PICU & A&E

PICU & A&E Airway & Breathing Children under 6m = obligate nasal breathers All children are diaphragmatic breathers à tire easy & affected by full stomach Chest expansion is low as ribs lie horizontally at rest Serious parenchymal injuries can occur without rib # Respiratory Distress Stridor (upper airway obstruction, inspiratory – e.g. croup / epiglottitis) Wheeze (lower airway obstruction, expiratory – e.g. asthma) NB: noise doesn’t correlate to severity, Silent chest is BAD Grunting (expiration against a partially closed glottis à peak end expiratory pressure) Head Bobbing (use of accessory muscles) Nasal Flaring (esp. in < 6 months) Recession (sub-costal, intercostals, sternal, tracheal) Harrison’s Sulci (permanent line under rib cage) SpO2 < 70% NB: if signs, but resp. rate normal = exhaustion = pre-terminal sign Decreased respiratory drive in children = raised ICP, poison or encephalopathy Sats SpO2 of <85% = seriously low 92-85% = low >92% = normal Preterminal signs Exhaustion Bradycardia Cyanosis Hypotension ET tube sizes Internal diameter = (age/4) + 4 (in mm) Length = (age/2) +12 for oral (+15 for nasal) Circulation Systolic BP of little use in critically ill child (hypotension is a late pre-terminal sign) Diastolic hypertension is a warning sign for circulatory collapse Low pulse & poor perfusion à metabolic acidosis à increased RR Sternal capillary refill > 2 sec = poor perfusion / low temperature SBP = (age x 2) + 85 With cuff width > 80% of upper arm length and bladder > 40% of arm circumference Blood Flow Flow (Q) = pressure (P) / resistance (R) Resistance Flow (Q) = π P r4 / 8 h l Therefore control of vessel radius is essential for control of flow and pressure Elastic recoil of arteries maintains pressure difference during diastole à ensures forward flow Pulse pressure Pulse pressure = systolic – diastolic MAP = diastolic + 1/3 pulse pressure Veins can act as compliance vessels – usually partly collapsed but can hold up to 60% blood volume Local control of flow Vasodilator theory – lactic acid + CO2 produced by increased metabolism à increased dilatation à increased flow O2 demand theory – tissue is sensitive to low O2 à dilatation Auto-regulation – tissues respond to BP changes to ensure continual flow Chronic changes – e.g. athlete – chronic demand à increased vascular beds due to endothelial growth factors Neural control of flow Sympathetic autonomic – fibres secrete NA à vasoconstriction à increased HR + increased contractility Parasympathetic – ACh à vasodilatation & lowers HR BP regulation Acute Baroreceptors in carotid sinus & aortic arch – respond to stretch à brainstem à autonomic response Chemoreceptors respond to low O2, high acid / high CO2 à raise arterial pressure Most active when cerebral ischemia à sacrifice other tissues to protect brain Intermediate Transcapillary stress relaxation – veins stretch to absorb increased pressure. Takes 10-60 minutes Renin-Angiotensin system Angiotensinogen ¯ In plasma by Renin ¯ (from Juxtaglomerular cells) Angiotensin I ¯ in lungs Angiotensin II ¯ Vasoconstriction in kidney & acts at adrenals à increase aldosterone à salt and water retention Long term Aldosterone requires 2-3 hours for stimulation by angiotensin II. Takes a week for peak effect ADH (from thalamus) in response to atrial stretch receptor response à water retention AND if high concentrations à vasoconstriction (hence name vasopressin) Cardiac Output CO = HR x Stroke Volume = arterial pressure / total peripheral resistance Increased muscle stretch à increased force of contraction (until overload) = Starling’s Curve ECGs Left anterior hemi-block à Left axis deviation Left posterior hemi-block à Right axis deviation Bifascicular block = RBBB + Left Ant OR Post à RBBB & LAD LBBB – is always pathological à not possible to diagnose hypertrophy Newborn axis is +110 to +180 Fallots à pulmonary obstruction + RV hypertrophy à RAD PE à RAD Tricuspid atresia à LAD Secundum defect à often normal ECG, later develop RAD Urine output Min 1ml/kg/hr in children Min 2ml/kg/hr in infants Fluid boluses: Poor perfusion = 20mls/kg 0.9% saline Hypoglycaemia = 2mls/kg of 10% dextrose Disability Decorticate = flexed arms, extended legs Decerebrate = extended arms and legs Increased ICP à hyperventilation à apnoea Cushings response = hypertension & sinus bradycardia = compression & herniation GCS Score 1 2 Eyes Closed Pain 3 Voice 4 Open 5 6 Voice None Grunt / moan / irritable / crying inconsolable Inappropriate words / crying with pain / partially consolable Disoriented / inappropriate interaction /consolable crying Spontaneous / alert Motor None Extension to pain Flexion to pain Withdraws from pain Localises pain Spontaneous Exposure Check for rashes & any signs of injury (inc NAI) Remember to recover to prevent hypothermia Observations <1yr 1-2yrs 2-5yrs 5-12yrs >12yrs Resp Rate 30-40 25-35 25-30 20-25 15-20 Systolic BP Body weight (1-10yrs) PLS Resus Choking Pulse Rate 110-160 100-150 95-140 80-120 60-100 Systolic BP 70-90 80-95 80-100 90-110 100-120 = 80 + (age x 2) = 2 (age + 4) 5 rescue breaths, 15:2 5 back slaps, 5 abdo thrusts à CPR Urine output 2ml/kg/hr 1ml/kg/hr 0.5ml/kg/hr W E T F A G Weight Energy ET Tube Fluid Bolus Adrenaline Glucose (Age + 4) x 2 4J / Kg (Age / 4) + 4 (+/- 0.5 sizes available) 20mls / kg 0.1ml/kg of 1:10,000 (= 10mcg/kg) 5mls / kg of 10% Total blood volume = 80mls/kg (up to 2 yrs.) or 70mls/kg (over 2yrs) Hypotension due to blood loss in a child requires 25% loss Bicarb 1mmol/kg (if used) ONLY use if ventilation established as paradoxically worsens acidosis Atropine = 20mcg/kg For shock resistant dysrhythmias Amidoarone 5mg/kg Lidocaine 1mg/kg Inhibits conduction Assoc with methaemaglobinaemia Can be used as local analgesia IO access – anterior-medial tibia. 1-2cm below tibial tubercle Causes of arrest Hypoxia Hypovolaemia Hypothermia Hyper/Hypokalaemia Tension Pneumothorax Thrombus Tamponade Toxins Types of arrest Asystole = most common – Due to hypoxia / hypovolaemia PEA = Tamponade, Tension pneumothorax or hypovolaemia VF/VT = Hypothermia, hyperkalaemia, toxins Asystole / PEA Immediate Adrenaline (then repeat every 4 minutes) 10mcg/kg = 0.1ml/kg of 1:10,000 à increases coronary perfusion and contractility (If giving by ET tube then x100 dose) Bicarb ONLY once good ventilation established For cases of prolonged arrest, hyperkalaemia, TCA overdose 1mmol/kg = 1ml/kg of 8.4% NOT to be given via same line as Ca infusions as causes precipitates Inactivates adrenaline therefore use a big flush Ca2+ ONLY to be used if hypocalcaemia, hyperkalaemia, calcium channel blocker overdose or hypermagnesaemia VF / VT Shock 4J/kg Then immediate 2mins of CPR] Then recheck pulse Repeat shock every 4 mins Adrenaline (after 3rd shock, then alternate shocks) 10mcg/kg = 0.1ml/kg of 1:10,000 Amiodarone (after 3rd & 5th shocks only) 5mg/kg If not available then use lignocaine 1mg/kg Precordial thump Only if witnessed monitored arrest and defib not available Magnesium Only if low magnesium or torsades-du-points Post Arrest Aim for sats 94-98% (hyperoxia can damage tissues) Active cooling IF hyperthermia (aim form normal core temp) Ionotropes as required Fluids Maintenance Fluid Requirements Birth à 3 months = 150ml/kg/day 3 à 6 months = 120ml/kg/day After 6 months = 100ml/kg (1st 10kg) + 50ml/kg (next 10kg) + 20ml/kg (after that) If Dehydrated = Maintenance + Deficit + Ongoing Losses Level of Dehydration Weight loss (apparent or actual), Mild = <5% loss Moderate = 5-10% Severe = >10% 5% - decreased skin turgor, sunken fontanelle, sunken eyes, lethargic, NORMAL HR 10% - mottled, poor cap refill, deep fontanelle, deeply sunken eyes, increase HR, decreased vol, prostration, coma Behaviour, history, Mucous membranes (mouth, lips, eyes) Capillary refill (should be < 2 secs) Skin Turgor (check on tummy – should spring back in less than 2 sec) Fontanelle (if still palpable) HR = increased (but decreased pulse vol) BP = increased (if decreased = late sign) Urine Output (serious if decreased, see BLS for values) Management of Dehydration Mild = drinking / NG top up, only IV fluid if vomiting Moderate = oral if possible + IV if insufficient oral intake Severe = IV (or intraosseus if no IV access available) Isotonic = correct over 24hrs with 0.9% saline / 0.45% saline with 5% dextrose Hypotonic (low Na+) = replace salt & give isotonic fluid Hypertonic (high Na+) = correct over minimum 48hrs, with isotonic fluid aim to decrease Na+ by ½ in 1st day (if faster à cerebral oedema & fits) Types of fluids Normal Saline (0.9%) 154mmol/l of Na Dextrose-Saline 0.18% Saline + 4% Dextrose = 30mmol/L Na (& Cl) = 4g dextrose / 100mls = 40g / L = 160 calories / litre Ringers Lactate (Hartmann’s) 131 mmol/L of Na 111 mmol/L of Cl Balances to better replace extracellular loss Fluid & electrolyte abnormalities Osmo gap = difference in calculated and actual Osmolarity (estimated) = 2 (Na+) + 2 (K+) + Glucose + Urea NB: if lab osmolarity > estimated then consider alcohol, ethylene glycol or other additives Anion Gap Contribution of unmeasured anions to acidosis Calculate as K+ + Na+ - Cl- - Bicarb Normal range is 8-16 Doesn’t count PO4, Acetate or ketone Shock O2 2x large IV access Blds Abx If signs of shock present give fluid bolus Severe shock = 10-20ml/kg of normal saline over 30 mins Moderate shock = 10-20ml/kg of normal saline over 1 hr If requires above 40-60 mls/kg then arrange intubation, vasopressors, central access etc Cardiogenic shock – Causes Cardiomyopathy – dilated/hypertrophic/restrictive Myocarditis – infective/autoimmune Arrhythmias CHD – Aortic stenosis, hypoplastic left heart, coarctation Hypertension HTN = > 95% centile for height, weight & gender Small cuff à false high reading Causes Vascular – thrombosis, coarctation Renal – parenchymal disease / failure Drugs – steroids, cocaine Catecholamines – phaeochromocytoma, neuroblastoma Others – bronchopulmonary dysplasia, ECMO, renal tumours, Conns, Cushings, Congenital Adrenal Hyperplasia Ix - Urinalysis, cultures, UEs, LFTs, CRP, FBC, Renin & aldosterone levels, Spot urine for catecholamines, CXR, ECHO, ECG, Renal US Rx - Diet, exercise, decreased Na load. If no response à drugs Hyponatraemia Na < 130 mmol/l Fictitious = Increased plasma osmo (e.g. hyperglycaemia) Pseudo = normal P.osmo (e.g. increased lipid / protein) True Extra renal Na loss - (U.Na = < 20). Gastroenteritis, fistula, CF, adrenal insufficiency Renal Na loss - (U.Na > 20). DKA, diuretic, fanconi, mineralocorticoid deficiency Non-oedematous increased H2O - (U.Na > 20) SiADH, antidiuretic drugs Oedema – nephritic syndrome, cardiac failure NB: thirst is stimulated by osmolarity (usually > 280ml) so dehydrated with low osmolarity won’t be thirsty until… Thirst is overridden by low BP à RAA system activation à Na+ & H2O retention & some increase in osmolarity à thirst & ADH secretion (water retention)à drink This is VERY DANGEROUS as the water intake will reduce osmolarity further Hypernatraemia Dehydrated Reduced fluid intake – not available, coma, dysphagia, loss of thirst mechanism (head injury, meningitis, sarcoid) Loss of water (H2O with low Na+ content) – GI (vomit, diarrhoea, fistula), skin (sweating, burns), Lungs (hyperventilation / ventilated on dry air / tracheostomy), Urine (DM, DI) Oedematous Excess intake – dietary, psychogenic Sodium retention – Conns syndrome (primary hyperaldosteronism) à High (N) Na+ & water retention (to dilute Na+) with low K+ and low H+ (= high bicarb) = metabolic alkalosis Hypokalaemia Inadequate intake (U.K < 20) Extra renal loss (U.K < 20) Low plasma bicarb – diarrhoea, GI stoma, fistula High plasma bicarb – laxative abuse, excess sweating in CF Renal loss (U.K > 20) Normal BP - Low plasma bicarb – urine/GI diversion, fanconi, renal tubular acidosis, DKA Normal BP - High plasma bicarb – vomiting, diuretic, barters syn High BP - Low renin – steroids, cushings, cons, liquorice High BP - High renin – renovascular HTN, renin producing tumour à U waves on ECG Hyperkalaemia Pseudo – haemolysis Normal renal function, low aldosterone – CAH, Addisons, 1o hypoaldosteronism, ACEi, NSAID, ciclosporin Normal renal function, high aldosterone – tubular acidosis, obstructive uropathy, K sparing diuretics Impaired renal function – ARF, CRF, Increased oral intake, transfusion Redistribution – acidosis, insulin deficiency, B blocker ECG changes Peaked T, Prolonged PR, QRS widening, flattened P, heart block & arrythmias Other Sx include muscle weakness, paraesthesia and hypoactive reflexes. Treatment Calcium (to protect myocardium) Bicarbonate Glucose / Insulin B agonist (salbutamol) Loop diuretics Binders (resonium) Dialysis Hypomagnesaemia Causes Malabsorption Hypoparathyroidism Hyper / hypocalcaemia Renal tubular acidosis Primary hyperaldosteronism Alcoholism DKA Can also occur with prolonged diuretic use or incorrect IVI administration Assoc with tetany Hypocalcaemia Causes – decreased PTH, vit D metabolism errors, sepsis,burns, rhabdomyolysis, pancreatitis Sx – muscle cramps, spasma & tetany, seizures, hyperreflexia, paraesthesia, stridor, prolonged QT Hypercalcaemia Can be due to thyrotoxicosis Acidosis PaCO2 > 5.9 Y RESPIRATORY Lung/neuromusc/CNS problem N METABOLIC Anion Gap ↑ ? Ingestion Osmo Gap Normal Serum K Methanol / Ethylene Gylcol ↑ ↑ Normal Urine pH pH >5.5 Prox RTA (2) Dist RTA (1) Met acidosis of prem Acetazolamide Dilutional Acidosis Adrenal – Addisons, CA hyperplasia, pseudohypoaldosteronism Renal – obstruction, infection, nephritis etc Ingestion – ACEi / NSAID N DKA Renal Failure Ingestion – Aspirin, Paraldehyde, Metformin Metabolic – lactic acidosis / organic acidaemia pH <5.5 Severe RTA prox Bicarb loss – diarrhoea, ileo-ileal pouch, fistula, ureteral diversion Cl ingestion – HCl, cholestryramine Acetazolamine Metabolic Alkalosis Low urine Chloride (<10) Pyloric stenosis Pseudobarters (CF) Thiazide / loop diuretics (chronic) Vomiting / NG aspiration Cl- losing Diarrhoea High Urine Cl (>10) with NORMAL BP Barters (High urine Ca2+) Gitelman’s Syndrome (Low urine Ca2+) Thiazide/loop diuretics (acute) High Urine Cl (>10) with RAISED BP High Renin, High Aldosterone Renovascular disease Renin secreting tumour Low Renin, High Aldosterone Conns (1o hyperaldosteronism) Low Renin, Low Aldosterone Cushings Congenital Adrenal Hyperplasia Liquorice Ingestion Anaphylaxis IgE mediated response à angioedema, urticaria, bronchoconstriction IM adrenaline 1:1000 Over 12 yrs = 0.5mls (500mcg) 6-12 yrs = 0.25mls (250mcg) 6m – 6y = 0.12mls (120mcg) <6m = 0.05mls (50mcg) Acute Respiratory Distress Syndrome (and acute lung injury) Acute inflammatory reaction in lungs Hypoxic respiratory failure • Severe hypoxaemia • Tachypnoea • Diffuse bilateral pulmonary infiltrates on CXR With NO left atrial hypertension (ie excludes pulmonary oedema) High mortality Damage to alveolus at endothelium + interstitium + epithelium Causes Direct (pulmonary) Pneumonia Aspiration Lung contusion Inhalation injury Near drowning Emboli Indirect (non pulmonary) Sepsis Massive transfusion (TRALI) Pancreatitis Trauma Traumatic brain injury Post cardio-pulmonary bypass Pathophysiology Endothelium – swollen injured cells à inflammatory cytokines à activates neutrophils à altered barrier function, coag & changes to flow Interstitium – oedema due to extracellular fluid + inflammatory activated cells à disrupts structure & decreases gas exchange Epithelium – rich in protein rich oedema fluid + necrosis/apoptosis of type I pneumocytes + proliferation of type II pneumocytes + increased alveolar macrophages à cytokines à amplifies inflammation & inactivates surfactant à impairs gas exchange. Prognosis – 30-40% mortality Management Ventilation with PPV and lung protective strategy Tidal volumes low (6mls/kg) Permissive hypercapnia Accept sats of 85% Strict fluid control – restrict input, induce diuresis Rx infection Optimise nutrition Limit sedation / neuromuscular blockade Can use HFOV/ECMO *** No proven benefit in surfactant replacement Trauma Primary brain injury – laceration, contusion, dural tear, diffuse axonal injury Severity GCS 13-15 = mild 9-12 = mod 3-8 = severe Management ABC + C-spine Prevent secondary brain injury Avoid hypoxia (maintain sats > 96% / PaO2 > 10) Avoid Ischaemia – raised MAP à raised cerebral perfusion – volume expansion, ionotropes / vasoconstrictors Reduce ICP – sedation – control PCO2 (4.5-5), paralysis, head up 30o, mannitol Surgery if required Fluid bolus = 10mls/kg (as rapid rise in BP can à disrupt forming clots à worsening bleeding) Once 20mls/kg given à ensure surgical review Once 40mls/kg given à ensure blood available for next bolus Head Injury Most are minor < 5 min. LOC, GCS 15, no/mild headache, < 3 episodes of vomiting, minor external injury, > 2 yrs old Reassure + simple analgesia, advice on warning signs & send home NB: pallor & vomiting are common due to vagal activity Hospital admission if: Loss of consciousness Penetrating injury Persistent vomiting Convulsions or any abnormal neurology Clinical / Radiological evidence of skull # GCS A fall of 2 or more points requires a neurological assessment GCS < 8 requires intubation & CT/MRI V5 = social smile & orientated V4 = cries but consolable V3 = moaning, inconsistently consolable V2 = inconsolable V1 = no verbal Aim is to prevent 2o injury (hypoxia, poor perfusion, hypothermia or increased ICP) Raised ICP Controlled ventilation to maintain PaCO2 = 35-40mmHg Nurse at 30-45 degrees head up Minimise stimulus – suction etc Keep midline position Restrict fluids to 60% of normal If severe à mannitol / furosemide Coning Subfalcine (cingulate) herniation of the cingulate gyrus under the falx = Usually asymptomatic, can à diplegia, hemiplegia & visual symptoms Central tentorial herniation = diencephalon & midbrain through the tentorial notch à sunsetting sign (upward gaze palsy), dilated pupils, VI nerve palsy, decerebrate rigidity, irregular respiration, hypertension, seizures Uncal (lateral tentorial herniation) = uncus of temporal lobe through tentorial notch à unilateral fixed dilated pupils followed by III nerve palsy then contralateral hemiplegia & extensor plantars, then ipsilateral hemiplegia (kernohan’s notch) = false localising sign Tonsillar herniation = cerebellar tonsils through foramen magnum à results in compression of medullary centres à bulbar palsy, stridor, hypotension, hyperthermia, neck stiffness & cardiorespiratory arrest Spinal Injury Midline tenderness Focal neurological deficit / pain Painful distracting injury Sedation drugs Low GCS Before applying collar then check Distended neck veins Tracheal deviation Neck wounds Laryngeal crepitus Subcutaneous emphysema COMA Causes ? tamponade ? pneumothorax Hypoxic / ischemic - arrest Vascular – sudden onset headache + LOC Trauma – including suspected NAI – RTC / falls, Impact (sports), Penetrating (gunshot) Toxic/Poison – drug Hx, bizarre behaviour Metabolic – polyuria & polydipsia, odours Infection Post-ictal SOL – early morning headaches Neuroleptic Malignant Syndrome Hyperpyrexia, muscle rigidity, altered consciousness & autonomic disturbance Occurs in 0.5-1.5% of those given antipsychotics 15% mortality Treat with dantrolene or bromocriptime Raised ICP Signs Unequal / unreactive pupils Raised BP Relatively low HR Abnormal posture Focal neurology Abnormal respiratory pattern *** papilloedema is a late sign Management ABC + O2 Sedate (analgesia + hypnotic) Ventilate – normocapnia (aim for 4.5) 30o head up Osmotic dieresis (mannitol / 3% saline) Encephalopathy Sudden onset brain dysfunction +/- changed LOC Causes Hypoxic/ischaemic Infection Haemorrhagic Metabolic Toxic (inc ingestion) Epileptic *** Seizures can be symptom or cause Mx Neuro-protection Treat infection Seizure control Monitor / control ICP Non neonatal intracranial haemorrhage Trauma AV malformation Bleeding disorder (genetic / drug induced) Acute leukaemia Tumour Thrombosis Infection Purpura Acute onset with fever & systemic symptoms Meningococcus until proven otherwise Could be ALL / DIC / Viral illness Less acute / absent fever Immune / idiopathic / thrombotic thrombocytopenia Protein C deficiency Drugs Meningococcaemia Neiseria menigitidis Gr –ve diplococci In nasopharynx of 2-5% of ppn Grp B is most common Children usually acquire from colonised adults Majority of people mount bactericidal response SIRS Temp > 38 WCC > 20 Raised HR + RR } } } + infective cause Caution if: Spreading purpura Poor perfusion Low BP Low pulse vol Respiratory distress Low plts / neutrophils Abnormal coag Management Cefotaxime Aggressive IV fluids can à pulmonary oedema Therefore intubate early Ionotropes Dopamine/dobutamine peripherally NA / Adrenalin centrally Correct chemistry & coag problems NOTIFY public health Mortality = 20-40% (often within 12 hours) ALTE 1/50 infants Usually approx 2 months old Apnoea, pallor / cyanosis, change in tone (floppy), choking / gagging At least 50% have no finding on examination Episode frightening to observe Characterised by one or more of: Apnoea (central / obstructive) Colour change (cyanosis, pale, red) Change in muscle tone (usually decreased) Choking/gagging Mostly benign Most common cause is GOR (but RX doesn’t reduce incidence) Seizures = 2nd most common Resp infection (e.g. RSV) = 3rd SUDI Sudden unexpected death Of well infant < 1yr Remaining unexplained after Ix 1/1500 dies between 1 wk & 2 yrs Peak age = 2-5m Increased risk if prem, sleep prone, smoking, bed sharing, male, born in winter Tend to be: smaller (wt) than case controls with smaller HC = ? IUGR After death Document then remove all IV lines & attempted IV sites Confirm correct placement of ET tube, then remove Full examination – esp. liver size, livedo reticularis, pallor Samples of everything for MC&S, virology and then frozen samples Save nappy LP & blood sample for biochem 2x risk in siblings Floppy Infant Sepsis CVS – CHD/Arrhythmia / myo or pericarditis GI –dehydration, pyloric stenosis, intussusceptions Metabolic – electrolyte / inborn error / low BM Endocrine – CAH Neuro – bleeds (consider NAI) Muscular – SMA Hypothermia = rectal temperature below 35o Moderate = 32-35 Severe = < 32 Cold à increases peripheral vasoconstriction à worsens acidosis à reduces O2 delivery à decreased peripheral nerve and cardiac conduction à decreased HR & ventricular arrhythmias with J waves on ECG Apathy, food refusal, cold to touch Oliguria à oedema Low HR, apnoeas, hypoglycaemia, metabolic acidosis, haemorrhages Also lethargy, poor co-ordination, apathy, irritable, confusion, hallucinations DIC à haemoglobinuria < 32 degrees à atrial arrhythmia, VT and VF < 30 degrees = asystole < 20 degrees = silent EEG Aim to increase temp by 1o/ hr. Continue CPR until T 32o Hyperthermia Increased body temperature occurs physiologically in tropical climate, ecstasy, ovulation & after a large meal Tetanus cover Is required if: High risk wounds = Immunisations incomplete / unknown OR complete immunisations with high risk wound • • Burns Bites Any wound / burn > 6hrs before treatment started Any time if: Devitalised tissue Puncture wound Soil / manure Clinical evidence of sepsis At Home Hold under water 5-10 mins, cover & attend A&E. DONT use damp dressings as can à hypothermia In Hospital Ensure ABC (shock possible), assess extent & depth Assessment Superficial Painful, erythema, skin intact, will blanch Partial Painful, blistering, dermis in tact Full NOT painful, white/charred skin, dermis destroyed If > 10% à IV fluid (plasma + saline), monitor UO + haematocrit à Abx to prevent toxic shock syndrome from infection à Check tetanus status If full thickness transfer to specialist unit for grafting Reassess after 48 hours as may deepen Rule of 9s – is outdated – use Lund & Brower Charts Give fluids according to parkland formula Ringer’s lactate = wt (kg) x % burn area Give ½ over first 8 hours, then rest in next 16 hours Complications Decreased immunity à increased sepsis & multi-organ failure ONLY use antibiotics if confirmed bacteria 80% are dog bites – tend to be colonised with Pasteurella multocida Remainder are assorted inc. human – Viridans strep & S.aureus Drowning ¾ inland (swimming pool, bath etc), ¼ in sea Boys 3x more likely than girls Dry drown = laryngeal spasm, wet drown = water in lungs Resus until core temp > 32oC Observe for minimum 24hrs Risk of pneumonia / pulmonary oedema à 2o drowning if pollution Fractures 1/3 of childhood fracture involve epiphysis / metaphysis = SALTER HARRIS S (I) – Slipped only A (II) – # above L (III) - # below inc epiphisis T(IV) – transverse – # above & below E (V) – everything = epiphisis obliterated I & II don’t involve growth plate therefore don’t usually affect growth III & IV does involve growth plate therefore can affect growth V is a crushing of the growth plate and is often only diagnosed retrospectively when growth failure occurs Bennett’s – 1st MC base Galeazzis Monteggia Potts – Radial shaft + dislocated distal R-U joint – proximal ulna + anterior dislocation of radial head – ankle Adverse Drug reactions Reporting scheme is voluntary Both over-the-counter & prescription-only should be included Black triangle drugs – should have ALL adverse reactions reported When reporting – also include ALL drugs taken in last 3/12 to look for interactions NB: some drug reactions only occur in some groups e.g. Teratogenic substances in pregnancy e.g. Breast milk Harm from tetracyclines, ciclosporin, antimalarials & methotrexate e.g. Prems Heparin à low plts Iodine antiseptic à hypothyroid Bicarb à high risk of IVH Chloramphenicol à grey baby syndrome (marrow suppression & shock) Dexamethasone à GI bleed, high BM, high BP & increased sepsis risk IV vitamin E à shock & ascites e.g. Neonates Sulphonamides à liver damage à risk of kernicterus e.g. Epilepsy Mefloquine = contraindicated (risk of neuropsychiatric symptoms) Chloroquine & ciprofloxacin à lower seizure threshold Phenytoin à folate deficiency à macrocytic anaemia Hydroxyurea à macrocytosis & megaloblastic anaemia Heparin à thrombocytopenia Penicillin à can cause haemolytic anaemia Co-trimoxazole à can cause drug induced aplastic anaemia Poisoning / Overdose Risk increased if stress in family Management ABC Limit absorption (activated charcoal by NG tube) Observe for complications (consult Toxbase) Deadly Nightshade Anticholinergic = like atropine = dilated pupils, dry skin + mouth, fever, increased HR, abdo distension, excitement & confusion Paracetamol Is metabolised into glucaronide & sulphate conjugates à excreted in urine Hepatotoxic because small amount is metabolised to toxic metabolite (N-acetyl-pbenzoquinoneimine) à conjugated in liver with glutathione to safe substance Once stores of glutathione are used up à accumulation of toxic metabolite Acutely = nausea & vomiting Increased risk of toxicity if malnourished, enzyme inducers (e.g. carbamazepine, phenytoin or rifampicin), chronic alcohol abuse (enzymes induced) or HIV Check blood level after 4 hrs N Acetyl Cystine (parvolex = replaces glutathione stores) can be given up to 24 hrs later Risk of hepatic failure à specialist unit NB: can have an anaphylactic style reaction to NAC if has had previously Aspirin Phase 1 – direct respiratory stimulation à respiratory alkalosis. Obilgate alkuria with loss of K, Na & HCO3 Phase 2 – K+/H+ exchange in kidneys à acid urine with continued respiratory alkalosis Phase 3 – dehydration with low K & increased lactate à acidosis & acid urine Can also get Pulmonary oedema, haemorrhages & hypo/hyperglycaemia Nausea, Vomiting, Dehydration, Tinnitus, Fever, Restless, can à convulsions In teenagers stage 1 & 2 last 12 hrs. each (longer in infants) Can intubate & gastric lavage if presents soon enough Induce diuresis to increase excretion Iron Tablets Can overdose on as little as 2g à D + V, haematemesis, malena à seems well à iron encephalopathy (coma, fits, liver damage, circulatory collapse) à Deep scarring of stomach & pylorus Gastric Lavage if within 3 hrs (intubate to ensure airway) Give Iron Chelator (desferrioxamine) Tricyclics (most commonly Amitriptyline) Respiratory & CVS depression (can à heart block) Cerebral stimulation à irritable, hallucinations, fits, increased tendon reflex, choreoathetosis, pyramidal signs Atropine like à fixed, dilated pupils, blurred vision, dry red skin, increased HR, urine retention Treatment is symptomatic (diazepam for CNS effects, bicarb to correct acidosis) Alcohol Acute encephalopathy Severe hypoglycaemia Digoxin è Heart rhythm disturbance Beta blockers è Increased K+ Amiodarone Increases effect of warfarin Increases levels of Digoxin, phenytoin and cyclosporine Sx Renal impairment Hypo / Hyperthyroid Bradycardia, AV block & myocardial depression Also à hepatitis, photosensitivity, peripheral neuropathy and optic neuritis Theophyline OD Nausea, insomnia, irritable, tremor, headache è GI sx occur before CNS è If severe à tachycardia & hypotension è Also ataxia, hyperglycaemia, hypokalaemia & hallucinations è Severe seizures & death Rx – emesis, charcoal & peritoneal dialysis MDMA (ecstasy) Hyperpyrexia, hypertension, low Na due to SiADH à polydipsia, respiratory alkalosis Carbon Monoxide Nausea, vomiting, headache, confusion, coma, death “Cherry red” appearance (skin & lips) Give 100% O2 Lead From old paint, water pipes, burning car batteries, lead salt cosmetics (surma) Colicky abdo pain (AXR may show lead fragments) Can get Pica or anorexia Encephalopathy (irritable, drowsy, convulsions, coma) + papilloedema Hypochromic anaemia (affects Heam synthesis) + basophil stippling of neutrophils If Chronic Chronic low doses can à mental retardation à Dense epiphyseal plates on XR (lead lines) à Blue lines at gingival margins Management Monitor blood levels Remove lead by chelation (EDTA / dimercaprol / D-penicillamine) Treat cerebral oedema (mannitol / dexamethasone) Will have decreased levels of delta amnio levulinic acid in blood Kerosene (paraffin) Peak age 1-3 years Usually urban areas (used in heaters) Laxative effect High risk of aspiration Can cause pneumonitis, but bacterial infection is rare No indication to starve Methanol à optic neuritis à blindness Organophosphate poisoning Bind to cholinesterases à prevent ACh breakdown à Sx Constricted pupils Rhinorrhoea Muscle fasciculations Convulsions Resp Paralysis Rx – atropine, paralidoxime and diazepam (for convulsions) Warfarin Levels increased by drugs which inhibit metabolism e.g. omeprazole, metronidazole, cimetidine, amiodarone Levels decreased by rifampicin & oestrogen (e.g. cocp) Penicillamine SE include – N&V, rashes, marrow depression & decreased taste