Emergency/surgical conditions Flashcards
Causes of arrest - requiring CPR
- Hypoxaemia
- Hypovolaemia
- Hyper/hypokalaemia or metabolic disturbances
- Hypo/hyperthermia
- Tension pneumothorax
- Tamponade/cardiac
- Toxins
- Thrombosis - PE or coronary (incl spontaneous intracranial bleed)
- Trauma
How long to do CPR for?
30 minutes
What are shockable rhythms?
How many joules to give per shock?
VF
Pulsesless VT
4J/kg
Indications for giving three stacked shocks at the onset of a shockable rhythm
- in cardiac cath lab
- in ICU or cardiac ward post cardiac surgery
- in other circumstances when defibrillator is already attached
in all other cases the standard s to give one shock then bak to CPR
how many joules to give in SVT?
0.5-1J/kg - if haemodynamically unstable
Adrenaline in resus - MOA
Alpha adrenergic receptors: vasoconstriction and increase blood flow to cerebral and coronary artery circulation
Beta adrenergic receptors: inotropic and chronotrophic
Indications for amiodarone in resus
Shock resistant VF and atrial tachycardia
SE: hypotension, CHD, bradycardia
Cx of fluid boluses for hypovolaemia/shock
hyperchloraemic acidosis
oedema
hyponatraemia
Vasopressor vs inotrope
Vasopressor - causes vasoconstriction and incr MAP
Inotrope - cardiac and vascular effects -> incr contractility and CO
Noradrenaline
- effect
- receptor
- use
vasopressor
alpha 1
septic, cardiogenic and hypovolaemic shock
Adrenaline
- effect
- receptor
- use
vasopressor and chronotrope
alpha 1 and mod beta 1 and 2 effects and low dose
anaphylactic shock
add on for septic shock
Dopamine
- effect
- receptor
- use
dose dependent effects
- alpha 1 at high dose
- beta 1 med dose
- D1 and low dose
2nd lnie for septic shock
Incr SV -> incr CO
Incr splanchnic blood flow
Dobutamine
- effect
- receptor
- use
inotrope - incr cardiac contractility
beta 1 R
Use: low output cariogenic shock
2nd line for septic shock
Used post cardiac surgery
Milrinone
- effect
- receptor
- use
- inotrope
- beta 1 receptor
- use for refractory cariogenic shock
- cardiac contractility and incr HR
- Decr BP
Indications for CTB in head injury
PECARN/NICE guidelines
Impaired mental status
LOC >5 sec
Vomiting >2yo
Severe injury mechanism
Signs of basilar skull #
Severe headache
Abnormal behaviour if <2yo
Palpable skull # if <2yo
Palpable scalp haematoma (unless frontal)
Risks of CT scan
Risk of malignancy - 24% more likely in those who did not have CTB <19yo
extradural vs subdural haematoma (which metabolic disease is SDH seen in?)
EDH
- doesn’t cross suture lines
- can appear as a big egg on the head, convex/lense shaped and contained/limited in scope
SDH
- crosses suturelines
- crescent shaped
- can be extensive as not contained
- seen in SHAKEN infants (NAI)
- seen in metabolic disease glutaric aciduria type I
- can be chronic w progressive enlargement w hx of irritability, poor feeding, lethargy
Subarachnoid haemmhorage
Sx/presentation
- Intracranial bleed within cisterns and sulci
- ‘Worst headache of my life’ +/- LOC
- Meningism 6-12 hrs post beed
- SZ
- N&V
- CT sensitivities best within first 8-12 hrs, decr day 6-7
- LP: isolated RBC in CSF, non-clearing
Treatment of status epilepticus
Benzo (midaz) at 5 min, then another 5 minutes.
ConSEPT trial: re choice of 2nd line antiepileptic.
- no difference between phenytoin and keppra
- using BOTH may delay or prevent further seizures and thus need for intubation/need for PICU beds
C spine clearance
- If unconcious:
Spinally immobilise
Needs CT - IF conscious, able to communicate:
POsterior midline spinal tenderness
Painful distracting injury
Focal neurological defects
Opiod medications masking ability to communicate
–> needs plain imaging (X-rays); look for soft tissue swelling
–> re-examined if imaging looks good
–> if improved, can remove collar and clear spine
Examining C spine X-ray for ?fracture
Above C2: Normal soft tissue is <1/3 of vertebral body width
C3-C7: Normal is <1 vertebral body width, progressively narrowing towards C7
Any soft tissue swelling larger than this is abnormal , ?fracture
what does seat belt sign indicate?
significant risk of intra abdominal trauma
why are kids more prone to intraabdominal injury relative to adults?
small size so multiple system involved
thin abdo
ribs pliable, less protective
liver nad spleen relatively take up more space in abdo relative to adults
diaphragm is horizontal
seat belts ill fitting <8yo or <140cm
Potential injuries in intraabdominal trauma
Injury to liver/spleen/pancreas
-> LFTs, lipase
Intestinal rupture
GU - bladder rupture/kidney/urethral
–> need urine MCS
Management of abdominal truama
IV access x2
Bloods including lipase, LFT, UEC, FBE and crossmatch
Urine MCS
Fluid boluses +/- blood (if hypotensive, suspect intraabdominal bleed so replace like with like)
Tranexamic acid is suspect intra abdominal bleed
FAST scan - look for free fluid
-> needs CTAP as gold standard to detect haemoperitoneum
Surgery only if haemodyanamic instability (otherwise conservative mx)
Greenstick fracture
Distal radius fracture
Break of one cortical surface
requires below elbow plaster
Buckle fracture
Distal radius fracture
hairline fracture not breaching cortical surfaces
Manage with splint (same outcome as below elbow pOP)
Indications for reduction of distal radial #
Age dependent due to remodelling potential
<5yo: <20 degrees angulation
5-10yo: <15 deg angulation
10-15yo: <10deg angulation
Indications for referral to orthopaedic with fractures
Salter harris 3-4 fractures (ankle)
Open fractures
NV compromise
Monteggia fracture vs galeazzi
Moteggia (mountain - ‘top of the mountain’ and ‘ggiA’ -UlnA): Prox Rad-ulnar joint dislocation with associated fracture of ULNA
Galeazzi (ground): DISTAL Rad-ula joint dislocation with assoc fracture of RADIUS
Facial lacerations - mx
glue
- aponeurosis on view of <3cm
sutures
periosteum on view or >3cm
Intussusception
Surgical emergency <2yo
Intermittent colicky abdo pain
legs drawn up
pallor
lethargy
Pain
palpable sausage shaped abdo mass
red currant jelly stool
dx - abdo uss (target sign)
mx - air emema or surgical reduction +/- resection if air enema unsuccessful
often occurs at ileocolic junction
post viral aetiology (adenovirus)
or think of pathological lead points for recurrent episodes (lymphoma, meckel’s diverticulum, intestinal polyps)
Indications for removal of foreign body
- HIGH risk objects: all require imaging and referral for removal
- Sharp and remaining in oesophageal and stomach (ok if below diaphragm)
- Long/large (>5cm long or >2.5cm wide)
- Magnet x2 or 1xmagnet + metal object
- Disk or button batteries
- toxic objects (ex containing lead) - LOCATION
- In oesophagus (stomach and below ok as long as low-risk)
- -> upper oesophageal obstruction worse
- -> lower oesophageal obstruction can be obersved 24 hrs as long as asymptomatic to see if it resolves - Concern for clinical compromise:
- signs of airway compromise
- near or complete oesophageal obstruction
- signs or sx suggesting inflammation or intestinal obstruction
Points of obstruction for FB
thoracic inlet
aortic arch
gasto oesopageal junction
MDMA overdose
= 3,4-Methylenedioxymethamphetamine,
= Ecstacy
= Molly
Sympathomimetic and serotonin syndrome toxidrome:
anxiety
tachycardia
HTN
Diaphoresis
Dry mouth
dilated pupils
jaw clenching
dehydration
rhabdomyolysis
hyperthermia
arrhythmias (VF, astystole; infarct possible)
Supportive care
Fluids
Agitation - benzos, olanzapine, haloperidol or droperidol
GHB overdose (gammahydroybutyrate)
Commonly used as date rape drug (liquid, can be slipped into drinks)
Euphoria in first hour, rapidly
followed by a period of profoundly depressed level of consciousness-> can progress to coma
Coma/stupor alternates with extreme agitation/combativeness
Resp depression/apnoea
potential seizures
Seizure-like movements and myoclonus are common
Bradycardia
Hypotension
Need to be tubed, ventilated and sent to ICU for monitoring
Mx
- No reversible agents
- Supportive tx
- Gastric lavage/charcoal NOT indicated
Cannabis/THC overdose
Tachycardia
Paranoia, fear
Hallucination and disorientation
Dilated pupils
Fluctuations in BP
Synthetic cannabinoids/Marley - significant bradycardia and SEVERE paranoia/hallucinations etc
Repeated supra therapeutic ingestion of paracetamol
Paracetamol level and Alt
- if normal ALT and paracetamol <120, no risk of hepatotoxicity -> DC
- if abnormal -> NAC etc
It is safe to wait for the paracetamol concentration to decide on the need for NAC in all cases that present within 8 hours of ingestion AND where a paracetamol concentration result will be available for interpretation within 8 hours of ingestion
Single supra therapeutic ingestion of paracetamol
If paracetamol level >200mg/kg or unknown quantity ingested
It is safe to wait for the paracetamol concentration to decide on the need for NAC in all cases that present within 8 hours of ingestion AND where a paracetamol concentration result will be available for interpretation within 8 hours of ingestion
<8 hrs post ingestion- paracetamol level and plot on nomogram, commence tx if indicated
>8 hrs
- commence NAC immedicately
- get paracetamol and ALT level - can stop NAC if level is below tx threshold
MASSIVE quantities (30g) - seek advise from toxicologist
Iron toxicity
- Tablets can be seen on X-ray if not yet absorbed -> tx w whole bowel irrigation
- If absorbed (N xray) -> desferrioxamine which is an iron chelator
Mitochondrial Toxin to GI mucosa; also to liver, lungs, heart
Phase 1: first 6 hrs post ingestion, effects due to local corrosive effects
- haematemesis
- diarrhoea
- abdo pain
- early hypovolaemia from bleed +/- diarrhoea and third spacing due to inflammation
- -> tissue hypo perfusion and metabolic acidosis
- -> convulsions, shock and coma if decr circulating blood vol
Phase 2: 4-12 hrs post ingestion
- improvement in sx with absorption of Fe by various tissues
- Systemic acidosis
- End organ dysfunction begins (liver enzyme derangement etc)
Phase 3: 12-24 hrs post ingestion -> multi organ failure
- Fe2+ -> Fe3+ and is concentrated within mitochondria -> free radical formation and lipid peroxidation
- Worsening metabolic acidosis, cell death, tissue injury
- Hypovolaemic shock and cariogenic shock
- Coagulopathy (liver failure)
TCA overdose ECG changes
Due to Na channel blockade
ECG changes
- QRS prolongation >100ms (>100ms is predictive of seizures and >160ms is predictive of ventricular tachycardia)
- R axis deviation
- Tall R wave in AVR
- QTc prolongation
Pathophys and sx of TCA overdose
- Na channel blockage in His-purkinje bundle system
- > Incr duration of repolarisation and refractory period
- > ventricular dysrhythmias, tachycardia, hypotension - ACh receptor antagonist
- > anticholingeric syndrome (dilated pupils, dry mouth/eyes, constipation/ileus, urinary retension)
- > confusion, delirium, myoclonic jerks, seizures - alpha adrenergic blockage
- > hypotension
Mgmt of TCA overdose
ABCs (can be very sick)
Intubate and HYPERventilate (aim for pH 7.5-7.55 because systemic acidosis worsens the TCA poisoning)
IV access -> Sodium bicarb (if hypotensive, arrhythmias or QRS >100ms)
NGT and charcoal within 2 hrs of ingestion
Treat other things as they come up
- Midaz for seizures (phenytoin CI)
- Fluid bolus for hypotension (the Norad 2nd line)
- If further arrhythmias, repeat sodium bicarb, then lignocaine
CO poisoning
Presentation
Treatment
When is hyperbaric o2 indicated?
When to suspect: house fires, poor ventilation, heaters, cars etc
Binds 240x more efficiently to haem than O2 (displaces O2 so lower O2 concentration in blood and harder to offload O2 to tissues)
Confusion, headache, irritability, nausea, seizures, coma
Myocardial dysfunction
ABCs and supportive care
ABG/VBG
Give 100% O2 to washout CO
Hyperbaric oxygen indicated only if HbCO 25% on gas OR signs of end organ dysfunction (ie seizure)
What is most common cause of fatal snake bike
What is its hallmark/cause of death?
What are presenting features/complications that can arise?
- *Brown snak**e (Brown - colour of old BLOOD = coagulopathy)
- hallmark consumptive coagulopathy; prolonged INR >3, low/undetectable fibrinogen, elevated d-dimer
–> may present with bleeding gums or bleeding around the IV site, rarely this can manifest as an intracerebral haemorrhage or intraabdominal haemorrhage
–> can cause collapse and cardiac arrest (NO rhabdo and neurotoxicity is rare)
–> can cause TMA (Thrombotic microangiopathy): classic triad of thrombocytopenia, microangiopathic haemolytic anaemia and acute renal failure
Most common snakes causing paralysis and rhabdo
- Black snake (Eschar, dead tissue, is BLACK)
- N Australia and PNG
- characterised by lots of tissue necrosis at site
- coagulopathy rare - Tiger snake (tigers are black and brown -> has features of both black and brown snakes)
- Southern and eastern seaboard
- coagulopathy a big component
Sx/signs of snake bite
Sx
- headachce
- nausea/vomiting
- abdo pain
- collapse or confusion
Signs
- fang marks (single or paired) or scratch mark
- blurred vision, diplopia or ptosis (drooping eyelids)
- difficulty speaking, swallowing or breathing
- swollen tender glands in axilla or groin of BITTEN LIMB
- limb weakness/paralysis
- Rest weakness or arrest
Mx snake bike
Pressure immobilisation bandage
Indications for antivenin (give 1 vial brown and 1 vial tiger)
- significant coagulopathy (INR >3 or prolonged bleeding)
- evidence of neurotoxic paralysis
- hx of the 4 Cs: coma (LOC)/collapse/convulsions/cardiac arrest
No indication for use of venom detection kits
Mgmt of coaguloapthy secondary to snake bites
Give antivneom if significant INR derangement (>3) or prolonged bleeding time
- bleeding should cease within 20-30min of giving AV but coag profile can take 6 hours to normalise
- No role for giving MORE than 1 antivenom or for giving FFP (has not been shown to be beneficial to outcomes)
Red back side bite
Local intense pain 5-10min after bite
Sweating and piloreection within an hour
Mild erythma, puncture bites often NOT seen
Tender proximal lymph nodes
Pain ++++++
Tx simple analgesia -> opioids
Antivenom if severe pain and unwell, unrelieved by simple supportive tx (2 ampoules)
Box jelly fish
sx and mx
Deaths within 5 min of sting - direct cardiotoxicity
Severe pain and linear welts at site
Hypertension, Bradycardia or tachyardia, arrhythmia
Delayed reaction in 50%
Mx:
Liberal amounts of vinegar
No pressure/immob bandage
Antievenom if cardiac arrest
MgSO4 has not been validated
Irunkanji syndrome
Jellyfish bite
No welts or feel of sting
Envenomation causing massive catecholamine release -> toxic cardiomyopathy -> cariogenic shock, pulm oedema and sudden death
Mx - if not immediately fatal, tx w vinegar, IV fentanyl and GTB for mgmt of HTN
Use of ondans in head injury
Can mask Sx so frowned upon
- ie can have 2 vomits but any more than this, should have CTB
Ok to give for sx control in LOW RISK situation
oesophageal atresia +/- tracheo-oesophageal fistula
- presentation and diagnosis
Presentation
- maternal polyhydramnios (60%)
- recurrent aspiration pneumonia
- coughing episodes w cyanosis
- abdominal distension (air passing from lungs into gut via fistula)
- intermittent choking w feeds (H-type -> oesophagus to stomach, no atresia, with fistula between oesophagus and bronchus)
Diagnosis
- inability to pass NGT into stomach
- AXR - prominent gastric bubble +/- dilated distal oesophagus, NGT coiled in upper oesophagus
- CXR - areas of lung collapse
- contrast-study to define the lesion
Downs syndrome child p/w bilious vomiting - what do you suspect as ddx?
Duodenal atresia
Presentation of intestinal atresias
BILIOUS vomiting
Polyhydramnios antenatally
Abdo distension +/- visible peristalsis
Delayed or absent passage of mec
How to differentiate between gastroschesis and omphalocele and what are the differences between the two?
Omphalocoele: evisceration of abdominal contents through umbilicus, is covered by peritoneum
- Umbi cord attached
- Central location
- > Assocations: #1 BWS, Trisomy 13/18, Renal malformations, Wilms tumour, CHD
Gastroschesis evisceration of Gastric (G and G) contents through PARA-umbilical defect, is NOT covered by peritoneum.
- Doesn’t have its own umbi cord
- R sided location
- > Assocations: bowel atresia (15%), strictures, stenosis
What infection mimics appendicitis?
Yersinia enterocolitica
ddx croup
Alternative diagnoses include: bacterial tracheitis, inhaled foreign body, anaphylaxis
Assessment median nerve function
palsy = ?
what # is it assoc w?
Nerve roots C6-T1
Sensory - palmar aspect of thumb and fingers 2,3
Motor - finger (make a fist) and wrist flexion; forearm pronation
Palsy -> hand of benediction (see photo)
- If patient tries to make a fist, only the little and ring fingers can flex completely. This results in a characteristic shape of the hand, known as hand of benediction
- Compression in carpel tunnel syndrome
Injured w supracondylar fracture and radius and ulna fractures
Assessment radial nerve function
palsy = ?
what # is it assoc w?
C5-T1
Motor - elbow extension (triceps), wrist and MCP joint extension
Sensory - Back of thumb/radial asset of back of hand
Palsy -> wrist drop +/- inabilility to extend at elbow
Injured w humeral shaft fractures (travels in ‘radial groove’; get wrist drop), shoulder dislocation (cannot extend at elbow + wrist drop)
- Wrist laceration -> only sensory sx (no motor sx)
Assessment ulnar nerve function
Nerve roots
palsy = ?
what # is it assoc w?
Nerve roots - C8-T1
Motor - finger adduction and abduction (not thumb)
Sensory - fingers 5 and 1/2 of finger 4 front and back
- Palsy -> claw hand and interosseous wasting
- Froment’s sign is a test for ulnar nerve palsy – specifically paralysis of the adductor pollicis:
- The patient is asked to hold a piece of paper between the thumb and index finger, as the paper is pulled away.
- They should be able to hold the paper there with no difficulty (via adduction of the thumb).
- A positive test is when the patient is unable to adduct the thumb. Instead, they flex the thumb at the interphalangeal joint to try to maintain a hold on the paper.
Injured with supracondylar fracutres; also radius and ulnar fractures
Lead poisoning
Symptoms
Ix
Symptoms
o Low level exposure= Decreased learning and memory/lower IQ/cognitive dysfunction, behavioural disturbance (irritability, restlessness), myalgia, parathesias, fatigue/lethargy, abdominal discomfort
o Moderate exposure=arthralgia, vomiting/LOW/constipation, muscule fatigue/tremor
o High level exposure= lead line (blue discolouration) on gum margis, anaemia, paralysis, encephalopathy/seizures/death
Investigations
o FBE (microcytic hypochromic anaemia, basophilic stippling, sideroblasts)
o Whole blood lead concentrations
Causes of reduced conscious level/coma
CNS
- epilepsy (post ictal)
- traumatic brain injury
- Infection (meningoencephalitis)
- subarachnoid haemorrhage
- hypoxic ischaemic brain injury
- acute incr ICP (mass/CSF obstruction/coning)
- brainstem neoplasm/infarct/trauma
TOXINS
METABOLIC IMBALANCE
- Na
- Ca
- glucose
INBORN ERRORS METAB
TEMP INSTABILITY
SYSTEMIC ORGAN FAILURE
- renal
- lungs
- liver
- sepsis
signs of base of skull fracture
CSF rhinorrhoea
bilateral eyelid ecchymoses (panda or raccoon eyes)
Bruising over mastoid (Battle’s sign)
Features of a BRUE (brief resolving unexplained event)
- Infant less than 12 months old
- Duration <1 minute (typically 20-30 seconds)
- Sudden onset, accompanied by a return to a baseline state
- Characterised by ≥1 of the following:
- -> Cyanosis or pallor
- -> Absent, decreased or irregular breathing
- -> Marked change in tone (hypertonia or hypotonia)
- -> Altered level of responsiveness
- -> Not explained by identifiable medical conditions (diagnosis of exclusion)
Can be risk stratified
- > low risk can be DC home w close f/u
- > higher risk needs baseline ix and admission for observation
Features of low risk BRUE
A low risk BRUE occurs when there are no concerning features on history or examination AND all of the following:
- age >60 days
- born ≥32 weeks gestation and corrected gestational age ≥45 weeks
- no CPR by trained healthcare professional
first event - event lasted <1 minute
A low risk BRUE is unlikely to represent a presentation of a severe underlying disorder and is unlikely to recur
Does NOT require ix and can be discharged home w close medical follow-up (as long as parents reassured and capable of looking after child)
High risk req admission for observation and oximetry +/- telemetry
Differentials for BRUE (medical conditions)
Seizure
Central apnoea
GORD/laryngospasm
Hypoglycaemia
Sepsis/infection
Cardiac - arrhythmia or tet spell (TOF)
Encephalopathy
Suffocation
Toxin
In paracetamol overdose, what is the best predictor of need for liver support or transplant?
PT prolongation
MOA, sx, Cx and treatment of aspirin/ibuprofen/salicylate ingestion
MOA:
- irreversible block the COX-1 pathway and modify the COX-2 pathway resulting in a decrease in inflammation (reduced prostaglandin synthesis) and platelet aggregation
- impairs cellular respiration by uncoupling oxidative phosphorylation -> lactitc acid buildup -> metabolic acidosis
Sx (present within 4 hrs of ingestion)
- N&V -> Dehydration
- Headache
- Hyperventilation -> Respiratory alkalosis
- Blurred vision
- Tinnitis, deafness
- Disorientation/confusion
- Ataxia, dizziness
- Hypoglycaemia
Cx
- Rhabdomyolysis
- Acute renal failure
- Hypotension
- Pulmonary oedema
- Seizures
Ix: Initially resp alk -> high anion gap metabolic acidosis
Salicylate levels
UEC
Treatment
- Plasma level
- Activated charcoal/stomach pumping to empty stomach if <12hrs from ingestion
- If severe or renal impairment, IV bicarb (treat acidosis) or even dialysis may be necessary
what is the peak age range and metabolic disturbance that you get w pyloric stenosis?
2-6 weeks of age
hypochloraemic hypokalaemic metabolic alkalosis
When to correct pyloric stenosis surgically and why?
Surgical correction is usually delayed until correction of dehydration, acid / base status and electrolyte disturbances
It is particularly important to fully correct serum bicarbonate before surgery because of the risk of hypoventilation / apnoea post-operatively in the setting of a metabolic alkalosis
meckels diverticulum
what is it?
presentation?
ix/diagnosis
mx
Ileal remnant of the vitellointestinal duct, which mat contain ectopic gastric mucosa or pancreatic tissue
appx 2% of ppl affected
2 inches long
2 feet from ileocaecal valve
2 year olds
Presentation
- mostly asymptomatic but may present w rectal bleeding, intussusception (lead point), volvulus or acute appendicitis
Ix
- technetium scan: incr uptake by ectopic gastric mucosa identifies 75%
Mx
- surgical resection
where is hip pain referred?
knee
Abx for septic arthritis
fluclox +/- 3rd gen cephalosporin (cefotax/ceftaz/ceftriaxone)
proceed to joint washout if delayed response to abx alone
most common sites for OM
distal femur
proximal tibia
xray features of Osteomyelitis
swelling of adjacent soft tissues
joint effusion
xray changes appreciable 5-7 days from sx onset (normal initially)
- periosteal reaction/thickening
- focal bony lysis/cortical loss/lucent areas in bone
what causes DDH
examination
mgmt
incomplete shallow development of acetabulum allowing femoral head to dislocate
Barlow manoeuvre tests for instability - posterolateral force applied, attempting to dislocate femoral head from socket
Ortolani - attempt to relocate a dislocated hip back into socket
other - asymmetrical skin creases, leg length discrepancy, check for limitation of abduction
mgmt -
- stable dysplastic hip: Brace within first 7 weeks of life for min 6-8 weeks (or until normal hip USS)
- dislocated hip - brace within first 7 weeks with USS monitoring if no hip reduction achieved within 3-4 weeks, abandon bracing and wait until baby is ~6 months for surgical reduction.
BRACE: abducted position with hips and knees flexed to keep head of femur enlocated in acetabulum
What is perthes disease
presentation
prognosis/tx
xray findings
Osteochondrosis caused by avascular necrosis of the FEMORAL HEAD, often due to compromise of the nutrient artery (reduced blood supply to femoral head)
M > F, ages 4-10 at presention (median 8)
Sx
- intermittent referred pain to anterior thigh/knee/groin
- limp (may be painless)
- worse w activity
- decr internal rotation & abduction of the hip (at rest semi-flexed and externally rotated)
- leg length discrepancy
Prognosis
- can heal by self if <6y (mx w splint and bed rest)
- in older kids (>6) can cause degenerative disease later in life and can require casting or surgery to prevent this (osteotomy)
Need ‘frog leg’ xray for diagnosis
- Increased density of femoral head epiphysis
- radiolucency
- widened and flattened femoral head with joint space widening.
What is osgood schlatter disease
Population affected/ Presentation
Diagnosis/ix
Treatment
Osteochondrosis or traction apophysitis of the TIBIAL TUBERCLE
More common in boys aged 12-15yo (during growth spurt years); girls aged 8-12
RF - sports ++
Causes anterior knee pain, tenderness and SWELLING over the tibial tubercle
Diagnosis made clinically and supplemented w xray which shows irregularity and fragmentation of tibial tubercle (and helps r/o neoplasm, fracture, infection)
Treatment is nonoperative with NSAIDs, activity modification (acid jumping/kicking activities) with quadriceps stretching and typically resolves with physeal closure.
SUFE
Slipped upper femoral epiphysis
Affects ADOLESCENT males most commonly (10-16yo)
RF: obesity, polynesian, also hypogonadism (small testes), taking GH, hypothyroid/pituitary/renal dysfunction,
Presentation: groin/hip pain but can be referred to thigh or KNEE; shortening of affected limb; obligate external rotation (limitation of internal rotation) with antalgic outgoing gait
Diagnosis confirmed by xray (frog lateral view) - head of femur slips off femoral neck
Tx - URGENT ORTHO REFERRAL! Immediate NWB -> femoral pinning
Potential complications of SUFE
- Osteonecrosis - the risk is up to 50% in an unstable SUFE, even with treatment
- Chondrolysis - this can result from the process of the SUFE itself, but more commonly it is from unrecognised screw/pin penetration from surgical stabilisation. The overall incidence of this is approximately 7%
- Osteoarthritis - patients with a moderate or severe SUFE have higher risk of early degenerative joint disease
- Impingement - patients with a severe SUFE have a risk of deformity through the femoral neck when the SUFE is stabilised and healed. This can cause femoral acetabular impingement, and may require further surgical treatment to correct this
Associated illnesses with reactive synovitis
Affects children 3-10 yo most commonly
Common w viral illnesses
- GI illness
- EBV
- Influenza
Mycoplasma
Strep
Sudden onset joint pain or limp with NO pain at rest
Can have decr range of movement
In a well child +/- mild fever
ESR/CRP/neuts normal or mildly elevated
BC negative
May have assoc small effusion on xray or USS but otherwise N
Mx
Rest, NSAIDs -> remobilise
Management of tics/sterotypies
If child who is not distressed and whose function is not affected by the presence of tics, can educate and reassure child and parent that no ix/tx is required and they will likely wax/wane over time but should resolve ~ adolescence
- Tics are diagnosed clinically and in a child with retained awareness and typical tics, an EEG is not required.
- Treatment with clonidine, or other pharmacological management, is only indicated if tics are causing significant social or functional impairment for the child. Tics often cause more distress for the parent than the child and this is not a reason to treat.
Management of inguinal hernias in infants
Ultimately requires surgical repair - will not self resolve on their own.
Referral to a surgeon and the timing of the repair depend on whether or not the hernia is reducible.
- > Incarcerated or non-reducible hernias must be urgently reduced
- > Reducible hernias can be referred for semi-urgent elective repair (as increased wait time results in higher risk of incarceration)
Neurogenic shock vs spinal shock
Neurogenic Shock (permanent)
- Is the manifestation of loss of sympathetic output to the cardiovascular system
- Is seen immediately after complete cord injury at the level of T6 or above.
- The loss of sympathetic vasomotor tone after cervical spinal cord injury will result in vasodilatation, venodilatation, and reduced venous return to the heart, causing hypotension.
- Neurogenic shock can be more easily distinguished from haemorrhagic shock where there is an associated relative bradycardia for age.
- Neurogenic shock should not be confused with Spinal Shock
Spinal shock (temporary)
- Spinal shock is the reversible dysfunction of the spinal cord associated with injury
- Is like a concussion of the cord without permanent damage
- may exist alone, or in combination with permanent cord injury.
- in resolution, produces the improvement in neurologic function seen in the first few days post injury.
What is SCIWORA?
Spinal cord injury without radiographic abnormality is present when there are objective signs of myelopathy as a result of trauma, with no evidence of fracture or ligamentous instability on XRAY OR CT (ie - perform MRI if SCIWORA is suspected - better for soft tissue imaging)
SCIWORA is most frequently seen in younger children (especially <8 years of age), and in injuries of the cervical spine.
Postulated causes include
- Ligamentous laxity and bony immaturity allowing excessive, transient movement during trauma causing distraction or compression of the spinal cord;
- Cord ischaemia due to vascular injury or hypoperfusion.
- The incidence reported in children ranges from 1% to 10% of all spinal cord injuries.
- Younger children tend to have more profound neurological injury, and hence less long-term improvement.
- A number of children will present with minor neurological injury and progress to complete or partial spinal cord injury. -The incidence of this delayed presentation of the serious symptoms is reported to be between 5 and 50%.
The delay to presentation of full symptoms has been as long as 4 days.
Because of these delayed presentations, all children with symptoms of any neurologic deficit should be treated as potential spinal cord injuries.
Discitis
Age group affected
Presentation
Common causative agents and method of spread
Ix
Ddx
Most commonly occurs between ages 4-10, affects lumbar spine
Presentation: refusal to walk (63%), limp, back pain (27%), inability to flex the lower back (50%) and a loss of lumbar lordosis (40%) , refusal to bend over+/- low grade fever
Common causative agents: staph aureus, kingella; consider Tb. haematogenous spread most common, or local spread from OM
Ix - BC to determine causative agent; eSR >40, WCC usually normal, CRP may be normal/mildy increased
MRI preferred over xray (xray changes delayed by 2-6 weeks)
Ddx - vertebral body OM (usually slightly older age, longer duration of illness, fever and leucocytosis assoc with bony destruction on imaging)
Clinical effects of heroin
Mild hypotension and mild bradycardia are
commonly observed with heroin use.
-> These are attributable to peripheral
vasodilation, reduced peripheral resistance and histamine release, and inhibition of baroreceptor reflexes.
Respiratory depression, due to heroin’s effect on the brain’s respiratory centres is a hallmark.
What sites of bruising on body are suspicious for NAI?
Non bony part of body or face/ears:
- buttocks, genitals, back and back of the hands are less likely to be due to an accident
What types of # are suspicious for NAI?
- Multiple fractures in child without underlying predisposition for # (ex osteogenesis imperfect, r/o on xray and skeletal survey)
- Fractures of varying ages
- Metaphyseal corner fractures – reported as almost pathognomonic of NAI.
- rib fractures (grabbed by the chest and squeezed/shaken)
- Spiral fractures - result of twisting forces
What burn locations are suspicious for NAI?
Soles of the feet
Buttocks/back
Backs of hands
(areas you wouldn’t expect to come into contact w hot surfaces)
toddler’s fracture
what is it
mx
Toddler fractures occur in young ambulatory children (from 9 months to 3 years).
A toddler’s fracture is a spiral or oblique undisplaced fracture of the distal shaft of the tibia with an intact fibula. The periosteum remains intact and the bone is stable. These fractures occur as a result of a twisting injury.
The mechanism of injury may be very minor and not noticed by the parents
Mx - backslab
Eye signs of neuroblastoma
Proptosis and periorbital ecchymoses
-> sec to tumour mass effect on symp innervation of eye (assoc w stage IV metastatic disease, often fatal)
Horner’s syndrome and Opsoclonus (‘dancing eyes’)
-> sec to infiltration of cervical ganglia (associated with localized neuroblastoma and consequently demonstrates markedly better survival rates)
Tricyclic antidepressant (TCA) overdose
sx/presentation
Confused, altered mental status
Seizures
Dilated pupils
Hyperthermia (NOT sweaty)
Dry mucous membranes
Hypotension
Tachyarrhythmia (wide QRS and dominant R wave in aVR)
When to organise follow up imaging after a UTI
Seriously unwell children, those with renal impairment, and boys <3 months of age should have renal USS before DC to exclute renal tract obstruction
Children w recurrent UTIs - non urgent o/p ultrasound
Indications for CTB in setting of headache (ie suspected CNS tumour)
Persistent headache in the following settings:
- wakes a child from sleep; occurs upon waking; in any child less than four years of age; associated with disorientation or confusion.
- Persistent vomiting upon waking.
- Visual findings including papilloedema, optic atrophy, new onset nystagmus, reduced acuity not due to refractive error, visual field reduction, proptosis, and new onset paralytic (non-comitant) squint.
- Motor findings including regression in motor skills, focal motor weakness, abnormal gait and/or coordination, bell’s palsy with no improvement over four weeks, and swallowing difficulties without an identifiable local cause.
Anticholinergic toxidrome
- signs/sx
- meds/drugs that cause this
Pneumonic - Alice in Wonderland
1. ‘red as a beet’ - flushed
2. ‘dry as a bone’ - no sweat, no tears, dry mouth
3. ‘hot as a hare’ - hyperthermia
4. ‘mad as a hatter’ - delerium/hallucinations
5. ‘full as a flask’ - urinary retention
6. ‘Blind as a bat’ - Dilated pupils
+ tachycardia and hypertensive
+ absent bowel sounds
Causes
- Antihistamines
- TCAs
- Sleep aid medications
Cholinergic toxidrome
‘SLUDGE BBB’ (up regulation of Parasymp NS -> fluid pouring out of every orifice)
- Salivation
- Lacrimation
- Urination
- Defecation
- Gastric emesis (vomiting)
- Bronchoroea (airway secretions ++)
- Bradycardia with low/N BP
- Pupil constriction
Causes
- insecticides (contain organophosphates)
Serotonin syndrome
Signs/sx
- NM excitation (***differentiates from sympathomimetics and cholinergics)
- hyperreflexia, tremors
- clonus, muscle rigidity - Autonomic hyperactivity
- vomiting, diarrhoea
- HTN, tachycaria, dysrhythmias
- tachypnoea
- diarhoresis
- hyperthermia
- pupil dilation - Altered mental status
- anxiety, agitation, confusion
Causes
- Amphetamines
- Metoclopramide, ondansetron
- SSRIs and SNRIs
- TCAs
- Ecstacy
- Tramadol and methadone
Sympathomimetic toxidrome
Upregulation of sympathetic NS:
- Increase HR and BP (high doses can cause tachyarrhythmia)
- Hyperthermia (sec to motor activity and agitation)
- Tachypnoea
- Dilated pupils
- Diaphoresis
EX - ecstasy/MDMA
Opiod sx/effects
Pinpoint pupils
Resp depression
No effect on HR/BP, temp or skin/secretions
Sedation ++ May be comatose
Organophosphate ingestion - what toxidrome does this produce?
SLUDGE (cholinergic)
- secretions ++++++ from every orifice
Antidote to cholinergic toxidrome
Atropine
Antidote to opiod overdose
Naloxone
Antidote to anticholinergic syndrome
Physostigmine - controversial use. only as per toxicology team
Mechanism of paracetamol overdose and antidote
Hepatic metabolism to N acetyl-p-benzyguinone-imine (NAPQI) which is highly toxic.
In normal doses, NAPQI conjugated by hepatic glutathione (cyp450 system) to nontoxic substance that is excreted in urine
In overdose, glutathione rapidly depleted and NAPQI accumulates, causing hepatic injury and potentially fulminant liver failure.
NAC (antidote) replenishes glutathione and detoxifies NAPQI
At what earliest time point following paracetamol ingestion can you measure the level
4 hours post
Mercury poisoning
- RF for exposure
- Signs/sx (acute vs chronic)
- Complications
-Tx
Mercury found in natural metals in environment, medical preservatives, dental amalgam, fluorescent bulbs, batteries, paint , fungicides, pesticides
RF: dentists, hygienists, miners, ceramic workers, taxidermy
Poisoning can occur from inhalation >> ingestion (poorly absorbed)
Acute Sx:
- if inhaled: fever, chills, cough, dyspnoea, circulatory collapse
- If ingested (local GI corrosive effects): nausea, vomiting and bloody diarrhoea -> renal failure
Chronic sx: triad of tremor, gingivitis, neuropsychiatric problems (behavioural disturbance = ‘erethismos’)
Cx: resp/renal failure, hemorrhagic colitis, death
Tx: chelation tx with oral DMPS or DMSA or IV dimercaprol
Neuroleptic malignant syndrome
Causes
Sx
Ix
Complications
Tx
Caused by dopamine D2R antagonists
- antipsychotic medications (1st gen worse = haloperidol, levomepromazine, chlorpromazine; 2nd gen not as bad = risperidone, quetiapine, olanzapine)
Sx - Often slow onset /resolution (1-2 weeks after dose incr)
- Altered mental status (mutism, withdrawal, somnolence)
- Autonomic dysfunction (tachypnoea, tachycardia and labile BP; diaphoresis and dilated pupils)
- Fever (from muscle activity)
- Muscle RIGIDITY (lead pipe) and restlessness; hyporeflexia (can have parkinsonian like sx w tremor, chorea, dyskinesias)
Ix - elevated myoglobin, CK; low Ca, Mg; high Ph ; leukocytosis
Cx
- Rhabdomyolysis -> renal failure
- Seizures (fever or metabolic disturbances)
- Cardiac arrhythmias
- DIC
Tx
- Bromocriptine (DA agonist)
- Dantrolene (skeletal muscle relaxant)
Thyroid storm/crisis
Triggers
Sx
Ttx
Triggers: surgery, trauma, infection, childbirth
- abruptly stopping tx for hyperthyroidism
- taking too much thyroid hormone
Sx
- fever
- agitation, confusion, seizures, coma
- severe tachycardia -> cardiac arrhythmias, high output CO
- can cause death
Note- level of TH between storm and hyperthyroidism are similar; differ in way the hormones affect bodily tissues (incr sensitivity to thyroid hormone)
Treatment
- Block synthesis (i.e. antithyroid drugs - PTU or carbimazole);
- Block release (i.e. iodine - potassium iodide or lugs solution);
- Corticosteroids (hydrocort or dex) inhibits peripheral conversion of T4 into T3
- Beta-blocker (propanolol)
Addisonian crisis
Acute insufficiency in adrenal hormones (GC or MC)
Causes
- acute stress event (infection, trauma or surgery) with inadequate incr in steroid dose
- abrupt cessation of chronic steroid tx
- first presentation
Sx
- hypotension/shock
- fever
- vomiting, abdo pain
- mental status changes
- fatigue, anorexia, weight loss, muscle/joint pain (chronic)
Tx
- IV fluids
- IV Hydrocort
Sickle cell crisis
Presentation
Triggers
MOA
Homozygous mutation in Hb gene (HbS HbS)
Heterozygous for HbS -> carrier ‘sickle cell trait’
Acidosis, hypoxia or dehydration -> HbS changes shape into sickle/crescent shape -> results in vasodilation-occlusion and haemolysis (intra and extravascular ie liver/spleen)
Haemolysis results in
- Elevated unconjugated bilirubin
- Elevated LDH
- Anaemia
Vaso-occlusive crisis/sickle crisis results in tissue ischaemia and sudden onset pain:
- -> dactylitis is when it happens in hands
- -> priapism (painful prolonged erection)
- -> hip = AVN
- -> brain = stroke, moyamoya
- -> kidneys -> haematuria, proteinuria
- -> acute chest syndrome (chest pain, SOB, cough, hypoxia)
- -> splenic infarct and splenomegaly frmo sequestration –> rapid drop in Hb leading to hypovolaemic shock over a few hours (potentially fatal)
Triggers
- infection
- dehydration
- hypoxia
- sedatives
- surgery
- local anaesthetics
Mx
- call haem
- start alangesics (simple +/- morph)
- Fluids
+/- blood transfusion
+/- abx (3rd gen cephalosporin + rox or azithromycin) if acute chest syndrome, acute splenic sequestration or fever present
Paracetamol metabolism
how is this impacted by overdose?
The liver metabolises > 90% of a paracetamol dose to sulfate and glucuronide conjugates, which are water soluble and are then eliminated in the urine.
2% is excreted unchanged by kidneys
Remaining 8% is metabolised by hepatic cyp450 system (CYP2E1 enzyme) to form NAPQI (highly toxic) -> glutathione binds and conjugates NAPQI, detoxifying it and enabling excretion in urine
In overdose, glutathione is saturated so excess NAPQI cannot be detoxified so excess causes hepatic centrilobar necrosis
treatment of vesicular crusted rash in infant
LP + CSF
Swab for HSV, VZV PCR and bacterial MCS
IV fluclox and acyclovir
Metabolism of alchohol
Alchohol dehydrogenase oxidises
Ethanol -> acetaldehyde and reduces NAD+ -> NADH
Acetaldhyde -> acetic acid via aldehyde dehydrogenase
Posterior fat pad is associated with what #
Supracondylar # of humerus
CO poisoning
- what direction does curve shift?
left (harder to offload O2)
What nerves can be injured in shoulder dislocation?
- axillary nerve
- musculocutaneous nerve (supplies biceps and biceps tendon reflex)
components of the gait cycle
stance phase (2/3 of gait cycle; foot in contact w floor) swing phase (1/3; clearing foot and advancing limb)
Variation of normal leg/knee alignment in children
start with bow legs , with growth and development the knees/legs straighten out (by 18mo) then by age 4-5 have knock knees, then by age 7-8 should reach normal alignment
** only investigate for bow legs at age 3years of age on (below this, is variation of normal). Could do vit D to ensure doesn’t have rickets
Causes of bow legs
assoc with in-toeing
Physiological (normal variation if <3yrs old)
Pathological
- Rickets
- Blounts disease
- Skeletal dysplasia (dwarfism)
Causes of knock knees
often associated with flat feet and external tibial torsion and out-toeing
-> can be assoc w anterior knee pain in adolescents and patellar maltracking
Causes
- physiological/familial (main cause, should resolve with time)
- pathological
- > metabolic bone disease
- > post traumatic valgus
- > skeletal dysplasia (trevors disease)
- > asymmetric femoral growth
Adolescent knock knees may require time
-> by guided growth
blounts disease
What is it?
Mechanism
RF
Diagnosisa
mx
Progressive pathologic genu varum (bow legs) centered at the tibia in children 3 to 5 years of age.
Mechanism: related to mechanical overload in genetically susceptible individuals inducing osteochondrosis of MEDIAL PROXIMAL tibial physis and epiphysis (so essentially the medial growth plate slows/stops making new bone)
RF: overweight children, early walkers (<1 yr), hispanic or african american
Diagnosis is suspected clinically with presence of a genu varum/flexion/internal rotation deformity and confirmed on XR with an increased metaphyseal-diaphyseal angle
Mx
- bracing if <3yo or mild
- operative (osteotomy) if more severe or >3yo
Causes of limp
Pain
-> infection, #, tumour, jia, transient synovitis
Leg length discrepancy
-> acquired, congenital
Mechanical or anatomical abnormality
-> DDH, SUFE , perthes disease
Neurological abnormality
-> Cerebral palsy
Weakness
-> Muscular dystrophy
Metabolic
- rickets, hyperPTH
Inflammatory
- TS, JRA, HSP
Infectious
- SA, OM, disci tis, cellulitis
Neoplastic
- malignant vs benign
Traumatic
- Toddlers #, OCD, Osgood schlatter/overuse, dust, SUFE
Haematological
- sickle cell crisis
Iatrogenic
- AVN, LLD
Idiopathic
Most common cause of limp by age group
toddlers
children
adolescents
Toddlers and children - transient synovitis
Adolescents - OM/SA
What framework to differentiate between SA and transient synovitis?
Kocher criteria
- temp (Fever presence)
- NWB?
- ESR >40
- WCC >12
All 4 - 99% chance of SA
3 - 93%
only 2 - 50% chance of SA
1 - 30% chance
0 - 0% chance
What is most common malignant cause for limp?
ALL
RF for DDH
Female sex
Family history
Breech presentation
Other things that can incr risk
- ethnicity
- swaddling
Assoc
- Downs
- spina bifida
- larsens syndrome
Baby is born with multiple joint dislocations (hips, knees, elbows), B/L talipes, hand deformities and dysmorphic facies
What is the suspected condition and what is it caused by?
Larsens syndrome
Disorder of bone development -\> ligamentous hyperlaxity Inherited disorder (AD) caused by mutations in FLNB gene (filamin B) and carbohydrate sulfotransferase 3 deficiency
Main features:
- Clubfoot
- Multiple joint dislocations at birth (hips, knees, elbows),
- Hyperflexible joints
- Abnormal facial features
- flattened nasal bridge
- hypertelorism
- prominent forehead
- Cervical kyphosis
- Other: +/- cleft palate, short stature, hearing loss
What isn’t a RF for CP?
prematurity
LBW
placental disturbance
Infection
Drug or alcohol
Epilepsy
Hyperthyroidism
Toxamia
Birth trauma (forceps)
Incompetent cervix
3rd trimester bleeding
kernicterus
head trauma
(note not a comprehensive list)
Birth trauma (forceps)
Indication for botox in CP
Treatment of spasticity (NOT contractors)
SE: permanent atrophy and contractors. is a temporary fix whilst waiting for surgery or whilst undergoing PT
Bilateral acoustic neuroma is associated with what genetic condition?
NF2
orthopaedic manifestations of NF1
- Tibial dysplasia (50% of these are assoc w NF1)/pseudoarthrosis
- Dystrophic scoliosis
- Osteopenia
Surgical causes of short gut
NEC
Gastroschesis
Omphalocoele
Mec ileus
Midgut volvulus
Long segment hirschsprugs
Presentation of H type TOF
Note - this is the type of TOF where there is NO tof but there is a tracheo-oesoph fistula
Recurrent chest infections
Vomiting with feeds or apnoeas/blue or dusky discolouration with feed
Gaseous abdo distension (as swallowing air)
Effect of DKA on Na levels
Measured sodium is depressed by the dilutional effect of hyperglycaemia (actual ‘corrected’ Na will be higher)
Corrected sodium can be calculated with this formula:
Corrected sodium = measured sodium + 0.3 x (glucose – 5.5) mmol/L
ie 3 mmol/L sodium to be added for every 10 mmol/L of glucose above 5.5 mmol/L.
Effect of DKA on K levels
Children with DKA are deplete in total body potassium regardless of the initial serum potassium level
What type of IV fluids do u use for rehydration in DKA and why?
0.9% sodium chloride with glucose and potassium chloride (maximum 60 mmol/L) as required should generally be used for the duration of IV rehydration (unless initial K is >5.5 in which withhold K from fluid bag until the K level is 5.5 or less)
This is because children with DKA are deplete in total body potassium regardless of the initial serum potassium level
What is this presentation?
- Acute onset; opisthonos (dramatic abnormal posture due to spastic contraction of the extensor muscles of the neck, trunk, and lower extremities that produces a severe backward arching from neck to heel), ‘stereotyped cycling movements’ along with ketotic hypoglycaemia in neonatal period
Maple syrop urine disease
unable to break down branch chain AA (elevated serum levels of valine, leucine, isoleucine) -> unable to be made by body so must be consumed from external source
Mutation in gene that codes for alpha-ketoacid dehydrogenase (enzyme that breaks them down) - varying function of this enzyme wit phenotypic severity
Antagonist to benzo overdose
Flumazenil - selective GABAA receptor antagonist
