February 25, 2011

The Last Hours of Living: Practical Advice for Clinicians: When Death Occurs

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MedscapeCME - Linda Emanuel, MD, PhD; Frank D. Ferris, MD; Charles F. von Gunten, MD, PhD; Jamie H. von Roenn, MD

5. When Death Occurs

No matter how well families and professional caregivers are prepared, they may find the time of death to be challenging. Families, including children, and caregivers may have specific questions for health professionals.

Table 2. Signs That Death Has Occurred
The heart stops beating
Breathing stops
Pupils become fixed and dilated
Body color becomes pale and waxen as blood settles
Body temperature drops
Muscles and sphincters relax (muscles stiffen 4-6 hours after death as rigor mortis sets in)
Urine and stool may be released
Eyes may remain open
The jaw can fall open
Observers may hear the trickling of fluids internally, even after death

Basic information about death may be appropriate (eg, the heart stops beating; breathing stops; pupils become fixed; body color becomes pale and waxen as blood settles; body temperature drops; muscles and sphincters relax, and urine and stool may be released; eyes may remain open; the jaw can fall open; and observers may hear the trickling of fluids internally) (Table 2).[51,52]

There are no universally applicable rules that govern what happens when the patient dies (in any setting). If the patient dies an expected death at home, there is no need to call for emergency assistance. If a hospice program is involved, have the family call the hospice. If a hospice program is not involved, determine in advance who should be notified. Unless death is unexpected, or malice is suspected, involvement of the coroner's office is usually not required. State and local regulations vary. Healthcare professionals will need to familiarize themselves with the regulations in the areas in which they practice.

When an expected death occurs, the focus of care should shift from the patient to the family and those who provided care. Even though the loss has been anticipated for some time, no one will know what it feels like until it actually occurs, and indeed it may take hours to days to weeks or even months for each person to experience the full effect.

Many experts assert that the time spent with the body immediately after death will help people deal with acute grief.[53-55] Those present, including caregivers, may need the clinician's permission to spend the time to come to terms with the event and say their good-byes. There is no need to rush, even in the hospital or other care facility. Encourage those who need to touch, hold, and even kiss the person's body as they feel most comfortable (while maintaining universal body fluid precautions).

Because a visually peaceful and accessible environment may facilitate the acute grieving process, a health professional, usually the nurse, should spend a few moments alone in the room positioning the patient's body, disconnecting any lines and machinery, removing catheters, and cleaning up any mess, to allow the family closer access to the patient's body.[56,57]

REFERENCES
51. Aspen Reference Group. Palliative Care Patient and Family Counseling Manual. Gaithersburg, Md: Aspen Publishers Inc; 1996.
52. Martinez J, Wagner S. Hospice care. In: Groenwald SL, Frogge M, Goodman M, Yarbro M, Jones CH, eds. Cancer Nursing: Principles and Practices. 4th ed. Boston, Mass: Bartlett Publishers; 1997.
53. Sheldon F. Communication. In: Saunders C, Sykes N, eds. The Management of Terminal Malignant Disease. Boston, Mass: Edward Arnold: 1993:29-31.
54. The Hospice Institute of the Florida Suncoast, Hospice Training Program. Care at the Time of Death. Largo, Fl: The Hospice Institute of the Florida Suncoast; 1996.
55. Doyle D. Domiciliary palliative care. In: Doyle D, Hanks GWC, MacDonald N, eds. Oxford Textbook of Palliative Medicine. 2nd ed. Oxford, England: Oxford University Press; 1998:957-973.
56. O'Gorman SM. Death and dying in contemporary society. J Adv Nurs. 1998;27:1127-1135. Abstract
57. Weber M, Ochsmann R, Huber C. Laying out and viewing the body at home -- a forgotten tradition? J Palliat Care. 1998;14:34-37.

February 22, 2011

The Last Hours of Living: Practical Advice for Clinicians: Two Roads to Death

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MedscapeCME - Linda Emanuel, MD, PhD; Frank D. Ferris, MD; Charles F. von Gunten, MD, PhD; Jamie H. von Roenn, MD

4. Two Roads to Death

Decreasing Level of Consciousness

Most patients traverse the "usual road to death." They experience increasing drowsiness, sleep most if not all of the time, and eventually become unarousable. Absence of eyelash reflexes on physical examination indicates a profound level of coma equivalent to full anesthesia.

Communication with the unconscious patient. Families will frequently find the inability to communicate with their loved one distressing. The last hours of life are the time when they most want to communicate with their loved one. As many clinicians have observed, the degree of family distress seems to be inversely related to the extent to which advance planning and preparation occurred. The time spent preparing families is likely to be very worthwhile.

Although we do not know what unconscious patients can actually hear, extrapolation from data from the operating room and "near death" experiences suggests that at times their awareness may be greater than their ability to respond. Given our inability to assess a dying patient's comprehension and the distress that talking "over" the patient may cause, it is prudent to assume that the unconscious patient hears everything. Advise families and professional caregivers to talk to the patient as if he or she were conscious.

Encourage families to create an environment that is familiar and pleasant. Surround the patient with the people, children, pets, objects, music, and sounds that he or she would like. Include the patient in everyday conversations. Encourage family members to say the things they need to say. At times, it may seem that a patient may be waiting for permission to die. If this is the case, encourage family members to give the patient permission to "let go" and die in a manner that feels most comfortable. The physician, nurse, social worker, chaplain, or other caregivers might suggest to family members other words like:
  • "I know that you are dying; please do so when you are ready."
  • "I love you. I will miss you. I will never forget you. Please do what you need to do when you are ready."
  • "Mommy and Daddy love you. We will miss you, but we will be okay."
As touch can heighten communication, encourage family members to show affection in ways they are used to. Let them know that it is okay to lie beside the patient in privacy to maintain as much intimacy as they feel comfortable with.

Terminal delirium. An agitated delirium may be the first sign to herald the "difficult road to death." It frequently presents as confusion, restlessness, and/or agitation, with or without day-night reversal.[19] To the family and professional caregivers who do not understand it, agitated terminal delirium can be very distressing. Although previous care may have been excellent, if the delirium goes misdiagnosed or unmanaged, family members will likely remember a horrible death, "in terrible pain," and cognitively impaired "because of the drugs," and they may worry that their own death will be the same. Bruera and associates[20] have documented the distressing impact of delirium on patients and families.

In anticipation of the possibility of terminal delirium, educate and support family and professional caregivers to understand its causes, the finality and irreversibility of the situation, and approaches to its management. It is particularly important that all onlookers understand that what the patient experiences may be very different from what they see.

If the patient is not assessed to be imminently dying, it may be appropriate to evaluate and try to reverse treatable contributing factors such as pain, urinary retention, or severe constipation/impaction. The treatment of reversible delirium is to find and correct reversible causes. The drug class of first choice for symptomatic management of reversible delirium is the neuroleptics.[21,22] On the other hand, irreversible delirium can also affect patients in the final hours of living. In this setting, it is referred to as irreversible terminal delirium.[23] Irreversible delirium does not respond to conventional treatment for reversible delirium. Focus on the management of the symptoms associated with terminal delirium in order to settle the patient and the family[24]

When moaning, groaning, and grimacing accompany the agitation and restlessness, these symptoms are frequently misinterpreted as physical pain.[25] However, it is a myth that uncontrollable pain suddenly develops during the last hours of life when it has not previously been a problem. Although a trial of opioids may be beneficial in the unconscious patient who is difficult to assess, clinicians must remember that opioids may accumulate and add to delirium when renal clearance is poor.[26,27]If the trial of opioids does not relieve the agitation or makes the delirium worse by increasing agitation or precipitating myoclonic jerks or seizures (rare), then pursue alternative therapies directed at suppressing the symptoms associated with delirium.

Currently, no studies specifically address the management of terminal delirium. Palliative experts base their treatment recommendations on the goals of treatment and the mechanisms of action of classes of medication. Benzodiazepines are generally not recommended for first-line management of delirium, especially if the delirium is thought to be reversible, because they can worsen delirium and cause paradoxic excitation.[28] However, because they are anxiolytics, amnestics, skeletal muscle relaxants, and antiepileptics,[27] benzodiazepines are recommended by palliative care experts for the management of irreversible terminal delirium, where the goal of therapy is sedation. Benzodiazepines are also the drug class of first choice for management of delirium complicated by seizures or caused by alcohol or sedative withdrawal.[29] Common starting doses are:
  • Lorazepam, 1-2 mg as an elixir, or a tablet predissolved in 0.5-1.0 mL of water and administered against the buccal mucosa every hour as needed until agitation subsides. Most patients will be controlled with 2-10 mg per 24 hour period. It can then be given in divided doses, every 3-4 hours, to keep the patient calm. For a few extremely agitated patients, high doses of lorazepam, 20-50+ mg/24 hours, may be required.
  • Midazolam 1-5 mg/hour subcutaneously or intravenously by continuous infusion, preceded by repeated loading boluses of 0.5 mg every 15 minutes to effect, may be a rapidly effective alternative.
Barbiturates or propofol have been suggested as alternatives for management of refractory agitation.[30,31] Seizures may be managed with high doses of benzodiazepines or alternatively with other antiepileptics such as intravenous phenytoin, subcutaneous fosphenytoin, or phenobarbital 60-120 mg rectally, intravenously, or intramuscularly every 10-20 minutes as needed until control is established.

If benzodiazepines cause paradoxical excitation, the patient may require neuroleptic medications to control delirium. Haloperidol has fewer sedating and hypotensive effects, but in bedbound patients in whom sedation is desirable, chlorpromazine is a better choice:
  • Chlorpromazine 10-25 mg orally or rectally every 60 minutes, or subcutaneously/intravenously every 30 minutes until agitation is controlled. Titrate to effect, then give the summed dose nightly to every 6 hours to maintain control.[32]
  • Haloperidol 0.5-2.0 mg intravenously every 10 minutes, subcutaneously every 30 minutes, or rectally every hour until agitation is controlled (titrate to effect, then give the summed dose nightly to every 6 hours to maintain control).[33]
Respiratory dysfunction. Changes in a dying patient's breathing pattern may be indicative of significant neurologic compromise.[34-36] Breaths may become very shallow and frequent with a diminishing tidal volume. Periods of apnea and/or Cheyne-Stokes pattern respirations may develop. (Cheyne-Stokes is a disorder characterized by recurrent central apneas during sleep, alternating with a crescendo-decrescendo pattern of tidal volume.[37]) Accessory respiratory muscle use may also become prominent. A few (or many) last reflex breaths may signal death.

Families and professional caregivers frequently find changes in breathing patterns to be one of the most distressing signs of impending death. Many fear that the comatose patient will experience a sense of suffocation. Knowledge that the unresponsive patient may not be experiencing breathlessness or "suffocating," and may not benefit from oxygen (which may actually prolong the dying process) can be very comforting. Low doses of opioids or benzodiazepines are appropriate to manage any perception of breathlessness.

Some clinicians express concern that the use of opioids or benzodiazepines for symptom control near the end of life will hasten death. Consequently, they feel they must invoke the ethical principle of "double effect" to justify treatment. The principle of double effect applies in situations where there is a difference in the effects of an intended action (alleviating suffering) and the unintended possible consequences of the same action (hastening death). To be acceptable, the action must comply with the following requirements:
  • The treatment proposed must be beneficial or at least neutral (relief of intolerable symptoms);
  • The clinician must intend only the good effect (relieving pain or symptoms), although some untoward effects might be foreseen (hastening death or loss of consciousness);
  • The untoward effect must not be a means (not necessary) to bring about the good effect; and
  • The good result (relief of suffering) must outweigh the untoward outcome (hastening death).[38]
Although it is true that patients are more likely to receive higher doses of both opioids and sedatives as they get closer to death, there is no evidence that initiation of treatment or increases in dose of opioids or sedatives is associated with precipitation of death. In fact, the evidence suggests the opposite.[39]

Loss of ability to swallow. Weakness and decreased neurologic function frequently combine to impair the patient's ability to swallow. The gag reflex and reflexive clearing of the oropharynx decline and secretions from the tracheobronchial tree accumulate. These conditions may become more prominent as the patient loses consciousness. Buildup of saliva and oropharyngeal secretions may lead to gurgling, crackling, or rattling sounds with each breath.[40] Some have called this the "death rattle" (a term that should be avoided, as it is frequently disconcerting to families and caregivers).

Once the patient is unable to swallow, cease oral intake. Warn families and professional caregivers of the risk for aspiration. Muscarinic receptor blockers (anticholinergics) are commonly used agents to control respiratory secretions when death is imminent. These agents have been compared in several retrospective studies and in a recent prospective randomized trial, which compared subcutaneous administration of atropine with hyoscine hydrobromide (scopolamine) and hyoscine butylbromide (not available in the United States). All agents were found to be equally effective at controlling secretions, with an effectiveness of 37%-42% at 1 hour, increasing to an effectiveness between 60% and 76% at 24 hours. There was no significant difference in side effects or survival time, and effectiveness increased when treatment was initiated at a lower initial intensity of rattle.[41]

Other studies that compared glycopyrronium (glycopyrrolate) (which has a theoretical advantage over other agents because it does not cross the blood-brain barrier) with other agents such as hyoscine, have yielded conflicting reports of comparative efficacy, with no difference in side effects such as agitation.[42,43] Although atropine theoretically has the disadvantage of more cardiac effects or agitation,[44] this has not been borne out in clinical studies to date, which have found it to be equally effective without any evident increased incidence of side effects.[41] Although further studies are necessary to provide definitive evidence-based recommendations, current findings support the use of the commonly used agents in the United States: scopolamine, glycopyrrolate, atropine, and hyoscyamine sulfate. Common starting doses of these medications are:
  • Scopolamine, 0.2-0.4 mg subcutaneously every 4 hours, or
    Scopolamine, 1-3 transdermal patches every 72 hours (onset delayed 12 hours), or
    Scopolamine, 0.1-1.0 mg/hour by continuous intravenous or subcutaneous infusion
  • Hyoscyamine sulfate, 0.125-0.25 mg sublingually every 4 hours
  • Glycopyrrolate, 0.2 mg subcutaneously every 4-6 hours, or
    Glycopyrrolate, 0.4-1.2 mg daily by continuous intravenous or subcutaneous infusion, or
    Glycopyrrolate, 1 mg sublingually every 4-6 hours
  • Atropine, 0.1 mg subcutaneously every 4 hours, or
    Atropine eyedrops, 1 drop (1%) sublingually every 4 hours[45]
These drugs will minimize or eliminate the gurgling and crackling sounds and may be used prophylactically in the unconscious dying patient. Some evidence suggests that the earlier treatment is initiated, the better it works, as larger amounts of secretions in the upper aerodigestive tract are more difficult to eliminate. However, premature use in the patient who is still alert may lead to unacceptable drying of oral and pharyngeal mucosa.

If excessive fluid accumulates in the back of the throat and upper airways, it can be cleared by repositioning the patient or performing postural drainage. Turning the patient onto one side or into a semiprone position may reduce gurgling. Lowering the head of the bed and raising the foot of the bed while the patient is in a semiprone position may cause fluids to move into the oropharynx, from which they can be easily removed. Do not maintain this position for more than a few minutes at a time, as stomach contents may also move unexpectedly, increasing the risk for aspiration.

Oropharyngeal suctioning is not recommended. Suctioning is frequently ineffective, as fluids are beyond the reach of the catheter, and may only stimulate an otherwise peaceful patient and distress family members who are watching.

Loss of sphincter control. Fatigue and loss of sphincter control in the last hours of life may lead to incontinence of urine and/or stool. Both can be very distressing to patients and family members, particularly if they are not warned in advance that these problems may arise. If they occur, attention needs to be paid to cleaning and skin care. A urinary catheter may minimize the need for frequent changing and cleaning, prevent skin breakdown, and reduce the demand on caregivers. However, it is not always necessary if urine flow is minimal and can be managed with absorbent pads or surfaces. If diarrhea is considerable and relentless, a rectal tube may be similarly effective.

Pain. Although many people fear that pain will suddenly increase as the patient dies, there is no evidence to suggest that this occurs. Although difficult to assess, continuous pain in the semiconscious or obtunded patient may be associated with grimacing and continuous facial tension, particularly across the forehead and between the eyebrows. The possibility of pain must also be considered when physiologic signs occur, such as transitory tachycardia that may signal distress. However, do not overdiagnose pain when fleeting forehead tension comes and goes with movement or mental activity (eg, dreams or hallucinations). Do not confuse pain with the restlessness, agitation, moaning, and groaning that accompany terminal delirium. If the diagnosis is unclear, a trial of a higher dose of opioid may be necessary to judge whether pain is driving the observed behaviors.

Knowledge of opioid pharmacology becomes critical during the last hours of life. The liver conjugates codeine, morphine, oxycodone, and hydromorphone into glucuronides. Some of their metabolites remain active as analgesics until they are renally cleared, particularly the metabolites of morphine. As dying patients experience diminished hepatic function and renal perfusion, and usually become oliguric or anuric, routine dosing or continuous infusions of morphine may lead to increased serum concentrations of active metabolites, toxicity, and an increased risk for terminal delirium. To minimize this risk, discontinue routine dosing or continuous infusions of morphine when urine output and renal clearance stop. Titrate morphine breakthrough (rescue) doses to manage expressions suggestive of continuous pain. Consider the use of alternative opioids with inactive metabolites such as fentanyl or hydromorphone.

Loss of ability to close eyes. Eyes that remain open can be distressing to onlookers unless the condition is understood. Advanced wasting leads to loss of the retro-orbital fat pad, and the orbit falls posteriorly within the orbital socket.[46] Because the eyelids are of insufficient length to both extend the additional distance backward and cover the conjunctiva, they may not be able to fully appose. This may leave some conjunctiva exposed even when the patient is sleeping. If conjunctiva remains exposed, maintain moisture by using ophthalmic lubricants, artificial tears, or physiologic saline.[47]

Medications. As patients approach death, reassess the need for each medication and minimize the number of drugs that the patient is taking. Continue only those medications needed to manage symptoms such as pain, breathlessness, excess secretions, and terminal delirium and to reduce the risk for seizures. Choose the least invasive route of administration: the buccal mucosa or oral routes first, the transcutaneous/transdermal route if appropriate, the subcutaneous or intravenous routes only if necessary, and the intramuscular route almost never. Rectal administration can also be considered, especially if the oral route is not possible.

Dying in Institutions

The preceding discussion is relevant to patients dying in any setting (eg, at home, in hospitals, in nursing homes, other extended care facilities, prisons, etc.). However, there are particular challenges to ensuring a comfortable death in an institution where the culture is not focused on end-of-life care.[48]

When death is imminent, it is appropriate that patients remain with caregivers that they know rather than being transferred to another facility. Institutions can help by making the environment as home-like as possible. It is appropriate for the physician, nurse practitioner, or physician's assistant to order a private room where family can be continuously with the patient if they so choose and be undisturbed. The clinician will want to talk with the professional staff and encourage continuity of care plans across nursing shifts and changes in house staff.

Priorities and care plans at the end of life differ considerably from priorities and plans focusing on life prolongation and cure. It is frequently challenging for physicians, nurses, and other healthcare professionals to incorporate both kinds of care into a busy hospital or skilled nursing facility. For this reason, specialized units where patients and families can be assured of the environment and the skilled care they need have been developed in many institutions.[49,50]

REFERENCES
19. Ingham J, Breitbart W. Epidemiology and clinical features of delirium. In: Portenoy RK, Bruera E, eds. Topics in Palliative Care, vol. 1. New York: Oxford University Press; 1997:7-19.
20. Bruera E, Bush SH, Willey J, et al. Impact of delirium and recall on the level of distress in patients with advanced cancer and their family caregivers. Cancer. 2009;115:2004-2012. Abstract
21. Quijada E, Billings JA. Fast Fact and Concept #060: Pharmacologic management of delirium, update on newer agents. January 2002. Available at: http://www.mcw.edu/fastFact/ff_60.htm Accessed November 24, 2009
22. Campbell N, Boustani MA, Ayub A, et al. Pharmacological management of delirium in hospitalized adults- a systematic evidence review. J Gen Intern Med. 2009;24:848-853. Abstract
23. Fainsinger RL, Tapper M, Bruera E. A perspective on the management of delirium in terminally ill patients on a palliative care unit. J Palliat Care.1993;9:4-8. Abstract
24. Del Fabbro E, Dalal S, Bruera E. Symptom control in palliative care. Part III: Dyspnea and Delirium. J Palliat Med. 2006;9:422-436. Abstract
25. Shuster JL. Delirium, confusion, and agitation at the end of life. J Palliat Med. 1998;1:177-186. Abstract
26. Zaw-tun N, Bruera E. Active metabolites of morphine. J Palliat Care. 1992;8:48-50. Abstract
27. Maddocks I, Somogyi A, Abbott F, Hayball P, Parker D. Attenuation of morphine-induced delirium in palliative care by substitution with infusion of oxycodone. J Pain Symptom Manage. 1996;12:182-189. Abstract
28. Feldman MD. Paradoxical effects of benzodiazepines. NC Med J. 1986;47:311-312.
29. Twycross R, Lichter I. The terminal phase. In: Doyle D, Hanks GWC, MacDonald N, eds. Oxford Textbook of Palliative Medicine. 2nd ed. Oxford, England: Oxford University Press; 1998:987-988.
30. Truog RD, Berde CB, Mitchell C, Grier HE. Barbiturates in the care of the terminally ill. N Engl J Med. 1992;337:1678-1682.
31. Moyle J. The use of propofol in palliative medicine. J Pain Symptom Manage. 1995;10:643-646. Abstract
32. McIver B, Walsh D, Nelson K. The use of chlorpromazine for symptom control in dying cancer patients. J Pain Symptom Manage. 1994;9:341-345. Abstract
33. Liu MC, Caraceni AT, Ingham JM. Altered mental status in patients with cancer: a delirium update. Principles and Practice of Supportive Oncology Updates. Philadelphia, Pa: JB Lippincott Co; 1999:2.
34. Lichter I, Hunt E. The last 48 hours of life. J Palliat Care. 1990;6:7-15.
35. Twycross R, Lichter I. The terminal phase. In: Doyle D, Hanks GWC, MacDonald N, eds. Oxford Textbook of Palliative Medicine. 2nd ed. Oxford, England: Oxford University Press; 1998:985-6.
36. Voltz R, Borasio GD. Palliative therapy in the terminal stage of neurological disease. J Neurol. 1997;244(suppl 4):S2-S10. Abstract
37. Naughton MT. Pathophysiology and treatment of Cheyne-Stokes respiration. Thorax. 1998;53:514-518. Abstract
38. MacDonald N, ed. Palliative Medicine, a Case-Based Manual. Oxford, NY: Oxford University Press; 1998:263.
39. Sykes N, Thorns A. Sedative use in the last week of life and the implications for end-of-life decision making. Arch Intern Med. 2003;163:341-344. Abstract
40. Nuland S. How We Die. New York: Vintage Books; 1995.
41. Wildiers H, Dhaenekint C, Demeulenaere P, et al. Atropine, hyocine butylbromide, or scopolamine are equally effective for the treatment of death rattle in terminal care. J Pain Symptom Manage. 2009;38:124-133. Abstract
42. Hugel H, Ellershaw J, Gambles M. Respiratory tract secretions in the dying patient: a comparison between glycopyrronium and hyoscine hydrobromide. J Palliat Med.2006;9:279-284. Abstract
43. Hughes AC, Wilcock A, Corcoran R. Management of "death rattle." J Pain Symptom Manage. 1996;12:271-272. Abstract
44. Twycross RB, Lack SA. Therapeutics in Terminal Cancer. 2nd ed. London, England: Churchill Livingstone. 1990:134-136.
45. Bickel K, Arnold R. Fast Facts and Concepts #109. Death rattle and oral secretions. March 2004. End-of-Life Physician Education Resource Center. Available at: http://www.eperc.mcw.edu Accessed February 2, 2010.
46. Gray H. Anatomy of the Human Body, 29th ed. Philadelphia, Pa: Lea & Febiger; 1985:1303-1313.
47. Smeltzer SC, Bare BG, eds. Brunner and Suddarth's Textbook of Medical Surgical Nursing. 7th ed. Philadelphia, Pa: JB Lippincott Company; 1992:1657-1602.
48. Ferris TG, Hallward JA, Ronan L, Billings JA. When the patient dies: a survey of medical housestaff about care after death. J Palliat Med. 1998;1:231-239. Abstract
49. Kellar N, Martinez J, Finis N, Bolger A, von Gunten CF. Characterization of an acute inpatient hospice palliative care unit in a US teaching hospital. J Nurs Admin. 1996;26:16-20.
50. Walsh D, Gombeski WR, Goldstein P, Hayes D, Armour M. Managing a palliative oncology program: the role of a business plan. J Pain Symptom Manage. 1994;9:109-118. Abstract

February 19, 2011

International Training Courses for Clinical and Healthcare Professionals and Students

1 comment:
INTERNATIONAL TRAINING COURSES

INMED is pleased to announce two intensive training courses designed with you in mind! The 2011 International Medicine Intensive Course is a two-week course in June designed for healthcare professionals and healthcare profession students in the clinical fields. The 2011 International Public Health Intensive Course is a one-week course in June for healthcare professionals and students who are interested in public health.

February 12, 2011

18th Union Conference, African Region on TB, TB/HIV and Other Lung Diseases

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COURSES AND CONFERENCES

The African Region has made progress in the control of TB, TB/HIV, tobacco, asthma, and other lung diseases though serious challenges still exist for the Region to achieve the Millennium Development Goals by 2015.

February 09, 2011

Antihypertensives May Raise Blood Pressure In Some Patients

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WEDNESDAY, Aug. 25 -- Popular prescription medications taken to control hypertension may actually boost blood pressure in a "statistically significant" percentage of patients, researchers report.

The warning stems from a new study appearing in the online edition of the American Journal of Hypertension. The research involved 945 New York City residents participating in a program designed to control high blood pressure in the workplace from 1981 to 1998.

"Every clinician knows that there's a variation in response to antihypertensive treatment, and that some patients will have an elevation in blood pressure," study author Dr. Michael Alderman, a professor of epidemiology & population health and of medicine at the Albert Einstein College of Medicine of Yeshiva University and a former president of the American Society of Hypertension, said in a news release from the society. "The latter phenomenon is generally attributed to patients' failure to take their medications or to a random event. But these data show that it's not a random event."

None of the study participants, who all had systolic blood pressure of at least 140 mm Hg, had been treated for high blood pressure prior to enrollment in the study. Once enrolled, they were prescribed just one of two types of blood pressure medications: either a so-called "V" drug to lower blood volume (by means of a diuretic or a calcium channel blocker), or a so-called "R" drug (a beta blocker or ace inhibitor) to lower the kidney enzyme -- renin -- that is critical to blood pressure control.

After monitoring and reviewing both plasma renin activity (PRA) and systolic blood pressure levels during treatment, Alderman and his team found that the plasma renin levels predicted whether a "V" or an "R" drug would benefit or be problematic for a particular patient.

Overall, 7.7 of the patients had a clinically significant increase in blood pressure of 10 mmHg or more. The highest percentage of these responses -- 16 percent -- occurred in patients with low renin levels who were given an "R" drug (a beta blocker or an ACE inhibitor).

Rather than a random event, an elevation in blood pressure from a particular drug suggested "a mismatch between the patients' renin status and the drug," Alderman said. "Our findings suggest that physicians should use renin levels to predict the most appropriate first drug for treating patients with hypertension." For example, the researchers wrote, "our data indicate that patients with low PRA values are at highest risk" of a clinically significant increase in systolic blood pressure when prescribed an R drug.

Tracking renin levels would be particularly helpful for two groups of patients, Alderman and his colleagues noted: those taking blood pressure medications for the first time, and those already on a regimen incorporating several blood pressure drugs at the same time.

Renin level monitoring "would increase the likelihood of achieving blood pressure control and reduce the need for patients to take additional antihypertensive medication," Alderman added.

Plasma renin activity testing has been used for years to determine the underlying cause of an individual's hypertension (whether it is caused by too much blood volume or constricted blood vessels, or both), but the test was expensive and hard to perform accurately. On an encouraging note, the research team points out that in recent years testing for plasma renin activity has become more effective and more widely available than it was in the past.

Dr. Stephen A. Siegel, an assistant clinical professor of medicine at New York University, agreed that renin monitoring could be an "excellent approach" if clinicians are able to identify an enzyme level dividing line that clearly separates those patients who would benefit from a particular medication from those that might not.

"We've been looking at renin levels for a long time," he said, "but it's been of equivocal benefit in the past because it's been hard to agree on a particular stable level that would indicate trouble. So I'm a little hesitant to enthusiastically endorse this method for addressing the problem."

"However, we're getting more sophisticated with this, and improvements in the testing may now make it much more helpful for screening purposes," Siegel added. "And certainly, conceptually, the problem this paper addresses is real because not everyone is the same. Whereas in the 60s and 70s, our choices in anti-hypertensives were extremely limited and blunt, today there is a lot of work being done to individualize patients to see what treatment works best case by case, instead of lumping them all together in the single category of having high blood pressure. So, this type of work is very important."

More information
For more on high blood pressure medications, visit the National Heart, Blood, and Lung Institute.