Week 8 Flashcards
1
Q
Tetanus Microbiology
A
C tetani, anaerobic Gram positive bacterium, terminal spores ‘drumstick’ highly resistant. Found in the environment throughout the world. Pore-forming toxin ‘tetanolysin’ and a collagenase are needed for growth and toxin production. Only toxigenic C tetani causes tetanus
2
Q
Tetanus Pathophysiology
A
At the site of inoculation, tetanus spores enter the body and germinate in the wound. Germination needs particular anaerobic conditions, such as dead and devitalized tissue that has low oxidation-reduction potential. After germination, they release tetanospasmin into the bloodstream. This toxin enters the presynaptic terminals in the neuromuscular endplate of motor neurons and destroys a vesicular synaptic membrane protein resulting in the inactivation of inhibitory neurotransmission that usually suppresses motor neuron and muscle activity. This paralyzes muscle fibres. Subsequently, this toxin, via retrograde axonal transport, travels to neurons in the central nervous system, where it also inhibits neurotransmitter release; this occurs approximately 2 to 14 days after inoculation. Since glycine and GABA are major inhibitory neurotransmitters, cells fail to inhibit the motor reflex response to sensory stimulation, causing a tetanic spasm. This can cause such powerful unopposed muscle activity and contraction that bone fractures and muscle tears can occur.
3
Q
Tetanus Clinical features
A
Incubation period: Symptoms, Stiffness. Period of onset: Stiffness, spasms, autonomic dysfunction
4
Q
Tetanus Neonatal prognosis
A
Significantly improved with ventilation. Paralysis stops the spasms which stops much of the morbidity and mortality
5
Q
Tetanus Autonomic dysfunction
A
Difficult to differentiate from acute cardiac events in comorbid patients
6
Q
Tetanus Modified Ablett Score
A
Grade 1 No spasm. Grade 2 Mild short-lived spasms not interfering with respiration. Grade 3 More prolonged muscle spasm interfering with respiration. Grade 4 Grade 3 but autonomic nervous system dysfunction
7
Q
Tetanus Things you won’t read in the textbooks
A
Voice change, Spasms (can be mild in elderly patients, but beware), cardiovascular instability is early, pyrexia (can cause irreversible heat-shock), Cardiac events are common in elderly patients
8
Q
Tetanus Management
A
Remove toxin (debride, ANTIBIOTICS, ANTITOXIN), Support (control spasms, prevent cardiovascular complications), promote recovery, vaccinate
9
Q
Tetanus Antibiotic
A
Metronidazole for 7-10d (Penicillin potentiates GABA)
10
Q
Tetanus Antitoxin treatment
A
IM Safe, no large improvement by intrathecal administration (but much more expensive). No difference in mechanical ventilation, autonomic dysfunction, ICU stay or hospital stay between two administration methods Human half life 28d, Equine half life 2w.
11
Q
Tetanus Antitoxin prevention
A
Incomplete primary course: all wounds give booster, if dirty/high risk give passive immunisation. Incomplete vaccination all wounds give booster, if high risk give passive immunisation. Complete vaccination: no booster or passive immunisation required
12
Q
Tetanus Supportive
A
Airway (tracheostomy), Spasm control (Beno, MgSO4 may help reduce requirement for muscle relaxants but not mechanical ventilation), Autonomic disturbance (use short-acting drugs as the swings are huge, Mg may reduce catecholamine response), Gastrointestinal, Hospital acquired infection
13
Q
Tetanus Recovery
A
Important to remember QOL, critical illness in ICU for 3-4w and suffer longterm problems as other patients with prolonged ICU. Early rehab (use relatives in absence of physio) in low resource setting
14
Q
Tetanus Prevention
A
Prevention is a much more economical option in LMIC and the cost is borne by patients in low resource settings. Vaccination is cheap (challenges: remote communities, multiple doses [5] needed, and no herd immunity). Important to keep the programs running. Unvaccinated are vulnerable (natural disasters, unintended impact, vaccine hesitancy). If you can’t vaccinate people, prevent neonatal tetanus by clean delivery/wound management
15
Q
Tetanus Key messages
A
A toxin mediated disease with no herd immunity. Clinical course is relatively predictable at presentation. Specific therapies have limited impact on outcome and supportive management is the mainstay of treatment. Prevention is and will remain a priority.
16
Q
Mpox Virology
A
Zoonotic orthopox, multiple animal reservoirs (primarily rodents).
17
Q
Mpox Clinical features
A
Acute febrile illness. Incubation 1-2w, invasion period 0-5d (fever, headache, fatigue, LN), 1-2 into fever -> skin eruption - a few to several thousand lesions appear and evolve simultaneously. Centrifugal vs centripetal distribution. Often quite painful. Macules -> papules -> vesicles -> pustules then scab
18
Q
Mpox Clades
A
1 Predominantly West Africa. 2 Central Africa
19
Q
Mpox Epidemiology
A
Initially in small jungle villages from zoonotic jumps - rural and rare disease, but as time goes on spreading into other areas. Increased over 1970-2019 associated with urbanisation, increased populations. Smallpox vaccination ended in the 1980s, and worldwide waning immunity has likely contributed to increasing susceptibility. 2018-2022 imported cases, associated with animals in quarantine
20
Q
Mpox Clade 2b
A
May to October 2022. Sexual health clinic presentation with blistering lesions, systemic illness. 85,000 cases in non-endemic areas over 110 countries. UK epi - Clade 2b mpox - community engagement through Grndr. WHO PHEIC 2022. 25% of those infected living with HIV, 98% GBMSM aged 20-40. Prevention - immunisation, change in behaviour, infection-associated immunity
21
Q
Mpox Epi study
A
Used condoms collected - scavengers (brothels, public spaces) - tested for Mpox DNA found 1% had evidence of Mpox, looked for cooccurrence of other STIs - great example of lateral thinking and creativity
22
Q
Mpox Clade 1a
A
Geographically limited to DRC and other West African countries. Zoonotic, less person-person transmission. CFR 4.6%
23
Q
Mpox Clade 1b
A
Increasing incidence in DRC, ascertainment bias, initially CFR 4% (likely over estimated as the mild cases do not present, difficult to access testing, and if diagnosed may be asked to isolate which adds to stigma, and inability to go to work and support yourself/family) Retrospective review of HSV/VZV swab negative tests in Burundi - wide distribution M=F, children>adults - likely represents spread in childhood. WHO declares PHEIC 08/2024 - spread through DRC, Burundi, Rwanda, Kenya, Uganda, -> Sweden, Thailand, India, Germany, UK, Zambia, Zimbabwe. Epi: predominantly high-contact sexual networks. CFR 0.38%
24
Q
Mpox Key messages
A
Waning immunity to poxviruses. Global outbreak clade 2b controlled (mostly gay, bisexual and MSM). Clade 1 continues to occur with increasing geographic spread. Some sexual transmission clade 1. We don’t have much good data for clade 1 as diagnostics lacking
25
Mpox Transmission
Person-to-person: direct contact with infectious rash, scabs or body fluids, respiratory secretions, fomites (lower risk, but can occur), pregnancy transplacental. Also possible to contract from infected animals either by being scratched or bitten, or by preparing or eating meat, or using products from an infected animal
26
Mpox Incubation
1-2w, physicians are currently recommended to monitor patients up to 21d, typically prodrome first then rash 1-4d later
27
Mpox Key messages
Transmission data strongest in clade 2b. Sexual transmission, but also close skin contact. Transmission different in different clades (or is this about different populations?). Some sexual transmission of clade 1. Not much good data for clade 1
28
Mpox Diagnosis
PCR for DNA. Best diagnostic specimens are taken directly from the rash (deroof). In the absence of skin lesions, testing can be done on oropharyngeal, anal or rectal swabs
29
Mpox Differential diagnoses
Primary or secondary syphilis, VZV, disseminated Crypto, HSV, DGI, Molluscum, other causes genital/anal diseases and proctitis: Chancroid, LGV, Behcet's disease, Inflammatory bowel disease
30
Mpox Clase 2b case series
Male 97-100%, Fever 62-72%, Rectal pain 14-25%, Lesions 95-100%, genital 46-73% and anal/perianal 31-42%
31
Mpox Severe Mpox
Proctitis, genital deformity/abscess, pharyngitis, lymphadenopathy, bacterial superinfection, encephalitis, pneumonia, HIV infection - higher rates of complications, higher mortality - esp in those with CD4<50
32
Mpox Key messages
Fever and a rash. Examine thoroughly. Site of exposure/infection may determine clinical manifestations. Lymphadenopathy. Bacterial superinfection. Severe disease and death can occur. Gap in knowledge clade 1
33
Mpox Tecovirimat
Antiviral stockpiled for smallpox preparedness. Interfering with VP37 protein that is found on the surface of orthopoxviruses (inc smallpox, mpox, cowpox). Trials of tecovirimat did not reach statistical significance on the primary end point in lesion resolution. But probably does have clinical benefit (vs placebo) in those treated early, and those with severe disease - more trials required
34
Mpox Supportive care
Assess pain (mucosal lesions may not be visible on exam). Oral lesions (mouthwash, salt water gargle, viscous lignocaine), rectal lesions (stool softeners, sitz baths, topical lignocaine, avoid opioids). Stay in contact with patients in community. NSAIDs with caution. Tecovirimat may still have a place (trials). Most recover without complication.
35
Mpox Vaccines
Jynneos, Imvamune, Imvanex - live, non-replicating vaccinia virus. 2 doses, 4 weeks apart. Contraindicated: Mpox symptoms, severe allergy to egg, ciprofloxacin and gent in the insipient. Safe to administer to PLWHIV and atopic dermatitis. Fractional dosing as intradermal used during the outbreak, instead of the standard subcutaneous. There is a long lag time to create the vaccine due to the extensive passaging through cell lines required, so this was the strategy used to quickly achieve cover. Efficacy is what happens in trials under supervision. Effectiveness is what happens in the real world. Initially there was no access in Africa (acting CDC Director) - "This is a classic example of constrained access for Africa for a product, in this case, vaccines. Even if we wanted to buy, there is nowhere to buy, because they are manufactured in modest numbers and then countries stockpile them in case they need them, while where it is actually needed, on the continent of Africa, we don't have access"
36
Mpox Infection control
Fomite transmission in hospital room has been described. PPE recommended in hospital: gloves, gown, N95, eye protection. Dedicated footwear that can be decontaminated. Cover lesions. Avoid unnecessary movement around hospital. IPC at home: able to manage their self-care. Dedicated, well-ventilated room separate from others in the household. Cover lesions. items such as eating utensils, linens, towels, electronic devices or beds should be dedicated to the person with mpox.
37
Mpox Key messages
Nosocomial transmission can occur (protect staff and other patients), fomites are important, community based care for those at home
38
Mpox Conclusions
Increasing incidence mpox linked to waning of immunity. Transmission - don't forget fomites. We think clade 1 is like clade 2 but data is sparse. Vaccine available and effective. Supportive care. Good infection prevention and control practice. Endemic versus non endemic settings inequitable access to vaccine, drugs and diagnostics.
39
Zika Virology
ssRNA flavivirus. 2 strains - African and Asian 95% amino acid similarity. Asian strain responsible for known outbreaks. African strain has higher transmissibility and pathogenicity
40
Zika 2007 Yap Island
5000 of 6500 population infected. Highly competent vector, no population immunity. Possible underreporting in other countries due to similarities with other infections
41
Zika 2013 Pacific Islands
Unusual increase in Guillain Barre, first confirmed case of perinatal infection - 2 mothers developed symptoms just before delivery, babies tested positive just after birth - one was asymptomatic, the other had an isolated rash.
42
Zika 2015-2016 Americas
03/2015 Brazil notifies WHO of rash illness, cases soared, lots of epidemiological alerts of numbers of cases. 07/2015 reported patients with neurological symptoms, 10/2015 increase in microcephaly and increasing evidence of link to congenital abnormalities 01/2016 PHEIC. Cases dropped off in 2017, and still minimal cases since 2018
43
Zika Transmission
Vector: Aedes aegypti, day biting, well adapted to urban environments, multiple meals from multiple hosts - established in many countries. Mosquito borne transmission major driver in outbreaks. Aedes albopictus is secondary vector - more widespread global distribution including in Europe, extends into more northern latitudes than A aegypti - has not supported large scale ZKV outbreaks yet. Both can spread to newer areas. Other transmission (cannot sustain outbreaks): sexual, blood, transplacental. Has been found in breast milk, no reports of transmission. Case report in NEJM - transmission through tears and sweat
44
Zika Clinical features
Incubation 3-12d, 80% asymptomatic. Rash (macular, non-distinct in ~93%) and fever most common - arthralgia, arthritis, myalgia, conjunctivitis headache, back pain, mild, self-limiting
45
Zika Congenital Zika
Severe microcephaly is key marker, but can get congenital without microcephaly. Multi organ phenotype. Pointed occiput, redundant scalp skin, contractures, cerebral calcifications, less frequently raised hemidiaphragm. Eye problems also very common: focal retinal mottling and macular scarring, cataracts, glaucoma, optic nerve atrophy. Deafness. Seizures, tremors, hypertonia, hyperreflexia, irritability. Neurodevelopmental abnormalities may appear later in life and not be obvious at birth eg visual loss, developmental delay, seizures may develop months later. 11x more likely to die in the three years of life - <12m sepsis, hydrocephalus, microcephaly. >12m nervous system, cerebral palsy, diseases of circulatory system. Emerging evidence indicates adverse neuro effects in infants following postnatal infection. Asian strain linked to CZS, but the lack of data on African strain - possibly more severe in Africa and loss of pregnancy. No surveillance to know. Animal models suggest African strain is more pathogenic, caused embryonic death rather than live births.
46
Zika Congenital Zika risk
Highest risk of birth defects is infection in T1, but can occur throughout pregnancy. Asymptomatic infection can still have devastating congenital impact
47
Zika Dengue vs Zika in pregnancy
Dengue more severe disease in pregnancy, increased risk of death, increased risk of fetal loss, but no congenital signal. Zika no increase in maternal complications, but does result in congenital disease
48
Zika Neurological complications
Primary CMV and Campylobacter are still more likely to cause GBS, but Zika dose have increased rate 6d post Zika infection 24 cases per 100,000 infected with Zika virus. CNS involvement very rare (myelitis, encephalitis, optic neuritis)
49
Zika PCR
Short viraemic 3-5d after onset of sx. Pregnant women longer viraemic period - the longer the viraemia, the higher the likelihood of congenital. Urine excellent sample, says positive for at least 3 weeks. In principle test blood 1w, urine 3w. Can also be performed on semen, CSF, amniotic fluid, placental and umbilical cord tissue. The longest reported 'serial interval' between symptom onset in a man and symptom onset in his female sexual partner is 44 days
50
Zika Serology
IgM positive first week after symptom onset, can persist for weeks, can get false positives (non-specific reactivity, cross-reactivity), ask for repeat to see if develop IgG. IgG also appears early, may persist for years possibly life long. Cross reactivity with other flaviviruses - if previous flavivirus infection/vaccination subsequent exposure to related flavivirus cans a rapid and brisk rise in IgG against multiple flaviviruses (including Dengue) - may not develop IgM in patients with previous dengue
51
Zika Pregnancy advice
If planning: don't travel to endemic area. Avoid pregnancy for 2m if only woman travelled, 3m if both/male partner travelled. If already pregnant: use barrier contraception. If living in an endemic country - mosquito avoidance
52
Zika Dengue and Zika
Relationship asymmetric. Prior Zika can worsen and enhance future dengue with DENV2,3,4, prior dengue infection protective for Zika/ May have implications for Zika and dengue vaccinations
53
Zika Reinfection
Emerging evidence that immunity to ZIKV does not last longterm. We do not know the duration of durable immunity
54
Zika Summary
Flavivirus, usually causes a mild infection. Similar to dengue, chikungunya. Major issue is potential for sexual transmission. Development of congenital Zika syndrome and neurological complications. Unanswered questions: Aedes mosquito widespread, future epidemics. No currently approved Zika vaccination to date. Don't know how long immunity lasts for, don't have the data for this. Cross immunity between flaviviruses/implications for vaccine. Unsure of the long-term outcomes in CZS, post-natal infection.
55
FGM Definition
WHO definition: Partial or total removal of external female genitalia, or injury to the female genital organs for non medical reasons. FGM is a violation of the rights of the child and woman and form of child sexual abuse
56
FGM Four types
1 Partial or total removal of the clitoral gland and sometimes the prepuce. 2 1+ labia minor with or without excision of labia majora. 3 Infibulation or Pharaonic circumcision - narrowing of the introitus through creation of a covering seal. 4 All other harmful procedures to the female genitals for non-medical purposes. Such as pricking, piercing, incising, cauterising or nicking without flesh removed. Pulling and stretching the labia and clitoris. Damage during sexual violence or abuse?. A normal genital examination cannot exclude type 4 FGM/C. Diagnosis should be based on the woman's history
57
FGM Differential diagnoses
Labial adhesion following inflammatory processes or lichen sclerosis can be confused with infibulation. Small irregularities in the skin of the vulva or clitoris can be a result of congenital variation.
58
FGM Deinfibulation
Opening procedure for women with type 3, sometimes called 'reversal', it can alleviate some physical symptoms but cannot replace tissue that has been replaced.
59
FGM Reinfibulation
The re-closure of a woman with type 3, usually after childbirth. Illegal in UK. Some women may be deinfibulated and then reinfibulated several times with the birth of each child. Common in Saudi Arabia, Somalia, Sudan
60
FGM Reconstruction
Where skin/tissue is grafted so that appearance is of a woman who is not cut. Clitoral tissue is pulled upwards and exposed in order to improve sexual pleasure. WHO and RCOG stated that evidence to support reconstructive surgery is not robust enough to recommend it. Evidence suggests reconstruction may alleviate genital pain, increase sexual pleasure, treat body image concern. Not available in UK
61
FGM Prevalence
230 million girls and women worldwide. >5% of global female population. >140,000 in UK
62
FGM Changes in prevalence
Change in mode: girls cut younger, less public cutting ceremonies, type 3 less common, increasingly performed by healthcare professionals. Overall chance that a girl will be cut today is 1/3 lower than 3 decades ago
63
FGM Myths to justify
Custom and tradition, religion, hygiene and cleanliness, virginity and chastity, increasing sexual pleasure for men, social pressure/norms, becoming a woman, family honour, preparing for marriage, enhancing fertility, a sense of belonging to the group or conversely a fear of social exclusion, peer pressure
64
FGM How
usually traditional birth attendants or circumcisers. 18% performed by health care providers. Anaesthetic rarely used and child often held down by group of adults. Special knives, scissors, razors, sharp stones or pieces of glass. Wound may be held together with thorns. Girls legs are bound together until wound is healed. Age of FGM varies from a few days old to adulthood. Usually 5 to 14 years
65
FGM Short term consequences
Haemorrhage, severe pain and shock, urine retention, injury to adjacent tissue, tetanus, HIV, HBV, HCV, fracture or dislocated limbs from being restrained. Death - severe bleeding leading to haemorrhagic shock. Neurogenic shock as a result of pain and trauma. Infection, septicaemia.
66
FGM Long term consequences
Dysuria, recurrent UTIs, candida infections, vulvodynia, clitoral pain, abscesses due to infected cysts/thorns, dysmenorrhoea, infertility, chronic PID, clitoral neuroma and chronic scar formation, sexual dysfunction and dyspareunia, problems in childbirth, psychological trauma (the fact that FGM is embedded in culture does not protect from developing PTSD)
67
FGM Obstetric problems
May not be identified antenatally. Difficulty with Ves, applying FSE/FBS. Scarring and stricture of vaginal canal. Possible obstructed labour. Psychological trauma, flash backs. Limited knowledge of birth attendant. Increased risk of CS, PPH, fetal asphyxia/anoxia and perineal trauma. Women with Type 3 can get pregnant
68
FGM How to ask about FGM
I notice you come from a country where some people practice FGM. Do you know what FGM is? Have you been cut or circumcised when you were a child? Ask directly and sensitively. Avoid retraumatising. Take time. Use health advocate/interpreter. Don't forget women may never have spoken about FGM before. Trauma informed care - establishing trust and yielding control to the patient, minimising discomfort, retraumatisation or shame. Creating a safe, private space by clearly describing the purpose of the evaluation. Provide concrete description of each step of the genital assessment and reassure her she may pause or stop the evaluation at any time. Taking time, being respectful and sensitive. In UK, flag on summary care record of female babies born to women with FGM - removed when child turns 18.
69
FGM Antenatal deinfibulation
Ask all women at booking whether they have FGM. If type 3 offer and recommend antenatal deinfibulation in T2, if woman declines, perform intrapartum deinfibulation at the end of 1st stage if soman has epidural or, (if no epidural) at the beginning of 2nd stage). Why recommend antenatal deinfibulation? Expert clinician available. Procedure is not an emergency. If woman has precipitate labour. Wound site has time to heal prior to labour (prevent extending anteriorly). Less UTIs/infections in pregnancy. No difficulties assessing labour. No baby to look after. Perform the anterior incision first, may not need the mediolateral episiotomy in labour.
70
Gender based violence Definition
Gender-based violence is violence directed against a person because of that person's gender or violence that affects persons of a particular gender disproportionately
71
Gender based violence WHO statement
Violence against women – particularly intimate partner violence and sexual violence – is a major public health problem and a violation of women's human rights. Estimates published by WHO indicate that globally about 1 in 3 (30%) of women worldwide have been subjected to either physical and/or sexual intimate partner violence or non-partner sexual violence in their lifetime. Most of this violence is intimate partner violence. Worldwide, almost one third (27%) of women aged 15-49 years who have been in a relationship report that they have been subjected to some form of physical and/or sexual violence by their intimate partner. Violence can negatively affect women’s physical, mental, sexual, and reproductive health, and may increase the risk of acquiring HIV in some settings. Violence against women is preventable. The health sector has an important role to play to provide comprehensive health care to women subjected to violence, and as an entry point for referring women to other support services they may need.
72
Gender based violence Murad code
Overarching principles (1 understand survivors as individuals, 2 respect survivor control and autonomy, 3 be responsible and have integrity, 4 add value or don't do it) Preparation principles (1 preparation is the foundation, 2 know and understand the context, 3 build systems, competency and support) Implementation principles (1 gather information from other sources, 2 take the time, create the space, 3 Ensure respectful and safe interactions)
73
Gender based violence Essential package
Information (SV, DV), Medical care (HIV PEP 72h, Emerg contraception 3-5d, HBV vax) Psychosocial (suicide, anxiety, depression, PTSD, referrals - refuge/counselling/social support) - can also consider DoxyPEP
74
Gender based violence Honour based abuse
Is a crime committed to protect or defend the 'honour' of a family or community, occurs when it is felt the individual's behaviour has broken the 'honour code' bringing disgrace to their family or social group. Is a broad umbrella term used to describe a combination of practices. Although predominantly associated with women and girls, male members of a family can also be victims. Perpetrators will feel that they need to restore their loss of face and standing within their community. There is often an element of approval and social acceptance from other family members and the community. HBA is a custom deep rooted in certain communities where the family or group is considered foremost rather than an individual, though many different societies believe in the honour code. Most prevalent in cultures originating from South Asia, Africa and the Middle East with the highest victim group being Asian females.
75
Gender based violence Types of Honour based abuse
Forced marriage, child marriage, domestic abuse, sexual harassment and sexual violence (rape and sexual assault or the threat of), threats to kill, physical and emotional violence and murder. Pressure to go or move to another country. Being kept at home with no freedom. Not allowed to use the telephone, internet, or have access to important documents like your passport or birth certificate. Isolation from friends and members of your own family. Virginity testing. Enforced abortion. Female genital mutilation
76
Gender based violence Statistics
~5000 honour killings internationally per year. 1000 in India, 1000 in Pakistan, 12 in UK per year. Likely a significant underestimate
77
Gender based violence Child Sexual Abuse
Involves forcing or enticing a child or young person to take part in sexual activities, not necessarily involving a high level of violence, whether or not the child is aware of what is happening. The activities may involve physical contact, including assault by penetration (for example, vaginal or oral rape ) or non-penetrative acts such as masturbation, kissing, rubbing and touching outside of clothing. They may also include non-contact activities, such as involving children in looking at, or in the production of, sexual images, watching sexual activities, encouraging children to behave in sexually inappropriate ways, or grooming a child in preparation for abuse. Sexual abuse can take place online, and technology can be used to facilitate offline abuse. Sexual abuse is not solely perpetrated by adult males. Women can also commit acts of sexual abuse, as can other children.
78
Gender based violence Child sexual exploitation
Child sexual exploitation is a form of child sexual abuse. It occurs where an individual or group takes advantage of an imbalance of power to coerce, manipulate or deceive a child or young person under the age of 18 into sexual activity: in exchange for something the victim needs or wants, and/or for the financial advantage or increased status of the perpetrator or facilitator.
79
Gender based violence Far more children are sexually abused than services identify
2,700 children on a child protection plan due to CSA. 50,000 children assessed at risk of CSA. 103,000 CSA offenses recorded by the police. 500,000 children are estimated to be sexually abused every year. Children are disproportionately likely to be victims of sexual offences. They are victims in 40% of all sexual offences. Yet make up to 20% of the population. We must formally recognise that children represent a significant proportion of victims and ensure their specific needs are met with sufficient and appropriate support.
80
Gender based violence How does sexual abuse present?
Allegation, Physical symptoms/signs, Behavioural/emotional/mental health difficulties. Poor school performance/learning. Other maltreatment. REMEMBER Most do not present. Even if they do it may NOT be recognised
81
Gender based violence How to manage a child presenting with history of sexual assault
Don’t panic! Have Systematic approach. Ask open questions. Be trauma informed (Believe them! Understand what the child or young person wants Reduce the number of times they have to tell their story) Document verbatim. Be aware of the law where you are. Assess for and manage medical symptoms (Medical treatment takes priority, Assess and manage bleeding etc) Assess risk of pregnancy - Give Emergency Hormonal Contraception. Assess risk for and give Hep B vaccination. Assess risk for and give HIV-PEP. Consider forensic need (forensic window) (What happened, When did it happen). Consider their safety (Are they safe at home? Who is the assailant and what contact do they have. Childrens social care (childrens services) referral. Police report (in UK if U13 no choice, but if 13 and over can choose)). Mental health risk assessment, Sexual health follow up, Pregnancy testing
82
Gender based violence How to manage genital presentations in children
Based on UK setting. Would need to be adapted in some settings. Will provide a basis and an approach. For all (Systematic approach, Detailed history, Examination). Remember open questions consider space for disclosure. History of presenting complaint: when did it start, how much, how long for, needing pads? History of trauma? Past medical history: bleeding problems, other bruising, other injuries, warts elsewhere, oral herpes, Social history – CSC involvement, where is child cared for? (school, nursery, child minder, friends etc), Developmental history, Pubertal status.
83
Gender based violence How to examine genital presentations in children
Inspect genitalia for: Hygiene, Active bleeding, Inflammation / rash, Infection (e.g. warts, worms, ulcers), Injury (e.g. lacerations, bruising, excoriation), Discharge, Urine, Scar tissue, Lump or bumps, Foreign bodies. Inspect anus for: Hygiene, Active bleeding, Inflammation / rash, Infection (e.g. warts, worms), Injury (e.g. fissures, lacerations, bruising), Venous congestion, Scar tissue or skin abnormalities (skin tag), Anal dilatation, Faeces.
84
Gender based violence Causes of 'blood in underwear'
Anal causes: (fissures/lacerations), constipation, inflammatory bowel disease, worms, trauma, Skin conditions: vulvo-vaginitis, lichen sclerosis, haemangioma, Infections: urinary tract, worms, STIs including HPV, HSV, Labial fusion, Injury – straddle injury, Foreign body, Urethral prolapse, Oestrogen (endocrine) (exogenous - neonatal oestrogen withdrawal, endogenous - ovarian tumour, precocious puberty), Exogenous medications (hormones, anticoagulants), Bleeding disorders, Sexual abuse.
85
Gender based violence Genital discharge in a pre-pubertal child
Discharge: A collection of fluid in genital tract that is not blood or urine. Can be physiological or pathological. Affects both male and female. Physiological: Females (not male), Under 3m or post pubertal, Varies with oestrogen levels, Keeps genital tract lubricated and health, Changes with hormone fluctuations, menstrual cycle, hormonal treatments, pregnancy. Pathological: Anal – IBD, infection, Vulvovaginitis, Infections (Streptococcus/Staphylococcus, STI (NG, CT, TV), Candida, Bacterial vaginosis, Threadworm (symptoms). Foreign body, Poor personal hygiene, Trauma, CSA (Discharge is uncommon if no abuse (seen in <1 – 2% in studies of prepubertal girls selected for non-abuse))
86
Gender based violence Infections
Pathogen common but not always found: Streptococcal – commonly Group A β-haemolytic Streptococcus (May have had recent sore throat / recurrent tonsillitis, Can co-exist with other bacteria e.g. staphylococcus, Treatment: sensitive antibiotic), Staphylococcal (Co-infections, Treatment: sensitive antibiotic), Candida (Inflammation of vulva, NOT found in pre-pubertal girls) unless recent ABx, immunocompromised, in nappies. Not STI but pathogenic: (H. influenzae, Moraxella catarrhalis, S. pneumoniae, N. meningitidis, Shigella, Yersinia entercolitica). Neisseria gonorrhoea: Copious discharge, greenish. Chlamydia trachomatis: Blood stained, discharge, spotting between periods. Trichomonas vaginalis: Heavy discharge, frothier, yellowish, alkaline, fishy odour, pain.
87
Gender based violence Penile discharge
Always pathogenic (unless it's not discharge!) (Overgrowth, Hygiene, STI, Other infection), +/- Balanoposthitis or balanitis, Consider if urethral or penile? Urethral discharge (is assessed by milking the length of the urethra from the base to the tip, indicates STI)
88
Gender based violence Genital warts in a child
Frequent cause of concern, Caused by human papilloma virus (multiple types >100, Some cause cervical cancer), Majority of infections latent or subclinical, In children the latency and incubation periods are not known, in adults they can be transient or latent for many years. Transmission can be through (Sexual contact, Vertical transmission (from mother during birth), Autoinoculation (from non genital warts), Heteroinoculation (contact between genitalia and infected carer or contaminated object). Typing is not routinely done. CSA must always be considered. Referral to Police/CSC for all children <13 and consider in young people > 13
89
Gender based violence Genital HSV in a child
Type 1 (most common- increasingly genital) or type 2 (genital). Can remain latent for long periods. Can reactivate at any time. Transmission (Contact with blisters or ulcers, Asymptomatic viral shedding, autoinoculation). Often has no symptoms (Initial episodes may be severe with extensive ulceration and systemic features, Recurrent ano-genital ulcers or blisters, Erythema with itching or tingling, Urethritis or cervicitis). Complications (Neuropathic bladder (initial episode), Increases risk of HIV transmission). CSA always needs to be considered. Consider autoinoculation. In UK advise to refer to children's social care. Positive diagnosis of genital herpes in mother does not exclude the possibility of CSA
90
Gender based violence Summary
Gender based violence is a major public health problem. Approaches will be tailored to the setting you are working in, resources and local law. A medical approach can be a basis that you adapt. It is challenging work and self-care is vital.
91
Ophthalmology - Adult Introduction
Most common and frequent causes are treatable - cataracts. The impact on a family and community is significant - children end up looking after adults instead of going to school, adults are unable to cook for their families
92
Ophthalmology - Adult Definitions
Visual acuity: ability to resolve two things in space, Snellen chart (letters) Tumbling E chart (not dependent on literacy) - not interested in what direction, it is about the ability to resolve the two lines in space = the minimum angle of resolution. On Snellen - the top number says how far away from the chart to stand, the bottom is the angle of resolution distance x over y line. WHO definitions blind <3/60, visual impairment 6/24 to 3/60, mild 6/12 to 6/18, normal 6/6 to 6/12. Definition of blindness is not darkness - it is not being able to see the top letter at 3m. If they can't see that at 1m, then we go to 'count finger' at 40cm, then we move to hand movement, and then light perception (when do you see the light come on, tell me when it goes away) the difference between light perception is very important to remember they are categorised by the vision in the 'better' eye. Blind person can't see in both eyes, near vision - ability to perform close tasks measure with both eyes open 40cm.
93
Ophthalmology - Adult Epidemiology
WHO: Blind 43 million, 295 mod-severe, 258 mild vision impaired. Distribution is not equal by age - from 50 the rate increases (80% aged 50 or above, >90% occur in LMIC). Trends 25% decrease in 25 years, interventions and collaborations have improved this, but the overall number has gone up - the World's population is growing and ageing, therefore this contributes to the overall prevalence.
94
Ophthalmology - Adult Causes
Uncorrected refractive error and cataract are the leading cause of impairment (cataract leads blindness), They are very treatable and occur everywhere. Glaucoma and diabetic retinopathy - partially preventable (slow progression), screening and treatment. Macular degeneration and other causes have no public health strategy. Consider the iceberg - underneath are those at risk of vision loss, and eye health issues not affecting vision - there are a huge number needing eye care
95
Ophthalmology - Adult Cataract
As collagens change in structure, the lens goes cloudy - happens at different paces in different people in different countries. It is gradual slow decline. Easy operation to replace lens and fix refractive error at the same time
96
Ophthalmology - Adult Refractive error
Glasses are needed by 1 billion people
97
Ophthalmology - Adult Trachoma
C trachomatis - flies, hand washing, fomites. Recurrent conjunctivitis (infection and inflammation), pattern of recurrent infection and inflammation, once recurrent causes scarring, upper lid curls and tightens - eyelashes rub on front of eye (very uncomfortable. Endstage scarred cornea and loss of sight. Pathophysiological cascade, public health approach is about breaking that cycle.
98
Ophthalmology - Adult River blindness (Onchocerciasis)
Onchocerca volvulus, intense itching and subcutaneous nodules. Second leading infectious cause of blindness.
99
Ophthalmology - Adult Glaucoma
Complicated disease with eye manifestation - not well understood. Optic nerve (collection of all nerve fibres in the retina - think of it as the cable leaving the house), inner tube within it allows entry of arteries and exit of veins, and the outer is the nerve tissue. Loss of nerve fibre layer around the optic nerve, looking at the eye, can see thinning of the cup - the blood vessels come in over the edge of the cup - look at cup to disc ratio (once over a certain ratio know it is going to cause trouble). Slowly lose peripheral vision, many people will not notice until the central island is affected, and it is not reversible once it is established. Pressure is only one small component - but helps to identify those at risk
100
Ophthalmology - Adult Diabetic retinopathy
Can grade this based on view at back of eye. Pathology 1 Basement membrane thickened, 2 endothelial cell damage 3 RBC changes 4 platelet stickiness - all of this together --> occlusion, loss of pericytes (scaffolding of blood vessel) -> weakening and tiny aneurysms. Eventually vasculature between arteries and veins starts to degrade and the area of retina becomes starved of oxygen -> releases vascular growth factors (inappropriate response to grow new blood vessels to oxygenate the retina) - they are tiny fragile vessels and prone to bursting and bleeding -> sudden events with bleeding and loss of vision. Diabetic retinopathy screening programs are monitoring and trying to control diabetes to reduce this from occurring. Sight threatening when it affects the macula (central point) and/or proliferative retinopathy (new blood vessels, burst)
101
Ophthalmology - Adult Age-related macular degeneration
Disease of ageing, under the retinal pigment epithelium, deposits of drusin (waste material from epithelium layer) - deposits around the retina, as disease progresses, it breaks through basement membrane, allows blood vessels through, which can allow bleeding in the back of the eye 'wet' = bleeding -> scarring , and symptoms of loss of central vision (opposite of glaucoma) and distortion of vision. Test using the Amsler grid.
102
Ophthalmology - Adult Interventions
From public health perspective, important to consider primary, secondary or tertiary. Cataract ?YY, URE NYY, Trachoma YYN, Onchocerciasis YYN, VitA def YY?, Glaucoma NYN, Diabetic retinopathy YY?
103
Ophthalmology - Adult Summary
The problem is the ongoing ageing of the population, and need to be able to deliver the care and glasses to wider population
104
Ophthalmology - Child Why children are different from adults
Children do not complain of poor vision. Children's vision can be hard to assess. Late presentation can lead to permanent visual loss as the visual cortex fails to develop normally (amblyopia)
105
Ophthalmology - Child Impact
More likely to die in childhood, less likely to obtain education, lower earning potential, social stigma - low esteem, impacts whole family
106
Ophthalmology - Child Magnitude
~1 million blind children worldwide, the regional prevalence is much higher in Sub-Saharan Africa and South Asia, and lowest in Central Europe
107
Ophthalmology - Child Causes
Preventable: corneal scar. Treatable: cataract, glaucoma. Treatable and preventable: retinopathy of prematurity. The others are 'unavoidable'. ROP is a middle income country issue - premature babies survive, but the resources to manage and prevent ROP are limited.
108
Ophthalmology - Child Priorities for control
Low income: corneal scarring (preventable), cataract (treatable). Middle income ROP (preventable and treatable), cataract (treatable), and high income: myopia increasing (treatable), genetic eye disease
109
Ophthalmology - Child Corneal scarring causes
Vitamin A deficiency, measles, ophthalmia neonatorum, harmful traditional eye medicines
110
Ophthalmology - Child Vitamin A deficiency
Occurs in low resource settings. Contributes to child mortality. Risk factors: (3Ms measles, malabsorption, malnutrition) Impact: mucin comes from goblet cells, first change in VitA def is loss of goblet cells - changes in columnar cells - the conjunctiva becomes squamous, Bitot's spot, corneal xerosis [dryness] and ultimately ulceration. Clinical features: Night blindness, conjunctival xerosis, Bitot spots (chronic vit A deficiency), corneal ulcer is acute vit A deficiency and danger of going blind, ulcer/scarring indicates it has been there in the past. Acute decompensation can occur with underlying vitamin A deficiency, then measles tips the balance, and they go blind within 2 days - it is not a slow trajectory
111
Ophthalmology - Child Vitamin A deficiency intervention
Community surveillance strategy: Bitot spots in 6yo, signals that VitA deficiency is in the community, and the younger siblings at home are at risk of going blind. Treatment: Vitamin A replacement on day 1, 2 and day 14 in a liquid capsule - response is excellent if the ulcer/scarring is not established. Prevention: Short term: high dose vit A supplementation every 6 months, Medium term: food fortification (usually sugar), Long term: change eating/food behaviours, socioeconomic development. Issue with food fortification is that it causes discolouration
112
Ophthalmology - Child Measles
Corneal ulcer - treatment with Vit A 200,000 IU oral day 1, 2, 14 and topical antibiotic ointment x3/d. Measles may predispose of vitamin A deficiency (child suddenly decompensates and has a vitamin A deficiency associated ulcer), can get secondary herpes simplex ulceration (dendritic ulcer) - end result of all of these is corneal scar. Administration of vitamin A has no risk, but will cause good.
113
Ophthalmology - Child Ophthalmia neonatorum
Conjunctivitis in first 28d of life. Clinically swollen lids with pus discharge. Causes; NG/CT from vaginal tract - CT subgroups D to K, and tends to be less pus. Prevention: clean eyelids at birth (mechanical removal of vaginal discharge), apply ocular tetracycline. Treatment: clean eyes with swab/saline, 3-hourly tetracycline 1%, Cefotaxime 100mg/kg single dose IV (x3 for 7d if concern for meningitis)
114
Ophthalmology - Child Cataract
~200,000 children blind form cataract worldwide. Incidence 1/1000 live births. May be bilateral or unilateral. May be present at birth (congenital) or develop later (developmental). It may be isolated or with other ocular abnormalities (microphthalmos). Leucocoria (mother notices 'something white in the eye', abnormal retinal/red reflex. Differential: retinoblastoma). Management - referral to a tertiary level eye department for assessment for cataract surgery. Early surgery improves the visual prognosis
115
Ophthalmology - Child Retinopathy of prematurity
20,000 new blind infants/year, once blind it is not reversible. Due to retina not being fully developed when child is born. Stages 1-2 usually ok, Stage 3 treat, Stage 4-6 late (detachment/blind). Screening criteria: UK <31/40 or birth weight <1500g. MIC: more mature babies can be affected if neonatal care is inadequate and exposed to oxygen; then screen babies <36/40 and 2000g. Prevention: steroids to mother prior to preterm delivery, high quality neonatal care (good O2 management), screen newborn babies at risk. Management: laser or intraocular injection by an experienced ROP ophthalmologist, longterm follow up to detect eye complications
116
Ophthalmology - Child Summary
Main causes of avoidable blindness in children: corneal scar due to vitamin A deficiency (low income settings. Cataract (all countries, late presentations in low income settings), Retinopathy of prematurity (middle and high income settings). Challenge is to learn from Coca Cola - marketing strategies for distribution (same with glasses to poor regions)
117
Ophthalmology principles History
1 Red painful eye (with or without injury, one or both eyes), 2 cannot see well (one or both eyes, gradual or sudden), 3 Cannot read (everyone as they get older), 4 All other specific symptoms (decide if serious or not). Then measure the visual acuity
118
Ophthalmology principles Examine with a torch
Arclight (also has blue light which is useful for ulcers), also ophthalmoscope - designed for use in LMIC. Examine: do the eyelids open and close normally? Is the white of the eye white? Is the cornea clear? Is the pupil black and circular?
119
Ophthalmology principles Other tests
VA with a pin hole (used to diagnose that poor vision is due to refractive error), Intraocular pressure with a tonometer (used to assess the risk of glaucoma and monitor treatment), retina examination with an ophthalmoscope (used to diagnose retinal and optic nerve disease), slit lamp microscopy (used to give a magnified view of the contents of the eye)
120
Ophthalmology principles Acute red eye
1 Conjunctivitis (microbial, discharge - mucus or pus, clear cornea, Rx antibiotic ointment 3x/d) 2 Corneal ulcer (stromal infiltrate [white inflammation], fluorescein staining, Rx hourly topical antibiotics), 3 Deep corneal ulcer (hypopyon [pooling of pus in eye], corneal infiltrate, Rx hourly topical antibiotics - may also give 0.5ml Gent under the conjunctiva) 4 Herpes simplex - dendritic ulcer (Rx aciclovir eye ointment x5/d for 10d - avoid steroids, it will make it worse), 5 Acute iritis (clear cornea, irregular pupil, Rx dilate the pupil: topical predsol [if sure] - lots of causes include TB, leprosy, Brucella), 6 Acute glaucoma (dilated pupil, reacts poorly to light, hazy cornea due to oedema, Rx Diamox 50 stat then 250 x4 may use pilocarpine drops x4. Will need surgery/laser)
121
Ophthalmology principles Acute red eye summary
Conjunctivitis (normal cornea, discharge, usually both eyes, Rx Ab ointment 3x/d for 5d). Ulcer (white or grey mark on cornea, Rx intensive topical Abx), Iritis (irregular pupil, Rx dilate the pupil, steroids if sure), Glaucoma (hazy cornea, dilated pupil - diamox 250x4, pilocarpine drops)
122
Ophthalmology principles Eye injury
1 Corneal foreign body (remove - lie flat, local anaesthetic, light (dark room with torch on eye), loupe (magnification), lift off (saline wash, corner of card, ?needle) - trick is to rub the 'good' eye it will make the 'bad' eye lacrimate) 2 Hyphaema blunt injury (rest - it usually resolves, if 'full' watch for raised pressure) 3 Perforation of globe sharp injury (prolapse of tissue, irregular pupil, refer for repair of perforation - use cone to cover eye without adding pressure)
123
Ophthalmology principles Treatment summary
Antimicrobial (antibacterial, antiviral, antifungal), Pupil dilator (phenylephrine, cyclopentolate, atropine), Antiinflammatory (prednisolone, betamethasone, dexamethasone), Pressure lowering (Diamox, pilocarpine drops, Timolol drops)
124
Ophthalmology principles Cannot see
Visual acuity OK 6/6-6/12, Mild <6/12-6/60, Blind/Severe <6/60-LP, Blind to light - if <6/12 Causes: 1 Refractile error (improves with pin hole, the rest do not, Rx glasses), 2 corneal scar (white mark on cornea Rx protect the good eye) 3 cataract (grey/white pupil Rx unilateral surgery) 4 chronic glaucoma (pupil reacts poorly - late Rx refer as the good eye may be salvageable) 5 retina and optic nerve disease (normal cornea and pupil) refer
125
Ophthalmology principles Basic diagnostic equipment
1 Visual acuity chart (with 6/12 and 6/60 lines), 2 Arclight (torch and ophthalmoscope), 3 Pin hole (check for refractive error), 4 Cyclopentolate 1% (to dilate the pupil)
126
Ophthalmology principles Summary
The number of blind and visually impaired people is increasing due to population growth and ageing. At least 75% of visual impairment is curable, due to cataract and refractive error. The major causes of childhood visual loss are refractive error (myopia), cataract, vitamin A deficiency and retinopathy of prematurity. The major causes of red eye are conjunctivitis, corneal ulcer, iritis, acute glaucoma and eye injuries. The major causes of poor vision globally are refractive error, cataract, chronic glaucoma and corneal scar. Difficulty in reading occurs in nearly everyone as we grow older and is treated by reading spectacles.
