While I was in nursing school, I wrote on this blog about death rattle . Family members responses to that post revealed a lack of reassurance provided from the explanation. And some nurses I worked with reported that the interventions typically suggested (turning and repositioning and anticholinergic medications) sometimes either had no effect or even made the sound worse. So... I decided to do my Master's thesis on the death rattle (often referred to as "excessive respiratory secretions" in the medical field). Here is a brief summary of my dissertation.
Death rattle occurs in 51% to 70% of patients within the last 48 to 57 hours of life (Lichter & Hunt, 1990; Morita, Tsunoda, Inoue & Chihara, 1998; Bausewein & Twycross, 1995; Power & Kearney, 1992).
Anticholinergic medications, which are typically used to treat death rattle, block the parasympathetic innervation of the salivary glands by inhibiting muscarinic actions of acetylcholine on autonomic effects innervated by post-ganglionic cholinergic neurons thus reducing the production of saliva (Hockstein, 2004; Springhouse, 2002). As the death rattle does not always respond to these interventions, Bennett conducted further research into this phenomenon and came up with the conclusion that there is more than one type of death rattle.
Physiological Theory: Causes of Death Rattle
Bennett (1996) identified two different types of death rattle. Type I is caused by an accumulation of salivary secretions when swallowing reflexes are inhibited and type II is caused by an accumulation of bronchial secretions in patients too weak to cough effectively (Bennett, 1996).
Salivary glands have an average output of 1000 to 1500 mL per day (Marieb, 1998). Salivation with eating is controlled by the parasympathetic division of the autonomic nervous system and the facial (CNVII) and glossopharyngeal (CNIX) cranial nerves; however, the sympathetic nervous system causes continuous release of a thick mucin-rich saliva irrespective of digestion (Marieb, 1998). Both the parasympathetic and sympathetic nervous systems have nerve endings in the salivary glands (Zeppetella, 1999). The constriction of blood vessels serving the salivary glands inhibits the release of saliva through the sympathetic system. Dehydration also inhibits salivation because low blood volume results in reduced filtration pressure at the capillary beds of the salivary glands (Marieb, 1998). There is no evidence, however, that salivary secretion decreases nor continues at the same rate in the end of life.
Impaired Swallow and Cough Reflexes
Swallowing and coughing reflexes are regulated by the autonomic reflex enter of the medulla (Marieb, 1998). The involuntary component to swallowing (pharyngeal-esophageal phase) is controlled by the vagus nerve (Marieb, 1998). Although many research articles empirically support the theory that the coughing and swallowing reflexes cease at the end of life, physiological explanations for this phenomenon are as of yet unknown (Bennett, 1996, Ellershaw, et. al., 1995, MacLeod, 2002).
Current Management Guidelines
Current practice guidelines for the management of death rattle include repositioning the patient to mobilize the secretions, anticholinergics, suctioning and reassurance or education (Poor & Poirrier, 2001; Enck, 2002; Doyle, Hanks & MacDonald 1998; Hughes, Wilcock & Corcoran, 1996; Spruyt & Kausae, 1998; Dudgeon, 2001). Morphine and midazolam have also been suggested concomitantly with anticholinergics to increase sedation and prevent central nervous system excitement caused by anticholinergics (Enck, 2002; Doyle, Hanks & MacDonald, 1998); morphine may also improve the frequency of death rattle by decreasing the respiratory rate. No research has been completed to evaluate the effectiveness of repositioning, suctioning nor education as management strategies for the distress caused by death rattle.
Suctioning may not be an effective means of treating death rattle for multiple reasons. For one, the secretions are pooling farther in the hypopharynx or the bronchial tree than an oral or Yankauer suction can reach. Even when a nasal trumpet is used to suction farther back in the nasooropharynx, repeated suctioning causes local trauma to the mucous membranes. This leads to inflammation and swelling, which eventually complicates further suctioning. Death rattle secretions may need to be suctioned as frequently as every two hours. Based on my clinical observations, after as few as four or five episodes of suctioning, edema may occur and may occlude the airway, preventing further suctioning. Suctioning is also thought by some to be undignified for the patient and may cause the patient distress if the patient is alert or semi-conscious. Nevertheless, it is frequently advocated in literature (Poor & Poirrier, 2001; Enck, 2002; Doyle, Hanks & MacDonald 1998; Hughes, Wilcock & Corcoran, 1996; Spruyt & Kausae, 1998).
In practice, many palliative care units and hospices limit intravenous fluids. The rationale for this practice is that intravenous fluids are forcing fluids into the body that the body is unable to utilize. Dying patients frequently have decreased serum protein levels, which shifts the plasma’s osmotic pressure; this causes fluid to leak from the vasculature, causing edema (Guyton, 1996). These fluids may collect in the lungs, the ankles and the oropharynx.
Type II Death Rattle
When anticholinergics are used consistently, yet the death rattle continues, there may be another underlying cause. These cases have been referred to by Bennett (1996); Morita, Tsunoda, Inoue and Chihara (2000); and Wildiers and Menten (2002) as type II death rattle. In most cases, it is difficult to distinguish between the two types because scientific investigation is rarely indicated in the last days of life. However, some causes may be identified and thus treated appropriately.
Identify each dying patient’s particular risk factors for developing death rattle to assess whether type I or type II death rattle is most likely to occur.
Family members should be encouraged to report any audible sounds to their health care provider as soon as they notice it to ensure early intervention.
Consider prophylactically treating patients at increased risk for type I death rattle by repositioning the patient every two hours and by applying a scopolamine patch. Simultaneously, the frequency of mouth care must be increased to every one to two hours in order to maintain the integrity of the oral mucosa with the reduction of salivary secretions. Risk factors include: prolonged dying phase
If scopolamine is ineffective in preventing the occurrence of type I death rattle, administer an additional anticholinergic around-the-clock for continuous coverage, such as atropine ophthalmic 1% 1 drop sublingually every 2 hours.
If the death rattle does not respond to the second anticholinergic, treat the patient empirically for possible type II death rattle causes (CHF, pneumonia, pulmonary tumor). If patient is known to have heart failure, treat with a diuretic. If the cause is suspicious for neurogenic pulmonary edema, treat with osmotic diuretics (i.e., mannitol), morphine (to decrease respirations), and/or corticosteroids (to reduce intracranial pressure). If the patient’s secretions are malodorous, suspect pneumonia and consider giving a single dose of Ceftriaxone. However, it should be noted that there are challenges in performing some of these interventions outside of a hospital setting.
Evidence has repeatedly suggested that death rattle is distressing to patients, family members and nursing staff and needs to be adequately managed in dying patients. Our goal is to provide for a “good,” peaceful, dignified death, one in which family members are assured of their loved ones’ comfort. Therefore it is imperative that we, as health care providers, address the treatment of death rattle.