Hyperkalemia
JOYCE C. HOLLANDER-RODRIGUEZ, M.D., and JAMES F. CALVERT, JR., M.D.,Oregon Health & Science University, Portland, Oregon
Am Fam Physician. 2006 Jan 15;73(2):283-290.
http://www.aafp.org/afp/2006/0115/p283.pdf
Once potassium is ingested, it goes to the pancreas and causes release of insulin. The insulin drives the potassium from the extracellular space into the cells. The increase of potassium also causes the release of renin, which stimulates the conversion of angiotensin I into angiotensin II. The ATII causes secretion of aldosterone, which causes renal excretion of potassium and retention of sodium.
When evaluating a patient for hyperkalemia, the first step is to rule out the artificial causes, such are hemolysis in the test tube (pseudohyperkalemia), traumatic venipuncture, lab error, and repeatedly making a fist during the blood draw. The three true causes of hyperkalemia are;
1. medication side effects
2. altered distribution of potassium between the cells and the extracellular space
3. impaired renal excretion
Medication induced hyperkalemia is commonly seen in patients who take ACEI with spironolactone. NSAIDs will decrease renin, which will decrease potassium excretion. Adrenal insufficiency will cause hyperkalemia, hyponatremia, and muscular weakness. Impaired renal excretion is caused by renal failure, renal hypoperfusion, and hypoaldosteronism. Congential causes include pseudohypoaldosteronism, which is aldosterone resistance of the kidney. Hyporeninemic hypoaldosteronism is associated with RTA IV. It can be treated with fludrocortisone.
Symptoms of hyperkalemia include muscular weakness, flaccid paralysis, ileus, and ECG changes (peaked T waves, loss of P wave, widened QRS). Lab tests include serum electrolytes, spot urine, transtubular potassium gradient, and fractional excretion of potassium. Patients may also present with decreased renal function and metabolic acidosis.
ECG changes, acidosis, or a potassium level of 6.0 mEq is typically the cutoff point for emergent potassium reduction. If the ECG is abnormal and the potassium is elevated, then calcium gluconate can be given. Calcium gluconate will protect the myocardium against the potassium, but does not lower it. Insulin or a beta-2 agonist can be used to drive the extracellular potassium into the cell, but the total body potassium is not lowered. Kayexalate will bind the potassium in the colon and excrete it, thus lowering the potassium. Sorbitol can be given with it to reduce constipation. Furosemide can be added to reduce volume overload from the increased sodium (it was exchanged for the potassium in the colon). Potassium can be excreted renally by using loop diuretics as well, as long as the renal function is intact.
Tuesday, October 1, 2013
"Infectious Endocarditis: Diagnosis and Treatment" (A Synopsis)
Infectious Endocarditis: Diagnosis and Treatment
DEBORAH PIERCE, MD, MPH; BETHANY C. CALKINS, MD; and KRISTEN THORNTON, MD, University of Rochester School of Medicine and Dentistry, Rochester, New York
Am Fam Physician. 2012 May 15;85(10):981-986.
http://www.aafp.org/afp/2012/0515/p981.pdf
Infectious endocarditis occurs when bacterial or fungus attach to endocardium or to a prosthetic valve, and form vegetations and thrombi. Risk factors include dialysis, IVDA, congenital disease, valve disease, and rheumatic heart disease. Early infection occurs within 2 months of a valve replacement or operation. Late infections occur after 12 months. Symptoms include unexplained fever, night sweats, and signs or a systemic infection. The Duke criteria classifies the endocarditis into definite (2 major, 1 major + 3 minor, or 5 minor), possible (1 major + 1-2 minor, or 3 minor), or rejected.
The major criteria are;
2 separate blood cultures infected with endocarditis bacteria, or
positive blood cultures drawn 12 hours apart, or
positive blood cultures from all 3 or most of 4 cultures drawn an hour apart, or
blood positive for Coxiella burnetii or IGG ab titer, or
positive findings on echo.
Minor criteria include;
fever of 100.4F or more,
glomerulonephritis, osler nodes, roth spots, RF,
positive blood cultures that don't meet major criteria,
history of IVDA or predisposing heart condition,
vascular phenomenon (arterial emboli, pulmonary infarct, mycotic aneurysm, intracranial hemorrhage, janeway lesions)
Evaluation starts with a cardiac evaluation. Physical exam may reveal heart failure, a regurgitant murmur, roth spots on the retina, hemorrhagic janeway lesions on the palms or soles, painful osler nodes on the palms or soles, or petechiae on the mucus membranes. Blood cultures should be drawn before antibiotics. Urinalysis may show hematuria, proteinuria, or pyuria. An ECG can be done as a baseline. TEE may be necessary in patients with staphylococcal bacteremia, obesity, mechanical ventilation, or a prosthetic valve that obscures visualization.
Treatment includes antibiotics. Empiric therapy consists or vancomycin or ampicillin/sulbactam plus an aminoglycoside. Cultures and sensitivity can can help guide therapy. Anticoagulation should be held for the first two weeks of antibiotic therapy. Patients with fungal infection, aggressive bacterial infection, multiple embolic events, left sided endocarditis, valve dehiscence or rupture, or perivalvular abscess will need a surgical consult.
DEBORAH PIERCE, MD, MPH; BETHANY C. CALKINS, MD; and KRISTEN THORNTON, MD, University of Rochester School of Medicine and Dentistry, Rochester, New York
Am Fam Physician. 2012 May 15;85(10):981-986.
http://www.aafp.org/afp/2012/0515/p981.pdf
Infectious endocarditis occurs when bacterial or fungus attach to endocardium or to a prosthetic valve, and form vegetations and thrombi. Risk factors include dialysis, IVDA, congenital disease, valve disease, and rheumatic heart disease. Early infection occurs within 2 months of a valve replacement or operation. Late infections occur after 12 months. Symptoms include unexplained fever, night sweats, and signs or a systemic infection. The Duke criteria classifies the endocarditis into definite (2 major, 1 major + 3 minor, or 5 minor), possible (1 major + 1-2 minor, or 3 minor), or rejected.
The major criteria are;
2 separate blood cultures infected with endocarditis bacteria, or
positive blood cultures drawn 12 hours apart, or
positive blood cultures from all 3 or most of 4 cultures drawn an hour apart, or
blood positive for Coxiella burnetii or IGG ab titer, or
positive findings on echo.
Minor criteria include;
fever of 100.4F or more,
glomerulonephritis, osler nodes, roth spots, RF,
positive blood cultures that don't meet major criteria,
history of IVDA or predisposing heart condition,
vascular phenomenon (arterial emboli, pulmonary infarct, mycotic aneurysm, intracranial hemorrhage, janeway lesions)
Evaluation starts with a cardiac evaluation. Physical exam may reveal heart failure, a regurgitant murmur, roth spots on the retina, hemorrhagic janeway lesions on the palms or soles, painful osler nodes on the palms or soles, or petechiae on the mucus membranes. Blood cultures should be drawn before antibiotics. Urinalysis may show hematuria, proteinuria, or pyuria. An ECG can be done as a baseline. TEE may be necessary in patients with staphylococcal bacteremia, obesity, mechanical ventilation, or a prosthetic valve that obscures visualization.
Treatment includes antibiotics. Empiric therapy consists or vancomycin or ampicillin/sulbactam plus an aminoglycoside. Cultures and sensitivity can can help guide therapy. Anticoagulation should be held for the first two weeks of antibiotic therapy. Patients with fungal infection, aggressive bacterial infection, multiple embolic events, left sided endocarditis, valve dehiscence or rupture, or perivalvular abscess will need a surgical consult.
Thursday, September 26, 2013
A Review of AFPs "Frontotemporal Dementia: A Review for Primary Care Physicians"
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.
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.
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.
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