Adam- Diabetic Ketoacidosis

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  • Created on: 18-04-16 13:52


Body tries to intervene with physiological adaptations to

attempt to overcome shock; Changes in nursing observationscan be detected.

One of the first compensatory indications of shock can be:

• an increase in respiratory rate • an accompanied tachycardia • and a decrease in urine output 

The blood pressure is maintained during this stage of shock

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Homeostatic mechanisms

  • Activation ofsympathetoc division of ANS (Adrenaline & Noradrenaline)
  • Neural regulation (Baroreceptor reflex & Chemoreceptors)
  • Endocrine response (release of ADH)
  • Renin-angiotensin pathway activation. 
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Cardiovascular responses to shock

To understand the cardiovascular response to shock it is necessary to understand the relationship of the various factors that contribute to the maintenance of BP. 


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Initial stage of shock

During this stage there are often no outward clinical signs to observe or document. = Hard to recognise

Cells are being starved of oxygen and there is a reduction in production of adenosine triphosphate (ATP) for energy.

Anaerobic metabolism takes place resulting in the production of lactic acid - detected by chemoreceptors 

The body will compensate. 

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Stages Of Shock

- Initial 

- Compensatory 

- Progressive 

- Refractory 

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Classification of shock


-Blood or fluid loss. Deceased intravascular circulatory volume


Pump failure – Failure of the heart to pump adequately


•Neurogenic- neurological trauma causes widespread vasodilation by loss of sympathetic control

•Anaphylactic- systemic allergic reaction causes vasodilation

•Septic - bacterial endotoxins cause vasodilation and fluid loss into the tissues due to capillary leakage 

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Hypovolaemic shock

Hypovolaemic shock – results from a reduction in circulatory blood volume


- burns 

- dehydration 

- D&V


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Common to all classification of shock

Shock is a life threatening condition where tissue perfusion is inadequate to maintain the supply of oxygen and nutrients necessary for normal cell function

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Renal response to shock 1

•Decrease blood flow to the kidneys is detected by the juxtaglomerular cells.

•Renin is secreted into the blood.

•Renin converts angiotensinogen, a plasma protein produced by the liver, into angiotensin 1, which is converted to angiotensin 2 (potent vasoconstrictor)by a plasma enzyme in the lungs.

•This stimulates the adrenal cortex to produce aldosterone (increases sodium reabsorption and water follows)

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Renal response to shock 2

Anti-diuretic hormone (ADH-vasopressin) is produced by hypothalamus and released from the posterior pituitary in response to blood osmotic pressure and blood volume

Elevated blood osmotic pressure (or decreased blood volume) activates the osmoreceptors.

These activiate cells in hypothalamus to synthesize and release ADH

  Properties of ADH

•Arterioles constrict •Kidneys retain more

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Fluid compartments

INTRACELLULAR FLUID (25 L) Enzymes and ions in solution (electrolytes)

EXTRACELLULAR FLUID: Interstitial fluid (12 L) Surrounds cells of body and allows gaseous diffusion, movement of nutrients, hormones, wastes, etc. between capillaries and cells

Plasma (3L) Non-cellular part of blood.  Similar to interstitial fluid but contains more proteins – albumins, clotting factors, immunoglobulins, lipoproteins, etc.

Transcellular Fluid (1L) The fluid contained within epithelial lined spaces; CSF, GI secretions, joint fluid etc

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Movement of fluid between blood and interstitium

There are two forces that determine the movement of fluid between blood and interstitium

Hydrostatic pressure – the physical pressure of fluid (e.g. blood pressure) that pushes fluid from one compartment to another

Osmotic pressure – the difference in concentration of solutes (e.g. plasma proteins) in a solution that ‘pulls’ fluid from one compartment to another

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Osmotic pressure

Adam has a change in osmotic pressure due to the increased glucose. This causes increased urination. 

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Fluids and Electrolytes

Water makes up a high proportion (60%) of the adult human body.The amount of total body water decreases with age and obesity.

Water in the body is distributed between two compartments:

Intracellular fluid (ICF) - water inside cells

Extracellular fluid (ECF) - water outside cells.

Homeostasis maintains body fluid volume, distribution and composition.

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ABCDE Assessment- Adam


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Progressive stage of shock

The reduction in blood pressure ultimately signifies the onset of progressive shock as compensatory mechanisms begin to fail. (Positive Portsmouth)

The mean arterial pressure (MAP) is insufficient to perfuse organs and multiple organ failure follows.

The patient presents with a metabolic acidosis as the reduction of oxygen to tissues is diminished.

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Refractory stage of shock

If a patient reaches this stage of shock then death is imminent. Shock can no longer be reversed due to widespread cell death

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Assessment Tools

The aim of using an assessment tool is to link clinical variables with measurement of clinical intervention

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Definition of shock?

‘Shock can be defined as a dynamic syndrome in which there is inadequate tissue and organ perfusion. This inadequate perfusion seriously reduces the delivery of oxygen and other essential substances to a level below that is required for cellular function 

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DKA Causes

Any physiological stress has the potential to initiate an episode of DKA. Some common causes are:

Medication (particularly corticosteroids, sympathomimetics, alpha and beta blockers, diuretics) Infection Inadequate insulin Non compliance Medical illness (e.g. pancreatitis, PE, MI, stroke)

However the cause remains unknown in 4-33% of cases

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DKA Pathophysiology (1)

Absolute or relative insulin deficiency Increase in counter-regulatory hormones(Glucagon, Cortisol growth hormone and epinephrine)          

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DKA Pathophysiology (2)

Increase in lipolysis (breakdown of fats)

•free fatty acids are metabolized as an alternative source of energy

•this process is called ketogenesis

•it results in an accumulation of a large quantity of ketone bodies

•ketones are H+ ion donors so this leads to metabolic acidosis

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DKA Incidence

DKA is more common in :

Younger diabetics Females than males

Approx 20% of DKA episodes are thought to occur in undiagnosed type 1 diabetics

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Life threatening metabolic disorder characterized by the presence of;

Hyperglycemia (BM >11 mmols/l)

Acidosis (Bicarbonate <15 mmol/l or venous pH < 7.3

Ketonaemia (Ketones >3 mmol/l or significant ketonuria- more than 2+ on standard urinalysis sticks) 

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Components of Effective Assessment Tools

Simple Acceptable to patients Have a clear & interpretable scoring system Demonstrate reliability & validity

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Levels of care

  • level 1- A normal ward with no particular monioring 
  • level 2- (HDU) monitored but not intubated, frequency of obs has increased 
  • level 3- ITU, 1:1, often intubated 
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DKA Pathophysiology (3)

Impact of the metabolic acidosis on respiration

When a fall in blood pH occurs

the respiratory system will attempt to increase the blood pH by increasing the elimination of CO2

Kussmaulsrespirations develop when metabolic acidosis becomes very severe

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DKA Pathophysiology (3b)

Kussmaul’s Respirations are a form of hyperventilation that reduces CO2.

It appears as a deep and laboured breathing pattern.

Breathing at first may be rapid and shallow but as the acidosis worsens it can become deep, laboured and gasping.

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Key Interventions (Secondary Care) 0-60 mins (2)

Rehydrate with IV fluid. Different regimes depending on whether systolic BP compromised or not. Up to 1 litre of 0.9% Sodium chloride given in the 1st 30 mins if systolic BP has fallen.

Potassium replacement in iv fluid, as required

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Key Interventions 1 (Primary Care)

NICE (2004) Adam should be offered:

timely and ongoing access to mental health professionals….may experience psychological disturbances such as anxiety, depression, behavioural and conduct disorders and family conflict’.

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Key Interventions 2 (Primary Care)

Also (NICE 2004):

Review of medication. Needs to be culturally sensitive, respectful of his needs, motivation and skills to manage it.

Must acknowledge and integrate his views and preferences into daily injection regime

Annual screening retinopathy, microalbuminuria, BP

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Key Interventions 3 (Primary Care)

24 hour access to advice from diabetes care team

Be involved in decision making about his care

Young people should be offered an alcohol education program

Nutritional review

Access to support group

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Key Interventions (Secondary Care) 0-60 mins (1)

Measurement of blood ketones

Measurement of venous pH, electrolytes, glucose and bicarbonate

Commence fixed rate, weight based, IVI insulin. Continue long acting insulin analogue as normal

Involve diabetes specialist team (DST)

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DKA Pathophysiology (4)

An osmotic diuresis develops causing severe dehydration

Typically 5-7 litres of water can be lost from the body during an episode of DKA.

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Osmotic diuresis explained

Nephrons (kidney) are designed to reabsorb all of the glucose that enters the filtrate  If the amount of glucose in the filtrate is above 11 mmol/l this exceeds the renal threshold. Some glucose will enter the urine

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Additional causes of dehydration


General underlying illness-poor fluid intake

Eventual inability to take in fluid due to altered level of consciousness (LOC)

Increased BM draws fluid from interstitial and intracellular fluid spaces

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Osmotic movement

When soluble substances (solutes) are dissolved in a solution, water will be ‘pulled’ into that solution from an area where solutes are in lower concentration

The solute does not diffuse toward the area of low concentration because cell membranes are selectively permeable and only allow the movement of water

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Hydrostatic pressure

The high hydrostatic pressure in the blood tends to force fluid from the blood into the interstitium

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Balancing hydrostatic and osmotic pressures

In the healthy individual there is a balance between hydrostatic and osmotic pressures, slightly favouring the movement of fluid out of the capillaries

The net small movement of plasma from the blood into the interstitium is returned to the blood via the lymphatic system

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Lymphatic system

Excess fluid in the interstitium is returned to the circulation via lymphatic vessels

These vessels act as a drainage system for tissues

Lymphatic fluid eventually empties into thoracic veins near the heart

Lymph nodes contain immune cells – B and T lymphocytes

Diseases that impede lymph flow can result in lymphoedema

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Maintenance of fluid balance

Blood volume is maintained by various (complex) systems

Renin-angiotensin Aldosterone system – conserves body fluid by vasoconstriction and adjusting Na+ balance

Anti-diuretic hormone (ADH) - adjusts urine production according to state of hydration

Plus other (complex) mechanisms promote increased diuresis in fluid overload

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Fluid Imbalance - fluid depletion (N)

Inadequate fluid intake or excessive fluid loss result in an imbalance - fluid depletion

Fluid depletion will cause BP to fall, triggering compensatory mechanisms

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Fluid depletion (N)

Perioperative Fluid Losses 

•Prolonged pre-operative fasting

•Mechanical bowel preparation

•Vomiting and nasogastric drainage

•Stoma & fistula losses – particularly in the jejunum and ileum

•Drains & Wound exudate

•Loose stool/diarrhoea •Insensible losses (respiration, sweat, stool)

Third space losses 

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Fluid Imbalance - fluid overload (N)

Fluid overload may have various causes, especially circulatory, kidney and liver problems

Fluid overload will cause fluid to accumulate in the interstitial spaces and is associated with oedema

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Conditions resulting in oedema

•Heart failure •Renal insufficiency

•Liver insufficiency

•Lymphatic disorders (lymphoedema)

•Medication e.g. steroids



•Post operative – increased aldersterone and ADH common after surgery

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Clinical Biochemistry Tests

Clinical biochemistry can determine abnormalities in body chemistry

Abnormalities can indicate disease and aid diagnosis

Urine and blood are most commonly sampled

Common  tests include...

• Urinalysis

•Urea and Electrolytes (U & Es)

•Full blood count

• Liver and renal function tests

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Urea (the ‘U’ in U & E’s)

Urea is formed in the liver from the metabolism of amino acids - ‘amine’ in amino acids refers to nitrogen

The liver removes the nitrogen from breakdown of amino acids and converts it into urea

The kidneys then excrete urea in the urine

Typical serum urea 2.5 – 7.8 mmol/L

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Urea (the ‘U’ in U & E’s) 2

Urea is normally measured as Blood Urea Nitrogen (BUN)

Higher levels of BUN can indicate renal insufficiency

Creatinine is also commonly measured with BUN

Creatinine is a waste product from muscle metabolism, excreted by the kidneys – high levels can indicate renal failure

Typical values BUN - 2.9–7.1 mmol/L

Typical values creatinine - 61.9–115 μmol/L

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Electrolytes (the ‘E’ in U & E’s)

Sodium (Na+)  133 – 146 mmol/L 

Potassium (K+)   3.5 – 5.3 mmol/L
Chloride (Cl-)   95 – 108 mmol/L
Bicarbonate (HCO3-)   22 – 29 mmol/L
Phosphate (PO43-)   0.8 – 1.5 mmol/L
Magnesium (Mg2+)   0.7 – 1.0 mmol/L

Electrolytes are ions dissolved in plasma

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Why is acid - base important?

Generally the body compensates for minor acid-base fluctuations

When compensation mechanisms are compromised there may follow severe, multiple cardiovascular, respiratory, neurologic and metabolic consequences

This is why monitoring and interventions to maintain acid-base balance is so important

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What is an acid (and a base) solution?

Pure water is neutral with a pH of 7.0


An acidic solution is one with a pH less than 7.0

A basic (alkaline) solution is one with a pH greater
than 7.0

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What is pH?

pH is the measure of the concentration of hydrogen ions (H+) in a solution

The more H+ the more acidic is a solution

The fewer H+ the more basic (alkaline) is a solution

The pH scale is an inverse scale so the more H+ the lower the pH and the greater the acidity – and vice versa

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Other determinants of pH

Bicarbonate ions

•HCO3- are more basic in nature and tend to counter the acidity of H+

Carbon Dioxide (CO2)

•An increase in CO2 causes a decrease in blood pH (i.e. increases blood acidity)

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Carbon dioxide

CO2 is produced in energy metabolism and is transported from the tissues to the lungs for excretion

Most CO2 is transported in red blood cells

In the capillaries of the lungs CO2 is exhaled

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Plasma pH

Plasma pH is maintained by homoeostasis within the
 range 7.35 – 7.45 mmol/L

most cell enzymes work best at physiological pH

An abnormal pH can result in disturbances in a wide
 range of body systems…

          - Abnormal respiratory function

          - Abnormal cardiac function

          - Abnormal nervous activity

So blood gas analysis is essential in acutely unwell patients           

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Regulation of acid-base balance

1. Chemical buffer* system - acts immediately

2. Respiratory compensation - acts in 1-3 minutes

3. Renal compensation - acts in hours or days

*a buffer is a substance that resists (pH) change 

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Respiratory compensatory system

Peripheral chemoreceptors and respiratory centres in the brain stem are sensitive to an increase in CO2 and H+ (decrease in pH)

Breathing is stimulated to “blow off” CO2 and thus reduce acidity by reducing H+ concentration

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Renal compensatory system

If the blood is too acidic the kidneys increase the excretion of H+ and reduce the excretion of HCO3-

So, urine becomes more acidic and blood becomes less acidic

If the blood is too basic (alkaline) the kidneys decrease the excretion of H+ and increase the excretion of HCO3-


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Respiratory acidosis

Respiratory acidosis – any problem that interferes with the excretion of CO2

•Pulmonary obstruction or respiratory depression
        e.g. from opiates
•Circulatory problems- pulmonary embolism (DVT)

CO2 can build up rapidly (hypercapnia) and exceed buffering capacity of blood

H+ conc. increases and pH falls

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Metabolic acidosis

Metabolic acidosis occurs when the body produces acid

Lactate acidosis occurs when cells are starved of oxygen (hypoxia)

In order to maintain energy production they switch metabolic pathways and produce lactic acid

Causes include…

       - Pulmonary obstruction

       - Respiratory depression

       - Circulatory problems

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Metabolic acidosis

Diabetic ketoacidosis (DKA) occurs when insulin levels are low in Type 1 diabetics

Insulin is needed for glucose to enter cells
Cells starved of glucose start metabolising more lipids, which produces acidic ketones such as acetoacetate and beta-hydroxybutyrate

As blood ketones increase, blood pH falls

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Causes of acid-base disorders

Acidosis is more common than alkalosis

Increase in H+ - lactate acidosis, DKA, poisoning etc.

Accumulation of H+ - renal failure

Depletion in HCO3 - renal failure, diarrhoea

Retention of CO2 – respiratory failure

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Base excess

Base excess (or base deficit) is defined as…

The amount of acid (in mmol) required to restore 1.0 litre of blood to its normal pH, at a PCO2 of 5.3kPa

CO2 is eliminated from the measurement so BE refers only to metabolic content

In alkalosis, acid would need to be added to the blood so the base excess figure is positive

In acidosis, acid would need to be subtracted from the blood so the base excess figure is negative 

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Arterial blood gases – typical values

  pH 7.35 – 7.45   (H+ 36 – 45 nmol/L)

    PaO 11 – 13 kPa

    PaCo 4.7 – 6 kPa                  Respiratory function

    SO (SATS) 96% - 99%

    HCO3-  22 – 26 mmol/L

    Base Excess +2 to -2               Metabolic measures

    Lactate <2 mmol/L

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Analysing the arterial blood gas (ABG)

STEP 1. pH (normal pH 7.35-7.45)

•Is this acidic? •Is this alkaline?

STEP 2. PCO2 (normal 4.7-6.0 KPa)

•Is this high or low? •To what extent?

STEP 3. PO2 (normal 11-13 KPa)

•Is there a hypoxia? •Has little relevance to acid base but does indicate respiratory function.

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Analysing the arterial blood gas (ABG)

STEP 4. Bicarbonate (normal 22-26 mmol/L)

•Indication of compensation

•Aids in classification of imbalance

STEP 5. Base excess / deficit (normal +2 to -2)

       •Provides an indication of severity

       •+ve = base excess

       •-ve = base deficit

STEP 6. O2 saturation (normal >95%)

       •If low shows an inadequate perfusion of Oxygen

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Management of respiratory acid base disturbances

•Mechanical ventilation may be necessary (possibly NIPPV first)

•Administration of drugs e.g. bronchodilators

•Oxygen therapy (with caution-COPD)

•Physiotherapy/ Suction

•Paper Bag (Respiratory Alkalosis)

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Management of metabolic acid base disturbances

•(e.g. hypovolaemia- give fluids/ blood, vomiting/ diarrhoea)

•Renal Dialysis/ Haemofiltration

May need IV bicarbonate in acute state or oral sodium in chronic state

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Cerebral lobes and their functions

 Frontal lobe

voluntary motor activity speech thought

Temporal lobe

processes sound / speech

Occipital lobe

processes visual input

Parietal lobe

processes sensations ( touch, pressure, heat, cold)

proprioception; awareness of body position.   

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Why is neurological assessment important?

To determine if someone’s level of consciousness and general neurological condition is: static improving deteriorating

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Common causes of altered consciousness have reduce

       •Direct causes: head / spinal injury, brain damage (hypoxia, CVA, etc), neuromedical conditions, trauma, metabolic changes

        •Secondary causes: drugs (sedatives / opiates / anaesthetics), environmental factors, homeostatic changes

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What is the Glasgow Coma Scale?

A standardised and practical method of assessing impaired consciousness

Allows a baseline of neurological function to be established

Determines any changes in the patients neurological condition over a period of time

Detects life threatening situations & those which need medical intervention

Establishes the impact a condition has on the patients independence.

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The Glasgow Coma Score (GCS)

Determining the degree of stimulation required to elicit a response. 

•Three components

•Eye opening (max. 4 points)

•Best verbal responses (max. 5 points)

•Best motor response (max 6 points)

The maximum score is 15

•Fully alert, orientated  and responsive

Performed in conjunction with pupillary response to light

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Best eye opening response

Closely linked to being awake, and that arousal mechanisms are functioning

Relates to function of brain stem, hypothalamus and thalamus (RAS)

Eye opening does not always indicate intact neurological function

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Best eye opening response

Score  Response

4  Patient opens eyes spontaneously when nurse approaches bedside

3  Patient opens eyes in response to speech (normal, then increase volume if necessary)

2  Patient opens eyes in response to pressure (painful stimuli) (touch normally before using painful stimuli)

1  There is no response from the patient at all following sufficient stimuli

NT  To be recorded if patients eyes are closed due to peri-orbital swelling

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Best verbal response

          Examines comprehension (understanding) of sensory input & verbal stimuli

          •Reflects patients ability to articulate and express a reply

          •Involves cognition of stimuli

           •May be affected if there has been damage to speech centres i.e. dysphagia

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Best verbal response

5   Patient is orientated to time (month), place (where they are & why) + person (their name).  Allowances are made for minor inconsistencies.

4  Patient is confused (able to converse but gives wrong answers)

3  Patient speaks only (inappropriate) words (minimal verbal response, no structure or sentence)

2  Patient makes only (incomprehensible) sounds (grunts or moans to verbal or painful stimuli)

1  Patient makes no response

NT  Factor interfering with communication i.e. endo- or tracheal tube in situ

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Best motor response

Testing ability to identify sensory input & translate into motor response

Focuses on performance of limbs

Scores from highest level of brain involvement to lowest

Purposeful response excludes automatic or reflex reaction. 

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Best motor response (best arm response is recorded

6  Patient can obey commands which have 2 parts of instruction, such as ‘raise and lower your arm’.

5  Localises to pain (moves hand to remove a source of irritation). Needs to be specific response to source of sensory stimulation, usually to head or neck.

4  Attempts to withdraw (normal flexion) from the source of pain; flexion of arm towards pain but not localising.

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Best motor response (best arm response is recorded

3(Abnormal) flexion to pain (decorticate posturing). Pt will flex arm & rotate wrist. Legs may extend

2  Extension to pain (decerebrate posturing).    Arms extend – elbow straight, arm rotates inwards. Legs may extend.

1    No response, even to painful stimuli, in any limb

NT  Factor ie. Patient paralysed 

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Abnormal Flexion (decorticate)

In abnormal flexion the arms are flexed at the elbow and wrists rotate outwards.  Legs are extended.

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Extension (decerebrate)

In extension the body can become rigid, with the arms externally rotated and toes pointing down, legs extended.

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Pain/Noxious Stimuli

•Central stimuli: –Trapezium squeeze

  -  advocated best   practice

–Supraorbital pressure

But not…….

–Jaw margin pressure - Sternal rub

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Pain/Noxious Stimuli

•Peripheral Stimuli: –Finger pressure

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Pupillary reflex assessment

Clinical test for brain stem function

The light reflex tests two cranial nerves.

        1.Optic Nerve (II) - the sensory nerve of visual acuity

2.Oculomotor nerve (III) - the motor nerve that controls pupillary response

Light shone into eyes causes

direct reflex response to light falling on retina

Consensual constriction of both pupils.

Involves the autonomic nervous system

sympathetic- pupil dilation

parasympathetic- pupil constriction

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Pupillary reflex assessment

Clinical test for brain stem function

The light reflex tests two cranial nerves.

        1.Optic Nerve (II) - the sensory nerve of visual acuity

2.Oculomotor nerve (III) - the motor nerve that controls pupillary response

Light shone into eyes causes

direct reflex response to light falling on retina

Consensual constriction of both pupils.

Involves the autonomic nervous system

sympathetic- pupil dilation

parasympathetic- pupil constriction

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Pupil assessment

Size – look before shining light in.  Pupils size can be affected by certain drugs for eg….



Be aware of any pre-existing eye problems.  Check each pupil reacts equally, or are unequal? Are they mishapen? Notice how sluggish, or briskly each pupil reacts to this light.

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Pupil Documentation

Pupil size should be noted before proceeding to test pupil response to direct light. Score pupil size 1-6mm + is used to indicate a brisk response - is used to indicate no response SL is used to indicate a sluggish response C is used to indicate closed eyes due to perirobital oedema.

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Altered pupil responses

            •Pupils should remain round throughout. 

          –If pupils are sluggish, oval or unequal may be a sign of raised ICP, haemorrhage or compression of cranial nerves

         –However some people do have unequal pupils and are healthy

           •Raised ICP constricts oculomotor (parasympathetic) nerve so eye remains dilated in response to light


            •Abnormalities can include either constriction or dilation of pupils

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Timings of neurological Observations

Neuro obs should be carried out thoroughly and frequently until GCS =15 half hourly for 2 hours Then 1-hourly for 4 hours 2 hourly thereafter

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What factors may affect the patient’s neurological

Time of day Is the patient usually asleep? Pain individual response to pain Pain induced increased BP, HR, RR Medication Sedatives, anticonvulsants, opiates. Individual interpretation

-    Assessment is subjective, seek second opinion when unsure.

Other factors

- Glucose

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Changes to GCS

Consistency important; do GCS at handover New or evolving neurological signs need to be reported immediately GCS of 8 or below indicates coma; immediate help is required. A, B, C. Helpful to note scores for each component as well as total i.e. GCS 10/15 (E=4, V=T, M=6) Pupil changes are often a late sign of deterioration 

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Emergency management of altered level of conscious

Ensure the patient airway is patent –adjuncts as necessary

Place patient horizontally in the lateral recovery position

Oxygen therapy If patients breathing is inadequate, provide assisted ventilation using a manual resuscitator / bag-valve-mask

Administer intravenous fluids to maintain adequate systolic BP

Measure blood glucose & treat hypoglycaemia

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Emergency management of altered level of conscious

Ensure the patient airway is patent –adjuncts as necessary

Place patient horizontally in the lateral recovery position

Oxygen therapy

If patients breathing is inadequate, provide assisted ventilation using a manual resuscitator / bag-valve-mask

Administer intravenous fluids to maintain adequate systolic BP

•Measure blood glucose & treat hypoglycaemia

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Glasgow Coma Scale

Advantages: Universal scale Relatively simple to use Aims to ensure changes in patients condition are detected and acted upon at the earliest opportunity 

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Glasgow Coma Scale

Disadvantages: Can be misused / misunderstood GCS score not always helpful Some patients could score lower i.e. if intubated/ tracheostomy, or if on sedation etc

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