Frontotemporal Dementia: A Review for Primary Care Physicians
ROBERTO CARDARELLI, DO, MPH, University of North Texas Health Science Center, Fort Worth, Texas ANDREW KERTESZ, MD, University of Western Ontario, London, Ontario, Canada JANICE A. KNEBL, DO, University of North Texas Health Science Center, Fort Worth, Texas
Am Fam Physician. 2010 Dec 1;82(11):1372-1377.
http://www.aafp.org/afp/2010/1201/p1372.pdf
Frontotemporal dementia (formally known as pick disease) is a disease which causes progressive decline in behavior and communication. It is due to atrophy of the frontal and temporal lobes of the brain. There are three categories:
behavioral variant FTD,
semantic dementia, and
progressive nonfluent aphasia.
They can be differentiated by histology. Tau-positive inclusions are more common in progressive nonfluent aphasia. Ubiquitin-positive inclusions are seen in semantic dementia. Behavioral variant FTD will contain both tau and ubiquitin inclusions. Pick bodies in inclusions are still called Pick disease.
The variations can also be determined through a good history, family history, and physical exam. In all variants, the onset is gradual and insidious, and memory is not affected (unlike in alzheimer's disease patients). Behavioral variant FTD is identified as having changes primarily in personality, leading to inappropriate social behaviors, emotional dulling, apathy, loss of insight, inappropriate sexual comments and inappropriate physical contact. Semantic dementia is characterised as having speech that is meaningless and generic. It will lack specific meaning and have semantic general terms instead of the correct words. They will also not be able to recognize familiar or famous faces (like of family or celebrities). Progressive nonfluent aphasia is characterised as having a hard time with speech. They will have hesitant, stuttering, nonfluent and agrammatic speech. They will also have anomia (problem naming objects) and agrammatism (omitting of grammatical terms). Alzheimers will present with memory and visuospatial deficits. Lewy body dementia will have memory and cognition problems, as well as visual hallucinations. Vascular dementia will present with problems with focal neurological deficit, gait problems, and changes in mood and personality.
Treatment consists mostly of SSRIs and antipsychotics, if there is aggressive behavior. Nonpharmacologic treatment includes addressing the caregivers needs, functional issues with ADLs, social stressors, counseling for the caregivers and family members, and providing education about the disease.
Thursday, September 26, 2013
Wednesday, September 25, 2013
A Review of AFPs "Hemolytic Uremic Syndrome: An Emerging Health Risk"
Hemolytic Uremic Syndrome: An Emerging Health Risk
SAMIYA RAZZAQ, M.D., University of Arkansas for Medical Sciences, College of Medicine, Little Rock, Arkansas
Am Fam Physician. 2006 Sep 15;74(6):991-996.
http://www.aafp.org/afp/2006/0915/p991.pdf
I choose to write about HUS (hemolytic uremic syndrome) because I am attending a dinner lecture on it and I thought it would be a good excuse to brush up on the topic (there is no reason to look like a fool if it can be avoided). There are two types of HUS. There is the diarrhea-positive HUS, which occurs more commonly in children and is due to an E.coli born shiga toxin. The other type is due to genetics, drugs (cyclosporine, tacrolimus, radiation), cancer, or it may be idiopathic.
The pathophysiology is not well understood. Damage to the endothelial cells are due to prothrombotic and proinflammatory states. This leads to MAHA (microangiopathic hemolytic anemia), thrombocytopenia, and renal injury (this is a triad). The E.coli O157:H7 can come from undercooked beef, unpasteurized goat's milk and apple juice, sprouts, petting zoos, contaminated lakes, or person to person contact (its a reportable disease). In the infectious type, antibiotics and antidiarrheal medications will only make it worse.
Hemolytic anemia is needed for the diagnosis. A hemoglobin at or below 6 will need a blood transfusion. Platelet transfusion will exacerbate the thrombosis and is not recommended. The microthrombi from the hemolysis will deposit in the kidneys and cause acute renal failure (or maybe you would rather me use the term acute kidney injury, but this article is from 2006, so there goes being politically correct). The CNS can can be affected and cause irritability, seizures and altered mental status. Other lab abnormalities include azotemia, decreased haptoglobin, elevated CRP, burr cells, helmet cells, leukocytosis, elevated reticulocyte count, platelet count less than 50,000, hematuria, and proteinuria.
HUS is self limiting and treatment consists of proper nutrition and close monitoring of electrolyte and volume status. Dialysis is an option for some patients. Hemoglobin and the platelet count need to be monitored regularly as well. Diarrhea associated HUS has a very good prognosis. The other type has a poor prognosis , with incomplete recovery and a 10% mortality rate.
SAMIYA RAZZAQ, M.D., University of Arkansas for Medical Sciences, College of Medicine, Little Rock, Arkansas
Am Fam Physician. 2006 Sep 15;74(6):991-996.
http://www.aafp.org/afp/2006/0915/p991.pdf
I choose to write about HUS (hemolytic uremic syndrome) because I am attending a dinner lecture on it and I thought it would be a good excuse to brush up on the topic (there is no reason to look like a fool if it can be avoided). There are two types of HUS. There is the diarrhea-positive HUS, which occurs more commonly in children and is due to an E.coli born shiga toxin. The other type is due to genetics, drugs (cyclosporine, tacrolimus, radiation), cancer, or it may be idiopathic.
The pathophysiology is not well understood. Damage to the endothelial cells are due to prothrombotic and proinflammatory states. This leads to MAHA (microangiopathic hemolytic anemia), thrombocytopenia, and renal injury (this is a triad). The E.coli O157:H7 can come from undercooked beef, unpasteurized goat's milk and apple juice, sprouts, petting zoos, contaminated lakes, or person to person contact (its a reportable disease). In the infectious type, antibiotics and antidiarrheal medications will only make it worse.
Hemolytic anemia is needed for the diagnosis. A hemoglobin at or below 6 will need a blood transfusion. Platelet transfusion will exacerbate the thrombosis and is not recommended. The microthrombi from the hemolysis will deposit in the kidneys and cause acute renal failure (or maybe you would rather me use the term acute kidney injury, but this article is from 2006, so there goes being politically correct). The CNS can can be affected and cause irritability, seizures and altered mental status. Other lab abnormalities include azotemia, decreased haptoglobin, elevated CRP, burr cells, helmet cells, leukocytosis, elevated reticulocyte count, platelet count less than 50,000, hematuria, and proteinuria.
HUS is self limiting and treatment consists of proper nutrition and close monitoring of electrolyte and volume status. Dialysis is an option for some patients. Hemoglobin and the platelet count need to be monitored regularly as well. Diarrhea associated HUS has a very good prognosis. The other type has a poor prognosis , with incomplete recovery and a 10% mortality rate.
Tuesday, September 24, 2013
A Synopsis of AFPs "Acute Lumbar Disk Pain: Navigating Evaluation and Treatment Choices"
Acute Lumbar Disk Pain: Navigating Evaluation and Treatment Choices
DAVID S. GREGORY, MD; CRAIG K. SETO, MD; GEORGE C. WORTLEY, MD; and CHRISTINE M. SHUGART, MD, Lynchburg Family Medicine Residency, Lynchburg, Virginia, and University of Virginia, Charlottesville, Virginia
Am Fam Physician. 2008 Oct 1;78(7):835-842.
http://www.aafp.org/afp/2008/1001/p835.pdf
Low back pain is the leading cause of missing time at work and it is the most common reason that patients go to the doctor. Low back pain that radiates down the thigh and leg is known as sciatica. Patients who complain of this must first look for any red flags, which include saddle anesthesia, urinary retention, fecal incontinence, unexplained fever, chronic steroid use, history of cancer, IVDA, and focal neurological deficits. The most common cause of sciatica (in patients without red flag symptoms) is lumbar disk herniation. A full neurological exam needs to be completed including a straight leg raise test. Disk herniation can usually resolve with conservative management, which includes NSAIDs, acetaminophen, muscle relaxants, and opioids.
Sciatica will present with a dermatomal pattern, depending on the level of involvement. A disk herniation at the L3/L4 level with affect the patellar reflex. The patient will have difficulty with ankle dorsiflexion and sensory loss along the medial malleolus and medial foot. A disk herniation at the L4/L5 level will cause difficulty with great toe dorsiflexion and sensory loss at the dorsal third MTP joint. A herniation at the L5/S1 disk will affect the achilles reflex and cause motor issues with ankle plantar flexion. Neurological symptoms will present as pain, numbness and a cold sensation. A late finding may also be calf muscle wasting.
Imaging is not always required and the findings on MRI do not usually correlate with the neurological findings. If there are not red flags, then conservative management will be implemented. If there are red flags then then imaging will be done. If the imaging correlates with the symptoms, then the patient can be referred to surgery. If the patient is on conservative management for two weeks and there is still severe pain, then the patient can be referred for epidural steriod injections. Otherwise, the patient can continue conservative management and supplement it with physical therapy and manipulation. If there is no change after six weeks then imaging should be considered. Bed rest should be discouraged because it may lead to muscle deconditioning.
Physical therapy and manipulation do not have high quality studies but it does appear to have benefit in pain relief. The is no long term benefit in disease outcome. The same goes with surgery where the patient does not have any long term benefit after two years.
DAVID S. GREGORY, MD; CRAIG K. SETO, MD; GEORGE C. WORTLEY, MD; and CHRISTINE M. SHUGART, MD, Lynchburg Family Medicine Residency, Lynchburg, Virginia, and University of Virginia, Charlottesville, Virginia
Am Fam Physician. 2008 Oct 1;78(7):835-842.
http://www.aafp.org/afp/2008/1001/p835.pdf
Low back pain is the leading cause of missing time at work and it is the most common reason that patients go to the doctor. Low back pain that radiates down the thigh and leg is known as sciatica. Patients who complain of this must first look for any red flags, which include saddle anesthesia, urinary retention, fecal incontinence, unexplained fever, chronic steroid use, history of cancer, IVDA, and focal neurological deficits. The most common cause of sciatica (in patients without red flag symptoms) is lumbar disk herniation. A full neurological exam needs to be completed including a straight leg raise test. Disk herniation can usually resolve with conservative management, which includes NSAIDs, acetaminophen, muscle relaxants, and opioids.
Sciatica will present with a dermatomal pattern, depending on the level of involvement. A disk herniation at the L3/L4 level with affect the patellar reflex. The patient will have difficulty with ankle dorsiflexion and sensory loss along the medial malleolus and medial foot. A disk herniation at the L4/L5 level will cause difficulty with great toe dorsiflexion and sensory loss at the dorsal third MTP joint. A herniation at the L5/S1 disk will affect the achilles reflex and cause motor issues with ankle plantar flexion. Neurological symptoms will present as pain, numbness and a cold sensation. A late finding may also be calf muscle wasting.
Imaging is not always required and the findings on MRI do not usually correlate with the neurological findings. If there are not red flags, then conservative management will be implemented. If there are red flags then then imaging will be done. If the imaging correlates with the symptoms, then the patient can be referred to surgery. If the patient is on conservative management for two weeks and there is still severe pain, then the patient can be referred for epidural steriod injections. Otherwise, the patient can continue conservative management and supplement it with physical therapy and manipulation. If there is no change after six weeks then imaging should be considered. Bed rest should be discouraged because it may lead to muscle deconditioning.
Physical therapy and manipulation do not have high quality studies but it does appear to have benefit in pain relief. The is no long term benefit in disease outcome. The same goes with surgery where the patient does not have any long term benefit after two years.
Monday, September 23, 2013
A Synopsis of AFP's "Management of Head and Neck Injuries by the Sideline Physician"
Management of Head and Neck Injuries by the Sideline Physician
JOHN W. WHITESIDE, M.D., Mayo Clinic, Scottsdale, Arizona
Am Fam Physician. 2006 Oct 15;74(8):1357-1364.
http://www.aafp.org/afp/2006/1015/p1357.pdf
A sideline physician must be well trained in detecting and managing sports injuries. This article focuses on concussions and head injuries. It is important to document the time of injury and how long symptoms and loss of consciousness lasts.
The neck should be evaluated in a certain order and if any of the tests are positive, then the testing can stop and the patient's neck needs to be immobilized. The patient should first be assessed for a loss of consciousness. If the patient is unconscious, then ACLS should be implemented. If the patient is suspected to have neck instability, it is important not to move the neck. Helmet and shoulder pads should be kept on. The patient should be immobilized and put on a backboard.
The next step is to assess the patients peripheral strength and sensations. The clinician should evaluate the paraspinal muscles and document any symmetrical spasm and tenderness. The patients isotonic neck strength should be evaluated. The neck should not be moved during this part of the test. Then, the active range of motion of the neck can be assessed. Next, the Spurling test, which compresses the cervical foramina is done. Pain or radiculopathy is a positive sign. If the test is negative, then the clinician can evaluate the patients neurological status. Questions should be asked to assess orientation and recent memory. A list of questions that may be asked include;
Where are we playing?
Who are we playing against?
How far into the game are we?
What is the score, who is winning, and who scored last?
Who did we play last week and who won?
Postural stability can be assessed with the balance error scoring system. The test is conducted by having the patient stand on either the ground or foam, while having his or her eyes closed. The patient is instructed to either stand with both feet side by side, one in front of the other, or with one foot in the air. Hands can be placed on the waist. Positive signs of balancing errors are stumbling, opening eyes, moving hands from waist, or moving out of testing position. A patient with usually make at least 12 errors after a concussion. The last step is to ask about symptoms such as headaches, nausea, dizziness, and blurred vision.
Sometimes the patient will complain of a "burner" or "stinger". This is described as a short period of weakness or numbness along the C5/C6 dermatome. They are unilateral and are not associated with any weakness or range of motion problems. Patients can usually return to play if the symptoms resolve quickly.
A concussion is defined as a quick, transient impairment of neural function after trauma to the brainstem. Symptoms include alterations in memory, blurred vision, fatigue, headache, coordination problems, loss of consciousness, nausea, vomiting, tinnitus, and sleep problems. Assessing for concussion is a little easier than for assessing the neck. The four steps are
1. asses for loss of consciousness
2. ask about symptoms
3. evaluate recent memory
4. evaluate postural stability.
According to the American Academy of Neurology Guidelines, there are three grades of concussion. Grade 1 has no loss of consciousness, transient confusion, and concussion symptoms lasting less than 15 minutes. These patient should be pulled out of the game and evaluated every 5 minutes on the sideline. They can return to play if they are symptom free for 15 minutes. If they get another grade 1, they should be held out for one week. A grade 2 concussion will present with symptoms lasting longer than 15 minutes. The patient should be pulled from the game for the day. The patient should be evaluated that day as well as the next day. The patient can return to play if asymptomatic for one day. Imaging can be done if the symptoms persist beyond a week. If the patient has a repeat grade 2 concussion, he or she cannot return until asymptomatic for two weeks. Any patient with loss of consciousness is considered to have a grade 3 concussion. These patients should be transported to the hospital if the loss of consciousness is prolonged, if there is persistent confusion. or if the neurological exam is abnormal. Imaging can be done if the patient is symptomatic beyond a week. The patient can return to play after 2 weeks of being symptom free. If the patient gets a second grade 3 concussion, they need to sit out for a month.
JOHN W. WHITESIDE, M.D., Mayo Clinic, Scottsdale, Arizona
Am Fam Physician. 2006 Oct 15;74(8):1357-1364.
http://www.aafp.org/afp/2006/1015/p1357.pdf
A sideline physician must be well trained in detecting and managing sports injuries. This article focuses on concussions and head injuries. It is important to document the time of injury and how long symptoms and loss of consciousness lasts.
The neck should be evaluated in a certain order and if any of the tests are positive, then the testing can stop and the patient's neck needs to be immobilized. The patient should first be assessed for a loss of consciousness. If the patient is unconscious, then ACLS should be implemented. If the patient is suspected to have neck instability, it is important not to move the neck. Helmet and shoulder pads should be kept on. The patient should be immobilized and put on a backboard.
The next step is to assess the patients peripheral strength and sensations. The clinician should evaluate the paraspinal muscles and document any symmetrical spasm and tenderness. The patients isotonic neck strength should be evaluated. The neck should not be moved during this part of the test. Then, the active range of motion of the neck can be assessed. Next, the Spurling test, which compresses the cervical foramina is done. Pain or radiculopathy is a positive sign. If the test is negative, then the clinician can evaluate the patients neurological status. Questions should be asked to assess orientation and recent memory. A list of questions that may be asked include;
Where are we playing?
Who are we playing against?
How far into the game are we?
What is the score, who is winning, and who scored last?
Who did we play last week and who won?
Postural stability can be assessed with the balance error scoring system. The test is conducted by having the patient stand on either the ground or foam, while having his or her eyes closed. The patient is instructed to either stand with both feet side by side, one in front of the other, or with one foot in the air. Hands can be placed on the waist. Positive signs of balancing errors are stumbling, opening eyes, moving hands from waist, or moving out of testing position. A patient with usually make at least 12 errors after a concussion. The last step is to ask about symptoms such as headaches, nausea, dizziness, and blurred vision.
Sometimes the patient will complain of a "burner" or "stinger". This is described as a short period of weakness or numbness along the C5/C6 dermatome. They are unilateral and are not associated with any weakness or range of motion problems. Patients can usually return to play if the symptoms resolve quickly.
A concussion is defined as a quick, transient impairment of neural function after trauma to the brainstem. Symptoms include alterations in memory, blurred vision, fatigue, headache, coordination problems, loss of consciousness, nausea, vomiting, tinnitus, and sleep problems. Assessing for concussion is a little easier than for assessing the neck. The four steps are
1. asses for loss of consciousness
2. ask about symptoms
3. evaluate recent memory
4. evaluate postural stability.
According to the American Academy of Neurology Guidelines, there are three grades of concussion. Grade 1 has no loss of consciousness, transient confusion, and concussion symptoms lasting less than 15 minutes. These patient should be pulled out of the game and evaluated every 5 minutes on the sideline. They can return to play if they are symptom free for 15 minutes. If they get another grade 1, they should be held out for one week. A grade 2 concussion will present with symptoms lasting longer than 15 minutes. The patient should be pulled from the game for the day. The patient should be evaluated that day as well as the next day. The patient can return to play if asymptomatic for one day. Imaging can be done if the symptoms persist beyond a week. If the patient has a repeat grade 2 concussion, he or she cannot return until asymptomatic for two weeks. Any patient with loss of consciousness is considered to have a grade 3 concussion. These patients should be transported to the hospital if the loss of consciousness is prolonged, if there is persistent confusion. or if the neurological exam is abnormal. Imaging can be done if the patient is symptomatic beyond a week. The patient can return to play after 2 weeks of being symptom free. If the patient gets a second grade 3 concussion, they need to sit out for a month.
Thursday, September 19, 2013
A Synopsis of AFP's "When to Order Contrast-Enhanced CT"
When to Order Contrast-Enhanced CT
JAMES V. RAWSON, MD, and ALLEN L. PELLETIER, MD, Medical College of Georgia at Georgia Health Sciences University, Augusta, Georgia
Am Fam Physician. 2013 Sep 1;88(5):312-316.
http://www.aafp.org/afp/2013/0901/p312.pdf
CT imaging is a common test ordered these days. The two contrast agents usually used are barium and iodine. They can be given orally, rectally, or IV. Oral is used to check out the bowel. Iodine contrast is water based and is also given orally. It is not nephrogenic, but may rarely cause an aspiration-induced pulmonary edema (this risk can be minimized if the contrast is given through an NGT). Rectal contrast is used if the clinician suspects that there is a penetrating colonic injury. Intrathecal contrast is used in patients with possible CSF leaks and spinal/ cisternal disease.
IV contrast is used if the clinician wants to look at vascular structures, abdominal, and pelvic organs. Nonionic contrast has a lower rate of adverse reactions, such as asthma and drug allergies. Although patients are always asked if they are allergic to shellfish before getting iodine contrast, there is no cross-reactivity between the two. Patients who have had a previous anaphylactic reaction (to anything) are at higher risk for a reaction to the contrast. A mild reaction need only be observed. A moderate reaction may need prompt treatment. A severe reaction may require rapid intervention and/or hospitalization. Patients with previous minor reactions may only need pretreatment with steroids and benadryl.
Patients with renal insufficiency should have their creatinine checked. Those with measurements above 1.5-2 mg/dL, or those with a level that is going up, should be considered for an alternate form of contrast. Patients with normal renal function do not need their creatinine checked.
Iodine contrast can cross the placenta and although it has not shown to cause any teratogenic or mutagenic effects, it should only be used when the results will affect the care of the fetus, or when the test cannot wait until after the pregnancy (and if other contrast/ imaging is inappropriate).
Patients who are being treated for thyroid disease with iodine 131 should not have iodine contrast because it will make the treatment ineffective. The contrast should be given two months prior to the thyroid treatment, otherwise a endocrinologist referral is warranted.
Patients who are on metformin who receive IV contrast will have an increased risk of metabolic acidosis because of the impaired metformin clearance. Patients on metformin with no renal impairment do not need to have their creatinine checked and can continue the contrast with the metformin. Patients with normal renal function but at least one comorbid condition should stop the metformin when the contrast is given. The metformin can be resumed after 48 hours as long as the patient is clinically stable. Creatinine does not need to be rechecked. Patients with known renal dysfunction should have the metformin stopped and it should be resumed only after the renal status have been reevaluated. High risk populations may be given sodium bicarbonate, hydration, acetylcysteine and smaller contrast volume to reduce risk.
Non-contrast CT can be used in patients with suspected acute stroke, closed head injury, lung disease, chronic dyspnea, soft tissue swelling, infection, trauma, kidney stones, and spinal trauma. Contrast enhanced CT is indicated for acute appendicitis, cancer staging, diverticulitis, pancreatitis, and pulmonary embolism.
JAMES V. RAWSON, MD, and ALLEN L. PELLETIER, MD, Medical College of Georgia at Georgia Health Sciences University, Augusta, Georgia
Am Fam Physician. 2013 Sep 1;88(5):312-316.
http://www.aafp.org/afp/2013/0901/p312.pdf
CT imaging is a common test ordered these days. The two contrast agents usually used are barium and iodine. They can be given orally, rectally, or IV. Oral is used to check out the bowel. Iodine contrast is water based and is also given orally. It is not nephrogenic, but may rarely cause an aspiration-induced pulmonary edema (this risk can be minimized if the contrast is given through an NGT). Rectal contrast is used if the clinician suspects that there is a penetrating colonic injury. Intrathecal contrast is used in patients with possible CSF leaks and spinal/ cisternal disease.
IV contrast is used if the clinician wants to look at vascular structures, abdominal, and pelvic organs. Nonionic contrast has a lower rate of adverse reactions, such as asthma and drug allergies. Although patients are always asked if they are allergic to shellfish before getting iodine contrast, there is no cross-reactivity between the two. Patients who have had a previous anaphylactic reaction (to anything) are at higher risk for a reaction to the contrast. A mild reaction need only be observed. A moderate reaction may need prompt treatment. A severe reaction may require rapid intervention and/or hospitalization. Patients with previous minor reactions may only need pretreatment with steroids and benadryl.
Patients with renal insufficiency should have their creatinine checked. Those with measurements above 1.5-2 mg/dL, or those with a level that is going up, should be considered for an alternate form of contrast. Patients with normal renal function do not need their creatinine checked.
Iodine contrast can cross the placenta and although it has not shown to cause any teratogenic or mutagenic effects, it should only be used when the results will affect the care of the fetus, or when the test cannot wait until after the pregnancy (and if other contrast/ imaging is inappropriate).
Patients who are being treated for thyroid disease with iodine 131 should not have iodine contrast because it will make the treatment ineffective. The contrast should be given two months prior to the thyroid treatment, otherwise a endocrinologist referral is warranted.
Patients who are on metformin who receive IV contrast will have an increased risk of metabolic acidosis because of the impaired metformin clearance. Patients on metformin with no renal impairment do not need to have their creatinine checked and can continue the contrast with the metformin. Patients with normal renal function but at least one comorbid condition should stop the metformin when the contrast is given. The metformin can be resumed after 48 hours as long as the patient is clinically stable. Creatinine does not need to be rechecked. Patients with known renal dysfunction should have the metformin stopped and it should be resumed only after the renal status have been reevaluated. High risk populations may be given sodium bicarbonate, hydration, acetylcysteine and smaller contrast volume to reduce risk.
Non-contrast CT can be used in patients with suspected acute stroke, closed head injury, lung disease, chronic dyspnea, soft tissue swelling, infection, trauma, kidney stones, and spinal trauma. Contrast enhanced CT is indicated for acute appendicitis, cancer staging, diverticulitis, pancreatitis, and pulmonary embolism.
Tuesday, September 17, 2013
A Synopsis or AFPs "Evaluation of Nausea and Vomiting in Adults: A Case-Based Approach"
Evaluation of Nausea and Vomiting in Adults: A Case-Based Approach
WILLIAM D. ANDERSON, III, MD, and SCOTT M. STRAYER, MD, MPH, University of South Carolina School of Medicine, Columbia, South Carolina
Am Fam Physician. 2013 Sep 15;88(6):371-379.
http://www.aafp.org/afp/2013/0915/p371.pdf
Nausea and vomiting is a very common symptom with a wide differential. The clinical presentation can hint towards the diagnosis. The differential is extremely large, but the most common cause is viral, norovirus in adults. If the presentation is acute, then it may suggest cholecystitis, gastroenteritis, medication side effects, or pancreatitis. A viral gastroenteritis may also be associated with diarrhea, headaches and myalgia. Bilious vomiting may be due to a small bowel obstruction. Feculent or foul smelling vomit may be due to an intestinal obstruction. A gastric outlet obstruction may have non-bilious vomiting of partially digest food. It can also be due to achalasia, esophageal stricture, or a diverticulum. Projectile vomiting may be due to an intracranial disorder. It is important to assess the patient's' vital signs and hydration status to quantify the severity of the illness.
When evaluating nausea and vomiting, the illness can be divided by length of symptoms into acute (less than a week) and chronic (more than a month). If there is an obvious cause (based on history and physical), then it should be treated. If it is not obvious, then it must be determined if the patient has any of the alarm signs, which include;
age above 55 years,
unintentional weight loss,
progressive dysphagia,
persistent vomiting,
GI bleeding,
family history of GI cancer,
altered mental status,
abdominal pain,
feculent vomiting,
hematochezia,
melena, and
focal neurological deficit.
If any of these warning signs are present, then a battery of labs need to be ordered, including UA, pregnancy test, CBC, CMP, lipase, TSH, stool studies, abdominal imaging, EGD, and possibly a head CT (if an intracranial issue is suspected). If there are no alarm signs and the symptoms are acute, then the clinician will give supportive care and provide reassurance and education. If the symptoms are chronic, then the clinician may consider a gastric emptying study if gastroparesis is suspected. Psychiatric causes can also be considered.
Imagining is very helpful in the evaluation of nausea and vomiting. X rays are good for bowel obstruction and kidney stones. CT can also find stones and obstruction, as well as infectious inflammation, such a appendicitis and cholecystitis. A patient with appendicitis may also need a ultrasound. Patients with cholecystitis may need a HIDA scan if the gallbladder cannot be visualized with ultrasound. Patients suspected of H. pylori can get a urea breath test and an serum immunoglobulin G level. The labs ordered for pancreatitis are amylase (>300 U/L), lipase (>135 ukat/L), and alanine transaminase.
Migraines are a common cause of nausea and vomiting. The patient should have a headache with at least four of the following characteristics; pulsatile, unilateral, disabling, lasting 4-72 hours, and nausea and vomiting. These patients may also need a head CT to rule out intracranial pathology.
The mainstay of management is supportive treatment, such as avoiding triggers, rehydration, and antiemetics. Patients with BPPV may benefit from meclizine. Those with gastroenteritis can use ondansetron or promethazine. GERD patients can have H2 blockers or PPIs. Erythromycin and metoclopramide can help patients with gastroparesis. Management of migraines can be done with NSAIDs, metoclopramide, and prochlorperazine. Motion sickness can be prevented with antihistamines and scopolamine. Symptoms associated with pregnancy can be treated with doxylamine, ginger and B6.
WILLIAM D. ANDERSON, III, MD, and SCOTT M. STRAYER, MD, MPH, University of South Carolina School of Medicine, Columbia, South Carolina
Am Fam Physician. 2013 Sep 15;88(6):371-379.
http://www.aafp.org/afp/2013/0915/p371.pdf
Nausea and vomiting is a very common symptom with a wide differential. The clinical presentation can hint towards the diagnosis. The differential is extremely large, but the most common cause is viral, norovirus in adults. If the presentation is acute, then it may suggest cholecystitis, gastroenteritis, medication side effects, or pancreatitis. A viral gastroenteritis may also be associated with diarrhea, headaches and myalgia. Bilious vomiting may be due to a small bowel obstruction. Feculent or foul smelling vomit may be due to an intestinal obstruction. A gastric outlet obstruction may have non-bilious vomiting of partially digest food. It can also be due to achalasia, esophageal stricture, or a diverticulum. Projectile vomiting may be due to an intracranial disorder. It is important to assess the patient's' vital signs and hydration status to quantify the severity of the illness.
When evaluating nausea and vomiting, the illness can be divided by length of symptoms into acute (less than a week) and chronic (more than a month). If there is an obvious cause (based on history and physical), then it should be treated. If it is not obvious, then it must be determined if the patient has any of the alarm signs, which include;
age above 55 years,
unintentional weight loss,
progressive dysphagia,
persistent vomiting,
GI bleeding,
family history of GI cancer,
altered mental status,
abdominal pain,
feculent vomiting,
hematochezia,
melena, and
focal neurological deficit.
If any of these warning signs are present, then a battery of labs need to be ordered, including UA, pregnancy test, CBC, CMP, lipase, TSH, stool studies, abdominal imaging, EGD, and possibly a head CT (if an intracranial issue is suspected). If there are no alarm signs and the symptoms are acute, then the clinician will give supportive care and provide reassurance and education. If the symptoms are chronic, then the clinician may consider a gastric emptying study if gastroparesis is suspected. Psychiatric causes can also be considered.
Imagining is very helpful in the evaluation of nausea and vomiting. X rays are good for bowel obstruction and kidney stones. CT can also find stones and obstruction, as well as infectious inflammation, such a appendicitis and cholecystitis. A patient with appendicitis may also need a ultrasound. Patients with cholecystitis may need a HIDA scan if the gallbladder cannot be visualized with ultrasound. Patients suspected of H. pylori can get a urea breath test and an serum immunoglobulin G level. The labs ordered for pancreatitis are amylase (>300 U/L), lipase (>135 ukat/L), and alanine transaminase.
Migraines are a common cause of nausea and vomiting. The patient should have a headache with at least four of the following characteristics; pulsatile, unilateral, disabling, lasting 4-72 hours, and nausea and vomiting. These patients may also need a head CT to rule out intracranial pathology.
The mainstay of management is supportive treatment, such as avoiding triggers, rehydration, and antiemetics. Patients with BPPV may benefit from meclizine. Those with gastroenteritis can use ondansetron or promethazine. GERD patients can have H2 blockers or PPIs. Erythromycin and metoclopramide can help patients with gastroparesis. Management of migraines can be done with NSAIDs, metoclopramide, and prochlorperazine. Motion sickness can be prevented with antihistamines and scopolamine. Symptoms associated with pregnancy can be treated with doxylamine, ginger and B6.
Monday, September 16, 2013
A Synopsis of AFPs "Functional Decline in Older Adults"
Functional Decline in Older Adults
CATHLEEN S. COLÓN-EMERIC, MD, MHS; HEATHER E. WHITSON, MD, MHS; JULIESSA PAVON, MD; and HELEN HOENIG, MD, Duke University Medical Center, Durham, North Carolina
Am Fam Physician. 2013 Sep 15;88(6):388-394.
http://www.aafp.org/afp/2013/0915/p388.pdf
Functional decline is the progressive inability to carry out activities of daily living. It increases with age. It is a dynamic and episodic disability due to chronic diseases, such as diabetes, dementia, cancer, obesity, vision, hearing, and other disorders. For example, heart disease may affect aerobic activities, and a stroke may affect activities of limbs use. Synergistic effects of multiple chronic conditions is also an important factor to consider in functional decline.
Evaluating new functional decline begins with characterizing the disability. It is necessary to find out the the time course, the associated symptoms, the compensatory strategies, and the effect the disability has on specific activities. Identifying the underlying health disorders is another part of the evaluation. The focus of the physical examination can be driven by the organ system that is affected. Identifying impairments and screening for impairments, such as mood disorders, cognitive impairments, nutrition, pain, medication side effects, and gait disorders is the next step. There are multiple tools and tests that can be done. Having the patient clasp his or her hands behind his or her neck can assess the ability for a patient to use their shoulders for ADLs, such as dressing and bathing. Having the patient get up out if a chair without using his or her arms can assess the patient's' leg strength and assess their ability to use the toilet or bathe. The get up and go test is a similar test that tests lower extremities, as well as gross motor coordination. Having a patient pick up a penny from the floor cans assess fine motor coordination, pinch strength, balance and vision. Common sensory tests include the whisper test and using a snellen eye chart. The clock drawing test can assess executive function. Common questions that you can ask the patient include (these I copied out of the article)
"Do you have trouble with stairs?"
"Are you confidently able to shower, bathe or use the toilet?"
"Who would be able to help you if you needed it?"
Other important factors include assessing social support, financial resources and environmental factors should be addressed.
Treatment of functional decline includes increasing the patients ability and reducing demands. This includes exercise, proper diet, oxygen supplementation, assistive devices (wheelchair, hearing aid, raised toilet seat or cane), referrals for adjunctive care (PT, OT, social worker,etc) and medical intervention (cataract surgery, more appropriate medication). A multifocal approach is effective and proven to improve function and quality of life.
CATHLEEN S. COLÓN-EMERIC, MD, MHS; HEATHER E. WHITSON, MD, MHS; JULIESSA PAVON, MD; and HELEN HOENIG, MD, Duke University Medical Center, Durham, North Carolina
Am Fam Physician. 2013 Sep 15;88(6):388-394.
http://www.aafp.org/afp/2013/0915/p388.pdf
Evaluating new functional decline begins with characterizing the disability. It is necessary to find out the the time course, the associated symptoms, the compensatory strategies, and the effect the disability has on specific activities. Identifying the underlying health disorders is another part of the evaluation. The focus of the physical examination can be driven by the organ system that is affected. Identifying impairments and screening for impairments, such as mood disorders, cognitive impairments, nutrition, pain, medication side effects, and gait disorders is the next step. There are multiple tools and tests that can be done. Having the patient clasp his or her hands behind his or her neck can assess the ability for a patient to use their shoulders for ADLs, such as dressing and bathing. Having the patient get up out if a chair without using his or her arms can assess the patient's' leg strength and assess their ability to use the toilet or bathe. The get up and go test is a similar test that tests lower extremities, as well as gross motor coordination. Having a patient pick up a penny from the floor cans assess fine motor coordination, pinch strength, balance and vision. Common sensory tests include the whisper test and using a snellen eye chart. The clock drawing test can assess executive function. Common questions that you can ask the patient include (these I copied out of the article)
"Do you have trouble with stairs?"
"Are you confidently able to shower, bathe or use the toilet?"
"Who would be able to help you if you needed it?"
Other important factors include assessing social support, financial resources and environmental factors should be addressed.
Treatment of functional decline includes increasing the patients ability and reducing demands. This includes exercise, proper diet, oxygen supplementation, assistive devices (wheelchair, hearing aid, raised toilet seat or cane), referrals for adjunctive care (PT, OT, social worker,etc) and medical intervention (cataract surgery, more appropriate medication). A multifocal approach is effective and proven to improve function and quality of life.
Friday, September 13, 2013
A Synopsis of AFP's "Diagnosis and Management of Acute Interstitial Nephritis"
Diagnosis and Management of Acute Interstitial Nephritis
CHARLES M. KODNER, M.D., and ARCHANA KUDRIMOTI, M.D. University of Louisville School of Medicine, Louisville, Kentucky
Am Fam Physician. 2003 Jun 15;67(12):2527-2534.
http://www.aafp.org/afp/2003/0615/p2527.pdf
Acute interstitial nephritis (AIN) is acute renal failure with inflammation of the interstitium and renal tubules. AIN is due to one of three causes; drug-induced, infection, and immune/ neoplasia. There is a wide spectrum of drugs that can cause AIN, including antibiotics, NSAIDs, antivirals, omeprazole, sulfa drugs, ranitidine, captopril, furosemide, thiazides, and many, many more. The side effects may not appear for up to two weeks. It is also not dose dependent. Infections that cause AIN include acute bacterial pyelonephritis, renal TB, and fungal nephritis. Systemic infections can indirectly cause AIN by lowering cell mediated immunity (HIV, sarcoid, lead exposure). Immune disoirders responsible for AIN include sjogren's, SLE, and wegeners.
AIN is caused when inflammatory cells invade the interstitium, leading to edema . Patchy or diffuse fibrosis will occur in the cortex and medullocortical junction. AIN presents with nonspecific features such as oliguria, anorexia, malaise, fever, rash, nausea and vomiting. The pathology varies widely depending on which drug has caused the problem. Immune-induced AIN is due to granuloma formation with epithelioid giant cells. Lab studies are generally nonspecific and variable. An elevated creatinine and BUN represent a rapid deterioration of renal function. The renal biopsy is the definitive diagnosis. A positive biopsy will show patchy plasma and lymphocytic infiltration in the peritubular area. Poor prognostic factors on biopsy include diffuse inflammation, neutrophilia, and excessive interstitial fibrosis.
When AIN is suspected, the first step is to stop the offending medication. If this leads to clinical improvement, then the patient is managed with supportive care. If the patient does not show clinical improvement, then a biopsy can be done. If there is a contraindication to biopsy, a renal ultrasound or gallium scan can be considered. If the patient is positive for AIN on biopsy, and their is no fibrosis, steroids can be started. If the steroids do not improve renal function, then they can be discontinued and supportive therapy can be started. Supportive therapy includes fluid and electrolyte management, symptomatic relief of fever and rash, and avoiding dangerous drugs. Immunosuppressive therapy is another option if warranted. Uncontrolled hyperkalemia, azotemia, mental status changes, and fluid/ electrolyte issues are indications for dialysis.
Most patients will recover in a weeks after discontinuing the medication. There is initial rapid phase of recovery lasting up to 8 weeks and a slow phase which may last up to a year.
CHARLES M. KODNER, M.D., and ARCHANA KUDRIMOTI, M.D. University of Louisville School of Medicine, Louisville, Kentucky
Am Fam Physician. 2003 Jun 15;67(12):2527-2534.
http://www.aafp.org/afp/2003/0615/p2527.pdf
Acute interstitial nephritis (AIN) is acute renal failure with inflammation of the interstitium and renal tubules. AIN is due to one of three causes; drug-induced, infection, and immune/ neoplasia. There is a wide spectrum of drugs that can cause AIN, including antibiotics, NSAIDs, antivirals, omeprazole, sulfa drugs, ranitidine, captopril, furosemide, thiazides, and many, many more. The side effects may not appear for up to two weeks. It is also not dose dependent. Infections that cause AIN include acute bacterial pyelonephritis, renal TB, and fungal nephritis. Systemic infections can indirectly cause AIN by lowering cell mediated immunity (HIV, sarcoid, lead exposure). Immune disoirders responsible for AIN include sjogren's, SLE, and wegeners.
AIN is caused when inflammatory cells invade the interstitium, leading to edema . Patchy or diffuse fibrosis will occur in the cortex and medullocortical junction. AIN presents with nonspecific features such as oliguria, anorexia, malaise, fever, rash, nausea and vomiting. The pathology varies widely depending on which drug has caused the problem. Immune-induced AIN is due to granuloma formation with epithelioid giant cells. Lab studies are generally nonspecific and variable. An elevated creatinine and BUN represent a rapid deterioration of renal function. The renal biopsy is the definitive diagnosis. A positive biopsy will show patchy plasma and lymphocytic infiltration in the peritubular area. Poor prognostic factors on biopsy include diffuse inflammation, neutrophilia, and excessive interstitial fibrosis.
When AIN is suspected, the first step is to stop the offending medication. If this leads to clinical improvement, then the patient is managed with supportive care. If the patient does not show clinical improvement, then a biopsy can be done. If there is a contraindication to biopsy, a renal ultrasound or gallium scan can be considered. If the patient is positive for AIN on biopsy, and their is no fibrosis, steroids can be started. If the steroids do not improve renal function, then they can be discontinued and supportive therapy can be started. Supportive therapy includes fluid and electrolyte management, symptomatic relief of fever and rash, and avoiding dangerous drugs. Immunosuppressive therapy is another option if warranted. Uncontrolled hyperkalemia, azotemia, mental status changes, and fluid/ electrolyte issues are indications for dialysis.
Most patients will recover in a weeks after discontinuing the medication. There is initial rapid phase of recovery lasting up to 8 weeks and a slow phase which may last up to a year.
Thursday, September 12, 2013
A Brief Synopsis of AFPs "Polymyalgia Rheumatica and Giant Cell Arteritis"
Polymyalgia Rheumatica and Giant Cell Arteritis
BRIAN UNWIN, COL, MC, USA, CYNTHIA M. WILLIAMS, CAPT (R), MC, USN, and
WILLIAM GILLILAND, COL, MC, USA, Uniformed Services University of the Health Sciences, Bethesda, Maryland
http://www.aafp.org/afp/2006/1101/p1547.pdf
Am Fam Physician. 2006 Nov 1;74(9):1547-1554.
Giant cell arteritis (CGA) and polymyalgia rheumatica (PMR) are very similar inflammatory vascular disorders and oftentimes, patients end up with both. CGA usually presents with temporal pain, headache and vision problems. PMR presents with pain and stiffness in the girdle (hip and shoulder) muscles. Both are more common in patients over 50 years old. Findings associated with PMR include age over 50 years, ESR above 50 mm/hr, mild anemia, pain with morning stiffness of the proximal muscles, and inflammatory symptoms (fever, night sweats, weight loss, anorexia, and depression). Other symptoms include asymmetric wrist and knee arthritis, hand and feet swelling, carpal tunnel syndrome, shoulder/ hip bursitis, and extremity tenderness. Findings associated with GCA include age over 50 years, ESR above 50 mm/hr, anemia, headache, jaw claudication, PMR, arthralgia, visual problems, inflammatory symptoms, and an abnormal temporal artery. The patient may present with a low grade fever and a red, tender, thickened, nodular, or pulseless temporal artery. A detailed vision exam, joint exam, and temporal artery biopsy should be considered. Steroid treatment should not be delayed in lieu of lab work or biopsy. Ultrasound may help determine the best section of the artery for biopsy. The differential diagnosis for GCA and PMR includes fibromyalgia, multiple myeloma, OA, RA, and polymyositis. A negative ESR will usually rule out CGA (and PMR). Corticosteroid use will give a falsely low ESR. A rough estimate of a normal ESR is the patients age divided by 2 (then add 5 if it is a woman). Other lab abnormalities include elevated CRP, thrombocytopenia, elevated LFTs, and microscopic hematuria. Treatment consists or prednisone. PMR requires low dose steroids for 2-4 week after the disease symptoms resolve, followed by a slow taper (lower the dose by 1 mg/day each week). A disease activity score has been developed for PMR to help monitor and adjust therapy. The five variables are;A visual analog pain scaleA visual analog scale for the physician's assessmentCRPLength of time with morning stiffnessAbility to elevate armsA score less than 7 suggests low disease activity, 7-17 is medium disease activity, and above 17 is high activity. GCA requires high dose intravenous steroid treatment. The treatment will not affect the quality of the temporal artery biopsy. It is useful in preventing permanent blindness, reduce fever, headache, and myalgia. Treatment can be tapered after 6 months, and should last 2-3 years. The treatment dose can be increased if a flareup or relapse occurs. Excessive steriod therapy may lead to side effects including osteoporosis, myopathy, bruising. hypertension, elevated cholesterol, diabetes, insomnia, restlessness, hypomania, and depression. The osteoporosis can be treated with vitamin D. calcium, weight bearing exercises, and bisphosphonates. Antidepressants can be used for emotional issues, while avoiding hypnotics and benzos. Hypertension may be due to subclinical vasculitis and may be assessed by comparing upper and lower extremity blood pressures.
BRIAN UNWIN, COL, MC, USA, CYNTHIA M. WILLIAMS, CAPT (R), MC, USN, and
WILLIAM GILLILAND, COL, MC, USA, Uniformed Services University of the Health Sciences, Bethesda, Maryland
http://www.aafp.org/afp/2006/1101/p1547.pdf
Am Fam Physician. 2006 Nov 1;74(9):1547-1554.
Giant cell arteritis (CGA) and polymyalgia rheumatica (PMR) are very similar inflammatory vascular disorders and oftentimes, patients end up with both. CGA usually presents with temporal pain, headache and vision problems. PMR presents with pain and stiffness in the girdle (hip and shoulder) muscles. Both are more common in patients over 50 years old. Findings associated with PMR include age over 50 years, ESR above 50 mm/hr, mild anemia, pain with morning stiffness of the proximal muscles, and inflammatory symptoms (fever, night sweats, weight loss, anorexia, and depression). Other symptoms include asymmetric wrist and knee arthritis, hand and feet swelling, carpal tunnel syndrome, shoulder/ hip bursitis, and extremity tenderness. Findings associated with GCA include age over 50 years, ESR above 50 mm/hr, anemia, headache, jaw claudication, PMR, arthralgia, visual problems, inflammatory symptoms, and an abnormal temporal artery. The patient may present with a low grade fever and a red, tender, thickened, nodular, or pulseless temporal artery. A detailed vision exam, joint exam, and temporal artery biopsy should be considered. Steroid treatment should not be delayed in lieu of lab work or biopsy. Ultrasound may help determine the best section of the artery for biopsy. The differential diagnosis for GCA and PMR includes fibromyalgia, multiple myeloma, OA, RA, and polymyositis. A negative ESR will usually rule out CGA (and PMR). Corticosteroid use will give a falsely low ESR. A rough estimate of a normal ESR is the patients age divided by 2 (then add 5 if it is a woman). Other lab abnormalities include elevated CRP, thrombocytopenia, elevated LFTs, and microscopic hematuria. Treatment consists or prednisone. PMR requires low dose steroids for 2-4 week after the disease symptoms resolve, followed by a slow taper (lower the dose by 1 mg/day each week). A disease activity score has been developed for PMR to help monitor and adjust therapy. The five variables are;A visual analog pain scaleA visual analog scale for the physician's assessmentCRPLength of time with morning stiffnessAbility to elevate armsA score less than 7 suggests low disease activity, 7-17 is medium disease activity, and above 17 is high activity. GCA requires high dose intravenous steroid treatment. The treatment will not affect the quality of the temporal artery biopsy. It is useful in preventing permanent blindness, reduce fever, headache, and myalgia. Treatment can be tapered after 6 months, and should last 2-3 years. The treatment dose can be increased if a flareup or relapse occurs. Excessive steriod therapy may lead to side effects including osteoporosis, myopathy, bruising. hypertension, elevated cholesterol, diabetes, insomnia, restlessness, hypomania, and depression. The osteoporosis can be treated with vitamin D. calcium, weight bearing exercises, and bisphosphonates. Antidepressants can be used for emotional issues, while avoiding hypnotics and benzos. Hypertension may be due to subclinical vasculitis and may be assessed by comparing upper and lower extremity blood pressures.
Tuesday, September 10, 2013
A Brief Synopsis of AFPs "Update on the Evaluation and Management of Functional Dyspepsia"
Update on the Evaluation and Management of Functional Dyspepsia
RYAN A. LOYD, MD, and DAVID A. McCLELLAN, MD, Texas A&M Health Science Center College of Medicine, Bryan, Texas
Am Fam Physician. 2011 Mar 1;83(5):547-552.
http://www.aafp.org/afp/2011/0301/p547.pdf
The ROME II criteria defines functional dyspepsia a having at least one of the following:
postprandial fullness
early satiety
epigastric pain
epigastric burning
no evidence of structural disease
Functional dyspepsia can be divided into two categories; epigastric pain syndromes and postprandial distress syndrome. Pathophysiology is unclear, but may be involved with gastric motility, low pH, and infection.
Whenever a patient is considered to have dyspepsia, a proper history and physical should be done to rule out other more common causes. There is a large differential and thus functional dyspepsia is a diagnosis of exclusion. If the patient has significant risk factors
(age greater than 55 years,
unintentional weight loss,
dysphagia,
persistent vomiting,
gastric bleeding, or
family history of cancer),
then an endoscopy should be done. Any results should be treated accordingly. If the patient has no risk factors or the endoscopy is negative, then the patient can be tested for H.pylori, or treated empirically for the infection. If symptoms resolve, then continue treatment and reevaluate as needed. If it does not resolve, then an endoscopy can be done. Due to cost and the sensitivity of endoscopy, it is better to start with empiric therapy before invasive testing. Cochrane recommends testing first and then treating (makes sense to me!) Testing for H. pylori includes serology, stool antigen, and urea breath testing. H2 blockers and PPIs appear to be the best medication. Prokinetics may have a benefit in treatment. Metoclopramide is a prokinetic that is associated with serious side effects, including tardive dyskinesia and parkinsonian symptoms. Erythromycin is another prokinetic (or irritant, depending on who you ask) which may have benefit. Antidepressants may assist with associated depression and actually improve the dyspepsia.
RYAN A. LOYD, MD, and DAVID A. McCLELLAN, MD, Texas A&M Health Science Center College of Medicine, Bryan, Texas
Am Fam Physician. 2011 Mar 1;83(5):547-552.
http://www.aafp.org/afp/2011/0301/p547.pdf
The ROME II criteria defines functional dyspepsia a having at least one of the following:
postprandial fullness
early satiety
epigastric pain
epigastric burning
no evidence of structural disease
Functional dyspepsia can be divided into two categories; epigastric pain syndromes and postprandial distress syndrome. Pathophysiology is unclear, but may be involved with gastric motility, low pH, and infection.
Whenever a patient is considered to have dyspepsia, a proper history and physical should be done to rule out other more common causes. There is a large differential and thus functional dyspepsia is a diagnosis of exclusion. If the patient has significant risk factors
(age greater than 55 years,
unintentional weight loss,
dysphagia,
persistent vomiting,
gastric bleeding, or
family history of cancer),
then an endoscopy should be done. Any results should be treated accordingly. If the patient has no risk factors or the endoscopy is negative, then the patient can be tested for H.pylori, or treated empirically for the infection. If symptoms resolve, then continue treatment and reevaluate as needed. If it does not resolve, then an endoscopy can be done. Due to cost and the sensitivity of endoscopy, it is better to start with empiric therapy before invasive testing. Cochrane recommends testing first and then treating (makes sense to me!) Testing for H. pylori includes serology, stool antigen, and urea breath testing. H2 blockers and PPIs appear to be the best medication. Prokinetics may have a benefit in treatment. Metoclopramide is a prokinetic that is associated with serious side effects, including tardive dyskinesia and parkinsonian symptoms. Erythromycin is another prokinetic (or irritant, depending on who you ask) which may have benefit. Antidepressants may assist with associated depression and actually improve the dyspepsia.
Monday, September 9, 2013
A Synopsis of AFPs "Overview of Changes to Asthma Guidelines: Diagnosis and Screening"
Overview of Changes to Asthma Guidelines: Diagnosis and Screening
SUSAN M. POLLART, MD, MS, andKURTIS S. ELWARD, MD, MPH Department of Family Medicine, University of Virginia School of Medicine, Charlottesville, Virginia
http://www.aafp.org/afp/2009/0501/p761.pdf
Am Fam Physician. 2009 May 1;79(9):761-767.
I know that I just did an article on asthma thursday, but I printed this one out at the same time, and it was on top of the pile, so here we go again. Asthma is real common anyway so there is nothing wrong with a little repetition.
Asthma is categorized by severity and control. Treatment is categorized by current impairment and future risk. Patients with previously treated asthma are hard to classify because the parameters can be skewed by incomplete treatment. Older guidelines that categorized patients based on severity alone did not result in the best management.
The four asthma classifications are intermittent and three types or persistent (mild, moderate and severe). So the way that I remember which is which is by the phrase "less than 2, more than 2, daily, constant". What that stands for is that intermittent asthma occurs less than 2x a week, less than 2x a month at night, and short acting betas are needed less than 2x a week. Persistent/mild asthma occurs more than 2x a week, more than 2x a month at night, and short acting betas are needed more than 2x a week. Persistent/moderate asthma consists of daily symptoms, weekly nighttime symptoms, and daily beta usage. Persistent/severe asthma has symptoms throughout the day, nightly nighttime symptoms, and beta inhaler usage several times a day. For FEV1, it is above 80 for intermittent and persistent/mild. It drops to 60-80 in persistent/moderate and less than 60 in persistent/severe. FEV1/FCV goes down by 5% in persistent/moderate and persistent/severe.
All patients with asthma need to recognize when they are not adequately controlled with medication. The patients symptoms need to be classified into "well controlled, not well controlled, or very poorly controlled". This can be further evaluated with several questionnaires, that are provided in the original article (teaser). FEV1 and FVC are also helpful predictors of current impairment.
This article describes a stepwise treatment approach to determine where to start treatment based on the disease classification. Patients who are not well controlled can go up a step. A patient should be reevaluated 2-6 weeks after starting or changing a step. Those who are very poorly controlled can get a short course of oral steroids, go up 1-2 steps, and be reevaluated in 2-4 weeks. Patients who are well controlled for three months can step down. Patients with intermittent asthma need only be seen yearly, or 2-3 times if on a rescue inhaler.
Step 1 begins with an inhaled short acting beta blocker (with a spacer and proper spacer training). Step 1 is where intermittent asthmatics start. After each step, there should be proper patient education, environmental control, and management of comorbidities. Step 2 includes adding a low dose inhaled steroid. Step 3 recommends adding a long-acting beta agonist, or increasing the steriod from a low to a medium dose inhaler. Step 4 includes a medium acting steriod and the long acting beta agonist. With steps 2-4, allergy immunotherapy, a leukotriene antagonist, theophylline, or zileuton can be added. Theophylline and cromolyn are not preferred but are acceptable alternatives. Step 5 requires a high dose steroid, long acting beta agonist, and possibly omalizumab. Step 6 is basically just adding an oral steroid to the previous regimen.
As mentioned in the previous synopsis, a proper, individualized asthma action plan can help greatly.
SUSAN M. POLLART, MD, MS, andKURTIS S. ELWARD, MD, MPH Department of Family Medicine, University of Virginia School of Medicine, Charlottesville, Virginia
http://www.aafp.org/afp/2009/0501/p761.pdf
Am Fam Physician. 2009 May 1;79(9):761-767.
I know that I just did an article on asthma thursday, but I printed this one out at the same time, and it was on top of the pile, so here we go again. Asthma is real common anyway so there is nothing wrong with a little repetition.
Asthma is categorized by severity and control. Treatment is categorized by current impairment and future risk. Patients with previously treated asthma are hard to classify because the parameters can be skewed by incomplete treatment. Older guidelines that categorized patients based on severity alone did not result in the best management.
The four asthma classifications are intermittent and three types or persistent (mild, moderate and severe). So the way that I remember which is which is by the phrase "less than 2, more than 2, daily, constant". What that stands for is that intermittent asthma occurs less than 2x a week, less than 2x a month at night, and short acting betas are needed less than 2x a week. Persistent/mild asthma occurs more than 2x a week, more than 2x a month at night, and short acting betas are needed more than 2x a week. Persistent/moderate asthma consists of daily symptoms, weekly nighttime symptoms, and daily beta usage. Persistent/severe asthma has symptoms throughout the day, nightly nighttime symptoms, and beta inhaler usage several times a day. For FEV1, it is above 80 for intermittent and persistent/mild. It drops to 60-80 in persistent/moderate and less than 60 in persistent/severe. FEV1/FCV goes down by 5% in persistent/moderate and persistent/severe.
All patients with asthma need to recognize when they are not adequately controlled with medication. The patients symptoms need to be classified into "well controlled, not well controlled, or very poorly controlled". This can be further evaluated with several questionnaires, that are provided in the original article (teaser). FEV1 and FVC are also helpful predictors of current impairment.
This article describes a stepwise treatment approach to determine where to start treatment based on the disease classification. Patients who are not well controlled can go up a step. A patient should be reevaluated 2-6 weeks after starting or changing a step. Those who are very poorly controlled can get a short course of oral steroids, go up 1-2 steps, and be reevaluated in 2-4 weeks. Patients who are well controlled for three months can step down. Patients with intermittent asthma need only be seen yearly, or 2-3 times if on a rescue inhaler.
Step 1 begins with an inhaled short acting beta blocker (with a spacer and proper spacer training). Step 1 is where intermittent asthmatics start. After each step, there should be proper patient education, environmental control, and management of comorbidities. Step 2 includes adding a low dose inhaled steroid. Step 3 recommends adding a long-acting beta agonist, or increasing the steriod from a low to a medium dose inhaler. Step 4 includes a medium acting steriod and the long acting beta agonist. With steps 2-4, allergy immunotherapy, a leukotriene antagonist, theophylline, or zileuton can be added. Theophylline and cromolyn are not preferred but are acceptable alternatives. Step 5 requires a high dose steroid, long acting beta agonist, and possibly omalizumab. Step 6 is basically just adding an oral steroid to the previous regimen.
As mentioned in the previous synopsis, a proper, individualized asthma action plan can help greatly.
Friday, September 6, 2013
A Synopsis of AFPs "Evaluation and Management of Heart Murmurs in Children"
Evaluation and Management of Heart Murmurs in Children
JENNIFER E. FRANK, MD, and KATHRYN M. JACOBE, MD, University of Wisconsin Fox Valley Family Medicine Residency Program, Appleton, Wisconsin
Am Fam Physician. 2011 Oct 1;84(7):793-800.
http://www.aafp.org/afp/2011/1001/p793.pdf
Heart murmurs are exceedingly common in the newborn and are usually asymptomatic. Rarely, it is a sign of a structural heart disease. Although a murmur is often the only sign of a problem, other features that may suggest a structural problem include feeding problems. failure to thrive, chest pain, palpitations, dizziness, family history (SIDS, hypertrophic cardiomyopathy, or congenital heart disease), aneuploidy, connective tissue disorders, kawasaki disease, exposure to alcohol, toxins or SSRIs, and others. Symptoms or a structural problem include dyspnea, nausea, vomiting, exercise tolerance, fatigue and cough. A physical exam including vital signs, looking for other congenital anomalies (dysmorphic features), breath sounds, chest contour, and heart sounds are important in proper care of the child.
Heart murmurs are graded into 6 classes:
grade 1- barely audible
grade 2- faint but audible
grade 3- loud
grade 4- easily heard over wide area of chest
grade 5- loud with precordial thrill
grade 6- can be heard with stethoscope off chest
Innocent murmurs will often change in intensity with a change in patient position. Gallops may be normal. Examples of innocent murmurs include peripheral pulmonary stenosis, still murmur, pulmonary flow murmur, aortic systolic murmur, and venous hum. According to this article the seven key features of innocent heart murmurs include
1. sensitive (with change with a change in position)
2. short duration (not a holosystolic murmur)
3. single (gallops or clicks are absent)
4. small (murmur is only found in a small area and is not radiating)
5. soft (low amplitude)
6. sweet (murmur does not sound harsh)
7. systolic
Red flags for a structural disease include a holosystolic murmur, a harsh sound, an abnormal S2, maximal intensity in the upper left sternal border, a systolic click, a diastolic murmur, and a murmur that is louder with standing. Pathologic heart murmurs may also have systolic ejection murmurs such as ASD, pulmonary stenosis, coarctation of the aorta, aortic stenosis, transposition of the great vessels, total anomalous pulmonary venous connection, tetralogy of fallot, and hypoplastic left heart syndrome. ASD will have a wide fixed S2. In pulmonary stenosis, the murmur is heard best in the upper left sternal border. Aortic stenosis is best heard in the upper right sternal border. Coarctation may cause a delayed femoral pulse. Murmurs that may have holosystolic components (left lower sternal border), include tetralogy of fallot, transposition, tricuspid atresia, and truncus arteriosus (or a diastolic rumble). All the murmurs that start with "T" may present with cyanosis (tetralogy, transposition, truncus arteriosus, total anomalous...., and tricuspid atresia. More detail can be found on table 5 of this article.
ECG and x ray are usually not helpful in diagnosis of murmurs in children less than six weeks old. A diagnosis of an innocent murmur can be made if there are the following criteria; no abnormal findings on exam, negative review of systems, negative history of features that may increase the risk of structural heart disease, and positive auscultatory sounds of an innocent murmur. If this cannot be achieved, then a referral to a pediatric cardiologist should be made. Suspicion of a neonatal murmur should be referred as well. Evaluation includes 24 hour pulse oximetry monitoring.
JENNIFER E. FRANK, MD, and KATHRYN M. JACOBE, MD, University of Wisconsin Fox Valley Family Medicine Residency Program, Appleton, Wisconsin
Am Fam Physician. 2011 Oct 1;84(7):793-800.
http://www.aafp.org/afp/2011/1001/p793.pdf
Heart murmurs are exceedingly common in the newborn and are usually asymptomatic. Rarely, it is a sign of a structural heart disease. Although a murmur is often the only sign of a problem, other features that may suggest a structural problem include feeding problems. failure to thrive, chest pain, palpitations, dizziness, family history (SIDS, hypertrophic cardiomyopathy, or congenital heart disease), aneuploidy, connective tissue disorders, kawasaki disease, exposure to alcohol, toxins or SSRIs, and others. Symptoms or a structural problem include dyspnea, nausea, vomiting, exercise tolerance, fatigue and cough. A physical exam including vital signs, looking for other congenital anomalies (dysmorphic features), breath sounds, chest contour, and heart sounds are important in proper care of the child.
Heart murmurs are graded into 6 classes:
grade 1- barely audible
grade 2- faint but audible
grade 3- loud
grade 4- easily heard over wide area of chest
grade 5- loud with precordial thrill
grade 6- can be heard with stethoscope off chest
Innocent murmurs will often change in intensity with a change in patient position. Gallops may be normal. Examples of innocent murmurs include peripheral pulmonary stenosis, still murmur, pulmonary flow murmur, aortic systolic murmur, and venous hum. According to this article the seven key features of innocent heart murmurs include
1. sensitive (with change with a change in position)
2. short duration (not a holosystolic murmur)
3. single (gallops or clicks are absent)
4. small (murmur is only found in a small area and is not radiating)
5. soft (low amplitude)
6. sweet (murmur does not sound harsh)
7. systolic
Red flags for a structural disease include a holosystolic murmur, a harsh sound, an abnormal S2, maximal intensity in the upper left sternal border, a systolic click, a diastolic murmur, and a murmur that is louder with standing. Pathologic heart murmurs may also have systolic ejection murmurs such as ASD, pulmonary stenosis, coarctation of the aorta, aortic stenosis, transposition of the great vessels, total anomalous pulmonary venous connection, tetralogy of fallot, and hypoplastic left heart syndrome. ASD will have a wide fixed S2. In pulmonary stenosis, the murmur is heard best in the upper left sternal border. Aortic stenosis is best heard in the upper right sternal border. Coarctation may cause a delayed femoral pulse. Murmurs that may have holosystolic components (left lower sternal border), include tetralogy of fallot, transposition, tricuspid atresia, and truncus arteriosus (or a diastolic rumble). All the murmurs that start with "T" may present with cyanosis (tetralogy, transposition, truncus arteriosus, total anomalous...., and tricuspid atresia. More detail can be found on table 5 of this article.
ECG and x ray are usually not helpful in diagnosis of murmurs in children less than six weeks old. A diagnosis of an innocent murmur can be made if there are the following criteria; no abnormal findings on exam, negative review of systems, negative history of features that may increase the risk of structural heart disease, and positive auscultatory sounds of an innocent murmur. If this cannot be achieved, then a referral to a pediatric cardiologist should be made. Suspicion of a neonatal murmur should be referred as well. Evaluation includes 24 hour pulse oximetry monitoring.
Thursday, September 5, 2013
A Brief Synopsis of AFP's "Management of Acute Asthma Exacerbations"
Management of Acute Asthma Exacerbations
SUSAN M. POLLART, MD, MS; REBEKAH M. COMPTON, MSN, FNP-C; and KURTIS S. ELWARD, MD, MPH, University of Virginia Health System, Charlottesville, Virginia
Am Fam Physician. 2011 Jul 1;84(1):40-47.
http://www.aafp.org/afp/2011/0701/p40.pdf
According to this article, asthma can be classified into mild, moderate, severe, or life threatening (I'm not sure what happened to intermittent and the different levels of persistent, but let's go with it for now). The classes can be determined by lung function (PEF or FEV1). Mild asthma has symptoms of dyspnea with activity and a PEF of greater than 70% predicted (of their personal best peak expiratory flow). Moderate asthma is described as dyspnea affecting usual activity and a PEF between 40-69%. Severe asthma has dyspnea at rest and a PEF less than 40%. Life threatening asthma has a PEF of less than 25%. Signs of an exacerbation in a child include accessory muscle use, chest wall retractions, tachypnea, cyanosis, and wheezing. Lab tests are generally not helpful. ABGs or chest radiographs may be considered under certain circumstances.
The most effective home treatment of acute asthma is a proper action plan (a personalized, written algorithm based on symptoms and PEF). Serious exacerbations (PEF less than 50%) may require an immediate physician visit. Otherwise, initial treatment should be short acting beta agonists (two treatments, 20 minutes apart). If the treatment stopped the wheezing (PEF greater than 80%) then the patient can continue the beta agonist for 1-2 days or add an oral corticosteroid. If the response is incomplete (PEF 50-70%) and the patient is having persistent wheezing, the patient should continue the beta agonist and add the oral steroids, as well as contact the primary care physician. A poor response (PEF < 50%) usually requires a trip to the ER in addition to the previous medications.
treatment goals in the emergency room setting consist of fixing any hypoxia, reversing any airflow obstruction, and reducing the risk of relapse. The patient is given supplemental oxygen to maintain a saturation above 94%. inhaled short-acting beta agonists will be given, or continuous administration if the exacerbation is severe. Anticholinergics can be added to nebulized beta agonists. IV magnesium may also have a role. Systemic corticosteroids (either oral or parenteral will decrease the need for hospitalization.
On discharge, patients should be sent home with about a weeks worth of oral corticosteroids. If lon term oral steroids are not needed, then inhaled steroids may be used. They should also have a scheduled follow-up within a week of discharge. .
SUSAN M. POLLART, MD, MS; REBEKAH M. COMPTON, MSN, FNP-C; and KURTIS S. ELWARD, MD, MPH, University of Virginia Health System, Charlottesville, Virginia
Am Fam Physician. 2011 Jul 1;84(1):40-47.
http://www.aafp.org/afp/2011/0701/p40.pdf
According to this article, asthma can be classified into mild, moderate, severe, or life threatening (I'm not sure what happened to intermittent and the different levels of persistent, but let's go with it for now). The classes can be determined by lung function (PEF or FEV1). Mild asthma has symptoms of dyspnea with activity and a PEF of greater than 70% predicted (of their personal best peak expiratory flow). Moderate asthma is described as dyspnea affecting usual activity and a PEF between 40-69%. Severe asthma has dyspnea at rest and a PEF less than 40%. Life threatening asthma has a PEF of less than 25%. Signs of an exacerbation in a child include accessory muscle use, chest wall retractions, tachypnea, cyanosis, and wheezing. Lab tests are generally not helpful. ABGs or chest radiographs may be considered under certain circumstances.
The most effective home treatment of acute asthma is a proper action plan (a personalized, written algorithm based on symptoms and PEF). Serious exacerbations (PEF less than 50%) may require an immediate physician visit. Otherwise, initial treatment should be short acting beta agonists (two treatments, 20 minutes apart). If the treatment stopped the wheezing (PEF greater than 80%) then the patient can continue the beta agonist for 1-2 days or add an oral corticosteroid. If the response is incomplete (PEF 50-70%) and the patient is having persistent wheezing, the patient should continue the beta agonist and add the oral steroids, as well as contact the primary care physician. A poor response (PEF < 50%) usually requires a trip to the ER in addition to the previous medications.
treatment goals in the emergency room setting consist of fixing any hypoxia, reversing any airflow obstruction, and reducing the risk of relapse. The patient is given supplemental oxygen to maintain a saturation above 94%. inhaled short-acting beta agonists will be given, or continuous administration if the exacerbation is severe. Anticholinergics can be added to nebulized beta agonists. IV magnesium may also have a role. Systemic corticosteroids (either oral or parenteral will decrease the need for hospitalization.
On discharge, patients should be sent home with about a weeks worth of oral corticosteroids. If lon term oral steroids are not needed, then inhaled steroids may be used. They should also have a scheduled follow-up within a week of discharge. .
Tuesday, September 3, 2013
A Short Synopsis of AFP's "Diagnosis and Treatment of Peripheral Arterial Disease"
Diagnosis and Treatment of Peripheral Arterial Disease
DUANE R. HENNION, MD, and KELLY A. SIANO, MD, Tripler Army Medical Center, Honolulu, Hawaii
Am Fam Physician. 2013 Sep 1;88(5):306-310
http://www.aafp.org/afp/2013/0901/p306.pdf
Peripheral arterial disease is basically just angina of the extremities. Distal arterial stenosis causes decreased blood flow and claudication of the legs. Claudication is defined as leg pain reproduced with exercise, which resolves within 10 minutes of resting. Risk factors are the same as the risk factors for cardiovascular disease; age, smoking, diabetes, hypertension, cholesterol, renal insufficiency, and race. Claudication can be differentiated from spinal stenosis by the fact that stenosis is worse when walking down stairs. It is also not resolved as quickly after rest. DVT's will often have a "hot leg", skin changes, and decreased distal pulses. The best test to check for PAD is the ABI (ankle brachial index). An ABI of 1 is normal. An ABI of less than 0.9 is interpreted as PAD. Patients with an ABI of less than 0.9 have a higher risk of CVA. Universal screening is not recommended by the USPSTF. Patients with risk factors may benefit from ABI screening.
Treatment of PAD starts with modification of risk factors. Smoking cessation, exercise, diet, statins, and antiplatelet therapy are first line therapies. Lipid therapy is done with a treatment goal of less than 100 mg/dL. Low dose aspirin (or clopidogrel) will lower the chances of a cardiovascular event. Supervised exercise, such as 30 minutes on the treadmill, 2-3 times a week, can increase overall walking time and walking distance. It is as effective as angioplasty. Cilostazol (a phosphodiesterase inhibitor) will cause arterial vasodilation and suppress platelet aggregation. It has been shown to increase walking distances. Surgery may be considered in patients who do not respond to medication or exercise.
DUANE R. HENNION, MD, and KELLY A. SIANO, MD, Tripler Army Medical Center, Honolulu, Hawaii
Am Fam Physician. 2013 Sep 1;88(5):306-310
http://www.aafp.org/afp/2013/0901/p306.pdf
Peripheral arterial disease is basically just angina of the extremities. Distal arterial stenosis causes decreased blood flow and claudication of the legs. Claudication is defined as leg pain reproduced with exercise, which resolves within 10 minutes of resting. Risk factors are the same as the risk factors for cardiovascular disease; age, smoking, diabetes, hypertension, cholesterol, renal insufficiency, and race. Claudication can be differentiated from spinal stenosis by the fact that stenosis is worse when walking down stairs. It is also not resolved as quickly after rest. DVT's will often have a "hot leg", skin changes, and decreased distal pulses. The best test to check for PAD is the ABI (ankle brachial index). An ABI of 1 is normal. An ABI of less than 0.9 is interpreted as PAD. Patients with an ABI of less than 0.9 have a higher risk of CVA. Universal screening is not recommended by the USPSTF. Patients with risk factors may benefit from ABI screening.
Treatment of PAD starts with modification of risk factors. Smoking cessation, exercise, diet, statins, and antiplatelet therapy are first line therapies. Lipid therapy is done with a treatment goal of less than 100 mg/dL. Low dose aspirin (or clopidogrel) will lower the chances of a cardiovascular event. Supervised exercise, such as 30 minutes on the treadmill, 2-3 times a week, can increase overall walking time and walking distance. It is as effective as angioplasty. Cilostazol (a phosphodiesterase inhibitor) will cause arterial vasodilation and suppress platelet aggregation. It has been shown to increase walking distances. Surgery may be considered in patients who do not respond to medication or exercise.
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