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Reduced Consciousness

Introduction

'Mr H has become drowsier' - this is one of the common calls a junior doctor will receive. This happens not only in the neurology or neurosurgery department, but in other specialties as well. This is also a common scenario to be tested for in clinical exams. So what is consciousness? It is a state of being aware of one's thoughts and surroundings. Clinically, this can be assessed by using the Glasgow Coma Scale (GCS) which consists of the patient's eye, verbal and motor responses. In a more acute situation, for example during the primary survey for a trauma case, the AVPU (Alert, Voice, Pain, Unresponsive) scoring system is more convenient to use (see below). Reduced consciousness can vary in severity from mildly drowsy to obtundation, stupor and coma which is the most severe form.

 

Tools used to assess conscious level:



Pathophysiology of reduced consciousness

Consciousness is divided into 2 components:

 

  1. Content and cognition
  2. Arousal and wakefulness

 

The content and cognition component of consciousness depends on the cortical function of the cerebral hemispheres whereas arousal and wakefulness of an individual depends on the interaction between intact cerebral hemispheres and reticular activating system (RAS) within the brainstem. Lesions which can cause impaired consciousness include lesions that:

 

  • Affect the cortical function diffusely - E.g. metabolic or endocrine disorders. Focal damage to the cortex does not contribute to disturbed consciousness.
  • Cause direct pressure on the brainstem - E.g. increased intracranial pressure leading to tentorial herniation.
  • Damage the RAS system within the brainstem itself - E.g. brainstem infarction. 

    Causes of reduced consciousness

    Before managing a patient with reduced consciousness, it is essential to have a grasp on the common possible conditions that could have caused this (Figure 1). It is important to remember other non-neurological causes and to look out for these especially the ones which can be reversed rapidly. 

     



    Management of reduced consciousness

    The definite treatment for a patient with reduced consciousness depends on the underlying aetiology. However the immediate management for any of these patients irrespective of the cause includes thorough clinical assessment consisting of history and clinical examination.

     

    History is important in guiding towards a set of likely causes. If the patient is unable to provide an adequate history, information must be sought by those available such as family, friends and nursing staffs. Information as listed below should be elicited as accurately as possible:

     

    • Preceding events (e.g. recent or previous head trauma suggestive of intracranial haemorrhage )
    • Onset and duration of reduced consciousness
    • Progression (e.g. slow progression may be due to metabolic causes, rapid progression can be secondary to intracranial haemorrhage.)
    • Pattern (constant or intermittent)
    • Other signs & symptoms (e.g. limb twitching & incontinence suggestive of possible epilepsy)
    • Past medical history (e.g. diabetes predisposing to hypoglycaemia)
    • Drug history
    • Social history – ?Lives alone, occupation, next of kin (in situations where consent is required e.g. surgical intervention), history of recreational and alcohol abuse

     

    In an acute situation, a concise history is sufficient to help rule out or diagnose immediate life threatening situations. However, this must be re-visited in detail after making sure that the patient is not in immediate harm.

     

    When assessing a patient with reduced consciousness, it is essential to assess the patient going through the ‘ABCDE’ steps (Airway, Breathing, Circulation, Disability, Exposure/everything else):

     

    • Airway
      • Establish the patency of the patient’s airway
      • Is he/she able to maintain it? Generally if the GCS is less than 8, the patient will require intubation and an anaesthetist must be informed immediately.

     

    • Breathing
      • Respiratory effort.
      • Respiratory rate.
      • Oxygen saturations.
      • Administer high flow oxygen via non-rebreather mask – Important to maintain well oxygenated blood and protect the brain from hypoxic injury.
      • Oxygen therapy in patients with COPD should be titrated as appropriate however in the event of an acute life-threatening situation, it is essential to remember that hypoxia will cause serious acute harm to the patient compared to the gradual onset of expected hypercapnea.
      • Chest examination –chest expansion, mediastinal shift, percussion and auscultation of chest.

     

    • Circulation
      • Blood pressure (BP) and pulse – If the BP readings are not recordable ensure to check this again with a manual sphygmomanometer. If the carotid pulse is impalpable, it is important to call the cardiac arrest team immediately.
      • Listen for heart sounds.
      • Establish venous access – Ideally 2 large-bore cannula inserted.
      • Blood samples – These need to be sent urgently to the lab for tests necessary to find the possible causes of reduced consciousness. Blood tests required are full blood count, electrolytes, inflammatory markers and renal function. Depending on clinical suspicions, additional blood test such as toxicology screen, drug levels or blood cultures should be requested.
      • Arterial blood gas – Gives an accurate reading of the patient’s oxygen and carbon dioxide partial pressures and provides a rapid picture of the patient’s metabolic state (acidotic/alkalotic).
      • Intravenous fluids – IV fluids should be commenced especially if there are signs of shock such as hypotension and tachycardia. If the patient is hypotensive, it is advisable to give a fluid challenge to assess the responsiveness. Be wary with fluid boluses if the patient has a significant cardiac history e.g. heart failure or recent myocardial infarction. Normally 500ml of 0.9% sodium chloride is used however in patients with cardiac problems, it is recommended to start with a lower volume of 250ml of 0.9% sodium chloride instead. Gelofusin can also be used. There is no evidence currently to support the use of colloids over crystalloids however colloids are more expansive and do carry the risk of anaphylaxis.
      • Urine output – Patient should be catheterised if not already. Monitor the patient’s hourly urine output. The kidneys are one of the earliest organs to show signs of shock. Fluid resuscitation should aim to produce a minimum urine output of 0.5ml/kg/hr.

     

    • Disability
      • GCS – It is important to establish the patient’s current GCS (Figure 1) and always compare it to the patient’s baseline. Note that GCS ranges from a minimum of 3 to a maximum of 15. Scores for eye response ranges from 1 to 4, verbal response is 1 to 5 and motor response is 1 to 6.
      • Pupils – Pupils size and reaction can point towards presence of intracranial pathology or systemic disorder such as pin point pupils in opiate toxicity. A unilateral fixed and dilated pupil points towards likelihood of an intracranial pathology.
      • Glucose levels – Hypoglycaemia is essential to rule out as has detrimental effects to the brain and is rapidly reversible.
      • Drugs - Always check the kardex for any causative/contributing medications eg. opioids or other sedating drugs. 

     

    • Exposure/Everything else  
      • A full examination should be carried out looking for signs of trauma, bleeding, sepsis, drug/ alcohol abuse, seizures and other possible causes.
      • Relevant investigations arranged urgently - e.g. CT head scan for a patient with recent head injury.

     

    • Re-assessment
      •  It is important to reassess the patient after each step so that response to any treatment given can be evaluated and guide further management.

     



    It is useful to know the immediate medical treatment for some common conditions as listed below which can be commenced as appropriate after assessing the patient in the steps mentioned above (ABCDE). Different hospitals have different local guidelines for these so it is worth familiarising yourself with them. Management of patients with acute surgical problems must include input from the relevant surgical teams for example the general surgical team must be informed regarding a patient with intra-abdominal bleeding.

     

    • Hypoglycaemia
      •  10% dextrose IV with close monitoring of blood glucose levels.
      • Encourage oral diet when glucose levels are back to normal.

     

    • Hyponatraemia
      • Assess fluid status.
      • Obtain measurement of the sodium levels and osmolality of both the plasma and urine.
      • Management depends on the underlying cause and be classified into hypervolaemic, euvolaemic and hypovolaemic hyponatraemia.

     

    • Sepsis
      • Perform septic screen to locate source of infection.
      • Start broad spectrum antibiotics promptly after blood cultures and urine culture are being sent.
      • Refer to hospital guidelines for antibiotic therapy.
      • Provide analgesia if patient is in pain and antipyretic if patient is pyrexial.
      • Seek microbiologist advice regarding antibiotics choice when receive culture results.

     

    • Status epilepticus
      • Slow IV bolus of 2-4mg lorazepam over ~30 seconds.
      • If no response within 2 minutes another dose can be given. Alternatives include buccal midazolam, 10mg IV diazepam or per rectal diazepam.
      • If seizures do not stop after 2 doses of benzodiazepine, commence IV phenytoin, 18mg/kg at a rate <50mg/min. At this point patient should have a cardiac monitor on.
      • If seizures continue despite phenytoin infusion, contact an anaesthetist as patient will need ITU support.

     

    • Diabetic ketoacidosis (DKA)
      • Dehydration is more lethal in DKA than hyperglycaemia so aggressive fluid resuscitation is indicated.
      • Insulin infusion of 6units/hr should be started with IV fluids. 0.9% sodium chloride with 20mmol of potassium chloride (KCl) per litre is advised.
      • Generally the regime used for fluid replacement is 1L in the first hour followed by another litre in 2 hours, 4 hours and 6 hours.
      • Blood glucose and potassium levels should be monitored closely. Potassium levels should be monitored 2 hourly during aggressive fluid therapy.
      • As blood glucose levels decrease to 10-12mmol/L, fluid therapy should be changed to 1L of 10% dextrose with 20mmol of KCl per litre running at a rate of 6 hours with insulin infusion adjusted according to blood glucose.
      • The underlying cause for DKA to develop must be sought e.g. infection, non-compliance to insulin therapy.
      • Seek advice from the diabetic team to achieve an appropriate insulin regime for the patient.

     

    Summary

    Reduced consciousness can vary in severity and has many causes which include life-threatening emergencies. Hence it is essential to have an adequate history, assess the patient promptly in an ‘ABCDE’ stepwise and carry out appropriate investigations urgently as these direct towards the likely diagnosis which then dictates the appropriate management. 

     

    Bibliography

    1. Lindsay, Kenneth W., Ian Frcp Bone and Geraint Fuller. Neurology and Neurosurgery Illustrated. 5th ed. Edinburgh: Churchill Livingstone, 2010.

    2. Liebenberg, W. Adriaan and Reuben Johnson. Neurosurgery for Basic Surgical Trainees. 2nd ed. ed. Carnforth: Hippocrates Books, 2010.

    3. Loftus, Christopher M. Neurosurgical Emergencies. 2nd ed. ed. New York: Thieme ; Rolling Meadows, Ill. : American Association of Neurosurgeons, 2008.

    4. Longmore, J. M. Oxford Handbook of Clinical Medicine. 8th ed. / Murray Longmore ... [et al.]. ed. Oxford: Oxford University Press, 2010.

    5. Kumar, Parveen J. and Michael L. Clark. Kumar & Clark's Clinical Medicine. 7th ed. ed. Edinburgh: Saunders Elsevier, 2009.

    6. Perel, P. and I. Roberts. "Colloids Versus Crystalloids for Fluid Resuscitation in Critically Ill Patients." Cochrane Database Syst Rev 6,  (2012): CD000567.

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