Seriously ill Child Flashcards
In the primary assessment of the sick child, what are the 3 aspects of breathing that should be assessed?
- EFFORT
- RR, recessions, insp or exp noises, grunting, accessory muscle use, nasal flaring, gasping - EFFICACY
- degree of chest expansion, auscultation, sats measurement - EFFECT (on other organs)
- HR, skin colour, mental status
Name the 3 circumstances where an increased effort in breathing will not be present despite failure of the respiratory system?
- If severe respiratory problems have been present for a prolonged time, fatigue develops
- In presence of cerebral depression e.g. raised ICP, encephalopathy, poisoning. Depresses the respiratory drive
- Concurrent neuromuscular disease
T or F: central cyanosis is an early consequence of hypoxia
False.
Late sign, only occurs when SpO2 is < 70%
Note if child is anaemic may not be present at all
Aspects used to assess cardiovascular status in the primary assessment of the sick child?
Heart rate
Pulse volume
Cap refill
Pre-terminal cardiovascular signs?
Hypotension
Rapidly falling heart rate
Associated with poor systemic perfusion
Effect of cardiac inadequacy on the respiratory system?
increased respiratory rate, but wont have recessions
incr in RR is caused by the metabolic acidosis from circulatory failure
Systemic effects of cardiac inadequacy?
- mottled pale skin
- drop in urine output
- drop in mental status (poor cerebral perfusion)
Decorticate posturing
flexed arms, extended legs
Decerebrate posturing
extended arms, extended legs
What is Cheyne-Stokes breathing pattern
an abnormal pattern of breathing characterized by progressively deeper, and sometimes faster, breathing followed by a gradual decrease that results in an apnoea. The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes.
What is Cushing’s response and what does it mean
Systemic hypertension with sinus bradycardia
Indicates compression of the medulla oblongata caused by herniation of of the cerebellar tonsils through the foramen magnum
Fluid bolus in children if inadequate circulation
20mg/kg (crystalloid)
Signs of raised ICP
decreasing conscious level
asymmetrical pupils
abnormal posturing
abnormal ocular motor reflexes
Difference between acidaemia/alkalaemia and acidosis/alkalosis
acidaemia + alkalaemia represent the acidity of the blood outwith the normal range.
acidosis + alkalosis refer to the underlying processes that result in the acidaemia/alkalaemia
What is the carbonic acid reaction
CO2 + H2O – H2CO3 – H + HCO3
T or F: bicarbonate crosses the BBB.
What does this mean for CSF & serum levels of bicarbonate
False. Cannot cross. Secreted in the CSF as it is produced in the choroid plexus
CSF bicarbonate levels approximate serum levels some hours previously
T or F: CO2 crosses the BBB
What does this mean for CSF & serum levels of CO2
True.
CSF CO2 and serum CO2 are essentially equivalent concurrently
Rewrite the carbonic acid reaction, expressed as the concentration of hydrogen ions
[H+] = K x ( [CO2] / [HCO3] )
where K is the dissociation constant
Henderson-Hasselbach equation
pH = pK + log ( [HCO3] / PCO2 )
where pK is approx 6.1
How does the pH of CSF contribute to the respiratory drive
pH of CSF is a major contributor to the respiratory drive
If CSF becomes acidotic then there is increased respiratory drive to exhale CO2
Reverse also true
What is the role of bicarbonate
To act as an electrical buffer to accommodate other electrolyte changes
What cation has the greatest impact on the concentration of [HCO3] if it changes
Na
What anion has the greatest impact on the concentration of [HCO3] if it changes
Cl-
What is the anion gap
Incorporates all the other anions/cations for which measurements aren’t usually available in order to provide wider context for acid-base balance
Anion gap calculation
AG = (Na + K) - (HCO3 + Cl)
What cations/anions are incorporated into the anion gap
Alb (- ve)
Phos (- ve)
Xa (unmeasured weak acids) (- ve)
Lactate (- ve)
Ca (+ ve)
Mg (+ ve)
Why are Ca and Mg not routinely included in the anion gap calculation
The concentrations of these are small and vary minimally
Which anion can be included into the anion gap to expand the calculation and why is this done
Albumin
Forms a large component of the normal anion gap & can vary dramatically in acute injury or illness, so if not included it could mask the severity of the acidotic process
What is the anion gap calculation with albumin included and why is it like this
AG = (Na + K) - (HCO3 + Cl) + 0.25x(42-Alb)
0.25 because albumin is only slightly charged so add a quarter of the albumin deficit to remain realistic
What is base excess and what does it tell us in practice
The amount of acid or base that needs to be added to a blood sample in order to return the pH to 7.40 at a temp of 37C at a PCO2 of 5.3kPa
It removes the respiratory component and allows us to quantify the metabolic components of. The acid-base abnormality
Fluid requirement in a well, normal child
First 10kg - 100ml/kg (per day) or 4ml/kg (per hour)
Second 10kg - 50ml/kg (per day) or 2ml/kg (per hour)
Subsequent kg - 20ml/kg (per day) or 1ml/kg (per hour)
Approximate urine & stool losses
Urine 30ml/kg/day or 1-2ml/kg/hr
Stool 0-10ml/kg/day
Consequence of hypernatraemia
Brain damage - the brain shrinks as a result of intracellular dehydration and blood vessels can tear or clot up
Consequence of hypernatraemia that is too rapidly corrected
Cerebral oedema
Convulsions
Consequence of hyponatraemia that is too rapidly corrected
Demyelination
Permanent brain injury
Principles of Rx of hypernatraemia
- Treat shock first
- Calculate maintenance fluid and estimate fluid deficit
- Lower serum Na at rate no higher than 0.5mmol/h
- Check other electrolytes
- Monitor electrolytes frequently
- Clinical assess hydration and weigh frequently
Use isotonic saline e.g. 0.9% NaCl or 0.9% NaCl with 5% glucose
Causes of hypernatraemia
Excessive Na intake e.g. iatrogenic poisoning, NAI
Excessive water loss e.g. diabetes insipidus, diarrhoea
Or combo of both e.g. children with gastroenteritis given excessive sodium in rehydration fluid
Causes of hyponatraemia
Excess water intake or retention
Excessive Na loss
Or combo of both
Rx of hyponatraemia if child is fitting
Needs rapid partial correction of Na to stop the fitting
4ml/kg of 3% NaCl over 15 mins
- will raise serum Na by approx 3 mmol and usually stops the seizures
Rx of hyponatraemia if child asymptomatic
If due to excessive water intake or retention - fluid restrict to 50% of intake requirements
Principles of Rx of hyponatraemia
- If fitting use hypertonic (3%) NaCl at 4ml/kg
- Calculate maintenance fluid and estimate fluid deficit
- Raise serum Na at rate no higher than 0.5mmol/h
- Check other electrolytes
- Monitor electrolytes frequently
- Clinical assess hydration and weigh frequently
Is Na mainly extracellular or intracelluar ion
Extracellular
Is K mainly extracellular or intracellular ion
Intracellular
Causes of hypokalaemia
Diarrhoea Alkalosis Volume depletion Primary hyperaldosteronism Diuretic abuse
Causes of hyperkalaemia
Renal failure Acidosis Adrenal insufficiency Cell lysis Excessive potassium intake
What is the underlying mechanism of hypokalaemia in patients who are alkalotic or receiving insulin or salbutamol?
Total body potassium depletion hasn’t occurred, there has been redistribution of potassium into cells
Therefore management of underlying cause is indicated
Drugs causing hyperkalaemia
ACEI
ARBS
B blockers
Management of hyperkalaemia if > 6 or abnormal ECG
- Stabilise cardiac membrane
- calcium gluconate or calcium chloride - Shift K into cells
- Glucose/insulin infusion AND neb salbutamol
(Consider sodium bicarb if pH <7.2) - Remove K from the body
- Furosemide or Ca resonium
(Consider dialysis if appropriate)
Before using sodium bicarb in a hyperkalaemic patient, what other electrolyte should be checked and why
Calcium
Hyperkalaemia can be accompanied my marked hypocalcaemia, esp in prfound sepsis or renal failure
Giving Na bicarb in hypocalcaemia can provoke hypocalcaemic crisis - tetany, convulsions, hypotension, arrhythmias
Causes of hypocalcaemia
Can be part of any severe illness
Specific conditions:
- severe rickets
- hypoparathyroidism
- pancreatitis
- rhabdomyolysis
- acute and chronic renal failure
Causes of hypercalcaemia
- hyperparathyroidism
- hypervitaminosis A or D
- idiopathic hypercalcaemia of infancy
- malignancy
- thiazide diuretic abuse
- skeletal disorders
Symptoms of hypercalcaemia
long standing anorexia malaise weight loss failure to thrive vomiting
Pathophysiology of DKA
Relative or absolute lack of insulin
Therefore inability to metabolise glucose
Leads to hyperglycaemia and osmotic diuresis
No insulin, so fat is used as source of energy, leading to production of large quantities of ketones and metabolic acidosis
Initial compensation of the acidosis by hyperventilation & a respiratory alkalosis.
As it progresses, there is a combo of acidosis, hyperosmolality and dehydration, leading to coma
Rx of DKA
- ABCDE
Principles of DKA Mx:
- Only give fluid bolus if signs of shock
- Rehydrate with 48 hours of replacement fluid - use ‘reduced volume’ calculations (large volumes of fluid replacement can precipitate cerebral oedema)
- Replace insulin - start IV insulin infusion 1-2 hours after beginning IV fluids
- PICU involvement if considering use of inotropes if signs of hypotensive shock
Major complications of DKA
Cerebral oedema
- avoid by slow normalisation of osmolality and hydration
- monitor for headache, recurrence of vomiting, irritability, reduced GCS, inappropriate bradycardia, high BP
Cardiac dysrhythmias
- usually 2y to electrolyte disturbances
Pulm oedema
- careful fluid replacement required
Acute renal failure
