emergency paeds Flashcards
paeds resp rates infant (upto 1 year) toddler (1-3) preschooler (3-6) school-age (6-12) adolescent (12-18)
Infant (birth–1 year) 30–60/m Toddler (1–3 years) 24–40/m Preschooler (3–6 years) 22–34/m School-age (6–12 years) 18–25/m Adolescent (12–18 yrs) 12–16/m
paeds HR Infant (birth–1 year) Toddler (1–3 years) Preschooler (3–6 years) School-age (6–12 years) Adolescent (12–18 years)
Infant (birth–1 year) 100-160/m Toddler (1–3 years) 90 -150 /m Preschooler (3–6 years) 80 -140/m School-age (6–12 years) 70 -120/m Adolescent (12–18 years) 60 -100/m
immunisation history
Birth – BCG for at risk infants
2 months – DTaP, IPV, HIB, Hep B
PCV
Men B
Rotavirus
3 months – DTaP, IPV, HIB, Hep B
Rotavirus
4 months – DTP, IPV, HIB, Hep B
Men B
PCV booster
12 months – HIB/ Men C
PCV booster
Men B booster
MMR
3/4 years – DPT Polio
MMR
14 (School yr 9) Td/IPV
Men ACWY
when does a kid smile sit unaided walk talk handedness
Smile – 6 weeks Sit unaided – 6 months Walk – 12 months Talk – 12 months Handedness
clinical Sx
mechanism
Mx
of paracetamol
Early:
• abdominal pain, vomiting
Later (12 h to 24 h):
• liver failure
Mechanism initial gastric irritation Toxic metabolite (NAPQI) produced by saturation of liver metabolism
Mx
Risk assessed by measuring plasma paracetamol concentration
Treat with intravenous acetylcysteine if concentration is high or liver function abnormal
clinical Sx
mechanism
Mx
of button batteries
Abdominal pain
Gut perforation and stricture formation
mechanism
Leakage: corrosion of gut wall due to electrical circuit production
Mx
X-ray of chest and abdomen to confirm ingestion and identify position
Endoscopic removal is recommended if in the oesophagus, the object fails to pass, or symptoms are present (e.g. abdominal pain or melaena)
clinical Sx
mechanism
Mx
of CO
Early:
• headache, nausea
Later:
• confusion, drowsiness leading to coma
mechanism
Binds to haemoglobin causing tissue hypoxia
Mx
High-flow oxygen to hasten dissociation of carbon monoxide
The role of hyperbaric oxygen therapy is unclear
clinical Sx
mechanism
Mx
of salicyclates
Early:
• vomiting, tinnitus
Later:
• respiratory alkalosis followed by metabolic acidosis
Mechanism
Direct stimulation of respiratory centre
Uncouples oxidative phosphorylation leading to metabolic acidosis and hypoglycaemia
Mx
Plasma salicylate concentration 2–4 h after ingestion helps to estimate toxicity
Alkalinization of urine increases excretion of salicylates.
Haemodialysis also effectively removes salicylate
clinical Sx
mechanism
Mx
of TCAs
Early:
• tachycardia, drowsiness, dry mouth
Later:
• arrhythmias, seizures
mechanism
Anti-cholinergic effects, interference with cardiac conduction pathways\
Mx
Treatment of arrhythmias with sodium bicarbonate
Support ventilation
clinical Sx
mehcanism
Mx of
ethylene glycol
Early:
• intoxication
Later:
• tachycardia, metabolic acidosis leading to renal failure
mechanism
Production of toxic metabolites that interfere with intracellular energy production
Mx
Fomepizole inhibits the production of toxic metabolites; alcohol may also be used but has more adverse effects
Haemodialysis to remove toxic metabolites in severe cases
clinical Sx
mechanism
Mx
alcohol
Hypoglycaemia
Coma
Respiratory failure
Direct inhibitory effect on glycolysis in the liver and neurotransmission in the brain
Monitor blood glucose and correct if necessary. Support ventilation if required
Blood alcohol levels may help to predict severity
clinical sx
mechanism
mx
of iron
Initial: vomiting, diarrhoea, haematemesis, melaena, acute gastric ulceration
Latent period of improvement
6–12 h later: drowsiness, coma, shock, liver failure with hypoglycaemia, and convulsions
Long term: gut strictures
mechanism
Local corrosive effect on gut mucosa
Disruption of oxidative phosphorylation in mitochondria leads to free radical production, lipid peroxidation, and metabolic acidosis
Mx
Serious toxicity if >75 mg/kg elemental iron ingested
Serum iron level 4 h after ingestion is the best laboratory measure of severity
Intravenous desferoxamine chelates iron and should be administered in cases of moderate-to-severe toxicity
clinical Sx
mechanism
Mx of
hydrocarbons ie. paraffin, kerosene
Pneumonitis
Coma
mechanism
Low viscosity and high volatility makes aspiration easy, resulting in direct lung toxicity
Direct inhibitory effect on neurotransmission in the brain
Mx
No specific antidote – supportive treatment only
clinical sx
mechanism
Mx of
organophosphorus pesticides
Cholinergic effects:
• salivation, lacrimation, urination, diarrhoea and vomiting, muscle weakness, cramps and paralysis, bradycardia. and hypotension
Central nervous system effects:
• seizures and coma
Inhibition of acetylcholinesterase resulting in accumulation of acetylcholine throughout the nervous system
Supportive care
Atropine (often in large doses) as an anticholinergic agent
Pralidoxime to reactivate acetylcholinesterase
factors increased risk of recurrence for self harm
lack of regret, evidence of planning, e.g. leaving a note, and a lack of protective social factors
surgical cuases of abdominal pain
acute appendicitis
other causes if abdo pain that are not abdo originated
• lower lobe pneumonia may cause pain referred to the abdomen
• primary peritonitis is seen in patients with ascites from nephrotic syndrome or liver disease
• diabetic ketoacidosis may cause severe abdominal pain
• urinary tract infection, including acute pyelonephritis,
- pancreatitis -> acute abdo pain, serum amylase
Sx of acute appendicitis
– Anorexia
– Vomiting
– Abdominal pain, initially central and colicky (appendicular midgut colic), but then localizing to the right iliac fossa (from localized peritoneal inflammation)
signs of acute appendicitis
– Fever
– Abdominal pain aggravated by movement, e.g. on walking, coughing, jumping, bumps on the road during a car journey
– Persistent tenderness with guarding in the right iliac fossa (McBurney’s point). However, with a retrocaecal appendix, localized guarding may be absent, and in a pelvic appendix there may be few abdominal signs.
Mx of appendicitis
appendicectomy - uncomplicated
generalised guarding consistent w perforation -> fluid resuscitation and intravenous antibiotics are given prior to laparotomy
define non-specific abdominal pain
- abdominal pain which resolves in 24–48 hours.
- accompanied by an upper respiratory tract infection with cervical lymphadenopathy
what is intussusception
invagination of proximal bowel into a distal segment. It most commonly involves ileum passing into the caecum through the ileocaecal valve
most common cause of intestinal obstruction
3 m-2yrs
most serious complication of intussusception
stretching and constriction of the mesentery resulting in venous obstruction, causing engorgement and bleeding from the bowel mucosa, fluid loss, and subsequently bowel perforation, peritonitis and gut necrosis
presentation of intussusception
- Paroxysmal, severe colicky pain with pallor – during episodes of pain, the child becomes pale, especially around the mouth, and draws up the legs. There is recovery between the painful episodes but subsequently the child may become increasingly lethargic.
- May refuse feeds, may vomit, which may become bile stained depending on the site of the intussusception.
- A sausage-shaped mass – often palpable in the abdomen
Passage of a characteristic redcurrant jelly stool comprising blood-stained mucus – this is a characteristic sign but tends to occur later in the illness and may be first seen after a rectal examination.
• Abdominal distension and shock.
how to confirm diagnosis of intusussception
US and also monitor treatment TARGET SIGN
Unless there are signs of peritonitis, reduction of the intussusception by rectal air insufflation is usually attempted by a radiologist
what is the compression ventialtion ratio
compression:ventilation ratio: lay rescuers should use a ratio of 30:2. If there are two or more rescuers with a duty to respond then a ratio of 15:2 should be used
DDx for a red swollen eye
- pre-septal cellulitis • Orbital or Post-septal cellulitis. • Allergicconjunctivitis. • Bacterial conjunctivitis. • Trauma. - sub-periostal/orbital abscess - cavernous sinus thrombosis
Features of pre-septal cellulitis
- redness and discharge from one eye
- affected eye ‘stuck shut’ in the morninh
- colour/consistency depends on cause
- caused by bacteria (staph aureus, H strep, H.influenzae) chlamydia, viruses
Definition of preseptal cellulitis
inflammatory disease of the orbit limited to the tissues anterior to the orbital septum.
definition of orbital cellulitis
inflammatory disease of the superficial and deep structures of the orbit.
aetiology of preseptal
cellulitis
- Commonly follows URTI and sinusitis (ethmoid commonest).
- Respiratory pathogens (Streptococcus, Haemophilus) commonest. • Other sources: spread from skin, lachrymal ducts, middle ear etc.
Mx of cellulitis
- Admit. • IV access. • FBC/CRP, cultures. • Nose swab. • IV Ceftriaxone. • ± IV Metronidazole • (if sinuses involved) • Prompt ENT and ophthalmology review - 4h obs - Consider CT scan
Sx of meningitis
- Fever
- Irritability
- Lethargy / Drowsiness
- High pitched cry
- Loss of consciousness
- Seizures
- Poor feeding
- Vomiting
- Photophobia
DDx of fever headache and neck stiffness
- Bacterial meningitis.
- Viral meningitis.
- Viral encephalitis.
- Tuberculous meningitis.
- Cerebral abscess.
- Hydrocephalus.
- Non-accidental injury
acute Mx of bacterial meningitis
Call for senior help
Airway: apply 15L/min facial O2
Breathing: support as necessary
Circulation: IV or IO cannula
Bloods: Gas (HCO3, BE, lactate), glucose. FBC, CRP, clotting, U&E
check circulation (CRT, HR, BP) - Rx PRN
IV 20ml/kg 0.9% NaCl fluid bolus
Disability: assess: level of consciousness (GCS)
Neurology - cranial nerves, focal. Raised ICP.
Exposure - temperature rashes
LP contraindications
- cardiorespiratory instability
- signs of raised ICP: coma, low HR, high BP, papilloedema -> needs CT
- coagulation abnormalities , thrombocytopenia
- after seizures - until stabilised
- focal neurological deficits
- sogns of infection at the LP site
- concerns about menigococcal septicaemia
what is normal CSF
clear
<5 lymphocytes
0.14-0.4g/L
>50% BG
bacterial menigititis CSF
Appearance white cells protein glucose organisms
turbid
100-10000 neutrophils
increased protein
decreased glucose
S. pneumoniae - 14 days
H. influenzae - 10 days
N. Meningitis - 7 days
neonates
strep group B
Ecoli
Listeria
viral meningitis Appearance white cells protein glucose organisms
clear
<1000 lymphoctyes
normal protein
usually normal
Enteroviruses Echo, coxsackie Parechovirus Herpesviridae Herpesvirus 1 & 2 Varicella zoster CMV, EBV Herpesvirus 6 & 7 adenovirus influenza RSV measles mumps
TB meningitis Appearance white cells protein glucose organisms
turbid clear/viscous
10-500 lymphocytes
increased protein
decreased glucose
Mycobacterium TB
viral encephalitis Appearance white cells protein glucose organisms
clear
usually <1000 lymphocytes
normal protein
normal
same as viral menigitis
acute Mx of meningitis
<28 days: 3o cephalosporin + Amoxicillin + Gentamicin
1-3 mo: 3o cephalosporin + Amoxicillin
IV amoxicillin + IV cefotaxime
> 3 mo:
3m: IV cefotaxime (or ceftriaxone)
3o cephalosporin ± Amoxicillin (? Listeria)
+ Acyclovir (all age groups – until microbiology seen)
- Steroids
NICE advise against giving corticosteroids in children younger than 3 months
dexamethsone should be considered if the lumbar puncture reveals any of the following:
frankly purulent CSF
CSF white blood cell count greater than 1000/microlitre
raised CSF white blood cell count with protein concentration greater than 1 g/litre
bacteria on Gram stain - Fluids
treat any shock, e.g. with colloid - Cerebral monitoring
mechanical ventilation if respiratory impairment - Public health notification and antibiotic prophylaxis of contacts
oral ciprofloxacin is now preferred over rifampicin
