2- Emergency paediatrics (2/2) Flashcards
Poisoning of unknown origin
- Accidental incidents common in children <6
- Intentional ingestions and recreational drug use in older children and adolescents
–>Mental illness (suicide and attempted self harm) - Think of Munchausen
common poisoning of unknown origin in <6
o Prenatal iron supplements
o Antidepressants
o Cardiotoxic agents
o Illicit drugs
o Analgesics
o Aspirin
common non drug poisoning of unknown origin in
o Hydrocarbons
o Alcohols
o Cleaning products e.g. laundry detergent and bleach)
o pesticides
Presentation POUO
Poisoning of unknown origin should be considered in the differentials of children who present with acute onset of:
- Multiorgan system dysfunction
- Altered mental state
- Resp or cardiac compromise
- Unexplained metabolic acidosis
- Seizures
- Puzzling clinical pictures
Risk factors POUO
- 1-4 yo
- Previous history of ingestion
- Prior history of substance misuse
approach to POUO
Initial evaluation and stabilisation
A to E
Diagnosis of poisoning
- Obtain accurate history
- Location, activity just before injesting
- Risk assessment I.e. suidice and self harm
- Ask paramedics about what they saw e.g. open containers, empty bottles, spilled content
- Toxicology screen
- Clinical response to antedote
Definitive management will depend on substance
Example managements of POUO
- Decontamination using charcoal
- Antidotes
o E.g. naloxone e.g. opioid
o E.g. NAC e.g. paracetamol
o E.g. Flumazenil (diazepam and cocaine)
poisoning antidotes and substrates
Paracetamol overdose (acetaminophen)
Background
- Drug most commonly overdose on are paracetamol, ibuprofen , aspirin, iron, cough medicines and the contraceptive pill
- Children with features of poisoning should be admitted to hospital
- Children who have taken poisons with delayed actions should also be admitted
Pathophysiology of paracetamol overdose
- Toxic doses of paracetamol may cause severe hepatocellular necrosis and much less frequently renal tubular necrosis -> lack of glutathione
- Liver damage is maximal 3-4 days after paracetamol overdose
- Can lead to liver failure, encephalopathy, coma and death
Presentation of paracetamol overdose
- Nausea and vomiting- early features (also recur after 2-3 days)
- Right subcostal pain and tenderness – hepatic necrosis
History for paracetamol overdose
- Dose
- Timing
- Associated ingestions
investigations for paracetamol overdose
Delay sampling to 4h after ingestion
* Paracetamol level.
* U&E – baseline renal status/risk of AKD.
* LFT – monitor ALT levels for hepatotoxicity.
* Glucose – hypoglycaemia common in liver necrosis.
* Clotting screen – INR as PT best indicator of liver necrosis.
* Venous gas –acidosis in 10% of acute liver failure.
Management of paracetamol overdose
Paracetamol Children taking >150mg/kg need assessment
- <1 hour ago give charcoal (prevents absorption) alongside NAC
- N-acetylcysteine: PO or NG loading 140mg/kg, then 70mg/kg/ dose qds for 17 doses.
- IV used if GI bleeding. Repeat blood level at 24hr
N-acetylcysteine MOA
Acts to increase synthesis of glutathione in the liver; which acts as antioxidant and facilitates conjugation of toxins, esp toxic metabolites of acetaminophen.
- Acts to prevent or reduce severity of liver damage
- Can be given up to and possibly beyond 24 hours of ingesting paracetamol
- Most effective if given within 8 hours
paracetamol overdose prognosis
management of aspirin overdose
ACTIVATED CHARCOAL 1G/KG
FLUID REPLACEMENT
URINE ALKALINISATION with sodium bicarbonate
BENZOS FOR SEIZURES (0.1MG/KG)
HAEMODIALYSIS IF SEVERE (ITU)
management of iron overdose
Activated charcoal DOES NOT bind iron
Deferoxamine (DFO)
Metabolic acidosis: 1-2 mmol/kg sodium bicarbonate (1-2 mL/kg 8.4% or 2-4 mL/kg 4.2%) over 20 minutes. Repeat as necessary, aiming for a normal pH.
- administer into a large vein (or via a central line).
Large flush before and after (irritant to vein)
management of benzos overdose
ACTIVATED CHARCOAL 1G/KG (<1H)
FLUMAZENIL
fatal household poisens
CAMPHOR (VICKS / TIGER BALM)
ESSENTIAL OILS
BLEACH
SOLVENTS
WEED KILLER / INSECTICIDES
BUTTON BATTERIES
button batteries
- halo sign on x-ray
- surgical removal
- emergency
- battery acid erodes stomach and can cause catastrophic bleed
mucosal ulceration / necrosis > haemorrhage > perf: FATAL
pneumothorax background
Background
- Occurs in 2% of term infants
- Increased in prematurity and respiratory disease
Presentation of pneumothorax
- Asymptomatic (if small)- most resolve spontaneously
- If large: Respiratory distress
- Tension pneumothorax
-> Respiratory distress
-> Cyanosis
-> Mediastinal shift away from affected side
-> Reduced chest movement and air entry on affected side
-> Transillumination lights up affected side
investigation for pneumothorax
o Ipsilateral translucency
o Lack of peripheral lung markings
o Collapsed lung
management of pneumothorax
- If asymptomatic: none
- If symptomatic
o Give oxygen as required
o Needle aspiration (2nd intercostal mid clavicular)
o Chest drain (4th mid axillary)
o In an emergency do a needle aspiration before chest drain
Pneumothorax: In an emergency: needle aspiration procedure
- Insert a 21-23G butterfly into affected side at the 2nd intercostal space in the midclavicular line
- Butterfily can be placed under water following insertion
Chest drain procedure
- Lie the child supine with the affected side raised by 30–45° using a towel.
- Raise the arm towards the head.
- Suitable sites are the fourth intercostal space in the mid-axillary line (be careful to avoid the nipple), and second intercostal space in mid- clavicle line.
- Chest drain insertion should be performed using strict aseptic technique.
- Wash hands and put on sterile gloves, gown, +/– surgical mask.
- Clean skin over the insertion site with antiseptic solution.
- Prepare sterile field, then infiltrate small amount of local anaesthetic into the tissues down to the pleura.
- Wait 1–2min, then make a small skin incision with the scalpel just above and parallel to rib. Note: Blood vessels lie just below each rib.
- Using artery forceps make a blunt dissection down to and through the parietal pleura.
- Using forceps clamp chest drain and then insert into pleural space. Most clinicians remove the trocar before insertion.
- Aim to push the chest drain tip towards the lung apex. In the event of a small pneumothorax aim the tip in the direction of the pneumothorax remembering to aim anteriorly (air rises in the ill child lying supine).
- Connect the drain tightly to the underwater drainage system, unclamp drain, and apply negative pressure of 5–10cmH2O. Bubbling should start to occur.
hypoglycaemia
<2.6mmol/l
Pathophysiology of hypoglycaemia
- Hypoglycaemia is a sign of underlying disease that interferes with at least one of the following processes:
o Carbohydrate intake
o Carbohydrate absorption
o Gluconeogenesis
o Glycogenolysis - Gluconeogenesis is a metabolic pathway that results in the generation of glucose from non-carbohydrate substrates e.g pyruvate, lactate, glycerol. It mainly occurs in the liver but also to some extent in the cortex of the kidneys. The process occurs during periods of fasting, starvation, low-carb diets or intense exercise. It is often associated with ketosis.
- Glycogenolysis is the breakdown of glycogen and takes place in the cells of muscle (to provide energy for contraction) and hepatocytes (to release glucose into the bloodstream for uptake by other cells).
Causes of hypoglycaemia
Systemic/Nutrition
* Starvation
* Malnutrition
* Sepsis
* Malabsorption
Metabolic
* Ketotic hypoglycaemia “accelerated starvation”
* Glycogen storage disease
* Galactosaemia
* Organic acidaemia
* Carnitine deficiency
* Acyl CoA Dehydrogenase deficiency
Endocrine
* Hyperinsulinism
* Hypopituitarism
* Growth hormone deficiency
* Hypothyroidism
* Congenital adrenal hyperplasia
Hepatic
* Hepatitis
* Cirrhosis
* Reye Syndrome
Toxic
* Aspirin
* Alcohol
* Insulin
* Valproate
presentation of hypoglycaemia
investigations for hypoglycaemia
- BM
- Urine: ketones
management of hypoglycaemia
If Patient can tolerate oral fluids
- 50ml of Lucozade or glucogels
- Recheck BM in 15 mins
<2.6mmol/l (IV bolus of dextrose or IM glucagon)
Patient unable to tolerate oral fluids
- IV access: IV bolus 2ml/kg 10% dextrose followed by continuous infusion 3-5ml/kg/hr 10% dextrose
No IV access- IM glucagon
- Aim BM 4-8mmol
- All patients with hypoglycaemia of unknown origin require admission
Malnutrition
Background
Wide spectrum of nutritional disorders, varying from protein-energy mal nutrition to micronutrient nutritional deficiencies t
- Common cause of child mortality and morbidity
malnutrition causes
- Diets low in protein, energy or specific nutrients
- Strict fad or vegetation diets
- Disease causing malabsorption (coeliac, CF, crohns disease)
- Eating disorders e.g. anorexia nervosa
Investigations/diagnosis malnutrition
- Recent weight loss (t10% over 3mths is suggestive of impaired nutritional status).
- Accurately plot serial height and weight (falling across 2 centile lines or below 3rd centile may indicate nutritional impairment).
- Percentage weight for height (= [actual weight/expected weight for height centile] x 100); a value of d90% may indicate impairment.
- Body mass index (BMI) = weight (kg)/height (m)2.
- Mid-arm circumference divided by head circumference (malnutrition if <0.31).
- Detailed dietary assessment of 5–7-day food diary.
- Serum albumin.
presentation of malnutrition
Presentation
* Not growing or putting on weight at the expected rate (faltering growth)
* Changes in behaviour, such as being unusually irritable, slow or anxious
* Low energy levels and tiring more easily than other children
specific nutritional deficiencies
Kwashiorkor
Characterised by bilateral pitting oedema, in the absence of another medical cause of oedema
- Typically associated with dietary protein deficiency
- Most often seen in sub-saharan Africa
- Can be seen in children with severely restricted diets (children with ASG)
- Typically occurs at the time of weaning and up to 5 years of age
complications of kwashikor
- Infection
- Hypoglycaemia
- Hypothermia
- Xerophthalmia
- Electrolyte disturbance
- Cardiac failure
diagnostic factors for kwashikor
Investigations for kwashikor
- Urine dipstick
- FBC
- Serum electrolytes
- Serum protein
management of kwashikor
- Fluids
- Oral calorie intake restricted to maintenance requirements (prevent refeeding)
- Antibiotic therapy
Nutritional support indication
- Severely ill patients, e.g. ill preterm infants.
- Nutritional supplementation is required, e.g. FTT, cystic fibrosis.
- Swallowing difficulty, e.g. severe cerebral palsy.
- Metabolic diseases, e.g. phenylketonuria.
- Gastrointestinal failure, e.g. malabsorption, short bowel syndrome.
- Other primary disease state, e.g. chronic renal failure.
types of feeding support
oral supplementation
enteral tube feeding
parenteral
Oral supplementation
high energy milks, mineral/vitamin supplementation
Enteral tube feeding
- Can be: NG, orogastric, nasojejunal and gastrostomy
- Liquid foods are given as boluses or continuously e.g. overnight
Indication
* Swallow problems (severe cerebral aplsy, prematurity)
* Cardiorespiratory compromise
* GORD
* Anorexia
parental feeding
e.g. TPN
- Indication: post op, treatment of IBD, oral feeds contraindicated e.g. NEC, intestinal failure e.g. short bowel syndrome, GI obstruction, oncology e.g. graft versus host
complications of supportive feeding
Complications
* Sepsis: usually S. epidermidis, S. aureus, Candida, Pseudomonas, E. coli.
* Demanding: in expertise, cost, etc.
* Central-line: occlusion, breakage, displacement.
* Electrolyte/metabolic disturbances: e.g. glucose i or d.
* Vascular: thrombophlebitis, thromboembolism, extravasation injuries.
* Cardiac tamponade: avoid by placing IV line tip proximal to right atrium.
* From amino acids: PN-associated liver disease, including, steatosis, cholestasis, or, rarely cirrhosis or portal hypertension.
* From lipids: platelet dysfunction, hyperlipidaemia, fatty liver, pulmonary hypertension.
* Metabolic bone disease: due to insufficient Ca2+ and PO43 –.
Hypothermia background
- Body temp <35 degrees
–> In trauma patients <36 (hypothermic trauma patients can have devastating consequences)
Classified as mild, mod or severe according to clinical features
- Mild 32-35
- Mod – 28-32
- Sev -<28
mild hypotheramia
32-35
moderate hypotheramia
28-32
severe hypothermia
28-32
Stages of hypothermia
o Compensation
o Decompensation
o Failure of body’s defences against cold
Risk factors for hypothyroidism
- Neonates and young children
- Hypothyroidisms
- General anaesthetics use
Causes of hypothyroidism
- Not enough clothes in cold weather
- Staying outside too long
- Fall into cold water
- Wet clothes
- Live in cold house
Investigations for hypothermia
- Core body temp measurement
- 12 lead ECG
- UandE
12 lead ECG for hypothermia
Osborn wave – notch in the downward portion of R wave in QRS complex
hypothermia presentation
- Cold exposure
- Body temp <35 degrees
- Shivering
- Impaired mental state
- Mild: Tachypnea, tachycardia, hypertension
- Moderate: resp depression, bradycardia, hypotension
- Severe: coma and apnea
Management of hypothermia
Initial
- Stop further cooling
- Remove patient from cold environment
- Remove wet or cold clothing
- Insulate
- Warming of body
- Secure airway
- Monitor breathing and circulating
- Maintaining circulating using warm IV fluid
Rewarming
- Passive: remove cold and wet clothing and apply dry insulation e.g. blankets
- Active external warming e.g. forced air rewarming, radiant heat and chemical heat packs
Beware: active external rewarming may be ineffective and harmful in patients with severe hypothermia or absent circulation
Hyperthermia background
Body temp >40 degrees
- Occurs when the body absorbs or generates more heat than it can release
- different types
types of hyperthermia
Heat cramps
Heat exhaustion
Heat rash
Heat stress
Heatstroke
causes of hyperthermia
- Heat stroke e.g. overexertion in hot, humid conditions
risk factors for hyperthermia
Risk factors
- Children – may play in the heat without taking time to rest, cool off and stay hydrated
- Dehydration
- CF
Investigations for hyperthermia
- Rectal thermometer/ oesophageal probe in intubated patients
- FBC
- Liver function tests
- U&Es
presentation of hyperthermia
Presentation
- >40 degrees
- Irritability
- Confusion
- Coordination issues
- Flushes skin
- Dizziness, syncope
- Low blood pressure
- Reduced sweating (heat stroke)
- Tachycardia/ tachypnoea
- Seizures
- Intense thirst
management of hyperthermia
- Stop physical activity, remove heavy or tight clothing
- Drink electrolyte drink/ IV fluids
- Cool compresses/ col or ice water immersion
prevention of hyperthermia
- Take cool breaks in the shade
- Stay well hydrated
- Wear light weight, light colour clothing
Is hyperthermia the same as a fever?
Hyperthermia isn’t the same as a fever. When you have hyperthermia, your body temperature rises above a certain “set-point” that’s controlled by your hypothalamus (a part of your brain that controls many body functions). But when you have a fever, your hypothalamus actually increases your body’s set-point temperature. This intentional rise in body temperature is your body’s attempt to fight off an illness or infection.
