Pediatric Early Warning Score Essay

Pediatric Early Warning Score

Training Manual

PREPARED BY:

Joel Taller Basabe CN/ICU
EWS PROJECT MANAGER

Learning Objectives:

• Be able to recognise that children deteriorate more rapidly than adults.
• Be able to calculate a Paediatric Early Warning Score
• To be aware of responsibilities when a trigger score is met

• Be able to complete the age appropriate observation chart.

Introduction
The Paediatric Early Warning Score (PEWS) like the adult MEWS is a bedside score that is calculated by nursing staff to indicate early signs of a patient’s deterioration.

The PEWS looks at all the observations together, not just a single observation in
isolation. It includes respiratory rate and effort, oxygen use and saturations, heart rate, blood pressure, and central capillary refill.

The following chapters will highlight where applicable the differences in the physiology, assessment and management of the paediatric patient.

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A PEWS does NOT replace calling the Code team. If the patient meets the Code criteria, Code team should be called as per protocol

Central Nervous System (CNS)

Central Nervous System (CNS) Learning Objectives:
Identify common causes of depressed level of consciousness (LOC) Describe how to assess a patient’s level of consciousness Describe how to manage a patient with depressed level of consciousness Depressed level of consciousness is a common finding in acute illness. It can occur due to intracranial disease or as a result of systemic insults.

Intracranial disease
Meningitis, encephalitis

Epilepsy

Cerebrovascular disease, SAH

Head injury

CNS infection
Systemic conditions

Hypoxia, hypercapnia

Hypotension, hypo/hyperosmolar

Hypoglycaemia, hyponatraemia

Hypo/hyperthermia

Hypothyroidism, hypopituitarism, Addison’s disease

Sedative drugs

Hepatic encephalopathy, uraemic encephalopathy

Common causes of decreased level of consciousness
Assessment of CNS function is an important indicator of adequacy of tissue oxygenation called “end-organ function”. Thus CNS assessment is included in the EWS. CNS depression in itself can also be associated with life-threatening complications. The most important complication is the associated inability to maintain an adequate airway. Loss of gag or cough reflex is associated with a high risk of aspiration, often rendering the patient hypoxic and in respiratory failure.
CAUSES OF DECREASED LEVEL OF CONSCIOUSNESS
1. Inadequate Oxygen delivery
Neurones in the central nervous system, like all other cells in the body, are highly dependent on oxygen. Adequate oxygenation allows the formation of large amounts of ATP “energy packets” which are required for all cellular functions.
When oxygen supply is inadequate, insufficient ATP is produced, which leads to failure of some cellular functions. This causes the symptoms of confusion or depressed level of consciousness. Oxygen supplies to the cells in the brain depend on the same factors as oxygen supply to all other tissues in the body.
Thus confusion or decreased LOC can reflect a decrease in oxygen delivery.
A. A decreased cardiac output decrease stroke volume decrease heart rate
(This may be indicated by a decreased blood pressure)
B. A decreased arterial oxygen content decreased haemoglobin decreased arterial saturation
C. A decrease in blood pressure decrease in cardiac output decrease in peripheral vascular difference
2. Hypoglycemia
Many cells in the body can use glucose, fats or proteins as source for energy production. However neurones predominately use glucose as their source for energy production, therefore if serum glucose levels fall too low, neurones will stop producing adequate amounts of ATP, and cellular function will be compromised. Thus confusion or depressed level of consciousness could also result from hypoglycaemia.

Checking the Blood Glucose Level is one of the first things, which should be checked on an unconscious, or fitting patient, whether they are diabetic or not.

ASSESSMENT of CNS

A. Level of consciousness

A common method of measuring CNS function is the “Glasgow Coma Scale”. Patients with GCS 2
Critical Care Outreach Team call is indicated

GLASGOW COMA SCALE

MOTOR obeys commands 6 localises to pain 5 withdraws to pain 4 abnormal flexion to pain 3 extension to pain 2 no response to pain 1

VERBAL oriented 5 confused 4 inappropriate words 3 incomprehensible sounds 2 nil 1

EYE spontaneous 4 to speech 3 to pain 2 nil 1

B. Pupillary Size

Pupils should be checked when requested, as part of neurological observations, and when there is any reduction in the patient’s level of consciousness. A change in the size, equality or reactivity of the patient’s pupils is an important clinical sign. This can provide important diagnostic clues.

BILATERAL PUPILLARY dilatation Causes: sympathetic over activity, e.g. fear, stress, anxiety, hypoglycaemia sympathomimetic administration, e.g. administration of adrenaline in an arrest situation anticholinergic activity e.g. atropine, tricyclic antidepressants, ipratropium nebuliser

BILATERAL PIN POINT PUPILS Causes:
. opiods/opiates
. cholinergic drugs-neostigmine, organophosphates
. brainstem CVA

UNEQUAL PUPILS Causes:
. previous surgery
. prosthetic eye
. eye drops
. brain lesions, aneurysms, infections
. glaucoma

Previous surgery, cataracts or prosthetic eyes can affect pupil size and reaction.

Management of Decreased Loss of Consciousness

1. Check airway and breathing; ensure airway is patent
Head tilt, jaw thrust
Insert Guedel’s or nasopharyngeal airway

2. Give high-flow oxygen

3. Measure blood glucose, and correct if 2 points)

5. If respiratory rate or arterial oxygen saturation is decreased, may need ventilator assistance using self-inflating bag & mask

6. Ensure intravenous access; 500 mls intravenous fluid bolus maybe required if patient is hypotensive. (In a child 10 -20 mls/kg NS). Intraosseous access should be used if an IV cannula cannot be inserted into a child. 7. Reverse any drug-induced CNS depression, e.g. naloxone for opioid overdose

8. If the airway is patent, and the patient is breathing, place patient supine in lateral recovery position.

Once again remember to always incorporate all the vital signs in your assessment.

Paediatric differences in Central Nervous System

Assessment of Level of Consciousness It is important to choose the developmentally appropriate tool when assessing the level of consciousness in children. It is difficult to assess the early signs of neurological deterioration (reduced attention and dulled affect) in young child. Often the parent is the best resource as they know their child is “just not themselves”. The child who does not recognise their parent is a significantly compromised. In young children the “AVPU” scale is most often used as it is more developmentally adaptable than the Glasgow Coma Scale. Though it does not contribute to the total PEWS it is still a vital observation to be documented. A- Alert V- Responds to voice P- Responds to pain U- Unresponsive

Causes of loss of consciousness

Poisoning is a common cause of neurological deterioration especially in the toddler age range. depending on the substance ingested the pupils may be small (opiates, organophopshates) or large (amphetamine, atropine, tricyclic antidepressants).

Airway and Breathing

Paediatric Airway differences
The paediatric airway differs from the adult airway in several important ways:
A. Anatomically • The larynx is relatively high and anterior in position compared to the adult airway • The epiglottis is ” U” shaped and protrudes into the pharynx •The trachea is short and soft and can become compressed if the neck is hyper extended • The narrowest part of the airway in infants and children < 8 years of age is below the vocal cords at the cricoid cartilage • The vocal cords are short and concave • Large tongue in proportion to the oral cavity B. Physiologically • The lower airways are smaller and so are at greater risk from being obstructed by mucous, oedema or active constriction. • Minor decreases in the diameter of the small paediatric airway creates a large increase in the amount of resistance to airflow. • The diaphragm plays a more significant role in the generation of tidal volume of infants and children as the cartilage supporting the ribs is more flexible allowing for paradoxical movement of the chest wall. • The metabolic rate of children is higher than adults, so oxygen consumption is higher and hypoxemia can occur more rapidly. Like adults, airway obstruction can either be mechanical or functional.

Infant airway

Chin Lift in children

A. BREATHING

Breathing is required to move adequate oxygen in and carbon dioxide out of the lungs. Breathing requires intact respiratory centre in the brain intact nervous pathways from brain to diaphragm & intercostal muscles adequate diaphragmatic & intercostal musclefunction unobstructed air flow (large and small airways)

Examination of breathing
Assessing breathing is the second priority.
The “look, listen, feel” approach is a practical method of quickly determining causes for abnormalities in breathing.

• Look:

Respiratory rate is an important marker of a deteriorating patient. When you walk into a room and the first thing you notice is the patient’s breathing, there is a significant problem with the patient.
Look for signs of respiratory failure:
a. use of accessory muscles
b. sweating/pallor
c. central cyanosis
d. abdominal breathing
e. shallow breathing
f. unequal chest movement
• Listen:

Initially listen at the “end of the bed”, for noisy breathing, which may indicate secretions in the upper airways stridor or wheeze which may indicate partial airway obstruction
Then auscultate with a stethoscope to assess breath sounds: quiet or absent breath sounds may indicate the presence of a pneumothorax or a pleural effusion bronchial breathing may indicate the presence of consolidation • Feel: Generally done prior to auscultation
1. Palpation Palpate the trachea and chest wall
Tracheal deviation indicates mediastinal shift, which may be due to: A. a pneumothorax or pleural fluid -tracheal deviation away from the lesion B. lung collapse-tracheal deviation toward the lesion) chest wall crepitus (surgical emphysema) is highly suggestive of a pneumothorax, oesophageal or bronchial rupture asymmetrical chest wall movement may indicate unilateral pathology eg. consolidation, pneumothorax
2. Percussion hyper-resonance indicates pneumothorax dullness indicates consolidation or pleural fluid

B. Why respiratory rate is important

An increase in respiratory rate can reflect either a drop in arterial saturation or reflect compensation for the presence of a metabolic acidosis. Respiratory rate may be an important indicator of inadequate oxygen delivery to the tissues. As oxygen delivery to the tissues is reduced, cells revert to anaerobic metabolism. This increases the lactate production, resulting in build up of acid. The accumulation of lactic acid stimulates an increase in respiratory rate (tachypnoea).

Inadequate oxygen delivery at the tissue level

Anaerobic metabolism

Lactate production

Metabolic Acidosis

Stimulates respiratory drive

Increases the respiratory rate

How inadequate oxygen delivery to the tissues can increase in
Respiratory Rate

Metabolic acidosis can increase the Respiratory Rate even though the arterial oxygen saturation may be normal

The decrease in oxygen delivery to the tissues, which results in tachypnoea, can be due to problems at any point in the oxygen delivery chain.

A normal arterial saturation and tachypnoea.
There can be falling oxygen delivery despite normal arterial oxygen saturation. Therefore rises in respiratory rate can occur in patients with a normal or low arterial oxygen saturation and may well be a better indicator of a deteriorating patient than arterial oxygen saturation.

Management
Specific treatment will depend on the cause, and it is vital to diagnose and treat life-threatening conditions promptly, e.g. tension pneumothorax, acute pulmonary oedema, acute asthma and acute pulmonary embolus.

All deteriorating patients should receive oxygen, before progressing to any further assessment. In acute respiratory failure, the aim is to keep Pa02 as close to 100mmHg as possible, but at least 60mmHg (Sa02 90%) is essential. In most patients, this can be achieved by sitting them upright, and applying 12-15 litres/min of oxygen via a non-rebreather mask. If the patient does not improve they will require a Paediatrician and Critical Care Outreach Team review.

Monitoring and Titrating Oxygen Therapy

Oxygen therapy can be monitored clinically (patient’s colour, respiratory rate, respiratory distress), or by measuring arterial oxygenation with pulse oximetry or arterial blood gas.
The advantage of measuring an arterial blood gas is that both oxygen and carbon dioxide, and metabolic status (including lactate) is measured. If the carbon dioxide tension rises in someone with acute respiratory failure, it can be a sign that they are tiring and may require ventilatory support. If CO2 begins to rise in a patient with COPD, it may be prudent to reduce the inspired oxygen concentration, however always remember that the arterial oxygen tension should not be allowed to fall below pO2 60mmHg

Patients do not die from a raised CO2 alone: they die from hypoxaemia, the eventual consequence of which will be myocardial ischaemia, cerebral injury and cardiac arrest.

In an acute setting, when taking an arterial blood gas sample, do not remove the oxygen. It is unnecessary, and may precipitate sudden deterioration.

As long as the concentration of oxygen being delivered is recorded, the degree of hypoxaemia can be calculated using the alveolar-air equation & A-a gradient. The blood gas machine will calculate this for you (as long as the correct inspired oxygen concentration is recorded).

PAO2 = FIO2 - PaCO2/O.8
PAO2 should be close to PaO2 in normal lungs

PaO2 calculation

Pulse oximetry measures how well haemoglobin is saturated with oxygen (oxygen saturation). It uses a probe, which shines light of two wavelengths through the tissues, and detects that which passes through. Oxygenated and deoxygenated haemoglobin absorb different amounts of light, and this information is integrated to determine the arterial oxygen saturation.

Oximeters can be unreliable in certain circumstances, e.g. if peripheral circulation is poor, the environment is cold, arrhythmias, or if the patient is convulsing or shivering

If the pulse oximeter does not give a reading, do not assume it is broken, the patient may have poor perfusion!

Although pulse oximetry provides excellent monitoring of oxygenation, it does not measure the adequacy of ventilation, as carbon dioxide levels are not measured nor determines the adequacy of oxygen delivery to the tissues.

Oxygen saturation may be “normal” but the pCO2 may be high which reflects inadequate minute ventilation and hence respiratory failure.
Arterial oxygen saturation being “normal” does not rule out acute respiratory failure.
Normal SpO2 does not rule out respiratory failure

When assessing a patient remember to incorporate all the vital signs, do not just look at an individual reading. Also remember to think about where they sit in Oxygen delivery Chain.

Remember to incorporate all the vital signs in your assessment!

ABC-Oxygen delivery Chain

Paediatric Breathing Differences

In children an increasing respiratory rate maybe an early sign of inadequate oxygen delivery. It is important to note that the metabolic rate of children is higher than adults. This means oxygen consumption is higher and hypoxaemia can occur more rapidly. a. Examination of breathing
Look: The normal respiratory rate in children varies with age and it is important to recognise it for each age group.

Clinical signs of inadequate breathing include:
a) use of accessory muscles
b) pallor
c) central cyanosis
d) tachycardia or bradycardia in extreme hypoxia

It is important to note that breathlessness and cyanosis in infants and children may be a sign of serious cardiac pathology

• Listen: Timing and nature of airway noises can assist in determining the site of the airway problem. Hearing inspiratory noises like stridor, snoring, and bubbling sounds would suggest upper airway obstruction (croup, excessive nasal and oral secretions). Expiratory noises like wheezes suggest a lower airway obstruction (asthma, foreign body inhalation). If coughs are present identify their characteristics: moist, barky, dry or paroxysmal. A paroxysmal cough followed by an inspiratory “whoop” is suggestive of pertusis. A barky cough is associated with croup. The early stages of asthma may present with a dry cough especially at night. Grunting is an attempt to provide PEEP. Auscultate with a stethoscope to assess depth and equality of breathing and quality of breath sounds. Absent or decreased breath sounds could indicate foreign body obstruction, consolidation, pleural fluid or pneumothorax

• Feel: The thin chest wall of the infant and young child enables the palpation of vibrations, called fremitus. Increased fremitus may indicate fluid accumulation, while decreased fremitus may indicate chronic obstructive pulmonary disease.

Management

Specific treatment will depend on the cause, and it is vital to diagnose life threatening conditions immediately, e.g. acute asthma, severe croup, epiglottis and foreign body inhalation. All deteriorating infants and children should receive oxygen at the lowest concentration needed to maintain saturations at least 93%. It is important to remember that high concentrations of oxygen in pre-term infants up to 34 weeks can cause retinopathy and so should be avoided. The method of delivery needs to be determined by taking into consideration the cooperation of the infant/child and the concentration needed to maintain adequate arterial oxygen saturation.
A period of respiratory compromise, which leads to hypoxia and acidosis can lead to a cardiac arrest in an infant and child.

There are a small group of children ( chronic lung disease, cystic fibrosis, heart defects) who have an arterial oxygen saturation range that is normal for them far below normal range for well children. Any alteration to the PEWS should be decided by the admitting Consultant and documented in the modifications section on the observation chart

PAEDIATRIC OXYGEN DELIVERY SYSTEMS

There are many oxygen delivery systems used in paediatrics that are age and or size specific.

Fixed performance devices such as Venturi masks are used in paediatrics, however only occasionally. Variable performances devices such as nasal prongs, simple facemasks, partial rebreathing and non-rebreathing masks come in different sizes to suit the size of the child. Paediatric Hudson masks have a minimum flow rate of 4L/min. Nasal prongs come in neonatal, infant, paediatric and adult sizes. There are three types used in paediatrics

Micro flow nasal prongs can be used for neonates and infants who were born prematurely. These are placed on oxygen flow rates of up to 0.1 LPM.

Low flow nasal prongs for rates less than 2 L/min.
Infants are often placed on flows from 0.1 - 1.0 L/min via a low flow meter. Rates of 1- 2 LPM can be via a regular flow meter. However, once the infant/child is on 2L oxygen, switch to humidified high flow nasal prongs. This will improve the tolerance of the nasal prongs by the patient

Humidification helps to loosen secretions and improve mucocilliary transport, prevent nasal obstruction from hard dry secretions and decrease discomfort and irritation. This type of therapy is generally suitable for patients with:
• Bronchiolitis (usually up to 3 years of age)
• Bronchial asthma (usually up to 6 years of age)
• Other conditions deemed suitable by the consulting paediatrician

SUMMARY

• In rare cases, an airway obstruction may be due to mechanical factors, which may not be so easily treated, e.g. airway swelling, post-operative haematoma, infection. This is a medical emergency. A Code Team should be called.
• An increase in Respiratory Rate can occur even though the arterial oxygen saturation may be normal
• In a small subgroup of patients who have Chronic Obstructive Pulmonary disease (COPD) and are “CO2 retainers”, high concentrations of inspired oxygen can be disadvantageous by suppressing their hypoxic drive. However, these patients will also suffer end-organ damage or cardiac arrest if their blood oxygen levels fall too low. The aim in these patients is to achieve a PaO2 of 6OmmHg, or oxygen saturation of 9O% on pulse oximeter. So, in a patient with COPD who has a pCO2 > 6OmmHg but is also hypoxic, pO2 < 6OmmHg, do NOT turn the inhaled O2 down however do not leave them unattended. If their pO2 is > 6O mmHg, then you can turn the inhaled O2 down to maintain SaO2 > 9O%
• Oxygen flow rates less than 6L/min for Adult Hudson’s mask and 4L/min in children should not be used due to carbon dioxide retention in the mask.
• When taking an arterial blood gas sample, do not remove the oxygen mask, it is unnecessary and may precipitate sudden deterioration.
• If the pulse oximeter does not provide a reading, do not assume it is broken; the patient may have poor perfusion and be very unwell!
• Oxygen saturation may be “normal” but the pCO2 may be high, reflecting inadequate minute ventilation and respiratory failure.
• Remember to incorporate all the vital signs in your assessment!

• The metabolic rate of children is higher than adults. This means oxygen consumption is higher and hypoxaemia can occur more rapidly
• It is important to note that breathlessness and cyanosis in infants and children may be a sign of serious cardiac pathology
• Any alteration to the PEWS should be decided by the admitting Consultant and documented in the modifications section on the observation chart.

CIRCULATION

The Importance of Oxygen

Oxygen reaching the cells and mitochondria is dependent upon adequate amounts of oxygen being delivered. Without oxygen being delivered to the mitochondria, inadequate amounts of ATP are generated and cellular dysfunction occurs. Oxygen delivery’s key components are:
1. Cardiac output=Stroke Volume x Heart Rate
2. Arterial oxygen content=Haemoglobin concentration x Arterial Oxygen Saturation

Blood PRESSURE

A. Blood Pressure, Pulse and Oxygen delivery

Blood pressure is the product of cardiac output and total peripheral resistance (TPR).

A decrease in blood pressure can reflect a decrease in cardiac output and which can lead to a reduction in the amount of oxygen getting to the tissues.
An increase in heart rate may reflect a decrease in stroke volume, which may reflect a decrease in cardiac output which may lead to inadequate amounts of oxygen getting to the tissues.
Hence, the measurement of pulse and blood pressure is an important surrogate marker of whether there is adequate cardiac output and hence oxygen delivery to the tissues and their survival.

High pulse and low blood pressure may reflect inadequate oxygen delivery to the tissues B. Blood pressure and maintenance of organ function
There are some organs that require an adequate blood pressure for their optimal function as well as adequate oxygen delivery. The brain and kidney are two examples of these organs.
The body’s organs adapt over time to a person’s “normal” blood pressure. If blood pressure is always elevated, e.g. chronic hypertension; the brain and kidneys adapt and will require a greater blood pressure in order to function normally. Therefore it is important to know what your patient’s “normal” or “usual” blood pressure was prior to their current illness.

Possible Causes of Hypotension

If blood pressure is the product of cardiac output and total peripheral vascular resistance, blood pressure can either fall because of:
A fall in cardiac output
A fall in peripheral vascular resistance.
It is important to understand how cardiac output and total peripheral resistance are determined and what can affect them. Having understood these principles, it is then easier to know what management to put in place.

A. Cardiac output
Cardiac output is the product of stroke volume and heart rate (i.e. flow is the volume per unit time)

Factors affecting stroke volume:
1) Contractility
The ability of the heart to contract in the absence of any changes in preload or afterload i.e. it is the power of the cardiac muscle.

Major negative influences (negative inotropy) include: Myocardial ischaemia, acidosis, negative inotropes (beta-blockers, anti- dysrhythmic)

Major positive influences (inotropy) include: Sympathetic nervous system sympathomimietics (noradrenaline, adrenaline) Calcium digoxin

2) Pre-Load
How well filled is the heart at the end of filling (diastole)? i.e. the end diastolic volume. Increases in end diastolic volume will result in increases in stroke volume although if the end diastolic volume over-stretches the heart muscle, the stroke volume can start to decrease.

The major effect of pre-load is venous return to the heart, which is influenced by:

a. Intravascular blood volume
Absolute:
A decrease in intravascular blood volume (bleeding, electrolyte and water loss [diarrhoea, vomiting], water loss [diabetes insipidus]) will cause a decrease in venous return and hence a decrease in stroke volume.
Relative:
There is no actual loss of intravascular blood volume but with vasodilatation and pooling of blood (vasodilators, epidurals, sepsis) a decrease in venous return to the heart occurs and hence a decrease in stroke volume.

decreases in intravascular blood volume can decrease cardiac output and therefore decrease blood pressure.

b. Intrathoracic pressure
Increases in intrathoracic pressure (asthmatic attacks, positive pressure ventilation) will restrict the amount of blood returning to the heart decreasing venous return and therefore reducing stroke volume.

Increases in intrathoracic pressure can decrease cardiac outputand therefore decrease blood pressure.

3) After-Load This is the resistance to the ejection of blood from the ventricle. This resistance can either be caused by an outflow resistance from the heart (aortic stenosis) or resistance to flow in the systemic circulation. This resistance is determined by the diameter of the arterioles and per-capillary sphincters. As resistance rises, stroke volume is reduced.

An increase in peripheral vascular resistance can decrease cardiac output and hence oxygen delivery.

B. Heart Rate:
This is determined by the rate of spontaneous depolarisation at the sinoatrial node. The rate can be modified by the autonomic nervous system:
Parasympathetic stimulation: SLOWS the heart rate via the vagus nerve e.g. vasovagals, parasympathomimetics e.g.:anticholinesterases (neostigmine)
Sympathetic stimulation: QUICKENS the heart rate via the sympathetic cardiac fibres e.g.: stress response, temperature, sympathomemetics e.g.: adrenaline, noradrenaline, isoprenaline

In the absence of conduction through the atrioventricular node (Complete Heart Block), the ventricle will only contract at its intrinsic rate of 30-40 beats per minute.

Any changes in heart rate, can change the cardiac output. A faster heart rate can increase the cardiac output and this often occurs when the stroke volume is falling and any reductions in heart rate can cause a decrease in the cardiac output.

As the ability of the body to compensate for inadequate oxygen delivery decreases the signs include:
Altered mental state, in infants fatigue may be an early indication of altered mental state
Capillary refill > 3 secs
Heart rate and respiratory rate trending down to normal levels without the infant/child looking any better

Does a fast heart rate always increase cardiac output and blood pressure?
There are situations when an increase in heart rate may reduce the cardiac output because the ventricle does not have adequate time to fill with blood, reducing the end diastolic volume and therefore stroke volume. Cardiac output reduces and may cause a drop in blood pressure. A good example is atrial fibrillation with a rapid ventricular response.
Does a slow heart rate always decrease cardiac output and blood pressure?
Sometimes when the heart slows there may be no reduction in cardiac output. As the ventricle has a longer time to fill, the end diastolic volume is increased each beat, stretches the myocardial fibres and increases the stroke volume per beat, this may then compensate for the reduction in heart rate. Therefore, there may be no change or even an increase in cardiac output and blood pressure. A good example of this phenomena is a very healthy athlete.

Fall in cardiac output
Fall in stroke volume due to decreased contractility (heart muscle) decreased preload (volume)
Increased afterload
Fall in Heart Rate - e.g. Complete Heart Block
Fall in Peripheral Vascular Resistance (PVR)

C. Peripheral Vascular Resistance
Changes in peripheral vascular resistance (the cumulative resistance of the thousands of arterioles in the body) can increase or decrease blood pressure.
d. Increase in peripheral vascular resistance o Autonomic Nervous System
a. Stimulation of Sympathetic Receptors Sympathetic stimulation of the arterioles can cause vasoconstriction and a subsequent increase in blood pressure. This often occurs in response to a fall in blood pressure (perhaps as a result of falling cardiac output), which is detected by baroreceptors situated in the carotid sinus and aortic arch, reducing the discharge from them to the vasomotor centre with a resultant increase in sympathetic discharge.
e.g. Sympathomimetics that stimulate the receptor will cause vasoconstriction of arteriole, examples include noradrenaline, adrenaline.
b. direct action on arteriole smooth muscle.
Examples: include metaraminol, vasopressin, angiotensin, methylene blue (a vasoconstrictor by inhibiting nitric oxide action on the vasculature). Decrease in peripheral vascular resistance

a. Blockade of Autonomic Sympathetic Nervous System
Anything that causes a reduction in the sympathetic stimulation of the arterioles will result in vasodilatation, reducing vascular resistance and blood pressure.
Influences include, increasing the stimulation of the baroreceptors from a rise in blood pressure, which causes a reduction in the sympathetic outflow causing vasodilatation.
Any drug that blocks the sympathetic nervous system can cause vasodilatation and a fall in blood pressure.

Examples include a: agonists e.g.: clonidine,

epidurals.

b. direct action on arteriole smooth muscle

Molecules and drugs can have a direct effect on

the vascular smooth muscle in arteriole causing

vasodilatation.

Examples include:

Vasodilating brugs:

Calcium channel blockers, ACE

inhibitors

Vasodilating Molecules:

Nitric oxide (infection/sepsis)

Vasodilating conditions:

Acidosis, increases in temperature

Compensatory Mechanisms for Hypotension

An adequate blood pressure is important for the function of vital organs including the brain, heart and kidneys. Any reduction in blood pressure will trigger responses to maintain homeostasis. Depending on the cause of the reduction in blood pressure will depend on the compensatory response.

Causes:
A. Reduction in Cardiac Output:
1. Reduction in Stroke Volume
Response:
There will be a compensatory increase in heart rate (tachycardia) and a compensatory increase in peripheral vascular resistance (cool, blue peripheries).
Blood pressure can be returned to normal without influencing the stroke volume but there will still be the signs of tachycardia and cool peripheries and possibly evidence of inadequate oxygen delivery if the cardiac output has not been restored and oxygen delivery has not been restored.
Reduction in Pre-Load (hypovolaemia):
Hypotension with a postural drop, tachycardia and cool, blue peripheries
Reduction in Contractility(cardiac failure):
Hypotension, tachycardia and cool, blue peripheries with signs of heart failure.
2. Reduction in Heart Rate
Response:
There will be a compensatory increase in total peripheral vascular resistance to try and maintain blood pressure.

Clinical features of Reduction in Heart Rate:
Hypotension, bradycardia and cool, blue peripheries.

B. Reduction in Peripheral Vascular Resistance
Response:
There will be a compensatory mechanism to increase the cardiac output by increasing the heart rate (tachycardia). Cardiac output is further increased following treatment with intravenous fluids to improve venous return.

Clinical Features of a fall in Peripheral Vascular Resistance:
Hypotension, tachycardia and warm peripheries

Consequences of Hypotension:

The greatest concern is that hypotension may suggest that there is an inadequate amount of oxygen getting to the tissues because of a falling cardiac output, which is described as SHOCK.
A. Inadequate Cardiac Output
Cardiac output is integral to the amount of oxygen being delivered to the tissues. If the cardiac output falls, it is likely that oxygen delivery will fall.
If there is inadequate oxygen delivery to the tissues, inadequate amounts of ATP can be generated which is vital for cellular function.
This is turn leads to organ failure, lactate formation and shock. B. Inadequate Pressure Gradient
Clearly without a pressure gradient across the vasculature (from high pressure to low pressure) there can be no flow of blood and its constituents including oxygen which is vital for the generation of ATP and hence life.
Some organs are able to maintain blood flow through organs despite changes in blood pressure (autoregulation) e.g.: brain and kidney. However, there reaches a point when this can no longer occur if the blood pressure is too low and this in turn reduces blood flow and hence the amount of oxygen reaching the
tissues.
Inadequate blood flow to the organs results in inadequate oxygen delivery to the organs resulting in reduced generation of ATP and the formation of lactate. This will lead to organ failure (oliguria and altered mentation), lactate formation and shock.

When is hypotension not shock?
In order to demonstrate that there is shock there needs to be evidence that organs are failing and/or that there is evidence of anaerobic respiration by the presence of lactate.
For example: If a patient is hypotensive post anaesthetic and has warm hands (suggesting good flow to the hands i.e. good cardiac output), is not confused, has a good urine output with no signs of heart or respiratory failure and no lactate is found, then the patient is currently not shocked. However, in these situations it is important to continue regular monitoring of the vital signs and continually look out for evidence of organ failure.

Can a patient with normal or high blood pressure have shock?

cardiac output and arterial oxygen content. Only if either of these two are reduced can this result in a fall in oxygen getting to the tissues and result in shock. Sometimes, the compensatory mechanisms for a drop in cardiac output, increase in total peripheral resistance, can result in there being a normal or even high blood pressure measurement. So, despite there being a “normal” blood pressure, there are signs of organ failure and anaerobic respiration i.e. the patient is shocked with a seemingly normal blood pressure.

The Initial Management of Hypotension

It is important to remember what generates a blood pressure:
Cardiac Output (stroke volume x heart rate)
Peripheral Vascular Resistance

It is important to decide from history and clinical examination, which of these two has decreased leading to a fall in blood pressure

A. FALL IN PERIPHERAL VASCULAR RESISTANCE
Common causes include infection, and vasodilating drugs.
History: Chills, fever, symptoms of infection, ingestion/inhalation of vasodilators.
Examination: Signs of infections, usually accompanied by warm hands (a vasodilated vasculature) and tachycardia. There may be signs of organ failure (confused, oliguria, respiratory failure).
Laboratory Investigations:
Evidence of infection (rise or significant fall in white cell count)
Evidence of renal dysfunction (rising creatinine)
Evidence of lactate formation (metabolic acidosis on arterial blood gas sampling, a negative base excess, a lactate > 2 mmol/L)

Management Plan
In the absence of tachycardia, organ failure, lactate formation
If there is no evidence of organ failure (not oliguric, not confused) and no evidence of anaerobic respiration (lactate formation) and no associated tachycardia i.e. looks well from the end of the bed, then there may be no need to do anything other than closely monitor the vital signs over the next six hours to ensure that there is no downward trend of blood pressure.
In the presence of tachycardia, but absence of organ failure and lactate formation. The tachycardia could be in response to a fall in venous return (due to pooling in the vasculature) and fall in stroke volume that has not yet affected the amount of oxygen going to the tissues. It is important to improve venous return and stroke volume to maintain adequate cardiac output and oxygen delivery to the tissues:
Administer intravenous fluid bolus (500 mls of
Normal Saline for adults)
Continue to perform frequent vital signs to document any trends (e.g. 1/2hrly for 1 hr, followed by hourly for 4 hours, then subsequently 4-hourly if stable)
If there is an improvement in tachycardia and blood pressure, then the fluid bolus has been adequate to restore venous return.
If the tachycardia remains repeat the fluid challenge
Continue to observe response
If the patient continues to have hypotension, tachycardia and warm hands, further fluid can be administered particularly if there are no signs of heart failure
An intensive care review should be requested once three litres of fluid have been administered and the tachycardia and hypotension are still present.

Hypotension and evidence of organ failure
Administer intravenous fluid bolus
If there is an improvement in tachycardia and blood pressure, then the fluid bolus has been adequate to restore venous return.
If the tachycardia, hypotension and organ failure remains, repeat the fluid challenge
Call for an intensive care review particularly if the patient has received three litres of fluid
Continue to perform hourly observations to ensure that the trend of blood pressure, pulse and mental state are being monitored.

.Fall In Cardiac Output

There are two predominant causes of fall in cardiac output, both having very different presentations:
1. FaII in Pre-Load Common causes include bleeding, loss of fluids and electrolytes. History will describe histories relevant to bleeding, loss of fluid and electrolytes [diarrhoea, vomiting, and polyuria from hyperglycaemiaj, loss of water [diabetes insipidusj.
• Look at fluid balance chart and determine recent fluid balance.
• Can also describe symptoms of postural hypotension (feels faint when standing up, has actually “fainted”).

Examination
• Signs that are relevant to the fluid lost (bleeding into drains, melaena, nasogastric losses)
• Cool, blue hands, tachycardia, hypotension with a postural drop (a drop more than l0mmHg from lying to sitting) Laboratory Investigations
• Evidence of bleeding (fall in haemoglobin)
• Evidence of renal dysfunction (rising creatinine)
• Evidence of lactate formation (metabolic acidosis on arterial blood gas sampling [negative base excess], lactate rising)

Management
• Correct cause of loss of fluid (call surgeon for ongoing bleeding, m ay need to correct coagulopathy)
• Replace whatever fluid has been lost (blood if bleeding, saline if gut losses, 5% Glucose if diabetes insipidus)
• Estimate how much has been lost by looking at the fluid balance chart, how much is in the drains, how far has the haemoglobinfallen
• Continue to administer fluid rapidly until there is the desired response: Blood pressure returning to normal Heart rate returning to normal Improvement in organ function, particularly urine output

2. Fall in contractility
• Common causes include myocardial ischaemia or infarction.
• History
• May describe history of chest pain suggesting ischaemia
• May describe previous symptoms of heart failure (orthopnoea, swollen ankles, breathlessness)
• describe palpitations (suggesting a tachycardia- atrial fibrillation, ventricular tachycardia) or symptoms related to causes of cardiomyopathy)

Examination
• Cool, blue hands, tachycardia and hypotension.
• Signs of right heart failure (swollen ankles, raised jugular venous pressure)
• Signs of left heart failure (tachypnoea, fine inspiratory crackles that do not clear on coughing, third heart sound, low arterial oxygen saturation).
• Investigations
• Evidence of renal dysfunction (rising creatinine)
• Evidence of lactate formation (metabolic acidosis on arterial blood gas sampling [negative base excess], lactate rising)
• ECG- signs of ischemia, infarction, dysrhythmia

Management
• If the patient is hypotensive and has signs of organ failure including heart failure (cardiogenic shock), the patient will require inotropic support and referral to either the coronary care unit or intensive care unit

When assessing a patient remember to incorporate all the vitals signs not just look at an individual reading. Also remember to think about where they sit in the Oxygen delivery Chain

PAEDIATRIC DIFFERENCES’ FOR CIRCULATION

ALERT: A child’s pain, anxiety, anatomy or condition may hinder blood pressure measurements. The first BP readings should be interpreted with this in mind.

Hypotension in Paediatrics

Hypotension is a very late sign in children due to their excellent compensatory mechanisms. Hypovolemia causing circulatory collapse is one major precipitant of cardiac arrest in infants and children. The Seagull sign is not relevant to Paediatric patients as the normal heart rate is higher than the normal systolic blood pressure until they reach the adolescent age group. Hypotension in infants and children is most likely to occur because of fluid loss from conditions such as gastroenteritis, intussusception, or haemorrhage. Other reasons for hypotension can be from vasodilatation associated with sepsis, anaphylaxis, or poisoning. Infants and children have a greater percentage of body water compared to body weight than adults. They have the potential for greater insensible losses due to their relatively large surface area to volume ratio. This may result in more water loss and temperature loss. Newborns have larger extracellular fluid levels than infants and older children. This extracellular fluid decreases over time so that by one year the ratio of extracellular fluid to intracellular fluid is close to adult levels.

Hypotension in children is a late sign. Decompensation often happens quickly and if not treated immediately can quickly lead to death.

Paediatric Compensatory Mechanisms for Hypotension

Cardiac output
Cardiac output is calculated the same way for infants and children as it is for adults. It is the product of stroke volume and heart rate (i.e. flow is the volume per unit time).

Infant’s have a smaller stroke volume relative to size than children 2 years of age. This stroke volume is relatively fixed so that cardiac output is directly related to heart rate. Practically this means that increasing fluid volume only works up to a point as stroke volume cannot be increased significantly.

So an increasing heart rate in infants and children is often an early sign of falling stroke volume and inadequate oxygen delivery. This is accompanied by peripheral vasoconstriction to maintain blood pressure.

As the ability of the body to compensate for inadequate oxygen delivery decreases the signs include
Altered mental state, in infants fatigue may be an early indication
Capillary refill > 3 secs
Heart rate and respiratory rate trending down to normal levels without the infant/child looking any better

The Initial Management of Hypotension in Children

1. IV access should be established if not already present. If unable to cannulate within 1-2 minutes, obtain intraosseous access. The preferred site for intraosseous access is in the centre of the tibia, just distal to the tibial tubercle in neonates; in 6-12 month olds, insert 1 cm distal to tibial tuberosity, and in children > 1 year of age, insert 2 cm distal to the tibial tuberosity

2. If it has been determined that the child is hypovolaemia, give a fluid bolus of 20 mls/kg Normal Saline. Reassess. If necessary another 20mls/kg can be given. Inotropic support needs to be considered after boluses reach 40-60 mls/kg.

Remember to incorporate all the vital signs in your assessment!

Summary Blood Pressure Cardiac Output x Peripheral Vascular Resistance
Hypotension: High pulse and low blood pressure may reflect low oxygen delivery
Hypotension is a marker of a deteriorating patient and at risk of increased risk of death. Hypotension may mean the patient is “shocked” but there needs to be evidence of organs failing due to inadequate oxygen getting to them.
Decrease in cardiac output can be caused by decreases in intravascular blood volume can decrease cardiac output and therefore decrease blood pressure.
Increases in intrathoracic pressure can decrease cardiac output and therefore decrease blood pressure.
Increase in peripheral vascular resistance can decrease cardiac output and hence oxygen delivery
The greatest concern is that hypotension may suggest that there is an inadequate amount of oxygen getting to the tissues, which is described as SHOCK.
Infant’s have a smaller stroke volume relative to size than children 2years of age
Stroke volume is relatively fixed so that cardiac output is directly related to heart rate
Increasing fluid volume only works up to a point as stroke volume cannot be increased significantly.

URINE OUTPUT

Poor urine output (oliguria) is one of the most common triggers for a patient review. The kidney is an “end-organ”, thus poor urine output can be an indicator of patient deterioration due to many different causes, and is often one of the earliest signs of overall decline. It is important that the cause of poor urine output is correctly diagnosed. PATHOPHYSIOLOGY

Normal urine flow requires
1. Adequate oxygenation of the kidneys
2. Adequate perfusion pressure
3. Normal function of kidneys
4. No obstruction to urine flow, e.g. prostatomegaly, renal calculus, blocked catheter, urethral valve disorders, ureterocele

A. Oxygen delivery In order to function, renal cells require adequate oxygen delivery, just as all the other cells in the body. Oxygen delivery depends on cardiac output and arterial oxygen content. If oxygen delivery falls to the kidney, urine output will fall. If oxygen delivery is insufficient for renal function, it probably reflects inadequate oxygen delivery to other tissues as well. Therefore urine output can be a sign of the adequacy of whole-body oxygen delivery.

B. Perfusion Pressure

Renal blood flow is autoregulated (i.e. kept constant) throughout a wide range of mean arterial pressures (MAP) (70-170mmHg). The MAP is the perfusion pressure experienced by the organs (figure 18 & 19). This range is increased in chronically hypertensive patients, who then require a higher blood pressure to maintain normal kidney function.
If mean arterial blood pressure falls below the lower limit of autoregulation, renal perfusion pressure will decrease and thus urine output will fall.

MANAGEMENT OF LOW URINE OUTPUT

The cause of the decreased urine output needs to be determined:

1. Decreased renal blood flow in the face of decreased blood pressure, cardiac output or tissue oxygen delivery.
2. Obstructed urine flow - needs to be urgently corrected if this is the case, thus it is important to diagnose early.

Decreased Renal Blood Flow

This can be due to decrease in Cardiac Output, as a result of decreased stroke volume decreased pre-load decreased contractility decreased after-load
Alteration in heart rate
Change in peripheral vascular resistance

There is a small window of opportunity preventing acute renal failure.

Management of Pre-Renal Oliguria When oliguria is due to decreased perfusion i.e. decreased blood pressure or cardiac output, it is potentially reversible. In this circumstance, the most important initial management is to exclude hypovolaemia (decrease in cardiac preload) being the cause. If hypovolaemia is likely (relative or absolute) give an intravenous fluid bolus of 500 mls of Normal Saline (adults). Frusemide is not to be given unless you have ruled out all other possible reasons for low urine output, and the patient is clinically fluid overloaded. Giving a fluid bolus will increase circulating volume, thus increase preload, and ultimately increase cardiac output. This will result in increased blood pressure, increased renal perfusion pressure, and ultimately increase the patient’s urine output.

Management of Post-Renal Oliguria Absolute anuria should be seen as a sign of urinary tract obstruction until proven otherwise. assess bladder size check catheter patency if there is no catheter in-situ, the patient may need one inserted

DO NOT give Frusemide to oliguric patients unless you have ruled out all other possible reasons for low urine output, and the patient is clinically fluid overloaded.

PAEDIATRIC DIFFERENCES FOR URINE OUTPUT

Glomerular filtration rate increases throughout the first two decades of life. This means that infants and children cannot concentrate their urine as efficiently as adults.

Infants and children have a greater percentage of body water compared to body weight than adults. They have the potential for greater insensible losses due to their relatively large surface area to volume ratio. This may result in more water loss and temperature loss.

Newborns have larger extracellular fluid levels than infants and older children. This extracellular fluid decreases over time so that by one year the ratio of extracellular fluid to intracellular fluid is close to adult levels.

Urine output should be 1-2 mls/kg/hr i.e. 12-24 mls/hr for a 12 kg child SUMMARY

Checking the BGL is one of the first things, which should be checked on an unconscious, or fitting patient, whether they are diabetic or not.
If there is a sudden fall in consciousness, or a fall in GCS >2 a
Outreach team call is indicated Paediatric urine output should be 1-2 mls/kg/hr or 12- 24mls/hr for a 12 kg child
There is a small window of opportunity for reversing oliguria and preventing acute renal failure.
Do NOT give Frusemide to oliguric patients unless you have ruled out all other possible reasons for low urine output, and the patient is clinically fluid overloaded.

Communication, Team Work

And Management Plans

One of the most important factors in determining an acutely ill patient’s outcome is the quality of the communication of the team involved. In each team, each member has their strengths and weaknesses, varying skills and different levels of knowledge. The art of managing the deteriorating patient is determining the role of each member of the team, identifying their comfort zones and working together in this knowledge to affect the best outcome for the management of the particular patient.

OPTIMISING MANAGEMENT

Optimising the management of the deteriorating patient requires:
1. Gathering as much information as possible
2. Integrating this information into the presentation of the patient
3. Communicating any concerns about a patient to other members of the team
4. Addressing each team member’s concerns or respond adequately
5. Formulating, documenting and communicating a management plan with a provisional diagnosis
6. Actioning the management plan
7. Reassessment for possible re-review and escalation of the management plan

1. Gathering Information
Each member of the team provides vital information about the patient’s course in hospital and all of this information must be integrated to inform our assessments, decisions and subsequent actions.

Examples:
1. A nurse who has been caring for a patient who is deteriorating will convey significant information about the patient’s cognitive state both pre and post deterioration to a medical officer who has reviewed a patient for the first time. This information will further inform the medical officer of the significance of the deterioration.

2. The team physio may have noticed that a patient’s exercise tolerance or arterial oxygen saturations on exercise have significantly deteriorated. This may alert the team to either a lower respiratory tract infection or pulmonary emboli. This should be communicated to the medical staff and documented in the notes.

It is important in the management of the deteriorating patient, to gather as much information from different members of the team as possible. Information can be obtained from:
Verbal contact with members of the team
Reading the daily notes from each different member
Reviewing observation, fluid charts, and medication charts
Comparing current presentation with previous presentations
Family, friends or the patient themselves

2. Integration of Information
The next step is to integrate the information gathered to understand better the current situation of the patient. e.g.- the need to understand why a BP has fallen or why a heart rate or respiratory rate has risen. 3. Communicating Information
Once information has been gathered and thought has been given to what is going on, the next step is working out what to do with the information. This obviously depends on each individual’s level of knowledge and understanding. If an enrolled nurse finds abnormal arterial oxygen saturation, they may refer this information to the registered nurse who is working with them for more guidance about what to do. If a RMO is concerned by a deteriorating patient, then they need to discuss these findings with their registrar and possibly their consultant. The patient must be attended to appropriately.

For a medical officer to be able to appropriately triage and advise on a particular patient, they need to actually know the parameters that have caused the score rather than just a number. We must remember that each member of the team needs to prioritise and attend to many things.

This means health professionals have to:
Identify that there is a problem
Attempt to interpret the problem in the context of the patient we are caring for
Communicate the trigger to the appropriate people for further actioning. “ISBAR’ Communication

The Identification, Situation, Background, Assessment and Recommendation (ISBAR) technique is an easy, structured, and useful tool to help communicate concerns, and call for help or action.
Identification: Identify yourself, who you are talking to and who you are talking about

Situation: What is the current situation, concerns, observations, MEWS, etc

Background: What is the relevant background. This helps set the scene to interpret the situation above accurately.

Assessment: What do you think the problem is? This is often the hardest part for medical people. This requires the interpretation of the situation and background information to make an educated conclusion about what is going on.

Recommendation: What do you need them to do? What do you recommend should be done to correct the current situation? Paediatric Communication

Timely, accurate communication is vital in determining the outcome for an acutely ill infant or child. Infants and children generally deteriorate more rapidly than adults it is imperative that senior nursing and medical staff are involved early.
Parents will generally be at the bedside and be quite concerned with the changes in their child. Enlist an appropriate person to provide support to the parents while you concentrate on the urgent medical needs.

Paediatric ISBAR example: An 8 month old male infant with a history of prematurity and extensive bowel resection secondary to Necrotising Enterocolitis (NEC) is admitted to the ward with gastroenteritis. buring the morning shift there were large fluid losses through urine and faeces.
The baby is tachypnoeic, tachycardic, pale, crying and restless. You, as the nurse caring for the child, are concerned that the baby is acutely unwell.

IDENTIFY

My name is Rose from east paediatric ward, im phoning regarding room no 5. SITUATION
“I am looking after an eight month old male infant who has significant fluid losses and looks unwell” He has a PEWS of 4, his respiratory rate is 70 and he is tachycardic at 180. He has IV fluids prescribed.” BACKGROUND
“ He has a short gut from extensive resection following NEC. He came in with gastroenteritis” ASSESSMENT
“I think he is acutely unwell and may be moderately to severely dehydrated. He has lost 200 grams since admission”. RECOMMENDATION
“I think this patient needs more fluids, electrolyte levels and an arterial blood gas with an urgent medical review

DOCUMENTATION

Once you have you acted on a particular problem, you always must document what you have done. This may involve documenting low arterial oxygen saturation, and that you have contacted a doctor, or if you are medical officer what treatment you have advised. This documentation has a two-fold purpose.

It helps the flow of information from one shift to the next and often helps to clarify your own thought processes.
This is also a medico legal requirement.

You must always identify who needs to know about a deteriorating patient, communicate as much as possible, and document appropriately
When communicating information you must:
1. Identify who the most appropriate person is to inform when you encounter a deteriorating patient.
2. Communicate as much information as possible to the next in line to ensure that they have all the information needed to appropriately triage and advice on the situation. Use the ISBAR.
3. Document the steps you have taken to remedy the situation and actions taken.

4. Adequate response to information/concerns

After being involved in the management of a deteriorating patient, many people feel that things could have been done better. It might bethat they felt the root of the problem was not being addressed and something else was going on, or that they just felt that their particular views were not taken into account. Each member of the team has different priorities with respect to patient management and these need to be integrated into the management plan.

After communicating with more senior colleagues, an individual may feel as if they were not taken seriously or their particular concern about a situation wasn’t addressed. This can be remedied by specifically asking each member of the team what their concerns are, how they think this can be addressed, and integrating those concerns into their management plan.

Sometimes people looking after a patient are not sure what an abnormal result means.They feel worried about ringing someone, as they are afraid they might seem stupid or even get scolded for not knowing. This behaviour does not help anyone and there are various communication tools that you can use to overcome this.

Theoretically, in the event of a deteriorating patient (for example at a Outreach team call), all people involved in the patient should be present. ISBAR should be used for communicating during critical care outreach team calls.
It is the job of the team leader to voice their concerns, pre-empt other people’s concerns and integrate that into their management plan. By simply asking what are people’s main concerns the team saves time. Often issues are raised that had not been considered and if all team members feel as if their concerns are validated, in the end it benefits the patient’s care.

5. Formulating, documenting and Communicating Management Plan The make or break of patient care is often in the formulation of management plans. To allow successful flow of information from one team, one shift and one ward to the next, plans MUST be documented. They must be thorough, yet concise and most importantly understandable, both legible and logical. Optimal management plans include action plans for all members of the team and time frames in which things must be actioned. Medical staff must always document their impression that is the provisional diagnosis. When this is done, each member has a clear idea of their roles and responsibilities and no excuses for not following them!

1. Observation Orders
A change in frequency of observations being performed may be needed in a deteriorating patient, for example a person with a blood pressure falling from 150/90 to 98/50 after review, may need their frequency of observations changed so that vital signs are done every half an hour until the blood pressure is above a certain level and stable without intervention.

2. Nursing Orders
More intensive monitoring may be needed if a patient deteriorates, for example changing the bag of an indwelling catheter from a free drainage to an hourly measure bag to monitor urine output more closely. 3. Allied Health Orders
An example of an allied health order is a person who has been diagnosed with hospital-acquired pneumonia. The physiotherapist must know that they now need to do chest physiotherapy intervention on the patient.

4. Change in Therapy Orders
This may include changing antibiotics from oral to intravenous, or adding a diuretic.

5. Investigation/intervention orders
If it has been decided that the patient needs their electrolytes checked then this must be documented, as well as whose responsibility it is to check the results. It is often useful to write what is expected and what to do about abnormal results if this is predictable.

You may now realise that the patient requires IV access for antibiotics that have been ordered.

6. Notification Orders
Guidance from the team as to when to worry, or not to worry in the management of a deteriorating patient is very useful! Notification orders include notifying the doctor when the urine output is less than
0.5ml/kg/hr, or systolic blood pressure less than 100 mmHg. This can alleviate the phone calls from nurse to doctor and also give reassurance to nursing staff about when they need to be concerned in a particular patient. With the EWS there is the ability to alter the mandatory notification of the medical team in certain situations. These should be documented and communicated verbally to the relevant staff.

7. Actioning the management plan
Everyone must clearly know his or her role and responsibilities in the management plan of the patient. In particular what needs to be done, and then ensuring that it is done!

People must know what to do, must be skilled to do it, must perform the task and then follow-up the results of the task.

8. Reassess
When caring for a deteriorating patient, you must always review them to ensure that your plan or actions have made a difference to the patient. It is NOT adequate to say you have informed someone, discharge your responsibility and forget about the patient. It is as much your responsibility to ensure that something is done, as is the responsibility of the person you informed to come and attend to the patient. If there is change of shift, then you must ensure that you have verbally conveyed your concerns and outstanding issues with respect to a sick patient to the person taking over the care of the patient so that they will follow them up. If your patient is not improving then you need to reassess them and start at the beginning. Gather the information, initial management, ask for help, and come up with a definitive management plan.

This will be a continuous cycle of review until the patient starts to improve. When documenting a medical entry always document:
H-history
E-examination
I-impression/diagnosis
P-management plan

Management Plans should include:
a. Observation orders
b. Nursing orders
c. Allied health orders
d. Change in therapy orders
e. Investigation/intervention orders
f. Notification orders

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