PAEDS Flashcards
Intussusception
- age
- presentation
- ix
- mx
CROUP -Who is affected -What is the cause -What are the signs and symptoms -What are the RF -What are the ddx -What is the mx
-6months-6years -Caused by parainfluenza virus, rsv, adenovirus -Present with; inspiratory stridor, seal like barking cough that is worse at night, coryzal symptoms, hoarse voice, widespread wheeze, +/- fever (but not toxic) RF; congenital heart defect, pre-existing narrowing, neurological disorders, laryngomalacia, past admission for croup -Mx; 1. minimal handling and examining, IVC and investigations are not required in an uncomplicated case 2. if case is complicated may require CXR/IVC/FBC+UEC+BC+ VBG + oxygen therapy 3. If mild/moderate croup give dexamethasone or prednisolone (give 2nd dose at next evening as croup worsens at day 2-3) 4. If severe croup give IV dexamethasone + nebulised adrenaline –> if good improvement keep for 4 hours and d/c home if no stridor, if not good improvement give another round of adrenaline and call for help
BRONCHIOLITIS -Who is affected -What is the cause -What are the signs and symptoms -What are the RF -What are the ddx -What is the mx
-Under 1 year -Caused by LRTI (RSV, adenovirus, parainfluenza) -Presents as acute URTI followed by resp distress and fever and one or more; cough, increased RR, retraction, widespread crackles/wheeze!! -Peaks at day 2-3 and resolves after 7-10 days -Signs; pale, chesty cough, increased WOB or apnoea, high RR, high HR, dehydration RF; under 10 weeks old, congenital heart disease or chronic lung disease, immunosuppressed, downs syndrome, ATSI, neurological disease Mx; very contagious via resp droplet -Is a clinical dx so no ix needed if mild Mild mx; small regular feeds, paracetamol, isolate at home, educate family on GP review in 24hrs/takes 7-10days to resolve/return if deterioration Mod mx; admit and do hrly obs, maintain hydration and only give 2/3 hydration due to risk of SIADH, paracetamol, oral sucrose for pain relief, comfort feeds occasionally, minimal handling or stimulation Severe; ADMIT and inform PICU, IV fluids and oxygen, minimal handling, CPAP/ventilation may be needed D/C home when; tolerating feeds, no periods of apnea or resp distress, maintaining o2 dats, conducive fam situation
sAcute asthma in a child -What are the characteristics -What are the signs on examination; how do you assess severity -What are the ix?
-Often precipitated by a viral URTI or exposure to allergens such as smoke or pollen, if under 12mo think bronchiolitis instead -Present w sudden onset cough, increased WOB, wheeze (not a good marker of severity), distress/irritability, +/- pulsus paradoxus (rare and only if severe) -Severity is assessed based on mental state, WOB, signs of respiratory distress, alterations in HR, ability to talk (from normal sentences, to only single words, to nothing) (in babies who cannot yet speak judge the severity on how much they can feed) -IX are not done, it is a clinical diagnosis
Anaphylaxis -Signs and symptoms -Management; DRABCD, when do they need to be admitted, what must be done before discharge
Multisystem allergic response that occurs within 30min of allergen exposure -Has at least one CVS/RESP + one GIT/skin symptom RS; tongue swelling, stridor, hoarse voice, persistent cough, wheeze, dysphagia, swelling/tightness in throat CVS; pale and floppy infant, palpitations, hypotension, low LOC GIT; diarrhoea, n/v, pelvic/abdo pain Skin; urticaria, pruritus, conjunctival erythema, flushing, angioedema, headache Dx is clinical!! Mx; -Adjust posture; upright to help breathe better -IM adrenaline into lateral thigh–> 0.01ml/Kg of 1:1000 (max of 0.5mg/ml)-> repeat after 5 min if not improving but consult ICU if more than 2 doses given w/o improvement -IV fluid resus; 20ml/kg 0.9% saline bolus -Airway; only give salbutamol if upper airway obstruction present–> if not responding to adrenaline then need to intubate quickly -Urticaria; antihistamines -Admissions; all need to be observed for 4 hours but admission required if; more than 1 adrenaline dose given, needed fluid bolus, home setting not conducive to returning to hosp -D/C; must have anaphylaxis action plan, must be educated on and have epipen, refer to allergy specialist
Peritonsillar Abscess/Pharyngeal Abscess -Bacteria responsible -Signs and symptoms -Mx
Caused by polymicrobials; staph and strep -Presents as; severe sore throat, hot potato voice (muffled), odynophagia, dysphagia, drooling, trismus (lock jaw), torticollis (contraction of SCM), neck swelling, respiratory distress (UA obstruction), chest pain Mx; -Admit -ABx; benpen and metronidazole -Insert IVC; take bloods (FBC, UEC, LEFT, Blood culture) -Give analgesia (paracetamol, ibuprophen) -Fluids -NBM -ENT consult/surgical drainage ?
Epiglottitis -Cause -Age group affected -Signs and symptoms -Mx
-Caused by H.influenza-> not as common now due to immunisations -Affects 2-4 year olds Presents as; child appears toxic -Fever, stridor, muffled/hoarse voice, odynophagia/dysphagia (causing drooling), NO COUGH, respiratory distress (narrowed airway), tripod position Mx; -Admit and call for help (contact PICU + anaesthetist) -Organise OT for early intubation + IVC insertion -Collect bloods; FBC, UEC, LFT, BC -IV Abx -IV fluids -Analgesia -Rifampicin prophylaxis for contacts -Don’t extubate for at least 48hours
GAS pharyngitis -When should they be admitted -What Abx can be used -What analgesia is available -What complications can occur
Admit if; suspected UA obstruction, systemically unwel, evidence of complications (abscess formation), significant comorbidity (immunosuppression)
Abx; phenoxymethilpenicillin or amoxicillin
-only give Abx for high risk groups
Analgesia; sucrose, paracetamol, ibuprophen, corticosteroids (if severe pain not responding to other analgesia)
Complications; abscess, epiglottitis, sepsis, ARF, post-strep glomerulonephritis
Cystic Fibrosis -Pathophys -Presentation -IX/DX -MX -Prognosis / complications
Path; -Mutation in the F508 gene causing dysfunction of the CFTR protein–> chloride channel is defunct meaning chlorine doesn’t exit the cells and move to the surface–> causes poor osmotic gradient and less water in secretions causing the mucous to be sticky and viscous (affects respiratory tract, repro, pancreas, salivary and sweat glands, intestines) Presentation; Resp; chronic productive cough, chronic sinusitis, dyspnea/wheeze, bronchiectasis, recurrent infections GIT; steatorrhoea, constipation, diarrhoea, rectal prolapse, intestinal obstruction -Infertility (esp males), deficiency in vitamin A,D,E,K as these are fat soluble Exam; -nasal polyps, some coarse crackles and rales, finger clubbing, increased AP diameter, biliary cirrhosis (pruritus), failure to thrive, absent vas deference, salty skin, kidney stones IX/DX; -Immunoreactive trypsinogen assay; done at birth and if levels are high is followed by sweat and genetic testing -Genetic testing; assess for specific mutations (specifically F508) -Sweat chloride testing; GOLD STANDARD, assess chloride concentration Mx; -Immunise (influenza and pneumococcal) Respiratory; use Abx in acute exacerbations, use daily chest physio/exercise/coughing to remove mucous plugs, use regular bronchodilators and saline aerosols, Dornase-alpha nebuliser (breaks down DNA in mucous making it easier to clear) Pancreas; pancreatic enzyme supplements, fat soluble vitamin supplements, high calorie/protein diets, monitoring of BSL (as 25% become diabetic) Subfertility; ART and screening of parents Liver; ursodeoxycholic acid (aids in dissolving gallstones) Prognosis; -Rarely live beyond 40 w/o transplants -Death is usually from resp failure or drug resistant infections Complications; -pulmonary infection -pulmonary HTN–> leads to RHF -atelectasis -pneumothorax -GORD -Malnutrition
Bronchopulmonary dysplasia -What is it -RF -Dx -Mx -Prognosis
-Is the need for supplemental O2 in premature infants who have no other conditions that may require increased O2 (HF, pneumonia)- often seen after ventilation as prem lungs are more susceptible to inflammatory changes post ventilation (norm development is interuppted and lung architecture is changed so that there are fewer alveoli and the interstitium is thick and has abnormal vasculature) RF; prolonged mechanical ventilation, FIo2, infections, pulmonary interstitial emphysema, male sex Dx; -NICHD criteria; 28 days of >21% o2 -Xray shows diffuse haziness and cystic sponge like spaces with areas of atelectasis Mx; -nutritional support -fluid restriction to prevent pulmonary congestion (can use diuretics but need to monitor UEC) -O2 supplement as needed -RSV monoclonal Ab (to prevent infection) -Abx/bronchodilators in the event of resp infection -Wean mechanical ventilation as early as possible Prognosis; -varies with severity -try and transition from mechanical vent–> cpap–> low flow 02 over 2-4 months -infants have a higher incidence of growth and neurodevelopemental delay and at an increased risk of pulm infections
What is infantile colic
Paroxysms of unexplained crying for more than 3 hours on more than 3 days per week for longer than 3 weeks
HUS- haemolytic uremic syndrome
- what is the cause
- what is patho
- what is the presentation
- what is the ix
- mx
- what are some complications
- triad of MAHA, kidney failure and thrombocytopenia
- Occurs mainly in those under 5 years post diarrhoeal illness
- Caused by E.coli infection–> shiga toxin causes endothelial cell dysfunction in the glomerulus–> causes vasoconstriction and formation of platelet microthrombus–> GFR is reduced and blood cells flowing through are destroyed by the microthrombi (MAHA) → hemolysis and end-organ ischemia and damage, especially in the kidneys
Presentation;
- Low platelets (i.e., thrombocytopenia); Petechiae, purpura, Mucosal bleeding, Fatigue, dyspnea, pallor, Jaundice, oedema, Impaired renal function, Hematuria, proteinuria, Oliguria, anuria, HTN
- Can lead to chronic renal failure
Ix; -FBC, blood smear (schistocyte), haemolytic screen (high reticulocytes, high LDH, low haptoglobin) UEC, urinalysis (haemaglobinuria), stool cultures/PCR, LFT (high bilirubin)
Mx; -supportive; nutrition, hydration, +/- ventilation -monitor UEC and renal function, perform dialysis if electrolyte abnormality,
-STEROIDS ARE NOT HELPFUL, ABX IS CI DUE TO INCREASE TOXIN RELEASE
Complications;
- AKI; oliguria, hyperkalemia, hypertension
- Neruological–> irritability, seizures, ALOC
- bleeding
- Cardiac–> hypertensive cardiomyopathy, myocarditis
- gastrointestinal–> bleeding, perforation, pancreatitis
Kawasaki Disease
- Pathophys
- Age affected
- Features
- DDx
- Ix
- Mx
- Mainly affects 3mo-5y and mainly boys
- Thought to follow an infection–> immune system attacks arteries and damages endothelium-> exposes collagen in tunica media and causes platelet aggregation–> these promote clot formation +fibrin deposition-> aneurysms, decreased blood flow to coronary tissues
- Complications include coronary artery vasculitis, coronary artery aneurysm, cardiac failure
- Features; CRASH and Burn
- Conjunctivis but sparing of the limbus
- Rash; polymorphous but eventually desquamates and peels
- Adenopathy; mainly cervical
- Strawberry tongue; red tongue and pharynx
- Hands and feet swell
- Fever that is non-responsive to antipyretics
- Can also have diarrhoea and vomiting, cough and coryza, arthritis
DDx; don’t want to miss staph infection (toxic shock or scalded skin), strep infection (scarlet fever), measles, viral exanthems, steven johnson syndrome, drug reaction, juvenile RA
-Dx confirmed with 5 days of fever plus 4 of the 5 CRASH symptoms
Ix;
- ASOT and Anti-DNAse B–> looking for strep infection
- ECHO to look for complications
- Platelet count; will be high
- LFT; high transaminases
- ESR/CRP; high
Mx;
- ADMIT
- IV access; fluids and take blood if needed
- IVIG to decrease risk of coronary aneurysm and suppress immune response
- Aspirin; will inhibit COX and stop platelet aggregation; need to monitor child closely to ensure doesn’t develop Reye Syndrome (encephalopathy and liver damage)
Pyloric stenosis
- Etiology
- RF
- Presentation
- Ix
- Mx
Etiology; Progressive hypertrophy causing thickening of the pylorus; presents normally between 3 and 6 weeks of age
RF; male, 1st born, family history, caucasian
Presentation; recurrent vomiting after feeding that gets progressively worse, is projectile, is NON BILLIOUS, can be blood stained, the infant is still hungry after
- can have weight loss or inadequate weight gain, can be severely dehydrated
- pyloric mass- ‘golf ball like mass’ can be palpated in epigastrium
Ix;
Bedside - capillary BGL, VBG (hypochloraemic hypokalaemic metabolic alkalosis)
Bloods - BGL, UECs (hypochloremia, hypokalaemia), FBC (differential for vomiting)
USS - investigation of choice
Mx;
- DRABCE
- Insert NGT- drip and suck
- IV fluids
- Need to correct acid base balance; monitor 4-6hrly
- Surgical mx; pyloromyotomy
GOR in babies
- when does it present, when does it peak, when does it resolve
- what is the pathophys
- difference between GORD and GOR
- presentation
- how does GOR differ from pyloric stenosis
- hx questions
- mx
- Gatro-oesphoageal reflux; presents at or shortly after birth and will peak at 4 months and resolve by 6-12 months
- occurs in 2/3rds of kids- very common
- Caused by a weak LOS that allows regurgitation–> increases in tone with age
- GORD is GOR that has lead to complications like eosphagitis, poor growth/FTT/aspiration and is more common in CP, downs syndrome, cystic fibrosis, GI abnormalities
Presentation;
- GOR presents with; effortless vomiting that is non-expulsive, burping, mild irritability but no other symptoms and usually in those less than 12 months
- GORD is GOR that presents with 1 of the following; oesophagitis, FTT, aspiration (chronic cough with wheeze, coughing with feeds, apnea)
- Pyloric stenosis occurs at 3-6 wks and GOR presents at birth, vomiting after meals occurs in both but is projectile and forceful in pyloric stenosis, dehydration and metabolic derangement occur in PS but rare in GOR
- Examination; ask about irritability, haematemsis, refusing feeds, weight loss, SOB/spluttering/coughing
-Mx
-Reassure and educate; common in up to 2/3rs of infant and is benign and self limiting and normally resolves in 6-12 months
-Keep breastfeeding; never change breast to bottle
-Keep upright or on tummy (prone) for 20 minute after feed (only under supervision- risk of SIDS)
-Try feeding small frequent amounts
-Refer to paediatrician if extremely irritable
If GORD and not GOR
-employ general measures plus can use PPI (omeprazole)
Intusussception
- who is affected; when does it peak
- etiology
- pathology
- points on hx/presenting features
- exam findings
- ddx
- complications
- ix
- mx
- how successful is air enema/how many recur
- Occurs from 2 months-2 years of age w a peak at 5-9 months
- Mainly idiopathic in children (thought to occur after recent illness due to hypertrophic lymph tissue ie.peyers patches) however in adults is related to CRC or benign polyps
Path; is telescoping of the bowel where the proximal section of the intestine slides into the distal-mainly the ileum going into cecum/ascending colon thru ileocecal valve–> mesentery is incorporated and therefore venous return is compromised and causes oedema/arterial occlusion leading to ischemia and necrosis
Points on hx/features;
- Hx of preceding illness, onsent of intermittent colicky pain (associated with pallor and indrawing of knees- will occur with increasing frequencies), vomiting (bile stained is LATE), bowel motions (blood and diarrhoea typically, red current jelly stool is LATE), distened abdomen
- Exam; pallor, lethargic, distressed, hypovolemic/distended abdo +/- palpable mass in RUQ or midline that is classically sausage shaped/tenderness/high pitched bowel sounds/rebound tenderness/check for hernia or testicular torsion
- DRE only done by senior consultant
DDx;
-gastro, IBD, hirschprungs, appendicitis, pyloric stenosis
Complications; bowel obstruction, perforation with peritonitis
IX;
FBC, UECs, BGL, G&H (if going to theatre), VBG (lactate)
AXR;Exclude perforation and bowel obstruction - proximal dilation & air-fluid levels
USS; Diagnostic - target sign-Children occurs mainly by ileum –> cecum through the ileocecal valve
Mx;
- DRABCDE
- notify surgeon
- IV access, fluids, analgesia
- Monitor UO, NBM (NGT if obstructed)
- If perf= urgent laparotomy + abx
- If obstruction= NGT drip and suck then air enema
- Air enema; give Abx prior, gives retrograde air pressure to reduce intussusception–> CI IS PERFORATION/NECROSIS
- Surgical management only needed if the bowel has perforated or is necrotic and likely to perf
-Air enema is 75% successful, can recur in 10-15% of patients
Constipation
- how common is it
- what is soiling/what is encopresis
- what are some etiologies of constipation
- what is the path of functional constipation
- what is the Rome 4 criteria for functional constipation
- what are some pertinent history questions
- what is found on examination
- what are some red flags of constipation
- what is the management (pharm and non-pharm)
- occurs in 30% of children aged 4-7
- soiling is the faecal staining in underwear caused by leakage of liquid stool around impacted faeces
- encopresis is the voluntary soiling by a child mature enough to be continent and indicates behavioural issues
Etiologies; Functional constipation (most common), lifestyle (low fibre or water), ineffecicent peristalsis (hirschprungs, spina bifida, metabolic causes like hypothryoidism, hypercalcemia, hypokaelmia), anorectal (fissures, congenital abnormalities), surgical (GI obstruction, peritonitis, post-op ileus), coeliac, cows milk allergy
-Rome criteria; (must include ≥2 criteria for at least 1 month);
≤2 stools/week, History of withholding evacuation - retentive posturing or volitional stool retention, History of painful or hard bowel motions, History of large diameter stools, Palpable faecal mass, At least 1 episode per week of soiling in toilet trained children
Hx q;
- SOCRATES; onset, freq, timing, consistency, colour, straining, diarrhoea in between episodes
- Retentitive posture (sitting with legs straight or cross whilst straining to hold in stool), blood in nappy or on wiping, fissures, vomiting, diarrhoea, anorexia, distension, PR loss
- Paeds hx; developement, weight loss, growth, fever, feeding history, urine output
- PMHX, soial and developemental hx, family hx
Exam;
-look for weight loss, pallor, palpate abdo looking for palpable faeces, anus for fissures, can do neuro exam
-Red flags; <6wks of age, ribbon looking stools (hirschprungs), weight loss or poor growth, vomiting or PR bleed, abdo mass
Mx;
-Nonpharm; foot stool, increase fibre and hydration, encourage toilet sits/bowel motions
Pharm; outpatient disimpaction using movicol satchets (multiple per day for 1 week) + maintenance osmotic/libricant with movicol and paraffin oil
-Inpatient disimpaction using colonlytely
PLUS other causes ruled out
Hirschprungs disease
- What is it
- Who is affected/gene/indicence
- Symptoms/signs
- Mx
- complication
- Congenital aganglionosis where the bowel wall nerve plexus has less ganglion cells and is therefore non-innervated–> causes decreased peristalsis and the proximal bowel will dilate/intenal sphincter fails to relax
- Causes delayed passage of meconium by or after 24 hours and chronic constipation, symptoms of bowel obstruction (abdo distension, pain, bilious emesis), failure to thrive
- Commonest in boys, RET syndrome, 1 in 5000 births
- DX; barium enema and then rectal biopsy
- AXR w contrast will show narrow rectum and transition zone
-Mx remove narrow section with surgical resection and anastamosis of remaining intestine to anus
Complications; hirshprungs enterocolitis- toxic megacolon followed by sepsis and shock
- is caused by obstruction causing dilation–> thinnning of colonic wall and bacterial overgrowth–> translocation of gut bacteria into systemic circulation
- present with fever, abdominal distension, bloody diarrhoea, obstipation
- mx; DRABCDE, NGT decompression + rectal tube, broad spectrum abx, SURGERY
Enuresis
- what is it
- who is affected
- what are some common causes of primary enuresis
- what is the mx of primary enuresis
- what is a wet alarm
- what are some causes of diurnal (day and night) enuresis
- what is the mx
- what is secondary enuresis and some potential causes
- what are the red flags of enuresis
- Inability to control urination- mainly bedwetting
- primary enuresis occurs where bladder control has not been previously attained and is normally due to delay in normal sphincter control mechanisms- occurs in 10% of 6 year olds (more boys than girls)
- Not considered pathological until 7 years
- Common causes of primary= delayed matruation, low ADH, emotional stress, UTI, developemental disorder, polyuria from diabetes, normal variation (small bladder, deep sleep)
- Mx; time and reassurance (20% resolve in 1 yr), behaviour modification like spreading fluid intake throughout day/avoiding caffeinated drinks at night/voiding prior to sleep, conditioning (wet alarms- requires referral to paediatrician), medications (not for long term but useful for sleepovers/camps–> oral ADH)
- Wet alarm is a rubber mat this is placed under the child and wired to a box–> when wet will sound alarm
- Diurnal= wetting during day and night
- caused by micturition deferral (holding until last minute), UTI, severe constipation, structural anomaly, neurogenic bladder, psychogenic stressor (stress, abuse)
- mx through treating underlying cause and doing behavioural modification (scheduled toileting, chart incentive)
- secondary enuresis is bed wetting in a child who has been dry for the past 6 months
- due to new psychological stress (new sibling, family death), UTI, diabetes (DM, DI), neurogenic bladder, cerebral palsy, seizures, thread/pinworm infection
-red flags; secondary enuresis, persisting past 7 yrs old, diurnal, change in urine colour, FUNDWISE symptoms, odd odour, change in gait (neurogenic- pudendal nerve), stool incontinence, polyuria/dipsia/phagia
Henloch Schonlein Purpura
- what is it
- presentation
- exam findings
- ix
- mx
- prognosis
- immune mediated vasculitis of children affecting 2-8y- due to deposition of IgA
- often preceded by a GAS URTI and resolve within 4wks
- mainly affects GIT, joints, kidneys and skin
Presentation;
-typical traid of palpable purpura (due to deposition of immune complex), arthralgia, abdominal pain and glomerulonephritis
GIT; abdo pain, PR bleed, vomiting
Renal; glomerulonephritis, occasionally ARF, RBC casts/protein/HTN
Skin; palpable purpura, usually symmetrical, occurs in gravity dependent areas
Arthritis; lower limbs, no effusion or warmth
Exam;
- HTN, symmetrical palpable purpura, petechiae, painful subcutaneous oedema, arthritis/arthralgia, signs of bowel obstruction, peritonism, altered LOC/encephalopathy
- complications; diffuse alveolar haemorrhage, peritonism/necrosis of bowel, encephalopathy, intussusception (due to submucosal haematoma)
Ix;
- urinalysis, UEC, FBC–> only main ones indicated in classic HSP
- look for renal complications (proteinuria) and thrombocytopenia/infection
- other ix include LFT, CRP, blood culture, meningococcal PCR
Mx;
- Mild pain= elevation (for oedema), rest, paracetamol, ibuprofen
- Severe pain= steroids to reduce duration of joint/abdo pain (oral pred), regular paracetamol
Prognosis;
- those who get renal complications get so within the first 2 months
- however renal complications can still appear 6 months after
- risk of recurrence is 30% but will get a shorter/milder episode
Urinary tract infections in children
- common causes
- RF
- presentation
- hx
- exam
- UTI (cystitis) vs pyelonephritis
- ix
- mx
- More common in females than males
- Most commonly caused by E.coli but can also be caused by klebsiella, enterobacter, proteus, staphylococcus saphrophyticus
RF;
-Female, uncircumcised male, past UTI, IDC, vesico-ureteral reflux, obstruction (congenital or stones), immunosuppression
Features;
- non-specific symptoms commonly- irritability, lethargy, fever, poor feeding, pallor, vomiting
- older verbal children can describe FUND (frequency, urgency, dysuria, nocturia), loin/suprapubic pain
Hx;
-associated symptoms; fever, nausea, vomiting, diarrhoea, blood, odour
exam; often normal and just present with fever and tachy +/- loin/suprapubic tenderness
- UTI - dysuria, frequency urgency, lower abdominal pain
- Pyelonephritis - high fever, toxic, lethargy, vomiting, flank tenderness
IX;
- clean catch urine MCS (dipstick is good initially but MCS will guide the tx), urine mcs, bloods (UEC, if child is unwell do FBC and culture
- consider LP/CXR if very unwell
- USS KUB only if obstruction is thought to be the cause/very unwell/renal impairment/boys under 3 months
Mx;
-DRABCDE- fluids, paracetamol (only if fever causing discomfort)
Well (cystitis) and >3 months= Trimethoprim PO for 3-7 days as an outpatient
Unwell (pyelonephritis) or <3 months= Admission + Benzylpenicillin IV + gentamicin IV - must check renal function and gentamicin levels before giving 3rd dose –> Switch to PO trimethoprim when improved
Follow up; follow up with GP in under a week
-if having recurrent infections or not responding to tx order a USS
Testicular torsion
- age group affected
- presentation
- examination
- ix;
- mx
- mainly affects neonates of adolescents aged 13-16
- presents as sudden, severe +++ pain, unilateral, swelling, constant, may radiate to iliac fossa, associated n/v, non-pyrexial, can follow minor trauma/sport
- will impair gait, teste can be high and horizontal, teste is red and render to palpation with absent cremasteric reflex, negative phrens sign (no relief with lifting the affected teste)
ix;
-clinical but need immediate doppler to assess blood flow–> torted teste will have decreased blood flow
+/- urine MCS if unsure
mx;
- immediate surgical referral
- admit
- analgesia
- keep NBM
- teste will become
Neonatal jaundice
- what are the RF (maternal, perinatal, neonatal)
- what are the common causes of jaundice if the fetus is;
- under 24hrs
- 24-74 hrs
- over 1 wk
- what history q are important
- what is the ix
RF;
- Maternal; ethnicity (asian), breastfeeding, fam hx, complications during preg (GDM)
- Neonatal; prematurity, genetic factors, polycythemia, drugs, infection
-UNDER 24HRS IS ALWAYS PATHOLOGICAL
<24hrs= sepsis, haemolytic disease, Rh/ABO incompatibility, congenitcal infection (TORCH)
24-72hrs= dehydration, G6PD, hemolysis, sepsis, spherocytosis, pyruvate kinase deficiency
over 1 wk= breast milk jaundice, prolonged physiological jaundice in newborn, neonatal hepatitis, conjugation dysfunction (Gilber syndrome), hypothyroidism, inborn errors of metabolism (galactosemia), biliary tract obstruction (biliary atresia)
Hx= onset of jaundice (before 24 hours and persisting past 3 days is pathological), is the baby unwell? (git obstruction, sepsis), do they have to be woken for feeds (lethargy–> encephalopathy), dark urine/pale stool (biliary obstruction= conjugated jaundice), is there dehydration/poor weight gain (can exacerbate the jaundice), was there birth trauma/bruising, maternal hx (her blood type/serology), fam hx of haemolytic diseases
Ix;
- SERUM BILIRUBIN–> see whether it is conjugated or unconjugated jaundice (will help ascertain cause)
- others as needed; FBC, LFT, coombs test, haemolytic screen, TFT, septic screen
T1DM
- incidence
- path
- signs/symptoms
- initial presentation
- hx questions
- exam features
- Ix + diagnostic criteria
- Mx
- signs of poor control
- T1DM occurs in 10% of australians
- Autoimmune condition in which T1 cells lack self-tolerance and destroy the pancreatic islet cells (insulinitis and atrophy of islet cells–> type 4 hypersensitivity response)–> no insulin production or release–> hyperglycaemia
Presentation; polyuria, polydipsia, polyphagia, glycosuria
- present with FTT/poor weight gain, lethargy, thirst–> short 2-3wk history
- some can present in DKA (abdo pain, vomiting, lethargy, coma)
Hx;
- polyuria; bedwetting
- polydipsia, polyphagia?
- fam hx of other autoimmune conitions
Exam;
- signs of poor growth
- signs of lipodystrophy/atrophy from poor injection technique
- check BP–> looking for renal complications
- Fundoscopy
- Signs of coeliac or hypothyroidism
Ix;
- BSL–> need regular monitoring at home with finger prick–> T1DM aim between 4-8 when fasting and under 10 post prandial
- HBA1C–> monitor every 2-3 months–> T1DM aim for 7% or lower
- Urinalysis–> looking for glucose, ketones, microalbuminuria (first sign of diabetic nephropathy)
- Coeliac/thyroid screen
- annual retinal screen
- islet cells Ab/insulin Ab/GAD–> autoAb in T1DM
- Insuline/c-peptide levels (low in T1DM)
Dx criteria=
Finger prick BSL above 7 is instant diagnosis of T1DM in a child
HBA1C= above 7.1%
BSL= random above 7.1 on 2 occassions
OGTT= above 11.1
Mx;
-Immediate insulin management
-Can either do continuous pump (gives rapid acting insulin throughout day)
-Can do twice daily regimen (give mixture of long acting and rapid acting before breakfast ad dinner)
-Basal bolus regimen (give long acting at night and then short acting before each meal)
-ongoing follow up of HbA1C every 3 months, annual TFT/Coeliac serology, retinal check starting 10yrs after diagnosis
-educate family
Signs of poor control;
-DKA, repeated hypo or hyper episodes, poor growth, lipodystrophy
What are common causes of collapse/syncope in a child
Respiratory (major cause in children); Upper airway obstruction - anaphylaxis, foreign body, croup etc.
Neurological; Seizures, Raised ICP, TBI
- *Metabolic;** Hypoglycaemia - not true syncope as don’t spontaneously recover,
- *Toxin or poison exposure;** Toxic ingestion, Venomous bites
- *Cardiac;** arrhythmias (long QT, SVT, WPW), structural congenital heart disrase (HOCM, congenital heart disease)
- *Orthostatic;** autonomic dysfunction, hypovolema, dehydration
- *Neural mediated;** vasovagal, situational syncope, breath holding spell
Hypoxic encephalopathy
- what does it cause
- how does it present
- what is the pathophys
- how is it diagnosed
- what is the mx and prognosis
- Causes cerebral palsy and other severe neurological deficits
- Presentas as; low APGAR score at delivery, metabolic acidosis in cord blood, within first 24 hours of life infant may develop apnea and seizures, abnormal EEG
Pathophys; lack of sufficient blood flow causes decreased oxygen content in the blood–> leads to loss of normal cerebral autoregulation–> diffuse brain injury
-greatly affects myelinated areas as these are more metabolically active and therefore affected by hypoxia
Dx;
- dx on USS, MRI or EEG
- shows severe encephalopathy (cortical and basal ganglia anomalies)
Mx;
- secure airway + adequate ventilation and oxygenation
- maintain sufficient fluids
- hypothermic state + maintain stable BSL
Prognosis;
- infants with mild encephalopathy normally make a full recovery
- 20% of infants die
- 25% develop serious sequale
Sepsis in a child
- common causes in those; under 3 months, over 3 months
- what is the difference between cold and warm shocl
- what is the mx of a septic child
<3 months; GBS, E.coli
>3 months; N.meningitides, strep pneumo, staph aureus, GAS, MRSA
Warm; wide pulse pressure, bounding pulse, rapid CRT, vasoplegia
Cold; narrow pulse pressure, slow CRT, common in infants and neonates, due to septic cardiac dysfunction
Mx;
- look for signs; fever or hypothermia, tachycardia/pnea, altered LOC, hypotension is late sign
- look for signs of local infection
- get IV access–> take blood culture, VBG, blood glucose
- Give IV ABx empirical (ceftriaxone + fluclox) +/- vancomycin if MRSA suspected, or give piptaz if chemo child
- do fluid resus; bolus of 20ml/kg crystalloid
- ionotropes; adrenaline for cold shock, noradrenaline for warm shock
- do a complete septic sceen–>CXR, Urine MCS, LP when stable
Acute Otitis Media
- cause
- RF
- incidence
- signs/symptoms
- HX points
- examination findings
- complications
- mx
Common causes; viral (25%), streptococcus pneumonia (35%), HiB (25%), moraxella catarrhalis (15%)
- caused by negative pressure in middle ear due to obstructed eustachian tube–> causes neg pressure–> edema of mucosa with exudate/effusion-> causes bacterial stasis and infection of nasopharyngeal secretions
- 90% have one episode by school age
RF; smoking in household, defect in eustachian tube (those with cranial abnormalities like downs syndrome, cleft palate), allergic rhintis, overcrowding (kindy/preschool attendance),
Signs and symptoms;
- fever, URTI, coryzal symptoms
- ear pain/tugging at ear
- ear discharge
- anorexia, vomiting, lethargy
- ask about meningitic symptoms
- Hx points–> swimming, history of grommets, frequency of ear infections/URTIs
Exam;
- febrile, signs of URTI (red pharynx, enlarged tonsils, coryza, cough)
- TM has loss of light reflex, middle ear landmarks (handle of malleus, incus, stapes) are not well seen, TM is also dull and can be bulging or retracted
- Can be hyperemic (but can also be hyperemic if theyre crying)
Complications;
- Acute–> perforation of TM (purulent discharge but pain relief), febrile convulsions, mastoiditis, suppurative labyrinthitis, meningitis, intracranial abscess, facial nerve palsy, lateral sinus thrombosis
- Chronic–> chronic suppurative Otitis Media, cholesteatoma, hearing loss (, learning difficulties (secondary to hearing loss)
Mx;
- most are viral and resolve spontaneously
- Antibiotics are only for select cases–> ATSI, immunocompromised, no improvement in 48hrs, <12 months
- Analgesia–> paracetamol or short term lignocaine drops
- Parental advice; don’t smoke, dummies limited to settling, give information sheet
- Inform parents that Abx risk outweighs benefits (NNT is 1/20)
What rash is this
- where is it present
- why does it occur
- how is the dx made
- what is the mx
- what is the mx of a flare up
- what is the mx for an infection
- Eczema/atopic dermatitis
- Presents on the forehead/cheeks/elbow and knee flexures, ankles, wrist, groin
- Is erythematous, thick and dry scaly skin that is intensely itchy
- Aggrevated by heat, dryness and prickly material
- Is atopic response and associated with IgE release–> linked with allergies, sinusitis/rhinitis and asthma
- can cause sleep disturbance and prone to secondary infection (bacterial or herpes)
Dx;
- itch plus 3 or more of the following; involvement of skin creases, visible flexural eczema, onset under age of 2, history of dry skin in the last year, pmhx of asthma or hayfever
- use the SCORAD tool to determine severity (score atopic dermatitis)
Mx;
- individualised plan that involves daily treatments and flare management
- Non pharm; avoid irritants (soap, overheating, excessive soaking, scratchy clothing/sheets, scratching skin), parent education + advice, daily cool baths, cold compress/wet dressings (sooth itch, rehydrate skin), diet (breast feed as long as possible)
- Pharm; steroids (betamethasone for body, hydrocort for face and nappy area), moisturisers (use 4-6 times a day, put on over the steroid cream), antihistamines (benadryl- good for relieving itch but only use for a short period), treat secondary infection (topical antibacterials)
- Tx for a flare up involves tar for lichenified lesions, topical steroid creams, abx for infected lesions, cool compress
- Mx for eczema infection includes; remove crust, take skin swabs, give PO cephalexin or fluclox (acyclovir if herpes infection)
What rash is this
- where is it present
- why does it occur
- ix
- what is the mx
- what is the ddx
Urticaria
- is elevated pruritic lesions surrounded by an erythematous base
- caused by transient extravasation of plasma into the dermis (due to high vasc perm–> associated with anaphylaxis/hayfever)
- need to take a good history to determine cause (food, bites/stings, infections, physical triggers, medications (abx))
- need to look for signs of anaphylaxis
Ix;
- none needed for acute
- for chronic (lasting longer than 6 weeks) can test FBC, ESR, ANA cell count differential (eosinophils)
Mx;
- remove the causative aganet
- cool compress
- don’t modify diet
- can give anti-histamines to alleviate itching (promethaxine)
- refer on if turns chronic, not repsonding to antihistamines, has a severe life threatening allergy or the angio-oedema is causing airway compromise
DDx;
- erythema multiforme (not itchy and not transient)
- masocytosis, flushing, HSP, pityriasis rosea
What rash is this
- where is it present
- why does it occur/bacteria involved
- complications
- what is the mx
- what is the ddx
Impetigo
- high contangious–> occurs on exposed areas of face/hands
- starts with a blister that bursts and leaves a red crusting lesion
- multiple types; nonbullous (GAS or staph, no scar), bullous impetigo (staph, no scar), ecythyma (GAS; punched out necrotic lesion that can leave a scar)
- Predisposing factors; skin abrasions, lacerations or burns, exzematous skin, scabies
Complications;
-cellulitis, staph scalded skin syndrome, post-strep glomerulonephritis, ARF, toxic shock syndrome
Mx;
- Remove the crusts from the sores and start abx (topical muciprocin or if extensive use oral fluclox, for those in rural areas give benpen IM single shot)
- need to cover lesions with watertight dressings and give medication until sores have healed
- keep in isolation until after 24hrs since starting mx as it is highly contagious
What rash is this
- where is it present
- why does it occur
- ix and complications
- what is the mx
- what is the ddx
Erysipelas- superficial form of cellulitis
- caused by GAS-beta haemolytic
- affects the upper dermis of skin and can extend into the superficial cutaneous lymphatics –> mainly affects lower limbs + face (cheeks and over nose)
- presens with abrupt onset + fevers, bright red/well demarcated/swollen area of skin–> can cause lymphadenopathy, malaise, chills
-IX; clinically but can do FBC showing high WBC, and elevated CRP
Complications; cellulitis, asbcess, gangrene, toxic shock syndrome, ARF, PSGN, thrombophlebitis
Mx;
1) Cold packs and analgesics to relieve local discomfort
2) Elevation of an infected limb to reduce local swelling
3) Compression stockings
4) Wound care with saline dressings
Abx; Flucloxacillin Orally, 6-H for 5 to 10 days
Vancomycin is used for facial erysipelas caused by MRSA
What rash is this
- what are the common organisms
- what are the predisposing factors
- what is the presentation
- how is it dx
- what are the complications
- what are the ddx
- what is the mx
Cellulitis- infection of the lower dermis and subcut tissues
- often caused by GAS, Hib, pseudomonas (feet)
- RF; skin abrasions, lacerations, bites, burns, eczema, furuncles, DM, CKD, obesity
-Presentation; unilateral, often on limb, area of erythema/warmth, painful swollen skin, may have lympangitis/lymphadenitis, systemic symptoms (fever, chills), skin lesions (eczema, wounds)
Dx; mainly clinical +/- wound swab for MCS
-if systemic symptoms get FBC, CRP, BC
Complications; abscess, nec fascitis, gangrene, sepsis (if gets systemic)
DDx; eczema, tinea infection, drug eruption, allergic reaction from bites, psoriasis, impetigo
Mx;
-Mark involved area to monitor, Rest + elevate limb, Cold packs and analgesics to relieve local discomfort, Wound care with saline dressings, Maintain fluid intake
Abx;
MILD (no systemic signs) 7 days (or until cleared); Flucloxacillin Orally, 6H; OR o Cephalexin 25mg/kg po 6H
SEVERE/EXTENSIVE; Admit to ward, Fluids, IV antibiotics
Usual = flucloxacillin 50mg/kg iv 6H - Add vancomycin if MRSA + Amoxicillin and clavulanic if unusual
-Call surgeons of abscess, debridement or NF suspected Internal medicine if patient septic
FUTURE ADVICE
▪ Avoid trauma
▪ Keep skin clean + moisturised
▪ Cut Nails
▪ Treat fungal infections of hands and feet early
What rash is this
- what are the common organisms
- why doesn’t it occur in adults
- what is the presentation
- how is it dx/ix done
- what are the complications
- what are the ddx
- what is the mx
Staph scalded skin syndrome
- blistering due to epidermolytic toxins A and B of S.aureus–> comes secondary to infection
- Presents as a small local skin reaction (erythema and crusting), fever and irritability–> after 24 hours the skin is red and wrinkled and fluid filled blisters arise and rupture–> cause burn looking appearance
- skin is tender and painful to touch–> Nikolsky sign (skin separates when rubbed, child becomes irritable when picked up)
- Uncommon in adults as we are able to renally clear the toxin–> babies have immature renal clearance system
- DDx; drug eruptions (SJS, TEN, DRESS)- common as the infection is first treated with antibiotics, however staph scalded skin doesnt involve mucous membranes and TENS/SJS do
- Complications; secondary bacterial infection (cellulitis), sepsis, dehydration/electrolyte imbalances, hypothermia
Ix;
-FBC, UEC, LFT, CRP, BC, Lesion swabs, Tzank distinguishes SSSS from TEN/SJS, NPA to look for carrier
- Mx;
- IV Abx - flucloxacillin or vancomycin (anti-staph)
- Dressings with emollient cream (vaseline)
- Analgesia - paracetamol, NSAIDs, severe cases can use opioids being wary of respiratory depression
- IVFs - rehydrate, increase clearance of toxin, correct electrolytes
- Monitor temperature - hypothermia
What rash is this
- what are the common organisms
- what are the RF
- what is the presentation
- how is it dx/ix done
- what are the complications
- what is the mx
Necrotising fasciitis
- Often caused by GABHS (strep), staph aureus, anaerobes (clostridium, actinomyces)
- 4 main types; T1 (polymicrobial- T2DM), T2 (GAS-limbs), T3 (clostridium, vibrio), T4 (immunosuppression)
RF; DM, PVD, Renal failure, ETOH, malignancy, recent srug, penetrating trauma
Presentation; looks like cellulitis- dusky pink/purple appearance that rapidly spreads, swelling, very painful, can progress to gangrene, the tissue feels hard and ‘woody’
Ix; FBC, UEC, LFT, CRP, CK, Coags - low platelets
Mx;
- DRABCDE
- Admit, fluids, analgesia
- IV Abx; fluclox + clindamycin +/- vancomycin +/- meropenem
What rash is this
- what are the common organisms
- why doesn’t it occur in kids older than 8
- what is the presentation
- what are the RF
- what are the complications
- what is the mx
- Scarlet fever; follow GAS infection (strep throat or impetigo)
- By 10 the body has already formed Ab so is able to fight the infection
- Presents as a rash 12-48hrs after the fever–> starts below the ears, neck, chest, armpits and groin–> look like scarlet spots or blothces that spread, have rough sand-paper like skin–> skin will peel by day 6
RF; same as RF for strep and impetigo; overcrowding, day care, camps, age between 2-10, known contact with GAS
MX;
- Orap penicillin for 10 days (or one single IM shot)
- Paracetamol
- fluids
- antihistamines for itch
Complications;
-RF, OM, pneumonia, septiciaemia, PSGN, osteomyelitis
What rash is this
- what are the common organisms
- what is the presentation
- how is it dx/ix done
- what are the complications
- what are the ddx
- what is the mx
HSV Gingovstomatitis
- Caused by HSV –> trasmitted through direct contact, generally lasts 10-14 days
- presents as painful erythematous based lesions, drooling, refusal to eat/drink, fever, irritability, dehydration
Dx;
- clinical mainly
- if need to confirm HSV–> do scraping of lesion and then do direct immunofluorescence
Mx;
- analgesia–> topical lignocaine, codeine may help, cool compress
- if dehydrated–> admit, rehydrate, consider acyclovir
What rash is this
- what are the common organisms
- why doesn’t it occur in adults
- what is the presentation
- how is it dx/ix done
- what are the complications
- what are the ddx
- what is the mx
- Chicken pox
- Varicella zoster virus
- Incubation period of 2 weeks–> short prodrome of fever, lethargy and anorexia
- Presents with an eruption of a rash over 3-5 days; crops of papules which become vesiular and erythematous and then rupture and crust over
- all lesions are usually crusted by day 10
- lesions are commonly on the scalp/face/trunk/mouth/conjunctivae
Ix;
- usually clinical but PCR can detect varicella virus in a skin lesion
- can do serology (IgM, IgG) - mainly only in pregnant women
Complications; bacterial superinfection (GAS), dehydration, pneumonia, encephalitis, hepatitis, arthritis
Mx;
Well child–> symptomatic treatment with calamine lotion/cool compress/warm baths/moisturisers
-stop child from scratching, give paracetamol for fever/pain, antihistamines can help with itching for sleep
-DON’T give aspirin (already at risk of reye syndrome)
-keep isolated from 2 days pre-lesion until all lesions have crusted over
Unwell child–> admit all neonates, those who are immunocompromised, those with cellulitis, altered mental state, cough, SOB, high RR
- symptomatic treatments (as with well child)
- may need IV or oral acyclovir
Prevention;
- VACCINATION–> 12 months
- infection precautions–> keep out of school for infectious period, droplet precautions
- varicella immunoglobulin; used in those who are neonates, on immunosuppressive therapy or pregnant
What rash is this
- what are the common organisms
- why doesn’t it occur in adults
- what is the presentation
- how is it dx/ix done
- what are the complications
- what are the ddx
- what is the mx
Slap cheek syndrome/Parvovirus/Fifth disease
- caused by parvovirus B19
- virus targets RBC in bone marrow and causes non-specific symptoms (fever, headache), red cheeks develop and last 2-4 days, then lace like pattern appears on limbs
-Incubation of 7-10 days, spread via resp droplets
Complications;
-polyarthropathy, aplastic crises, spontaneous abortion, hydrops fetalis, encephalitis, hepatitis, thrombocytopenia
IX; is mainly a clinical dx
-can do FBC if child is severely unwell
MX;
- cool compress and paracetamol
- if in aplastic crises can do RBC transfusion or IVIG
What rash is this
- what are the common organisms
- why doesn’t it occur in adults
- what is the presentation
- how is it dx/ix done
- what are the complications
- what are the ddx
- what is the mx
- Hand foot and mouth disease
- caused by coxsackie virus, or enterovirus
- due to diet contact with the skin, nasal and oral secretions or through fecal contamination
- Presents in those under 10 with viral symptoms (fever, sore throat), mouth lesions (can be painful), lesions on the dorsal and palmar surfaces of the hands and feet (pink patches that can turn to grey blisters), small vesicles and ulcers around the mouth/palate/pharynx
- resolve in a week with no scar
Ix;
- clinical diagnosis
- those with severe infection can have high WCC and atypical lymphocytes
MX;
- no specific treatment
- ensure adequate oral intake
- use antiseptic washes/analgesia for pain alleviation
- keep child home from school until lesions have healed
Complciations; dehydration, myocarditis, meningoencephalitis, pulmonary oedema/pneumonia, acute transverse myelitis
What rash is this
- what are the common organisms
- why doesn’t it occur in adults
- what is the presentation
- how is it dx/ix done
- what are the complications
- what are the ddx
- what is the mx
Molluscum
-these are firm peary dome shaped papules with central umbilication that can occur anywhere on the body–> most resolve spontaneoulsy in 6-9 months but can persist for up to 1 year
Mx;
- educate parents
- most don’t require treatment
- scarring from tx is often worse than the lesion
- lesions can be removed with cryotherapy, curretttage, benzyl peroxide or imiquimod cream
What rash is this
- what are the common organisms
- what is the presentation
- how is it dx/ix done
- what are the complications
- what are the ddx
- what is the mx
SCABIES
-RF; contact transmission so overcrowding, poor hygiene, tropical areas–> lesions are a host immune response to the mite
-Presents as classic or crusted scabies
Classic; 5-15 mites, acral distribution (web spaces, wrists, buttocks, breasts, palms, soles of feet, scalp), obvious papules/burrows, intensely itchy and worse at night–> excoriation can cause secondary infection
Crusted; have millions of mites and more common in immunocompromised patients–> HTLV, HIV, steroids, DM
Complications; impetigo, cellulitis, abscesses, bacteraemia, sepsis, PSGN, ARF
DDX; insect bites, folliculitis, impetigo, dermatitis
Ix; normally clinical dx but can do skin scraping with light microscopy or dermatoscopy
Mx;
- Topical 5% permethrin cream; apply to whole body (below neck) and leave on for overnight (8 hours) and repeat in 7-10 days
- Second line is benzyl benzoate (25%) same as permethrin use, but more irritating to the skin
- Third line is oral ivermectin 2 doses (7 days apart)
- need to treat all contacts in the house and ensure clothes/laundary items/sheets are boiled, leave mattresses in sun
- can manage itch with topical CS or oral antihistamines
- can return to school after 2 treatments
What rash is this
- what are the common organisms
- what is the presentation
- how is it dx/ix done
- what are the complications
- what are the ddx
- what is the mx
Toxic epidermal necrolysis (TEN) or Stephen Johnson Syndrome (SJS)
-Caused by an immune complex mediated hypersensitivity reaction causing separation of the epidermis from the dermis –> very rare
- Caused by ABx, NSAIDS, allopurinol, antiepileptics, penicillins–> NOT INFECTION
- Will have excessive mucosal lesions, fever above 38, large painful bullae, nikolsky sign (skin separating when friction applied), erythema, full thickness necrosis
IX;
FBC, UEC, LFT, CRP, BC (if thinking staph scalded skin or pt unwell), skin swab (mcs)
Mx;
- DRABCDE
- cease offending drug
- burn dressings
- consider plasma exchange (IVIG)
What rash is this
- what are the common organisms
- what is the presentation
- how is it dx/ix done
- what are the complications
- what are the ddx
- what is the mx
MEASLES
- caused by measles virus–> spread via resp droplets
- contagious 2 days before symptoms to 5 days post onset of rash
- prodrome of coryza/cough/conjunctivitis/koplik spots, fever
- rash is erythematous macular rash over the face and trunk that fades after 3-4 days
Ix; NPA for PCR, bloods (check IgG and IgM for vaccination)
Complications; diarrhoea, AOM, pneumonia, bronchitis, croup, conjunctivitis, mouth ulcers, acute glomerulonephritis, febrile seizures, encephalitis
Mx; supportive and isolation- no curative medication
What rash is this
- what are the common organisms
- what is the presentation
- how is it dx/ix done
- what are the complications
- what are the ddx
- what is the mx
Rubella
- mild and of limited significance unless you are pregnant
- presents as fever, coryza, cervical LAN, petechiae on palate
- rash is mainly on trunk, small pink macules and after rash passes (5days) the skin with desquamate
- contagious for 7 days before and 7 days after rash dissapears
Complications; infection when pregnant can cause congenital rubella syndrome and cause baby to be blind/deaf, have mental retardation, meningoencephalitis, jaundice, DM, thyroid malfunction, congenital heart disease
Ix; PCR of blood/urine/skin swabs
- IgG/IgM
- management is supportive
