Death rattle or respiratory secretions in the dying patient is common with a reported prevalence that ranges from 23 % to 92 % and can occur between 17- 57 hrs before death. It is thought to happen due to accumulation of respiratory secretion in the airways.
prevalence varies widely one of the most common symptom in dying patient along with pain , nausea , dyspnoea and agitation by the time it occurs the level of consciousness is usually low and gag and cough reflexes are often absent studies to ascertain the prevalence of death rattle are generally difficult to conduct
What happens – pathophysiology is not fully understood simply said it is caused by air passing through and over accumulated secretions in the hypopharynx , trachea or main bronchus in association with the inspiratory and expiratory phases of respiration various mechanisms may contribute to death rattle and it may be seen in the terminal phase of a wide variety of diseases including cancer , neurological , circulatory and pulmonary diseases factors / theories proposed to explain death rattle include - ◘ increased production of airway secretions ◘ inefficient elimination of the mucus ◘ cough inefficiency due to muscle weakness and poor coordination ◘ gastric reflux ( dysphagia theory Manthous 2013 ) ◘ brain hypoxia theory ( Hipp and Letizia ) release of neurotransmitters as acetylcholine lead to activation of muscarinic receptors within the salivary glands and bronchial mucosa culminating in production of excessive secretions ◘ dehydration hypothesis – this may ↑↑ the viscosity of chest secretions making them more difficult to expectorate ◘ partial airway obstruction ( Carl & Butler 2009 ) ◘ two types of death rattle ( Wildiers and Menten 2009 ) real and pseudo-rattle
These are proposed mechanisms but it is important to note that the pathophysiology of death rattle is hypothetical and has been neither directly studied nor demonstrated through research
Discussion ? ethical issues
the impact of death rattle on the patient remains unclear as patients are generally unconscious when it develops considered a strong predictor of death relatives / carers may feel distressed when hearing sounds produced by secretions at the end of life ( this may also be seen as helpful by some as this demonstrates that the patient is alive or is seen as a sign of impending death ) treatment is often initiated based on the perceived distress of family members clinicians may consider some difficult facts ( ethical dilemma ) as ○ although routinely treated patient may not be in distresses ○ patient may not have consented to treatment ○ patient is unable to describe side – effects or benefits ○ little evidence of effectiveness and treatment may be initiated based on the emotional and psychological distress that the clinician or the family members may face.
Main aim of management is to – Main aim of management is to promote expectoration ↑ mucociliary clearance and conduct of the upper airway secretions improve cough effectiveness to manage /minimise the noisy effects of secretions by effective use of nursing and or pharmacological measures.
Rule out and address if situation permits other contributing conditions as ○ chest infection ○ pulmonary oedema ○ bronchorrhoea ( massive fluid production defined as the excess production of of watery sputum 100 mL/day often seen in association with lung diseases such as tuberculosis , chronic bronchitis , asthma , bronchiectasis or malignant disease in the lung or metastatic to the lung ) ○ gastric reflux ( may cause pooling of fluid in the hypopharynx ) ○ aspiration Consider pharmacological management if secretions are causing distress to the dying person or their family / carers and non pharmacological management has not worked
Hyoscine butylbromide Hyoscine hydrobromide Glycopyrronium , Consider anticipatory prescribing to avoid delay if symptoms occur – prescribe for prn use and frequent need should prompt a review.
Hyoscine butylbromide , Hyoscine hydrobromide , Glycopyrronium.
monitor for improvements and regularly for side effects ( atleast every 24 hrs ) no effect and secretions still causing distress after 12 hrs unacceptable side effects as dry mouth , urinary retention, delirium , agitation , sedation.
nurse on their side and reposition to other side every 3-4 hrs , this may encourage postural drainage elevate the bed head slightly -retain position of comfort ensure mouth care consider using background noise -music , fan suctioning is a uncomfortable procedure and can lead to complications as pain , uncontrollable coughing , infection ,atelectasis , hypoxemia , haemoptysis and airway injuries ( gentle suctioning is recommended in some guidelines but effectiveness has not been well studied – please check local guidance )
explain to the family about the current understanding and that this is normal process of dying that this is not distressing or uncomfortable for the patient explanation and reassurance is paramount
Pharmacological management – These agents inhibit salivary secretions more than bronchial secretions Rationale for use is supported by date from anaesthesiology where they are used to protect against vagal reflexes and to reduce oropharyngeal secretions during surgery They are used routinely in palliative care but there is little evidence to support their use in the dying patient and there is yet no compelling scientific evidence that our interventions for death rattle are effective Drugs do not remove secretions which have been formed already There is no significant difference seen in effectiveness between agents Hyoscine butylbromide and hyoscine hydrobromide are broadly similar in effectiveness , working in about 2/3 rds of cases Glycopyrrolate and hyoscine butylbromide do not cross the blood brain barrier and contribute less to delirium / sedation than hyoscine hydrobromide.
Hyoscine butylbromide ( Buscopan ) initial bolus of 20 mg s/c , assess response in 20- 30 mins with 24 hr s/c infusion dose from 60 – 180 mg less sedating than hyoscine hydrobromide as does not cross the blood brain barrier.
Hyoscine hydrobromide ( Hyoscine , scopolamine ) avoid in conscious patients as it may cause anti-cholinergic associated delirium and or sedation ( has anti-emetic activity as well ) can be given as a bolus of 200 – 400 microgram and assess response in 20 to 30 mins with total 24 hr dose for s/c infusion from 1200 to 2400 micrograms also available as a transdermal patch of 1 mg / 72 hrs which may be easier to use but works slowly and is not well absorbed.
Glycopyrronium bromide preferred in cardiac disease less likely to cause CNS side effects has longer 1/2 life than other muscarinic initial bolus of 200 to 400 mcg s/c , assess response in 30-60 mins with a 24 hr s/c infusion dose of 600 to 1200 mcg
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