Asia), Yellow Fever (Sth America and Africa - Aedes mosquito is found in other parts of the world, esp SE Asia, unclear reasons Yellow fever is not in this region. P knowlesi (Malaysia)

DTM&H 2024 (32 decks)

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