Joe had searched for evidence of anti-folate bone marrow effects of cotrimoxazole (trimethoprim-sulfamethoxazole). He had found conclusions that trimethoprim is a weak inhibitor of dihydrofolate reductase. ...Have found some more evidence...
This 1986 study found the number of circulating granulocytes in 12 health adults to be unaltered by five days of cotrimoxazole. But normal donor harvested cells in vitro had colony formation inhibited by trimethoprim. Sulfamethoxazole had no effect.
Inhibition could be reversed when folate was added to the culture. (They did not look at platelets.)
This weblog worked during this month to extend clinical teaching. It may have saved some time at the bedside with patients. ...May also have expanded independent learning. Certainly MovableType software allowed each team member to author entries to the weblog (from any computer's web browser).
The weblog concept was gradually introduced over the four week clinical internal medicine rotation at Good Samaritan Hospital, Cincinnati Ohio.
Content of the weblog, care of the patients, and stimulating discussions sprang from members of the March Team: Bart Choate (Pharmacy Student), Tom Imhoff (Clinical Pharmacist), Joe Kiehl (Medical Student 3rd-year), Eric Kirkendall (Medical Student 4th-year), Suganthi Kumarin (Senior Resident), Curt Mardis (Resident 1st-year), Nancy Samol (Resident 1st-year), and Carl Gandola (Attending).
A pleasure to work together.
Curt shed light on David Hume. Here are some leads for more on Hume and miracles, suicide, medical ethics, or his general life and writings.
This study confirms that resistance to triclosan can develop with pseudomonas aeroginosa. Triclosan is the antiseptic in Colgate Total, mentioned at lunch.
Less serious but interesting are these abstracts: one a head-to-head study of Colgate vs. Crest, and a Norwegian study that claims triclosan rinse reduces aphthous ulcers.
For several years there has been another smoldering safety concern (often not journal-published). Triclosan's structure is said to be similar to dioxin, an environmental toxin.
Published articles in an American Chemical Society journal from June of 2002 report lingering triclosan concentrations in a Swiss lake, and evidence that triclosan does photochemically degrade to dioxin. (Caveat: Full text not available online, have not seen the actual articles.)
Bring Udipi to your own kitchen with this collection of recipes.
Opioids can cause direct mast cell degranulation without the presence of specific IgE antibodies.
Although rarely observed, opioids are known to provoke allergic reactions, such as urticaria, pruritis, erythema, bronchospasm, &c --all of which imply histamine release. In fact, mast cells have been shown to possess opioid receptors, suggesting that allergic reactions are receptor-mediated side effects of opioids rather that IgE-mediated reactions. Researchers agree that opioids may directly cause mast cell degranulation without the presence of specific IgE antibodies. Since antihistamines tend not to relieve these allergic symptoms, they recommend the use of the mu-antagonist naloxone, which blocks further mast cell degranulation, in anaphylactoid type reactions produced by opioids.
In one British study, skin pricks for morphine and meperidine were tested on a group of opioid-sensitive subjects (i.e., those who experience allergic reactions to IV or PO opioids) and on a group of non-opioid-sensitive control subjects. The researchers reported no adverse reactions in either group and found no statistically significant differences between both groups for the size of wheals produced by the skin prick test (SPT) for morphine and meperidine. Although there were no methods available for detecting antibodies specific for opioids (if they indeed exist), these researchers concluded that opioid hypersensitivity is unlikely to be an IgE-mediated response, which generally demonstrates much larger wheals after SPT.
Reference:
1.) "Opioid-sensitivity: clinical characteristics and the role of skin prick testing"
Clinical and Expermental Allergy, 2001 Vol. 31 pp1014-1020
2.) "Generalised Prurtis with Opioids" The Lancet, Oct/1994 Vol344 p1031
3.) "Use of naloxone in opioid-induced anaphylactoid reaction"
British Journal of Anaesthesia, 1988 Vol. 61, p.371
South Indian food today? Udipi in Roselawn. Stay in touch with Suganthi for time (probably caravan around 1:00 or so).
The differential diagnosis of acute hypotension in a hospitalized patient forces the clinician to examine the 3 main classifications of shock. Any classification scheme simplifies the complex pathophysiology underlying the many individual causes of shock states. Three broad types of shock states are recognized: hypovolemic, cardiogenic, and distributive. Each type is characterized by one primary physiologic derangement. This entry will examine distributive shock.
Distributive shock results from a severe decrease in SVR, often associated with an increased cardiac output. Causes include:
1) Septic shock
2) Activation of the systemic inflammatory response (eg, by pancreatitis, burns, or multiple traumatic injuries)
3) Toxic shock syndrome
4) Anaphylaxis and anaphylactoid reactions
5) Drug or toxin reactions, including insect bites, transfusion reactions, and heavy metal poisoning
6) Addisonian crisis (which should be considered if clinical signs of sepsis exist without evidence of infection)
7) Myxedema coma
8) Neurogenic shock after a central nervous system or spinal cord injury
The symptoms and signs of adrenal insufficiency depend upon the rate and extent of loss of adrenal function, whether mineralocorticoid production is preserved, and the degree of stress. The onset of adrenal insufficiency is often very gradual and it may go undetected until an illness or other stress precipitates adrenal crisis.
ADRENAL CRISIS ? The syndrome of adrenal crisis (acute adrenal insufficiency) can occur in a patient with primary adrenal insufficiency (Addison's disease) who has a serious infection or other acute stress. It can also occur after bilateral adrenal infarction or bilateral adrenal hemorrhage. It is rare in patients with secondary or tertiary adrenal insufficiency.
The predominant manifestation of adrenal crisis is shock, but the patients often have nonspecific symptoms such as anorexia, nausea, vomiting, abdominal pain, weakness, fatigue, lethargy, confusion or coma.
Hypoglycemia is a rare presenting manifestation of acute adrenal insufficiency; it is more common in secondary adrenal insufficiency caused by isolated corticotropin (ACTH) deficiency. The major hormonal factor precipitating adrenal crisis is mineralocorticoid, not glucocorticoid, deficiency, and the major clinical problem is hypotension. Thus, adrenal crisis can occur in patients who are receiving physiologic or even pharmacologic doses of synthetic glucocorticoid if their mineralocorticoid requirements are not met.
Infection or other stress ? Adrenal crisis usually presents as shock in a previously undiagnosed patient with primary adrenal insufficiency who has been subjected to a major stress, or in a patient with known adrenal insufficiency who does not take more glucocorticoid during a bacterial infection or other major illness or has persistent vomiting caused by viral gastroenteritis or other gastrointestinal disorders.
Fever is usually caused by infection, and may be exaggerated by hypocortisolemia. It should be assumed that fever indicates infection that must be identified and treated. The combination of abdominal pain and fever may lead to the incorrect diagnosis of an acute surgical abdomen with potentially catastrophic surgical exploration.
In addition, septic shock itself may occasionally cause transient relative adrenal insufficiency.
Bilateral adrenal hemorrhage and infarction ? Adrenal crisis can also occur as a result of sudden bilateral adrenal necrosis caused by hemorrhage, emboli, sepsis or, very rarely, adrenal vein thrombosis after a back injury. These patients do not have evidence of preexisting adrenal insufficiency. Before computed topography (CT) became widely available, the diagnosis of adrenal hemorrhage was usually made at autopsy.
The presenting symptoms and signs (and the frequency with which they occurred in one report) include hypotension or shock (more than 90 percent); abdominal, flank, back, or lower chest pain (86 percent); fever (66 percent), presumably a response to inflammation; anorexia, nausea, or vomiting (47 percent); neuropsychiatric symptoms such as confusion or disorientation (42 percent); and abdominal rigidity or rebound tenderness (22 percent). Surprisingly, only about half the patients have hypotension before shock.
Evidence of occult hemorrhage, such as a sudden fall in hemoglobin and hematocrit, and progressive hyperkalemia, hyponatremia, and volume contraction are other signs that should suggest the diagnosis.
The major risk factors for adrenal hemorrhage or infarction are anticoagulant therapy or coagulopathy, and the postoperative state. In patients treated with an anticoagulant, the results of clotting tests are usually within the therapeutic range and spontaneous bleeding elsewhere is not evident.
Because adrenal crisis is difficult to recognize clinically, it must be considered whenever these symptoms develop in a patient with one or more risk factors. Without appropriate therapy, shock progresses to coma and death. If the patient survives, adrenal function may rarely return to normal months later.
References:
1) http://www.utdol.com/application/topic.asp?file=adrenal/5492
2) Briegel, J, Schelling, G, Haller, M, et al. A comparison of the adrenocortical response during septic shock and after complete recovery. Intensive Care Med 1996; 22:894.
3) Rao, RH, Vagnucci, AH, Amico, JA. Bilateral massive adrenal hemorrhage: early recognition and treatment. Ann Intern Med 1989; 110:227.
4) Xarli, VP, Steele, AA, Davis, PJ, et al. Adrenal hemorrhage in the adult. Medicine 1978; 57:211.
5) Streeten, DHP. Adrenal hemorrhage. Endocrinologist 1996; 6:277.
6) Migeon, CJ, Kenny, FM, Hung, W, Voorhess, ML. Study of adrenal function in children with meningitis. Pediatrics 1967; 40:163-183.
7) Margaretten, W, Nakai, H, Landing, BH. Septicemic adrenal hemorrhage. Am J Dis Child 1963; 105:346.
8) Dunlop, D. Eighty-six cases of Addison's disease. BMJ 1963; 2:887.
Oral anticoagulants are frequently prescribed during lactation. Because these drugs could affect the hemostasis of the newborn, a literature search was performed to find out whether precautions should be taken. It appeared that warfarin is not detectable in human milk. Besides the usual daily supplementation of 25 micrograms vitamin K for every breast-fed infant, precautions are not necessary.
here's an enquirer link re: the ethics questions we talked about today....
Hypertensive crisis (i.e., DBP > 120mmHg) consists of 2 classifications: 1) Hypertensive emergencies (i.e., the presence of end-organ damage) generally require a reduction in BP within a few hours using I.V. medications in an ICU. 2.) Hypertensive urgencies (i.e., the absence of such complications) require a reduction in BP over 24-48 hours. Oral agents are sufficient, usually administered in a closely monitored outpatient setting.
Therapy for hypertensive urgencies consists of a non-specific combination of drugs, scheduled or PRN, including an increased dose of the patient's current baseline antihypertensive agents.
Oral clonidine (0.1-0.2mg Q1H, max=0.6mg) has an onset of action of 30-60 minutes and a duration of 6-8 hours. Clonidine is a good choice for patients in whom rapid control of BP is not required. Sedation is a common side effect, along with dry mouth and occasional dizziness.
A 20mg bolus dose of I.V. labetolol (onset: 2-5min), followed by repeated incremental doses of 20-80mg Q10min (max=300mg) is recommended until therapeutic goal is achieved. After that, oral labetolol 200-400mg Q2-3H (onset 0.5-2 hours) is sufficient. Unlike most beta-blockers, labetolol maintains heart rate and cardiac output. It reduces peripheral vascular resistence while maintaining cerebral, renal, and coronary blood flow. Adverse effects include hypoTN and dizziness. Don't administer to patients with 1st heart block or CHF.
I.V. hydralazine (onset: 5-20 minutes) is dosed as: 10-20mg Q4-6H. Hydralazine causes a precipitous drop in BP lasting for 12 hours. Its prolonged and unpredictable effect makes it difficult to titrate. Hydralazine has been traditionally used for eclampsia, but labetolol and nicardipine are safe and effective alternatives for pregnant patients. Hydralazine is an arterial vasodilator that increases cardiac output, and should therefore be avoided in pts with aortic dissection, coronary insufficiency, and CVA (d/t incr'd intracranial pressure). Adverse effects include tachycardia, flushing, and angina aggravation.
ACEIs are useful for pts with CHF, but must be used cautiously in pts with severe renal insufficiency. Oral captopril (onset: 15-30min/duration: 6-8hrs) is dosed as 25mg x1 (SL or PO), then repeat TID PRN. The dose may be increased at 1-2 week intervals up to 150mg TID. I.V. enalaprilat (onset: 15min/duration: 24hrs) is dosed as 1.25-5mg Q6H for HTNsive emergency, but then decreased to 0.625-1.25mg Q6H after therapeutic goal. ACEIs also can cause a precipitous drop in BP. They're unpredictable, poorly titrable, and contraindicated in pregnancy.
Extreme leukocytosis with a predominance of granulocytes is associated with infection in only 48% of cases, based on a 100 patient retrospective study done at the Minneapolis Veterans Affairs Medical Center between March, 1993 and January, 1994. Glucocorticoid therapy accounted for 8% of cases of leukocytosis greater than 25,000.
Vitiligo has been found to be associated with the following conditions:
1. Polyglandular autoimmune syndrome II (Autoimmune thyroid disease, Type I Diabetes Mellitus, Primary adrenal insufficiency, Hypopituitarism )
2. Autoimmune hepatitis
3. Alopecia areata
4. Pernicious anemia
Usually occurs in the second or third decade. However can occur at any age, and can be precipitated by stress.
PATHOGENESIS: It is an autoimmune process directed against melanocytes.
TREATMENT: Corticosteroids, Ultraviolet light, Pseudocatalase cream, Surgery, Depigmentation treatement with hydroquinone, Immunemodulators like Cyclosporine, Levamisole.
Diagnosis of amyloidosis:
Tissue biopsy is necessary for the diagnosis of amyloidosis. The diagnosis is established by biopsy of the affected organ. A kidney or liver biopsy is positive in over 90% of cases. Abdominal fat pad aspirate (60-80%), rectal biopsy (50-70%), and bone marrow biopsy (50-55%) can also be used to make the diagnosis.
The amyloid fibrils bind Congo red, leading to green birefringence under polarized light.
Familial forms of amyloidosis:
The transthyretin (TTR or prealbumin) gene is located on chromosome 18. More than 80 TTR mutations have been found thus far. Nearly all mutant TTR gene products are amyloid proteins.
Different variants of the TTR gene have different clinical expressions. Familial neuropathic, cardiomyopathic, nephropathic, and ocular forms have been described. Certain populations have an increased prevalence of particular mutations.
In Portugal, one of 600 people carries a TTR gene leading to a methionine substitution for valine at position 30. This leads to a familial amyloidotic polyneuropathy.
Isolated cardiac amyloidosis is more common in African-Americans than Caucasians. Nearly 4% of black Americans are heterozygous for a substitution isoleucine for valine at position 122.
Other mutations in the TTR gene have been associated with late-onset cardiac amyloidosis. Amyloid may be deposited in other organs with this condition.
Prognosis for cardiac amyloidosis:
Prognosis for cardiac amyloidosis seems to depend on the type of amyloidosis present in the patient. Among 36 patients with amyloid cardiomyopathy, the 24 with familial amyloidosis had a better survival than those with primary (AL) amyloidosis. AL amyloid is due to deposition of protein derived from immunoglobulin light chain fragments. It is a plasma cell dyscrasia that is usually associated with production of a monoclonal protein.
After 35 months, only 10% of the patients with primary amyloidosis were still alive. In contrast, 60% of the patients with familial amyloidosis were still alive after 50 months.
The Drug Information Handbook indicates that >10% of patients who take Baclofen have adverse effects of the central nervous system, which include: drowsiness, vertigo, psychiatric disturbances, insomnia, slurred speech, ataxia, and hypotonia. For additional information on warnings/precautions, adverse reactions, drug interactions, and nursing implications, click below.
WARNINGS / PRECAUTIONS; Use with caution in patients with seizure disorder or impaired renal function. Avoid abrupt withdrawal of the drug; abrupt withdrawal of intrathecal baclofen has resulted in severe sequelae (hyperpyrexia, obtundation, rebound/exaggerated spasticity, muscle rigidity, and rhabdomyolysis), leading to organ failure and some fatalities. Risk may be higher in patients with injuries at T-6 or above, history of baclofen withdrawal, or limited ability to communicate. Elderly are more sensitive to the effects of baclofen and are more likely to experience adverse CNS effects at higher doses.
ADVERSE REACTIONS >10%: Central nervous system: Drowsiness, vertigo, psychiatric disturbances, insomnia, slurred speech, ataxia, hypotonia Neuromuscular & skeletal: Weakness
1% to 10%: Cardiovascular: Hypotension Central nervous system: Fatigue, confusion, headache Dermatologic: Rash Gastrointestinal: Nausea, constipation Genitourinary: Polyuria
<1%: Palpitations, chest pain, syncope, euphoria, excitement, depression, hallucinations, xerostomia, anorexia, abnormal taste, abdominal pain, vomiting, diarrhea, enuresis, urinary retention, dysuria, impotence, inability to ejaculate, nocturia, paresthesia, hematuria, dyspnea
Withdrawal reactions have occurred with abrupt discontinuation (particularly severe with intrathecal use).
DRUG INTERACTIONS Increased effect: Opiate analgesics, benzodiazepines, hypertensive agents
Increased toxicity: CNS depressants and ethanol (sedation), tricyclic antidepressants (short-term memory loss), clindamycin (neuromuscular blockade), guanabenz (sedation), MAO inhibitors (decrease blood pressure, CNS, and respiratory effects)
NURSING IMPLICATIONS; Epileptic patients should be closely monitored; supervise ambulation; avoid abrupt withdrawal of the drug
DENTAL HEALTH: EFFECTS ON DENTAL TREATMENT; No effects or complications reported
DENTAL HEALTH: VASOCONSTRICTOR/LOCAL ANESTHETIC PRECAUTIONS; No information available to require special precautions
MENTAL HEALTH: EFFECTS ON MENTAL STATUS; Drowsiness and insomnia are common; rare reports of depression, euphoria, and hallucinations
MENTAL HEALTH: EFFECTS ON PSYCHIATRIC TREATMENT; Concurrent use with psychotropics may produce additive sedation; concurrent use with MAO inhibitors may potentiate their hypotensive effects
Reference
Drug Information Handbook
Charles Lacy, RPh, PharmD
Copyright (1978 to present) Lexi-Comp, Inc.
Some causes of persistent and intractable hiccups include...
Central Nervous System
- Vascular lesions: head trauma, ischemic/hemorrhagic stroke
- Infections: meningitis, encephalitis, brain abscess
- Structural lesions: intracranial neoplasms, brainstem neoplasms, MS
Toxic - Metabolic
- Alcohol, uremia, DM, hyponatremia, hypocalcemia
Postoperative
- General anesthesia, intubation, neck extension (stretching phrenic nerve roots)
- Gastric distension
Drugs
- Alpha methyldopa, short acting barbituates, dexamethasone. diazepam
Psychogenic
- Stress, conversion reaction, malingering
Irritation of vagus and phrenic nerves
- Meningeal branches: meningitis
- Pharyngeal branches: pharyngitis, laryngitis
- Thoracic brances: pneumonia, empyema, bronchitis, asthma, peuritis, esophagitis, esophageal obstruction, aortic aneurysm, myocardial infection, pericarditis, mediastinits, mediastinal tumors, chest trauma, enlarged lymph nodes secondary to infection or neoplasm
- Auricular branches: gastric disteniton, gastritis, PUD, pancreatitis, CA of pancreas, gastric CA, abdominal abscesses, gallbladder dz, IBD, hepatitis
- Diaphragmatic irritation: MI, pericarditis, hiatus hernia, GE reflux, hepatic splenomegaly, subphrenic abscess
Reference: Lewis, JH. Hiccups: Causes and cures. J Clin Gastroenterol 1985; 7:539.
Recent screening advances of donated blood have led to lower risks of transfusion-related infections with blood-bourne pathogens like Hepatitis C and HIV.
An article in the NEJM (sign on first, article will appear after login) that studied blood donations through the Red Cross during 1992-3 showed that the estimated risk of contracting HIV through receiving blood transfusions was about 1 in 450,000 to 600,000 per donation (unit). Since the study, screening for HIV has increased in sensitivity and specificity, especially with the addition in August of 1995 of testing for the HIV-1 p24 antigen.
The CDC states that the current risk of contracting Hep C through blood product transfusions is about 1:100,000 per unit transfused. In addition, virtually all risk for transplant-related transmission of HCV has been eliminated through vigorous screening.
Carbohydrate Antigen 19-9, or CA 19-9 as it is more commonly known, is currently the most sensitive and specific tumor marker used for evaluation and diagnosis of pancreatic cancer. However, it's usefulness is limited by several factors.
Approximately 10-15% of all people do not produce CA 19-9 because of their Lewis antigen status. The marker's presence requires the production of Lewis antigen; 10-15% of the population are Lewis (-ve). Secondly, of those who are Lewis (+ve), the marker is also produced by other tissue and can be elevated in relatively benign conditions such as acute cholangitis or chronic pancreatitis.
Currently, CA 19-9 is most useful when it is greatly elevated (more indicative of cancer), or more commonly, it's decline signals an effective treatment course (levels often followed during chemotherapy).
In the future, CA 19-9 may become a more sensitive and specific marker when used in conjunction with other markers in the SAGE database, such as tissue inhibitor metalloproteinase-1 (TIMP-1), a gene expression product.
For more info, check out this article on MD Consult;
Early Detection of Pancreatic Carcinoma, Rosty et. al.
Hematology/Oncology Clinics of North America, vol 16, no. 1, Feb 2002.
Two types of stress tests, exercise and pharmacologic, are combined with echocardiography or perfusion imaging for determining the risks for coronary artery disease. Pharmacologic agents commonly used are adenosine, dipyridamole and dobutamine.
Radionuclide pefusion imaging uses Tc 99m-sestamibi, Tc 99m-tetroformin, Thallium 201 as perfusion agents. Types of perfusion imaging agents are discussed at this patient education site.
A New England Journal of Medicine review distinguishes between the agents. ...Thallium-201 emits "mercury x-rays" and has a half-life of 72 hours. The newer sestamibi agents are labelled with Technitium-99 and emit gamma rays. Sesamibi agents have a much shorter half-life of 6 hours.
Your patient has no insurance. Yet they need an expensive medication. They do not qualify for state assistance. What can you offer?
Try RxAssist. Use their search feature to find the manufacturer. Download forms to request financial assistance and medication supply from the pharmaceutical company. Instructions for most major companies can be found here.
Your patient has had a gastrointestinal hemorrhage (melena). Her BUN is 28, her creatinine is 1.1. Is the absence of a significant rise in BUN predictive of a lower GI source? (Discussion with Eric raised this issue).
A BUN/Creatinine ratio of less than 36 is not predictive of bleeding location. Two of three recent reports did find that a BUN/Creatinine ratio of more than 36 does predict an upper GI source. One other study found the ratio not to be helpful in those patients who were not vomiting blood (unfortunately the very group where the prediction would be most needed.)
EVIDENCE
Ernst[1] in an emergency room study found a BUN/Creatinine ratio of greater than 36 to have a 9% sensistivity and specificity = 27% for upper GI source.
However, Chalasani[2] studying 790 patients admitted to the GI service looked at patients who did not have hematemisis (a more obvious sign of upper GI bleeding). In patients without hematemesis, the value of BUN/creatinine ratio led to much overlap, and lessened predictability. They found it correlate best with transfusion requirement.
Stellato[3] emphasizes that the rise in BUN is more than can be accounted for simply by ingestion of blood. Hypovolemia plays a role. And if azotemia does not resolve in a day or so, this suggests that volume status needs to be addressed, or that there is continued bleeding.
Richards[4] looked at five years of GI bleeding. No patient with lower gi source had a BUN/creatinine ratio of more than 36. Of those with upper GI source, 38% had a ratio greater than 36--this suggests a specific test, but not a very sensitive one. So the positive predictive value would be high. A negative test is not predictive.
SUMMARY
Two of three recent reports[1,4] did find that a BUN/Creatinine ratio of more than 36 does predict an upper GI source. But a BUN/Creatinine ratio of less than 36 is not predictive of bleeding location. One other study[2] found the ratio not to be helpful in those patients who were not vomiting blood (unfortunately the very group where the prediction would be most helpful.)
References
1. Ernst, A.A., et al., Usefulness of the blood urea nitrogen/creatinine ratio in gastrointestinal bleeding. Am J Emerg Med, 1999. 17(1): p. 70-2.
2. Chalasani, N., W.S. Clark, and C.M. Wilcox, Blood urea nitrogen to creatinine concentration in gastrointestinal bleeding: a reappraisal. Am J Gastroenterol, 1997. 92(10): p. 1796-9.
3. Stellato, T., R.S. Rhodes, and W.S. McDougal, Azotemia in upper gastrointestinal hemorrhage. A review. Am J Gastroenterol, 1980. 73(6): p. 486-9.
4. Richards, R.J., M.B. Donica, and D. Grayer, Can the blood urea nitrogen/creatinine ratio distinguish upper from lower gastrointestinal bleeding? J Clin Gastroenterol, 1990. 12(5): p. 500-4.
Touched on treatment of depression in the palliative care setting.
...from
Tremblay, A. Psychiatric dimensions of palliative care. Neurol Clin, 2001; 19(4): 949-6
"Psychostimulants (dextroamphetamine, methylphenidate , and pemoline) offer alternative and effective pharmacologic approaches to the treatment of depression in patients with advanced illness. Psychostimulants improve attention, concentration, and overall cognitive performance in the medically ill. In relatively low doses, they also stimulate appetite and improve weakness and fatigue in cancer patients.
Treatment is usually initiated with the lowest possible dose (2.5 mg for dextroamphetamine and methylphenidate , 18.75 mg for pemoline) at 8 o'clock and at noon. The dosage is increased slowly over several days until the desired effect is achieved or side effects, such as overstimulation, anxiety, insomnia, paranoia, or confusion, are experienced. Tolerance can develop over time and dosage adjustments may be required."
To be sure you are displaying the most recent bedside.org, click the Refresh, or "Reload" button up top, on your web browser.
The Amercian College of Physicians (ACP) has put together some clinical tools for the Palm. Will bring some to rounds.
Earlier, here, other handheld resources had been mentioned (Pneumonia Severity Index and MedRules). In the course of a day MedRules, Tarascon Pharmacopeia, and Sanford Guide to antibiotics come in handy for me.
Post-stroke unilateral spatial neglect...does it predict prognosis?
Some references suggest that it often (60% of time) resolves soon after an acute stroke. When it persists that can suggest a poor prognosis. Need a rebilitation doctor's clarification on this question. Could not find it specifically linked to depression.
Interestingly, there is a Cochrane review that looked at the benefit of rehabilitation to resolve neglect. They found no conclusive evidence of support.
A helpful acronym.
"Indeed, simply inquiring about recent depressed mood or anhedonia will detect 90% to 95% of patients with major depression and has a sensitivity similar to much longer depression questionnaires"
Kurt Kroenke, MD.
SYMPTOMS ("SPACE DIGS")
Less Depression-Specific Symptoms
Sleep disturbance (either insomnia or hypersomnia)
Psychomotor retardation or agitation
Appetite disturbance (decreased or increased) or weight loss or gain
Concentration difficulties
Energy low (ie, tiredness, fatigue)
More Depression-Specific Symptoms
Depressed mood
Interest in activities is diminished or lost (ie, anhedonia)
Guilt or feelings or worthlessness excessive or inappropriate
Suicidal ideation or thoughts of death
DIAGNOSTIC CRITERIA
Major Depression. At least 5 of the 9 DSM-IV symptoms have been present nearly every day for 2 or more weeks, and at least 1 of the symptoms is depressed mood or anhedonia.
Dysthymia. Depressed mood plus at least 2 additional DSM-IV symptoms have been present more days than not for at least 2 years.
Minor Depression. Individual does not meet criteria for major depression or dysthymia but does have 2 to 4 depressive symptoms that have been present nearly every day for at least 2 weeks, and at least 1 of the symptoms is depressed mood or anhedonia. (Although not yet an official DSM-IV diagnosis, minor depression has been proposed as a mood disorder.) "
...from
Kroenke K. Discovering Depression in Medical Patients: Reasonable Expectations. Annals of Internal Medicine 15 March 1997. 126:463-465
(And don't forget to check a CBC, basic metabolic panel including calcium, liver enzymes and TSH, and other physiologic considerations that fit the individual.)
On rounds today we can put our minds together about this story.
41 year-old woman comes to your office, tearful, tremulous, "jumping out of her skin." She had been assaulted by a boyfriend the previous day--kicked in the ribs. Pain in her left lataeral ribs/chest is unbearable. "I know he broke my ribs! But the ER doctor says no. My x-rays were normal!" The emergency room doctor had given her Tylenol #3. It is not helping her pain. She has a history of past alcohol abuse.
Exam shows Blood Pressure 150/80, Pulse 120, RR 15. She is holding her left lower chest, in obvious pain, wincing with each breath. She is trembling. Lungs show bilateral breath sounds. She is not short of breath. But with each inspiration there is an audible crunch and palpable popping of bone over the antero-lateral left lower ribs.
Your assessment?
Any diagnostic or treatment plans?
Idiopathic Thrombocytopenic Purpura is a diagnosis of exclusion. Other common causes of isolated thrombocytopenia must be ruled out before a diagnosis of ITP can be made. There are two main types of ITP, an acute form (usually found in children 2-4yrs old) and a chronic form (found in adults from 20-50yrs old). The acute form usually resolves spontaneously within 2 months of onset, while the chronic, adult form may persist for 6 months or longer.
ITP manifests as unusual bleeding or hemorrhaging, which is the largest factor contributing to morbidity and mortality. A large part of the diagnosis relies on CBC and peripheral smear findings. A thorough history and physical can give clues that may lead to an alternative diagnosis. Therapy is guided by the presence and severity of bleeding and the platelet count on the CBC. The mainstays of treatment are corticosteroids, IVIG infusions, and platelet transfusions.
Tomorrow morning (March 12 at 8:00) Dr. Steven Blatt presents Grand Rounds on smallpox. (Smallpox resource: CDC website.)
The Jenner Museum describes the last naturally occurring case of small pox...
"The last case of smallpox in India occurred in 1975, but the disease persisted in Ethiopia and surrounding regions of Africa. In 1977 a hospital worker who had nursed a family in a Somali hospital became ill. Ali Maow Maalim had never himself been vaccinated! WHO officials literally sat on his doorstep, letting no one out or in until the last scab had fallen off his last pock. He recovered. He was the last person on Earth to catch smallpox by natural transmission."
"But ironically, in 1978 two more cases popped up in Birmingham, England, from smallpox virus escaped from a research lab. One of the patients died. The director of the laboratory committed suicide. These were smallpox's last victims. In 1979, a global commission certified that smallpox had been eradicated, and this certification was officially accepted by the 33rd World Health Assembly in 1980."
Bart reviewed potential medical therapy of alcoholism.
Alcoholics Anonymous and Secular Recovery are two non-medical avenues for recovery. You can find a meeting tonight in Cincinnati (351-0422) or anywhere.
The Medical Letter is now available for Palm ($20.00/year for students & residents).
Are orthostatic vital signs a reliable predictor of hypovolemia? A 1999 paper by McGee, Abernathy & Simel suggests, no. Euvolemic people can have orthostatic hypotension and hypovolemic people may not have a fall in blood pressure. Seems we put together a picture of severity from pieces of individually less-than-reliable evidence (dizziness, rise in pulse, electrolytes, and observed hemorrhage).
The Weekly Web Review of Emergency Medicine has published a helpful summary of the primary article. Also the American College of Physicians has published an extensive online bibiliography on the value of phsicial findings.
Angiotensin converting enzyme inhibitors are associated with thrombocytopenia. (Grosbois B, Milton D, Beneton C, Jacomy D. Thrombocytopenia induced by angiotensin converting enzyme inhibitors. Br Med J 1989; 298: 189-90.)
The FDA defines serious adverse drug reactions, and makes them easy to report online.
Anemia and other marrow effects of ACE-inhibitors are discussed in another reference from the Journal of Nephrology, an Italian journal with full text available online. (For more about free full text online journals go to freemedicaljournals.com)
Ways to hear better, BATHE.
In this review article Dr.Joseph A. Lieberman, who along with Dr. Marian R. Stuart described the BATHE technique of interviewing, continues:
By adding BATHE or BATHEing the patient, clinicians can supplement the information gathered using the problem-oriented approach to determine the patient's psychosocial status. The BATHE acronym stands for the following:
Background: A simple question will elicit the context of the patient's visit: "What's going on in your life?"
Affect: Questions such as "How do you feel about that?" or "What's your mood?" allow the patient to report the current feeling state.
Trouble: The question, "What about the situation troubles you the most?" helps both the physician and the patient focus on the situation's subjective meaning.
Handling: The answer to, "How are you handling that?" gives an assessment of functioning.
Empathy: A statement can legitimize the patient's reactions: "That must be very difficult for you."
The BATHE technique enables the practitioner to get at critical elements in the patient's presentation that are not readily accessible through standard interview techniques. It also has the advantage of being very focused, quickly employed and nonthreatening to the majority of elderly patients. The information helps to make a much better assessment of the patient's situation, the forces acting on the patient and the patient's perception of their state of affairs.
We had talked about alternatives to warfarin (Coumadin). Ximelagatran is promoted by its manufacturer, and early clinical studies are accumulating for its use in prophylaxis after knee surgery, and other orthopedic surgery (tested agains low molecular weight heparin). Studies in stroke prevention in atrial fibrillation are yet to come. The company anticipates a large market.
You can almost feel it. More disussions online about interpretation and value of this exam here and there.
Living will and healthcare durable power of attorney forms are presented in this thoughtful & practical brochure from the Ohio Hospice Organization, Ohio State Medical Association, the Ohio Osteopathic Society, and others.
What is the order of authority if a patient has no durable power of attorney for health care decisions?
In Ohio: Guardian, Spouse, Adult children, Parents, Adult siblings, Next reasonably close relative. (According to Dr. Lawrence Ulrich, author of Patient Self-Determination Act, 2000)
Usual recommendations include: your doctor, lawyer, family, and county registrar. US Living Will Registry is on the web. They will fax your forms to responsible requesting health care facilities.
You see a 42-year old man for a cough and pleuritic chest pain. He is not known to be immunocompromised.
Oxygen saturation: 90%. X-ray: no infiltrate, but there is slight blunting of his left hemidiaphragm. Pulse is 120. Tempurature 100.6. White blood cell count 21,000.
Do you admit him? ...Is your handheld Pneumonia Severity Index (PSI) a valid tool to help you decide? (You can download this tool free. Also comes as part of MedRules a collection of decision tools.)
A NEJM review (and the Infectious Disease Society of America) concludes that PSI is "a rational foundation for the decision regarding hospitalization"). [Halm, Ethan A., Teirstein, Alvin S. Management of Community-Acquired Pneumonia. N Engl J Med 2002 347: 2039-2045]
Still not clear to me what percent of patients admitted with pneumoni at Good Samaritan, or elsewhere, end up with a complicated course such as empyema, post-obstructive pneumonia, bacterial resistance, etc.
While the best first step is our sitting in a chair on either side of the bed, listening to the patient, the question has come up, "Why does tradition (habit) say a doctor should examine standing on the right?"
Answer is up for grabs.
Eric has suggested that postural drainage is of no benefit in adult pneumonia, and that N-acetylcysteine is of equivocal or no benefit to thin secretions.
Another question on the table is the role of antibiotics in exacerbations of COPD. Here is a review.
Does a 62-year old carpenter with complicated pneumonia, too young for Medicare but without insurance, get help with his hospital bill?
As in our example, this 62 year-old carpenter, 80% of people who are uninsured do, in fact, work.
In Ohio the Health Care Assurance Program (HCAP) can help with his hospital bills.
"In 1992, Ohio's General Assembly passed a law that required health care providers to provide basic, medically necessary services regardless of ability to pay. This 'Free Care Requirement' affects hospitals in that hospital level care must be provided at no charge to any Ohio resident with a family income of less than the federal poverty line at the time of service. This rule can be found in the Ohio Administrative Code in section 5101:3-2-07.17 ."