Week 10 Flashcards
Snake envenoming DDx Bullous swelling on hand
Snake bite, necrotising fasciitis, burn, phytotoxicity
Snake envenoming Viperidae
Relatively short, thick, short-tailed, often with colourful dorsal pattern (V or U), slow-moving but lightning-striking, cytotoxic bite.
Snake envenoming Treatment
Antibiotics (superadded infection), Tetanus toxoid is essential for deep penetrating wound, Antivenom is only required for systemic illness in the initial phase, Surgical debridement is essential to attain source control
Snake envenoming Elapidae
Beautiful, graceful, hooded body (cobra), bands of colouring
Tunga penetrans Summary
Jigger flea. Over 1 billion people live in areas suitable for transmission of tungiasis. Adult female sand fleas burrow into the skin-shady soil. Adult females burrow in the stratum granulosum (usually feet). Pain and itching -> difficulty walking, sleeping and concentrating on school or work. Tungiasis can be associated with abscesses caused by secondary bacterial infections. Rx: remove with sterile needle, aim to remove as a whole, if pierced, eggs are laid everywhere. Antibiotic cover. Control = One Health approach (treating the patients, sealing/spraying floors with insecticide, daily foot washing with soap, treating infected animals owned by affected families.
Mycetoma (Madura foot) DDx
Bacteria: Actino, TB/NTM, Botryomycosis, Bacterial OM. Viral: Kaposi Sarcoma, Fungal: Basidiobolomycosis, Chromoblastomychosis, Non infections: Podoconiosis, malignant tumour (sarcoma)
Mycetoma (Madura foot) Summary
Chronic, suppurative, granulomatous subcutaneous infection caused by bacteria (actinomycetoma) or fungi (eumycetoma). Usually soil/water transmitted via broken skin. Incubation period: 3 months to many years. RF: living in endemic areas, low socioeconomic status, working in agriculture/farming, history of trauma, having poor health education, poor accessibility to healthcare, M:F 3:1. Mycetoma belt (latitudes 15o South and 30o North. Central/South America & parts of Asia = actinomycetoma commonest (dry areas). Africa eumycetoma = commonest (high rainfall). Classic triad: painless woody swelling, sinus tracts, grains. Deep incisional biopsies are preferred to superficial samples. Polymerase chain reaction (PCR) is the most reliable method but has high cost. Leading bacterial cause Nocardia asteroides (white grain), fungal Madurella mycetomatis (black/brown grain. XR: periosteal reaction, osteoporosis, osteolysis. MRI: pathognomonic dot in circle sign in bone. Prevention: Footwear - also protects against Hookworm, Strongyloides stercoralis, Podoconiosis, Tungiasis, Venom bites and stings.
Mycetoma (Madura foot) Comparison
Fungal: extremities, mainly foot. Slow progression, well encapsulated, clear margin. Few sinuses. Late bone invasion, punched out lytic lesions on XR. Long term antifungal and surgical intervention (itraconazole for years). Bacteria: mostly feet, trunk and head involvement has been seen. Rapid, diffuse, unclear margins, inflammation and destruction. Many sinuses. Early invasion of bones. Osteolytic and osteosclerotic lesions on XR. Antibiotics. Surgery not usually indicated. SXT +/- second agent for months to years. Treatment options not based on comprehensive clinical trials - expert/local opinion.
Mycetoma Summary
Chronic, suppurative, disfiguring granulomatous subcutaneous infection caused by bacteria (actinomycetoma - commonest nocardia) or fungi (eumycetoma - commonest Madurella sp). Usually soil/water transmitted via broken skin. Incubation period 3 months to many years. High risk individuals are those in remote communities with limited access to healthcare and medications in tropical/subtropical areas. M:F 3:1. Clinical triad of painless tissue swelling, sinus tracts producing grains. Firm, painless masses under the skin, untreated can destroy muscle and bone. Treatment lasts months to years. Eumycetoma: Itraconazole +/- surgery. Actinomycetoma: SXT = gold standard. Can be prevented with footwear. Numerous adverse medical, health and socioeconomic consequences for patients, communities and health services. On the WHO Neglected tropical diseases list.
Myiasis Summary
Cordylobia nathropophaga (In Africa Tumbu, mango fly) US can sometimes see larvae under skin. Prevention: insecticides (BHC, DDT, pyrethroids), drying clothes inside or ironing. Vaseline over the top to oxygen deprive. South America: Bot fly: Dermatobia hominis (oval shaped maggots) - harder to get out, still use occlusive therapy but need cruciate incision to remove.
Polio Introduction
Ancient disease, Egyptians described, in the last century. Enterovirus (RNA), three serotypes. Faecal-oral transmission (or pharyngeal). Virus to mucosa to lymphoid to CNS. Incubation 7-14d (3-35d) - flaccid paralysis (‘AFP’). Case infection ration 1/100 to 1/2000 (serotype 1>3>2)- increases with age, increase during 20th century (improved hygiene meant that children were infected at an older age, and therefore were more likely to be paralysed when they were infected)
Polio Vaccines
Salk (killed IPV vaccine). Sabin (live OPV vaccine). Incredible response in HIC countries. Campaigns of twice yearly vaccines for children 1-5yo - Cuba 1962, Brazil 1980. 1974 added to the expanded programme of immunisation. 1985 PAHO declared target to ‘eradicate’ (though we would call this elimination) poliomyelitis from Americas, 1988 World Health Assembly declaration to eradicate poliomyelitis from the world by 2000.
Polio Eradication strategy
1 High routine immunisation coverage (emphasis on OPV) 2 National Immunisation Days (NIDs) (OPV to all children under five, more than 1 billion doses of OPV per year). 3 Acute Flaccid Paralysis (AFP) surveillance (expect at least 1 per 100,000 under age 15). 4 Mop up campaigns (house to house). GPEI Progress from 1988 350,000 cases in 125 countries, from 2000 no type 2, 2003 <1000 cases in 6 countries (>99.7% decline - talk of ‘end game’. Endgame challenges: To finish off wild virus, financial, certification, containment, stopping OPV, security against reintroduction. Vaccine hesitancy in northern Nigeria 2003 -> wild polio got into Hajj population and transmission moved from Nigeria through Middle East to India. Politics challenge. Fake vaccination used to seek Osama Bin Laden’s family (sequencing of the needles) - this has severely affected vaccination campaigns and hesitancy. India conversely is the most heavily vaccinated populations anywhere, in history. Israel ‘silent circulation of WP1’ OPV discontinued 2005, >92 coverage 4 doses IPV, widespread routine environmental sampling - transmission occurring as IPV does not prevent infection (it prevents disease) - OPV reintroduced 2013. Global approach 2014 >=1 dose IPV in addition to the OPV (move from trivalent to bivalent OPV). 2016 to stop introducing type 2 virus and hence VDPV-2. Global withdrawal of trivalent OPV and destruction of remaining stock - global substitution of bivalent 1-3 OPV. Every vaccination centre in every LIC and most MIC. Following this: wild type Afghanistan Pakistan, Nigeria, increasing cases cVDPV2 across Africa.
Polio OPV
Why? Easy to administer, less expensive than IPV (does not need as much antigen as it is self-replicating)), greater enteric immunity (very effective against infection), Transmissible - so immunises more than those vaccinated. Disadvantages: lower seroconversion in tropics (probably due to competing bugs within the gut of children in the tropics, competitive inhibition), causes paralysis approximately 1 per million doses (risk is first dose, many HIC moved to IPV as they could no longer accept that risk), transmissibility is a two-edged sword. Millions of field staff involved - vaccination of young children in nomadic populations is key
Polio Vaccine-derived polio viruses
First recognised 2000 in Haiti (genomic identification) Note cVDPV ‘circulating vaccine-derived polio virus’ - defined as having circulated for more than one year and associated with ?1% change in VP1 gene. Outbreaks by 2007: more and more viruses typed - reverts to wildtype virulence and transmissibility. Mainly type 2 (with limited wild-type immunity in the population as it had been eliminated)
Polio Current situation
WPV1 Afghanistan, Pakistan. cVPDV central Africa, VDPV2 Africa, Middle East, Indonesia - these are just the ‘cases’
Polio End game
Stop all wild virus circulation, stop all VDPV circulation, security against reintroduction, to stop all vaccination (but need 100% removal before this is possible)
Polio Stop all wild virus
Afghanistan and Pakistan - two of the most difficult countries - Geopolitics - Patience, diplomacy, high coverage, time and money. Need to give armed cover for vaccinators (they have been attacked and killed regularly)
Polio Stop all VDPV
New vaccines: novel’ OPV eg nOPV2 (less likely to circulate than Sabin OPV2 >1 billion doses since 2021 (including 0.5mil in Nigeria, despite the hesitancy and history). VLP (virus-like-particle vaccine under development - uncertain whether it will induce sufficient mucosal immunity)
Polio Security against reintroduction
Continued circulation: surveillance sensitivity: cVDPV2 in sewage in ten countries with no cases over past year. ‘Sensitivity’ difficult to define (very low case/infection ratio). Vaccine manufacture: live vaccines best for mucosal immunity, but may escape (security is an issue). Stored samples (eg faecal samples in labs). Immunodeficient carriers (rare, but can excrete for many years, without clinical signs)
Polio To stop all vaccination
Ideally, to maximise dividend (as long as virus circulates anywhere, the entire world is at risk). Unlikely in near future.
Disability, stigma and resilience Disability
Persons with disabilities include those who have long-term physical, mental, intellectual or sensory impairments which in interaction with various barriers may hinder their full and effective participation in society on an equal basis with others. - UN Convention on the Rights for Persons with Disabilities. Key messages: people with disabilities face stigma which leads to social exclusion, discrimination, reduced social support, and lack of access to healthcare. Unless stigma is adequately considered and addressed, we will continue to fail people with disabilities.
Disability, stigma and resilience Epidemiology
According to the WHO globally, approximately 1.3 billion people; 16% of the world’s population have a significant disability. 240 million children with disabilities worldwide, 53 million under 5 years old. According to the World Bank 80% live in LMIC and have limited access to services to meet their needs. Discrimination, distress, exclusion. More likely to report ill health: Diabetes 3x, HIV/AIDS 2x, Catastrophic health expenditure 50x, Malnourished and die as a child x2.
Disability, stigma and resilience Needs of people with disabilities
Regular health needs (like anyone else), Higher vulnerability to poor health. Specialised medical treatment or rehabilitation services (in some but not all cases). Inaccessible transport, cost, inaccessible buildings, inaccessible equipment, HCW skills and attitude - caregivers are often blamed or dismissed. Challenges: limited knowledge of disability restricted ability to provide care, need for training and awareness raising, pressure of work and numbers mean limited capacity to respond.
Disability, stigma and resilience The Missing Billion report
I perceive a need -> I decide to seek healthcare -> I reach healthcare venue -> I access healthcare services -> I engage with healthcare staff -> I receive treatment and follow up care
Disability, stigma and resilience Ways to provide inclusive healthcare
Map your network - social security, community leaders, nursing staff. Know your safeguarding and child safety policies and what to do. Communication. Attitude, Rights based approach. What that means as a healthcare worker: identify and tackle barriers across all levels, more and better data is needed, better inclusion services, better training of healthcare workers, better policies, laws, leadership and funding - and their enforcement, influence policy and programming
Renal Epidemiology
Worldwide access to end-stage kidney disease. 2.284 million people might have died prematurely. Largest treatment gaps in low-income countries - Africa (432000 people conservative model). Worldwide use of RRT is projected to more than double to 5.439 million people by 2030
Renal Patient journey in LMIC
Acute illness - evident. Recognised - locally. Treatment (easily) available. Shortterm, reversible. Low need for follow up. Well researched, managed, surveilled. Acute morbidity high, mortality high. Chronic illness - obscure. Recognised - distant (takes more steps up the line to be diagnosed). Treatment available. Long term, irreversible. Follow up crucial, Poorly researched, managed, surveilled. Acute morbidity low, mortality low. (Chronic diseases therefore attracts less funding). The double burden of disease: infections diseases <-> non-communicable disease (Lack of drugs, specialists and awareness to treat NCDs)
Renal Burden of CKD
850 million people are estimated to have CKD in the world. 13% of adults in sub-Saharan Africa have some form of kidney disease. 90% of adults living with CKD do not know they have it. USD 84 billion was spent on healthcare for people with CKD in 2017.
Renal Kidney disease in LMIC
Susceptibilities: decreased nephrons, genetics, pregnancy, comorbidities (HTN, DM, HIV, Sickle). Exposures: repeated subclinical injury. Endemic infections (Leptospirosis, Schistosomiasis, Leishmaniasis, Malaria, Hantavirus, Tuberculosis, SARS-CoV-2), repeated AKI episodes. Nephrotoxins (endogenous (myoglobin, haemoglobin), exogenous (allopathic and traditional medicines, environmental exposures), heat stress, dehydration and hypovolaemia)
Renal The problem
One in ten people have CKD worldwide. Up to 70% of ESKD reside in LMIC. All current eGFR equations have limited regional validation. These equations may be inaccurate in some instances. Delayed development of prevention and treatment strategies.
Renal CKD definition
Abnormalities in kidney structure and function, present for >3 months with decreased GFR (GFR<60) and/or markers of kidney damage. New eGFR equations that incorporate creatinine AND cystatin C but omit race are more accurate and led to smaller differences between Black participants and non-Black participants than new equations without race with either creatinine or cystatin C alone.
Renal Practical screening tools
urine protein dipstick, urine albumin/protein, GFR/creatinine/cystatin C. POC ultrasound. Urine protein dip: measures the presence of all proteins, including albumin. Graded as negative, trace or positive. While it is common, cheap and accessible, it is inferior to Albumin Creatinine Ratio (ACR). It can only be used for screening and not diagnosis.
Renal Symptoms and signs of CKD
Hypertension, pruritus, nocturia, restless legs, haematuria, dyspnoea, lethargy, vomiting, body swelling, anorexia
Renal Assessing for possible causes and complications of CKD
CKD in itself is not a primary diagnosis. Attempts should be made to identify the underlying cause. Ain Uganda this may include HIV, FBC, urine dipstick, urine sedimentation, lipid profile, HbA1c, EUC/LFTs, abdominal ultrasound scan (BPH, polycystic), ESR, ANA, cystatin C, serum calcium, phosphorous, albumin, vitamin D, parathyroid hormone, irone studies, kidney biopsy, CT scan
Renal Summary
Kidney disease occurs in 10% of adults. It is associated with high mortality. LICs have unique CKD risk factors. The eGFR equations may be poor in LICs. Cystatin C is good marker for CKD in native Africans. Determining CKD requires blood and urine examinations. Early screening and detection is key.
Renal Quality of life definition
An individual’s perception of their position in life in the context of the culture and value systems in which they live and in relation to their goals, expectations, standards and concerns. - WHO. Successful chronic disease management = improvement/minimisation of deterioration QoL. Calman gap - the difference between reality and hopes/aspirations
Renal Uganda
14 Nephrologists for 45 million population, dialysis support staff 49 nurses, 10 technicians, HD costs 104GBP/month (average income 90GBP/month). 13th leading cause of death, RF: female, >30, higher SES, BMI>25. Three care options: 1 Kidney transplant (almost available - 5 performed so far, live family donation only, costs GBP40,000 initially then GBP400 monthly for life. 1 in 5 allografts fail at 12 months, RF AKI post discharge and surgery >3.5h). 2 Haemodialysis (only available in 4 districts, twice weekly, costs GBP400 to start and GBP25 per week. Lots of complications; CLABSI, only 10% have a fistula). Anaemia is a proxy for overall management, the lower the Hb the lower the likelihood of treatment effect) or 3 Supportive care (Holistic management: physical, psychological, social and spiritual, improved quality of life
Renal Summary
Kidney disease is a silent killer in LMIC. Awareness, affordability and accessibility limit utilisation and growth of services. Prevention practices need to be enhanced. Renal supportive care can mitigate suffering.
Renal AKD Epidemiology
Burden of AKD is high, causes: Sepsis and hypoperfusion 87% (gastroenteritis, TB, malaria - preventable and treatable), nephrotoxins 3%, obstruction 5%, parenchymal kidney disease 3%
Renal AKD in LMIC
Common, patients are young, often severe, most commonly caused by infections and hypoperfusion, preventable and treatable, outcomes are poor, opportunity to ‘save young lives’. Challenges: Not many nephrologists, lack of kidney training for HCPs, inability to measure serum creatinine, infrastructure (including electronic health records) for patient follow up
Renal Management strategy
1 Risk assessment (tool kits, active surveillance), 2 Recognition (clinical [vomiting, low oral intake, weakness, oliguria reported by patient, hypotension, appetite loss, swelling], point of care testing [capillary creatinine at the bedside]), 3 Response (interventions: fluids./ medications, regional stations), 4 Renal support (implementation of PD, telemedicine for coordination, transfer to regional centres for critical cases), 5 Rehabilitation (follow up post AKI, a local level, point of care testing, guidance via telemedicine) - study in Malawi detected that 40% of patients with presumed AKD, actually had previously undiagnosed CKD
Renal PD for AKI
Simple: no machines/water plant. Effective: as effective as HD (no evidence for benefit of one modality over another). Affordable: cf establishing HD unit (commercial PD fluids expensive, but can be locally prepared). Can be done in all ages (inc neonates).
Renal AKD Summary
AKD is common in LMICs with poor outcomes in historical cohorts. Most cases are treatable with relatively simple means. The KCN proposes a novel approach to AKD management in LMICs. This approach is feasible and effective. Follow-up after AKD episode is essential as opportunities for CKD may be otherwise be missed. Acute PD is a good option for KRT in LMICs.
Renal HIVAN
A biopsy-diagnosis - limited to Black patients (APOL-1). Collapsing FSGS, microcystic dilatation of tubules, tubuloreticular inclusion bodies. CD4 not a good discriminator. A disappearing lesion?
Renal History of dialysis in Malawi
Robert Mugabe’s wife dialysis dependent, 1988 set up unit, used piped water - all patients died. 1998 vice president needed dialysis - it has been free of charge at the point of delivery ever since
