1. Passive Straight Leg Raise (SLR or Lasegue's sign)
-The normal leg can be raised 80 degrees; <80 degrees= tight hamstrings or a sciatic nerve problem. To differentiate, raise the leg to the point of pain, lower slightly, then dorsiflex the foot. Pain = sciatica, no pain= tight hamstrings.
-The test is positive if pain radiates down the posterior/lateral thigh past the knee. This radiation indicates stretching of the nerve roots (specifically S1 or L5) over a herniated disc.
-Pain will most likely occur between 40 and 70 degrees. Pain earlier than 30 degrees is suggestive of malingering.
-Pain in the opposite leg during a straight leg raise is suggestive of root compression due to central disc herniation.
-When compared to MRI, the straight leg raise test has a sensitivity of 0.36 and specificity of 0.74
The ipsilateral straight leg raise test has a sensitivity of 0.80 and a specificity of about 0.40.
2. Crossed Leg Raise: asymptomatic leg is raised
-Test is positive if pain is increased in the contralateral leg; this correlates with the degree of disc herniation. Such results imply a large central herniation.
-Cross SLR test is much less sensitive (0.25) but is highly specific (about 0.90). Thus, a negative test is nonspecific, but a positive test is virtually diagnostic of disc herniation.
3. Claims of weakness > a few weeks without signs of atrophy is suggestive of malingering.
4. Symptoms of Disc Herniation
-Classically, disc herniation is associated with exacerbation when sitting or bending; and relief while lying or standing.
-Icreased pain with coughing and sneezing
-Pain radiating down the leg and sometimes the foot
-Paresthesias
-Muscle weakness, such as foot drop
-Most disk herniation cases resolve spontaneously in 4-6 weeks.
5. Red flags for more serious etiology of low back pain: Cancer
-B symptoms: unexplained weight loss > 10 kg in 6 mos, night sweats
-Personal history of malignancy
-Age > 50 or <17
-Failure to improve with treatment
-Pain at night, at rest.
-Pain lasts > 4-6 weeks
6. Red flags for more serious etiology of low back pain: Infection
-Persistent fever
-Obvious source - endocarditis, septic joint, abscess, cellulitis, etc.
-Recent history of infection, esp bacteremia
-Immunocompromised (including diabetes, chronic steroid use)
-History of IV drug use.
7. Red flags for more serious etiology of low back pain: Cauda Equina syndrome
-Saddle anesthesia
-Urinary retention or incontinence
-Fecal retention or incontinence
-Bilateral lower extremity weakness/numbness
-Progressive neurological defecits
8. Red flags for more serious etiology of low back pain: Vascular
-Claudication
-Known PAD, or significant risk factors.
9. Red flags for more serious etiology of low back pain: Significant nucleus propulsus herniation
-Foot drop (L4, 5)
-Acute onset severe weakness (strength <3/5)
10. Red flags for more serious etiology of low back pain: Fracture
-History of trauma
-Osteoporosis/prolonged steroid use
-HIstory of mild trauma > 50 y/o
-Age > 70
Tuesday, February 25, 2014
Monday, February 24, 2014
1. Effect of cilostazol in patients with aneurysmal subarachnoid hemorrhage: A systematic review and meta-analysis.
Niu et al {J Neurol Sci, 2014}
"Two randomized controlled trials and two quasi-randomized controlled trials with a total of 340 patients were included. The incidence of symptomatic vasospasm (RR=0.47; 95% CI, 0.31-0.72; p<0.001), severe vasospasm (RR=0.48; 95% CI, 0.28-0.82; p=0.007), vasospasm-related new cerebral infarctions (RR=0.38; 95% CI, 0.22-0.67; p=0.001), and poor outcome (RR=0.57; 95% CI, 0.37-0.88; p=0.011) were significantly lower in the cilostazol group. The numbers needed to treat for these outcomes were 6.4, 6.3, 5.7, and 5.4, respectively. Mortality rate differences between the two groups were insignificant. No statistical heterogeneity was found for all outcomes. These results show that cilostazol can decrease the incidence of symptomatic vasospasm, severe vasospasm, vasospasm-related new cerebral infarctions, and poor outcome in patients with aneurysmal SAH."
"Cilostazol, a selective inhibitor of phosphodiesterase 3, may attenuate cerebral vasospasm because of its antiplatelet and vasodilatory effects. A multicenter prospective randomized trial was conducted to investigate the effect of cilostazol on cerebral vasospasm."
Inclusion criteria: Patients in Japan admitted with SAH caused by a ruptured anterior circulation aneurysm who were in Hunt and Kosnik Grades I to IV and were treated by clipping within 72 hours of SAH. Nov 2009 to Dec 2010
Comparison: usual therapy group (control group) vs add-on 100 mg cilostazol twice daily group (cilostazol group).
End points: onset of symptomatic vasospasm (primary), onset of angiographic vasospasm, new cerebral infarctions related to cerebral vasospasm, clinical outcome (mod rankin scale), and length of hospitalization.
Results: N=109
Symptomatic vasospasm occurred in 13% (n = 7) of the cilostazol group and in 40% (n = 22) of the control group (p = 0.0021).
The incidence of angiographic vasospasm was significantly lower in the cilostazol group than in the control group (50% vs 77%; p = 0.0055)
Multiple logistic analyses demonstrated that nonuse of cilostazol is an independent factor for symptomatic and angiographic vasospasm.
The incidence of new cerebral infarctions was also significantly lower in the cilostazol group than in the control group (11% vs 29%; p = 0.0304,).
Clinical outcomes at 1, 3, and 6 months after SAH in the cilostazol group were better than those in the control group, although a significant difference was not shown. There was also no significant difference in the length of hospitalization between the groups. No severe adverse event occurred during the study period.
3. Triple H therapy for SAH: hypertension, hypervolemia, hemodilution. Although hypertension may be the only one of these things that work, and additionally, hemodilution may counteract or worsen the benefit of hypertension in decreasing O2-carrying capacity of blood.
4. Hemodynamic management of subarachnoid hemorrhage.
Treggiari MM1; Participants in the International Multi-disciplinary Consensus Conference on the Critical Care Management of Subarachnoid Hemorrhage. {Neurocrit Care. 2011}
-Literature review (years 2000-2010) on hemodynamic augmentation therapies in patients with subarachnoid hemorrhage. Among the eligible reports identified, 11 addressed volume expansion, 10 blood pressure management, 4 inotropic therapy, and 12 hemodynamic augmentation in patients with unsecured aneurysms.
-Hypervolemia did not appear to confer additional benefits over normovolemic therapy, with an excess of side effects occurring in patients treated with hypervolemic targets.
-Hypertension was associated with higher cerebral blood flow, regardless of volume status, with neurological symptom reversal seen in two-thirds of treated patients.
-Limited data were available for evaluating inotropic agents or hemodynamic augmentation in patients with additional unsecured aneurysms. In the context of sparse data, no incremental risk of aneurysmal rupture has been reported with the induction of hemodynamic augmentation.
5. Effect of different components of triple-H therapy on cerebral perfusion in patients with aneurysmal subarachnoid haemorrhage: a systematic review.
Dankbaar JW et al {Crit Care 2010}
-Systematic literature review (until 2009, excluding case reports) on the effect of triple-H components on cerebral perfusion in SAH patients.
-Outcome: cerebral blood flow (CBF in ml/100 g/min).
-11 studies (4-51 patients per study) were included (one randomized trial).
-Hemodilution did not change CBF.
-One of seven studies on hypervolemia showed statistically significant CBF increase compared to baseline; there was no comparable control group.
-Two of four studies applying hypertension and one of two applying triple-H showed significant CBF increase, none used a control group.
-There is no good evidence from controlled studies for a positive effect of triple-H or its separate components on CBF in SAH patients. In uncontrolled studies, hypertension seems to be more effective in increasing CBF than hemodilution or hypervolemia.
-Literature review on hemodilution as a therapeutic modality in treatment of cerebral vasospasm.
-Evidence has been accumulating against the efficacy of HHH therapy and hemodilution in particular.
-Although HHH therapy and consequently hemodilution has wide support, the evidence for its effectiveness remains equivocal.
-At the time of this study, the burden of evidence appears to be tipped away from hemodilution as a therapeutic modality.
7. Standard workup in a young or middle aged woman who presents with lower abdominal pain:
-Pregnancy test
-GC/chlamydia
-Wet mount
-Urine dipstick
-Pelvic & abdominal exam.
8. Back pain descriptors and suggested diagnoses
-Pain worse with movement and sitting is suggestive of a mechanical cause of back pain, such as a lumbar strain, disc herniation, or degenerative arthritis.
-Pain radiating down the leg and numbness indicate nerve involvement, such as in disc herniation.
-Pain that improves with the supine position suggests spinal stenosis and disc herniation.
-Dull, throbbing pain that progresses slowly, and increases with recumbency or cough in an older patient with a history of cancer, malignancy is likely
-Aching back and posterior thigh discomfort that increases with activity or bending- think spondylolisthesis
9. Overview: physical exam for back pain:
1. Look at posture, contour and symmetry (lordosis, kyphosis, scoliosis)
2. Palpate for any tenderness, tightness, rope-like tension, or inflammation in the paraspinous muscles or tenderness over bony prominences. This checks for muscle spasm, vertebral fracture, or infection. Point tenderness is suggestive of fracture, infection, malignancy.
3. Range of Motion:
-Lumbar Flexion (normal is 90 degrees): Best measure of spine mobility. Restriction and pain during flexion are suggestive of herniation, osteoarthritis, or muscle spasm.
-Lumbar Extension (normal is 15 degrees): Pain with extension is suggestive of degenerative disease or spinal stenosis.
-Lateral motion (normal is 45 degrees): Most patients should be able to touch the proximal fibular head of the knee. Pain on the same side as bending is suggestive of bone pathology (osteoarthritis or neural compression). Pain on the opposite side of bending is suggestive of a muscle strain.
4. Gait: Heels and toe walk. Expect normal gait, even with disc herniation.
-Difficulty with heel walk is associated with L5 disc herniation
-Difficulty with toe walk is associated with S1 disc herniation
-Have the patient go from a standing to squatting position: With central spinal stenosis, squatting will reduce the pain.
5. DTR:
-0: none, 1: reduced, 2. normal, 3: hyperreflexive, 4: clonus
-Patella is L3/L4, Achilles is L4/L5. Reduced reflexes implies pathology at those respective levels
-Increased reflexes supports UMN disease, like spinal stenosis
6. Strength
-0: none, 1: flicker, not enough to move limb, 2: move limb, not against gravity, 3: move limb against gravity, no resistance 4: some resistance, 5: normal strength.
-Iliopsoas/Hip Flexion (L 2, 3, 4)
-Quads/Knee Extension (L 2, 3, 4)
-Hip Adduction (L 2, 3, 4)
-Hip Abduction (L 4, 5, S1)
-Ankle Dorsiflexion/Tibialis Anterior (L 4, 5)
-Great toe Dosriflexion/Extensor hallucis longus (L5... L4?)
-Knee Flexion/Hamstrings (L 5, S1, S2)
-Ankle Plantar Flexion/Gastrocnemius (S 1, S 2)
10. Focused neuro exam for lower back pain:
-Check the patellar and Achilles reflexes.
-Check muscle strength for hip flexion, abduction, and adduction; knee extension and flexion; ankle dorsiflexion and plantar flexion.
-Test for sharp and light touch along the dermatomal distribution of the great toe (L5), lateral malleolus and posterolateral foot (S1).
Niu et al {J Neurol Sci, 2014}
"Two randomized controlled trials and two quasi-randomized controlled trials with a total of 340 patients were included. The incidence of symptomatic vasospasm (RR=0.47; 95% CI, 0.31-0.72; p<0.001), severe vasospasm (RR=0.48; 95% CI, 0.28-0.82; p=0.007), vasospasm-related new cerebral infarctions (RR=0.38; 95% CI, 0.22-0.67; p=0.001), and poor outcome (RR=0.57; 95% CI, 0.37-0.88; p=0.011) were significantly lower in the cilostazol group. The numbers needed to treat for these outcomes were 6.4, 6.3, 5.7, and 5.4, respectively. Mortality rate differences between the two groups were insignificant. No statistical heterogeneity was found for all outcomes. These results show that cilostazol can decrease the incidence of symptomatic vasospasm, severe vasospasm, vasospasm-related new cerebral infarctions, and poor outcome in patients with aneurysmal SAH."
2. Effects of cilostazol on cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a multicenter prospective, randomized, open-label blinded end point trial.
Senbokuya et al {JNS}"Cilostazol, a selective inhibitor of phosphodiesterase 3, may attenuate cerebral vasospasm because of its antiplatelet and vasodilatory effects. A multicenter prospective randomized trial was conducted to investigate the effect of cilostazol on cerebral vasospasm."
Inclusion criteria: Patients in Japan admitted with SAH caused by a ruptured anterior circulation aneurysm who were in Hunt and Kosnik Grades I to IV and were treated by clipping within 72 hours of SAH. Nov 2009 to Dec 2010
Comparison: usual therapy group (control group) vs add-on 100 mg cilostazol twice daily group (cilostazol group).
End points: onset of symptomatic vasospasm (primary), onset of angiographic vasospasm, new cerebral infarctions related to cerebral vasospasm, clinical outcome (mod rankin scale), and length of hospitalization.
Results: N=109
Symptomatic vasospasm occurred in 13% (n = 7) of the cilostazol group and in 40% (n = 22) of the control group (p = 0.0021).
The incidence of angiographic vasospasm was significantly lower in the cilostazol group than in the control group (50% vs 77%; p = 0.0055)
Multiple logistic analyses demonstrated that nonuse of cilostazol is an independent factor for symptomatic and angiographic vasospasm.
The incidence of new cerebral infarctions was also significantly lower in the cilostazol group than in the control group (11% vs 29%; p = 0.0304,).
Clinical outcomes at 1, 3, and 6 months after SAH in the cilostazol group were better than those in the control group, although a significant difference was not shown. There was also no significant difference in the length of hospitalization between the groups. No severe adverse event occurred during the study period.
3. Triple H therapy for SAH: hypertension, hypervolemia, hemodilution. Although hypertension may be the only one of these things that work, and additionally, hemodilution may counteract or worsen the benefit of hypertension in decreasing O2-carrying capacity of blood.
4. Hemodynamic management of subarachnoid hemorrhage.
Treggiari MM1; Participants in the International Multi-disciplinary Consensus Conference on the Critical Care Management of Subarachnoid Hemorrhage. {Neurocrit Care. 2011}
-Literature review (years 2000-2010) on hemodynamic augmentation therapies in patients with subarachnoid hemorrhage. Among the eligible reports identified, 11 addressed volume expansion, 10 blood pressure management, 4 inotropic therapy, and 12 hemodynamic augmentation in patients with unsecured aneurysms.
-Hypervolemia did not appear to confer additional benefits over normovolemic therapy, with an excess of side effects occurring in patients treated with hypervolemic targets.
-Hypertension was associated with higher cerebral blood flow, regardless of volume status, with neurological symptom reversal seen in two-thirds of treated patients.
-Limited data were available for evaluating inotropic agents or hemodynamic augmentation in patients with additional unsecured aneurysms. In the context of sparse data, no incremental risk of aneurysmal rupture has been reported with the induction of hemodynamic augmentation.
5. Effect of different components of triple-H therapy on cerebral perfusion in patients with aneurysmal subarachnoid haemorrhage: a systematic review.
Dankbaar JW et al {Crit Care 2010}
-Systematic literature review (until 2009, excluding case reports) on the effect of triple-H components on cerebral perfusion in SAH patients.
-Outcome: cerebral blood flow (CBF in ml/100 g/min).
-11 studies (4-51 patients per study) were included (one randomized trial).
-Hemodilution did not change CBF.
-One of seven studies on hypervolemia showed statistically significant CBF increase compared to baseline; there was no comparable control group.
-Two of four studies applying hypertension and one of two applying triple-H showed significant CBF increase, none used a control group.
-There is no good evidence from controlled studies for a positive effect of triple-H or its separate components on CBF in SAH patients. In uncontrolled studies, hypertension seems to be more effective in increasing CBF than hemodilution or hypervolemia.
6. The evolving role of hemodilution in treatment of cerebral vasospasm: a historical perspective.
Chittiboina P et al {World Neurosurg. 2011}-Literature review on hemodilution as a therapeutic modality in treatment of cerebral vasospasm.
-Evidence has been accumulating against the efficacy of HHH therapy and hemodilution in particular.
-Although HHH therapy and consequently hemodilution has wide support, the evidence for its effectiveness remains equivocal.
-At the time of this study, the burden of evidence appears to be tipped away from hemodilution as a therapeutic modality.
7. Standard workup in a young or middle aged woman who presents with lower abdominal pain:
-Pregnancy test
-GC/chlamydia
-Wet mount
-Urine dipstick
-Pelvic & abdominal exam.
8. Back pain descriptors and suggested diagnoses
-Pain worse with movement and sitting is suggestive of a mechanical cause of back pain, such as a lumbar strain, disc herniation, or degenerative arthritis.
-Pain radiating down the leg and numbness indicate nerve involvement, such as in disc herniation.
-Pain that improves with the supine position suggests spinal stenosis and disc herniation.
-Dull, throbbing pain that progresses slowly, and increases with recumbency or cough in an older patient with a history of cancer, malignancy is likely
-Aching back and posterior thigh discomfort that increases with activity or bending- think spondylolisthesis
9. Overview: physical exam for back pain:
1. Look at posture, contour and symmetry (lordosis, kyphosis, scoliosis)
2. Palpate for any tenderness, tightness, rope-like tension, or inflammation in the paraspinous muscles or tenderness over bony prominences. This checks for muscle spasm, vertebral fracture, or infection. Point tenderness is suggestive of fracture, infection, malignancy.
3. Range of Motion:
-Lumbar Flexion (normal is 90 degrees): Best measure of spine mobility. Restriction and pain during flexion are suggestive of herniation, osteoarthritis, or muscle spasm.
-Lumbar Extension (normal is 15 degrees): Pain with extension is suggestive of degenerative disease or spinal stenosis.
-Lateral motion (normal is 45 degrees): Most patients should be able to touch the proximal fibular head of the knee. Pain on the same side as bending is suggestive of bone pathology (osteoarthritis or neural compression). Pain on the opposite side of bending is suggestive of a muscle strain.
4. Gait: Heels and toe walk. Expect normal gait, even with disc herniation.
-Difficulty with heel walk is associated with L5 disc herniation
-Difficulty with toe walk is associated with S1 disc herniation
-Have the patient go from a standing to squatting position: With central spinal stenosis, squatting will reduce the pain.
5. DTR:
-0: none, 1: reduced, 2. normal, 3: hyperreflexive, 4: clonus
-Patella is L3/L4, Achilles is L4/L5. Reduced reflexes implies pathology at those respective levels
-Increased reflexes supports UMN disease, like spinal stenosis
6. Strength
-0: none, 1: flicker, not enough to move limb, 2: move limb, not against gravity, 3: move limb against gravity, no resistance 4: some resistance, 5: normal strength.
-Iliopsoas/Hip Flexion (L 2, 3, 4)
-Quads/Knee Extension (L 2, 3, 4)
-Hip Adduction (L 2, 3, 4)
-Hip Abduction (L 4, 5, S1)
-Ankle Dorsiflexion/Tibialis Anterior (L 4, 5)
-Great toe Dosriflexion/Extensor hallucis longus (L5... L4?)
-Knee Flexion/Hamstrings (L 5, S1, S2)
-Ankle Plantar Flexion/Gastrocnemius (S 1, S 2)
10. Focused neuro exam for lower back pain:
-Check the patellar and Achilles reflexes.
-Check muscle strength for hip flexion, abduction, and adduction; knee extension and flexion; ankle dorsiflexion and plantar flexion.
-Test for sharp and light touch along the dermatomal distribution of the great toe (L5), lateral malleolus and posterolateral foot (S1).
Friday, February 21, 2014
1. Criteria for starting tPA:
-Disease: diagnosis of ischemic stroke that began <4.5 hrs ago and is causing significant symptoms that are not resolving, no seizure with post-ictal
-Patient: patient does not have major deficits, understands risks.
-Brain: no signs of ICH, SAH, no recent history of head trauma or stroke, no history of ICH, CT does not show diffuse multiloblar infarction (hypodensity >1/3 cerebral hemisphere-- this can increase risk of bleed after tPA)
-Body: no recent GI/GU hemorrhage (21 days), no major surgery in last 14 days, no arterial puncture in non-compressible aa in last 7 days, no evidence of acute injury/active bleeding now.
-Coags: INR<=1.7, PTT normal, platelets > 100
-Other labs /vitals: BP <185/110, glucose >=50
2. Left MCA stroke:
-R facial/body weakness
-Receptive or productive aphasia
3. Right MCA parietal stroke:
-L facial and body weakness.
-Hemineglect of L side
-Visuospatial compromise (misjudge distances, hold books upside down)
-Denial of stroke symptoms.
4. Anticoagulation for prevention of future stroke:
-Warfarin if high risk of stroke, past stroke (goal INR 2-3)
-Asprin if low risk, unable to tolerate anticoagulation
-Aspirin + Plavix = warfarin for bleed risk.
-CHADS2 score to predict risk of stroke in people with afib.
-Don't start anticoagulation for about 2 weeks after an ischemic stroke to lower risk of secondary hemorrhage.
5. About cochlear implants:
-In infants, you want to implant bilateral cochlear implants so they develop biauricular hearing and will be able to triangulate sounds later in life.
-If someone is born deaf, once they pass the critical period for brain development of auditory processing, don't give them a cochlear implant. They will not be able to interpret the sound. Few exceptions is if you just want to give someone "sound awareness" so they can hear alarms or such.
-In adults who have auditory processing capability (i.e. they were hearing as a child and lost it later in life), start with one cochlear implant. Some people will have complete restoration of hearing. Some people will have partial restoration. In this case, put in a second cochlear implant. If the first implant had zero benefit, don't put in a second.
-When operating on someone with one, don't use a bovie, it can mess up the electronics of the implant
-To put one in, cut behind the ear and drill through the mastoid air cells until you reach the bone that covers the facial nerve. Use it as a landmark to find the round window. Go through it to get to the cochlea. Insert the electrode into the cochlea. Make a pocket in the bone behind the ear to put in the rest of the implant. Suture it in.
-The battery is worn outside the ear, there is no internal battery.
-The device is activated 2-3 weeks after the surgery to give the electrodes a chance to heal in.
6. Why did sinuses evolve? Theories:
-To lighten the head
-To allow for blowout fractures that protect the brain and eyes from facial trauma.
-To act as reservoirs for humidified air that will humidify air before it enters the lungs. The turbinates channel the flow of air in, most of it goes through the inferior part, some is channeled upwards and will pass by the meatus and via the bernoulli effect (air passing by holes for sinus outlets sucks in humidified air into the stream) the appropriate amount of humidity is passed into the air stream. People who have their turbinates removed have chronic problems with dryness.
-In our aquatic mammal common ancestors, it may be useful for buoyancy.
7. About maxillary sinuses:
-The outlet is at the top of the sinus, into the space under the middle turbinate
-Coated with mucus that traps dust and bacteria
-Cilia push mucus up towards the top of the sinus
-The maxillary sinus mucosa should appear white. If it is red, full of blood vessels, inflamed appearing, something is wrong.
-In maxillary sinusitis, there is chronic inflammation of the mucosa of the sinuses, plugging of the ostia leads to entrapped mucus, bacterial overgrowth. Eventually the cilia are destroyed by the inflammation/infection, leading to worsening mucus trapping.
-To treat chronic maxillary sinusitis unresponsive to meds, drill open the natural ostia that drain the sinuses. If that fails, drill an additional ostium under the inferior turbinate into the sinus.
8. About sinus surgery:
-To control bleeding, before surgery soak cotton patties in a solution of cocaine, like 4% (max dose: 4mg/kg) and stuff them in the nose. Cocaine is more vasoconstrictive than other local anesthetics.
-In people who chronically abuse cocaine, this may trigger a vasoconstrictive crisis, so watch their vital signs.
-Speaking of people who chronically abuse cocaine, the vasoconstrictive effect is so intense that over time, the tissues of the nose and sinuses will be deprived of blood supply. This leads to death of the cartilage (septal perforation) and to severe destruction of the cilia in the sinuses, leading to a significant, unremitting chronic sinusitis.
-Also soak cotton in afrin solutions (a1/a2 agonist) to promote vasoconstriction
9. Local anesthesia max dose
-Lido without epi: 7mg/kg
-Lido with epi: 4-5mg/kg
-Marcaine: 2mg/kg
These are probably somewhat arbitrary. The data is of questionable quality and come from animal tests or extrapolations
10. About angioedema
-The inherited version is mediated by bradykinin and does not respond to steroids. Its associated with decreased levels of C1 inhibitor. Treat by giving purified C1 inhibitor protein, or bradykinin or kallikrein inhibitors.
-Acquired angioedema is mediated by histamine, and responds well to steroids.
-Disease: diagnosis of ischemic stroke that began <4.5 hrs ago and is causing significant symptoms that are not resolving, no seizure with post-ictal
-Patient: patient does not have major deficits, understands risks.
-Brain: no signs of ICH, SAH, no recent history of head trauma or stroke, no history of ICH, CT does not show diffuse multiloblar infarction (hypodensity >1/3 cerebral hemisphere-- this can increase risk of bleed after tPA)
-Body: no recent GI/GU hemorrhage (21 days), no major surgery in last 14 days, no arterial puncture in non-compressible aa in last 7 days, no evidence of acute injury/active bleeding now.
-Coags: INR<=1.7, PTT normal, platelets > 100
-Other labs /vitals: BP <185/110, glucose >=50
2. Left MCA stroke:
-R facial/body weakness
-Receptive or productive aphasia
3. Right MCA parietal stroke:
-L facial and body weakness.
-Hemineglect of L side
-Visuospatial compromise (misjudge distances, hold books upside down)
-Denial of stroke symptoms.
4. Anticoagulation for prevention of future stroke:
-Warfarin if high risk of stroke, past stroke (goal INR 2-3)
-Asprin if low risk, unable to tolerate anticoagulation
-Aspirin + Plavix = warfarin for bleed risk.
-CHADS2 score to predict risk of stroke in people with afib.
-Don't start anticoagulation for about 2 weeks after an ischemic stroke to lower risk of secondary hemorrhage.
5. About cochlear implants:
-In infants, you want to implant bilateral cochlear implants so they develop biauricular hearing and will be able to triangulate sounds later in life.
-If someone is born deaf, once they pass the critical period for brain development of auditory processing, don't give them a cochlear implant. They will not be able to interpret the sound. Few exceptions is if you just want to give someone "sound awareness" so they can hear alarms or such.
-In adults who have auditory processing capability (i.e. they were hearing as a child and lost it later in life), start with one cochlear implant. Some people will have complete restoration of hearing. Some people will have partial restoration. In this case, put in a second cochlear implant. If the first implant had zero benefit, don't put in a second.
-When operating on someone with one, don't use a bovie, it can mess up the electronics of the implant
-To put one in, cut behind the ear and drill through the mastoid air cells until you reach the bone that covers the facial nerve. Use it as a landmark to find the round window. Go through it to get to the cochlea. Insert the electrode into the cochlea. Make a pocket in the bone behind the ear to put in the rest of the implant. Suture it in.
-The battery is worn outside the ear, there is no internal battery.
-The device is activated 2-3 weeks after the surgery to give the electrodes a chance to heal in.
6. Why did sinuses evolve? Theories:
-To lighten the head
-To allow for blowout fractures that protect the brain and eyes from facial trauma.
-To act as reservoirs for humidified air that will humidify air before it enters the lungs. The turbinates channel the flow of air in, most of it goes through the inferior part, some is channeled upwards and will pass by the meatus and via the bernoulli effect (air passing by holes for sinus outlets sucks in humidified air into the stream) the appropriate amount of humidity is passed into the air stream. People who have their turbinates removed have chronic problems with dryness.
-In our aquatic mammal common ancestors, it may be useful for buoyancy.
7. About maxillary sinuses:
-The outlet is at the top of the sinus, into the space under the middle turbinate
-Coated with mucus that traps dust and bacteria
-Cilia push mucus up towards the top of the sinus
-The maxillary sinus mucosa should appear white. If it is red, full of blood vessels, inflamed appearing, something is wrong.
-In maxillary sinusitis, there is chronic inflammation of the mucosa of the sinuses, plugging of the ostia leads to entrapped mucus, bacterial overgrowth. Eventually the cilia are destroyed by the inflammation/infection, leading to worsening mucus trapping.
-To treat chronic maxillary sinusitis unresponsive to meds, drill open the natural ostia that drain the sinuses. If that fails, drill an additional ostium under the inferior turbinate into the sinus.
8. About sinus surgery:
-To control bleeding, before surgery soak cotton patties in a solution of cocaine, like 4% (max dose: 4mg/kg) and stuff them in the nose. Cocaine is more vasoconstrictive than other local anesthetics.
-In people who chronically abuse cocaine, this may trigger a vasoconstrictive crisis, so watch their vital signs.
-Speaking of people who chronically abuse cocaine, the vasoconstrictive effect is so intense that over time, the tissues of the nose and sinuses will be deprived of blood supply. This leads to death of the cartilage (septal perforation) and to severe destruction of the cilia in the sinuses, leading to a significant, unremitting chronic sinusitis.
-Also soak cotton in afrin solutions (a1/a2 agonist) to promote vasoconstriction
9. Local anesthesia max dose
-Lido without epi: 7mg/kg
-Lido with epi: 4-5mg/kg
-Marcaine: 2mg/kg
These are probably somewhat arbitrary. The data is of questionable quality and come from animal tests or extrapolations
10. About angioedema
-The inherited version is mediated by bradykinin and does not respond to steroids. Its associated with decreased levels of C1 inhibitor. Treat by giving purified C1 inhibitor protein, or bradykinin or kallikrein inhibitors.
-Acquired angioedema is mediated by histamine, and responds well to steroids.
Thursday, February 20, 2014
1. Causes of A-fib:
-Structural heart changes: MI, acute mitral valve failure, myocarditis, pericarditis
-Pulmonary: PE, acute onset pulmonary disease leading to vasoconstriction
-Endo: hyperthyroid,
-Iatrogenic: cardiac/thoracic surgery (postop a-fib very common)
-Alcohol intake "holiday heart syndrome"
-Electrocution
2. Mechanisms of Cerebral ischemia:
-Embolic: from heart (afib) or carotids
-Thrombotic: native cerebral vessel thromboses (85% of CVA are this)
-Cardiogenic: acute onset heart failure (arrhythmia, MI, acute valve failure)
-Hemorrhagic: brain bleed.
-Hematologic: hyperviscosity (polycythemia, myeloproliferative), hypercoagulable (coag factor mutations, lupus, etc), sickle cell
-Vascular: vasculitis, extrinsic vessel compression/kinking, vasospasm (c-o-c-a-i-n-e, migraine)
3. TIA predictive of stroke risk:
-TIA symptoms => 8-12% risk of stroke within a week
-11-15% risk of stroke within a month.
4. CI to tPA for stroke:
-Recent history of heparin or warfarin administration
-Unknown history of anticoagulation
-Clinical suspicion of bleeding risk/thromobcytopenia
5. Workup for stroke, before initiation of tPA
-Noncontrast head CT
-BMP: lytes, renal function
-EKG/cardiac enzymes: to look for concomitant heart disease (very common). Everyone should get a cardiac workup within 24 hours of a suspected stroke.
-CBC/Coags: tells you about bleeding risk, also infection risk, hypoxia 2/2 severe anemia.
-O2 sat
-Blood glucose
-Other tests per clinical suspicion (i.e. drugs, hepatic, seizures)
6. Cardiac Biomarkers:
-Troponin=marker of choice for the diagnosis MI, more specific than CK-MB. They rise 4-6 hours after MI, and remain up for ~10 days so can be hard to time injury.
-CK-MB rises 4 to 12 hours after the event, remains elevated for only 36 to 48 hours. An elevated serum CK-MB can help confirm the timing of an acute myocardial infarction; in addition, repeat elevations may indicate recurrent myocardial injury.
-Don't use total CK or LDH to diagnose MI.
-Myoglobin is small and rapidly released from damaged cells; sensitivity approx = CK-MB. Myoglobin and LDH are nonspecific for heart. Injury to skeletal mm can cause elevation, as can cocaine use in people with compromised renal function (decreased clearance)
-B-type Natriuretic Peptide (BNP) is 32-amino-acid polypeptide secreted by the ventricles 2/2 pressure overload. BNP elevation can indicate ventricular dysfunction (including from PE!), levels correlate with both severity of symptoms & prognosis.
7. Standard approach for diagnosing MI with cardiac enzymes:
-Serum troponin-T (cTnT) or troponin-I (cTnI) is measured at first presentation.
-If the troponin WNL, repeat at 6-9 hours, or earlier if if you think they are still having NSTEMI. Repeat again at 12-24 hrs if the first 2 came back neg but there is strong clinical suspicion of MI.
-CK-MB if you can't get troponin, or if you suspect MI within 2 weeks of a previous, known MI.
8. Management of A-fib with RVR: first, rate control
-Rate control until you can do the maneuvers for rhythm control
-Goal is to block the AV node (so class II/IV antiarrhythmics)
-If there is no evidence of heart failure, use B-blockers or non-dihydropyridine CCB (ditiazem drip, verapamil)
-if there is evidence of heart failure, use amiodarone or digoxin.
9. Management of A-fib with RVR: second, anticoagulation
-Start heparin drip (goal PTT 45-60), or lovenox subQ (don't need to monitor)
-Low risk: heparin drip, cardiovert soon after, then aspirin
-High risk: heparin drip, transition to warfarin, continue warfarin to goal of INR 2-3.
10. Management of A-fib with RVR: third, rhythm control.
-Cardioversion can temporarily increase the risk of thromboembolic events and stroke, so you don't want to cardiovert someone if you think there is a good chance they will embolize something.
-If someone is low risk for having an embolization (<48 hours since onset of a-fib, TEE shows no thrombus) then you can cardiovert once you start the heparin drip.
-If someone is high risk for embolization, or you saw a thrombus on TEE, wait until they are therapeutically, stably anticoagulated for 3-4 weeks on warfarin to cardiovert.
-Cardioversion can occur with direct-current under anaesthesia
-Cardioversion can also occur pharmacologically: use Class IC antiarrythmics (flecanide, propafenone) work better than Class III antiarrhythmics (ibutilide, amiodarone). Be careful as you can push the rate too fast or slow with these drugs.
-Structural heart changes: MI, acute mitral valve failure, myocarditis, pericarditis
-Pulmonary: PE, acute onset pulmonary disease leading to vasoconstriction
-Endo: hyperthyroid,
-Iatrogenic: cardiac/thoracic surgery (postop a-fib very common)
-Alcohol intake "holiday heart syndrome"
-Electrocution
2. Mechanisms of Cerebral ischemia:
-Embolic: from heart (afib) or carotids
-Thrombotic: native cerebral vessel thromboses (85% of CVA are this)
-Cardiogenic: acute onset heart failure (arrhythmia, MI, acute valve failure)
-Hemorrhagic: brain bleed.
-Hematologic: hyperviscosity (polycythemia, myeloproliferative), hypercoagulable (coag factor mutations, lupus, etc), sickle cell
-Vascular: vasculitis, extrinsic vessel compression/kinking, vasospasm (c-o-c-a-i-n-e, migraine)
3. TIA predictive of stroke risk:
-TIA symptoms => 8-12% risk of stroke within a week
-11-15% risk of stroke within a month.
4. CI to tPA for stroke:
-Recent history of heparin or warfarin administration
-Unknown history of anticoagulation
-Clinical suspicion of bleeding risk/thromobcytopenia
5. Workup for stroke, before initiation of tPA
-Noncontrast head CT
-BMP: lytes, renal function
-EKG/cardiac enzymes: to look for concomitant heart disease (very common). Everyone should get a cardiac workup within 24 hours of a suspected stroke.
-CBC/Coags: tells you about bleeding risk, also infection risk, hypoxia 2/2 severe anemia.
-O2 sat
-Blood glucose
-Other tests per clinical suspicion (i.e. drugs, hepatic, seizures)
6. Cardiac Biomarkers:
-Troponin=marker of choice for the diagnosis MI, more specific than CK-MB. They rise 4-6 hours after MI, and remain up for ~10 days so can be hard to time injury.
-CK-MB rises 4 to 12 hours after the event, remains elevated for only 36 to 48 hours. An elevated serum CK-MB can help confirm the timing of an acute myocardial infarction; in addition, repeat elevations may indicate recurrent myocardial injury.
-Don't use total CK or LDH to diagnose MI.
-Myoglobin is small and rapidly released from damaged cells; sensitivity approx = CK-MB. Myoglobin and LDH are nonspecific for heart. Injury to skeletal mm can cause elevation, as can cocaine use in people with compromised renal function (decreased clearance)
-B-type Natriuretic Peptide (BNP) is 32-amino-acid polypeptide secreted by the ventricles 2/2 pressure overload. BNP elevation can indicate ventricular dysfunction (including from PE!), levels correlate with both severity of symptoms & prognosis.
7. Standard approach for diagnosing MI with cardiac enzymes:
-Serum troponin-T (cTnT) or troponin-I (cTnI) is measured at first presentation.
-If the troponin WNL, repeat at 6-9 hours, or earlier if if you think they are still having NSTEMI. Repeat again at 12-24 hrs if the first 2 came back neg but there is strong clinical suspicion of MI.
-CK-MB if you can't get troponin, or if you suspect MI within 2 weeks of a previous, known MI.
8. Management of A-fib with RVR: first, rate control
-Rate control until you can do the maneuvers for rhythm control
-Goal is to block the AV node (so class II/IV antiarrhythmics)
-If there is no evidence of heart failure, use B-blockers or non-dihydropyridine CCB (ditiazem drip, verapamil)
-if there is evidence of heart failure, use amiodarone or digoxin.
9. Management of A-fib with RVR: second, anticoagulation
-Start heparin drip (goal PTT 45-60), or lovenox subQ (don't need to monitor)
-Low risk: heparin drip, cardiovert soon after, then aspirin
-High risk: heparin drip, transition to warfarin, continue warfarin to goal of INR 2-3.
10. Management of A-fib with RVR: third, rhythm control.
-Cardioversion can temporarily increase the risk of thromboembolic events and stroke, so you don't want to cardiovert someone if you think there is a good chance they will embolize something.
-If someone is low risk for having an embolization (<48 hours since onset of a-fib, TEE shows no thrombus) then you can cardiovert once you start the heparin drip.
-If someone is high risk for embolization, or you saw a thrombus on TEE, wait until they are therapeutically, stably anticoagulated for 3-4 weeks on warfarin to cardiovert.
-Cardioversion can occur with direct-current under anaesthesia
-Cardioversion can also occur pharmacologically: use Class IC antiarrythmics (flecanide, propafenone) work better than Class III antiarrhythmics (ibutilide, amiodarone). Be careful as you can push the rate too fast or slow with these drugs.
Wednesday, February 19, 2014
1. Exam after suspected TIA/CVA:
-Mental status, recent/remote memory
-Cranial nerves, with special focus on II (visual fields), III/IV/VI (gaze palsies), VII (facial strength asymmetry)
-Strength: Deltoid, Biceps, Triceps, Wrist extension, Grip, Intrinsic Hand, Quadriceps, Hamstrings, Tibialis Anterior (dorsiflexion), Gastrocnemius, Extensor hallucis longus.
-Pronator drift (very sensitive for UE weakness)
-Sensation to pin and touch
-Deep tendon reflexes: biceps, triceps, brachiorad, patellar, ankle. Babinski, Hoffman.
-Romberg: loss of balance may indicate vertebral-basilar ischemic pathology
-Gait: ataxia may indicate vertebral-basilar ischemic pathology
-Coordination
-FAST test: face-arm-speech to quickly assess for risk of CVA-- face (ask them to smile, look for asymmetry), arm (raise both arms, check for downward drift), speech (ask to repeat sentence, check for incorrect or slurred response). PPV ~65-75%
-NIH stroke scale for formal, standardized stroke testing. Video demonstration of this exam.
2. Cardiovascular exam after suspected TIA/CVA
-CV: listen to heart-- new onset murmur may indicate valve pathology, mural thrombi that led to CVA
-Auscultate carotids for bruits-- narrowing, thrombi.
-EKG: r/o MI or arrhythmia leading to decreased cerebral perfusion.
3. Get up and go test to assess mobility: have someone sit in a chair, and without using their arms, stand up, walk 10 feet forward, turn around and walk back. Time starts when they start getting up and ends when they sit down. Give them 1 practice round and 3 timed rounds, average 3 times.
If they complete it in an average of:
-<10 seconds: full mobility
-10-20 seconds: mostly independent
-20-30 seconds: variable mobility
->30 seconds: impaired mobility
4. DDx of suspected TIA: Seizure (acute onset weakness, syncope/near syncope, fall, temporary altered mental status, etc)
-Can have aura in the form of alterations in sensorium (vision, hearing, touch, etc; believed to originate from temporal lobe), or dizziness/lightheadedness.
-Can lead to fall
-Post-ictal AMS
-Post-ictal unilateral paralysis (Todd's paralysis, lasting 30 min-30 hours, median 15 hours) or neurologic findings.
-Generally associated with amnesia during and after the seizure event.
-Can be associated with temporary spike in blood pressure.
-A seizure is UNLIKELY if the following are true: patient was responsive during event or had recall of the experience, lack of post ictal confusion/amnesia, no focal neurologic signs, oral injury, or fecal/urinary soiling.
5. DDX of suspected TIA: Stroke
-Risk factors: heart (irregular rhythm, known a-fib or dilation), hypertension, hypercholesterolemia
-Can be preceded by dizziness or lightheadedness 2/2 mild ischemia to brain
-May presenent as sudden onset of focal neurologic deficit (weakness, changes in sensorium, dysarthria, ataxia) or sudden onset of confusion or severe headache.
-Visual changes can occur if the stroke occurred in an opthalmic/retinal artery, if the stroke affects the visual cortex, or if it grossly affects the R brain (visuo-spatial reasoning)
-+/- LOC
6. DDX of suspected TIA: Cardiac dysfunction
-Anything cardiac that leads to fluctuating CPP will lead to TIA like events.
-MI
-Acute valve failure
-PE
-Arrhythmias
7. DDx of suspected TIA: Medications that cause TIA like symptoms
-Anything that affects electrolyte levels (hypoK can cause numbness, weakness, arrhythmias leading to embolic CVA) - diuretics
-Anything that causes hypoglycemia - sulfonylureas
-Anything that causes hypotension - antihypertensives
-Anything that causes orthostatic hypotension - anything that has a-1 blocking effects, like prazosin, and all drugs that have been used for depression except SSRIs.
8. DDx of suspected TIA: space-occupying lesion
-Generally not associated with dizziness/lightheadedness
-Generally associated with headache, n/v
-25% of patients with brain tumor report weakness in UE, 25% report visual changes
-Gradual changes in behavior and cognition are common, sudden LOC or AMS are less common (unless there is a bleed)
9. DDx of suspected TIA: hypoglcyemia
-Can present with weakness, dizziness, focal neuro findings, ataxia, paresthesias, sweating.
-Treat with glucose immediately to prevent long-term damage.
10. DDx of suspected TIA: Zebras
-Temporal arteritis: amaurosis fugax, jaw claudication, headache, TTP/pain over temporal bone, mostly women in their 70s.
-Hemiplegic migraine: migraine + unilateral weakness or sensory deficits, more common in childhood/adolescence, tends to fade by adulthood.
-Hypokalemic periodic paralysis: periodic events of general or focal paralysis, often occurs in rest period after physical activity. Often begins in childhood.
-Mental status, recent/remote memory
-Cranial nerves, with special focus on II (visual fields), III/IV/VI (gaze palsies), VII (facial strength asymmetry)
-Strength: Deltoid, Biceps, Triceps, Wrist extension, Grip, Intrinsic Hand, Quadriceps, Hamstrings, Tibialis Anterior (dorsiflexion), Gastrocnemius, Extensor hallucis longus.
-Pronator drift (very sensitive for UE weakness)
-Sensation to pin and touch
-Deep tendon reflexes: biceps, triceps, brachiorad, patellar, ankle. Babinski, Hoffman.
-Romberg: loss of balance may indicate vertebral-basilar ischemic pathology
-Gait: ataxia may indicate vertebral-basilar ischemic pathology
-Coordination
-FAST test: face-arm-speech to quickly assess for risk of CVA-- face (ask them to smile, look for asymmetry), arm (raise both arms, check for downward drift), speech (ask to repeat sentence, check for incorrect or slurred response). PPV ~65-75%
-NIH stroke scale for formal, standardized stroke testing. Video demonstration of this exam.
2. Cardiovascular exam after suspected TIA/CVA
-CV: listen to heart-- new onset murmur may indicate valve pathology, mural thrombi that led to CVA
-Auscultate carotids for bruits-- narrowing, thrombi.
-EKG: r/o MI or arrhythmia leading to decreased cerebral perfusion.
3. Get up and go test to assess mobility: have someone sit in a chair, and without using their arms, stand up, walk 10 feet forward, turn around and walk back. Time starts when they start getting up and ends when they sit down. Give them 1 practice round and 3 timed rounds, average 3 times.
If they complete it in an average of:
-<10 seconds: full mobility
-10-20 seconds: mostly independent
-20-30 seconds: variable mobility
->30 seconds: impaired mobility
4. DDx of suspected TIA: Seizure (acute onset weakness, syncope/near syncope, fall, temporary altered mental status, etc)
-Can have aura in the form of alterations in sensorium (vision, hearing, touch, etc; believed to originate from temporal lobe), or dizziness/lightheadedness.
-Can lead to fall
-Post-ictal AMS
-Post-ictal unilateral paralysis (Todd's paralysis, lasting 30 min-30 hours, median 15 hours) or neurologic findings.
-Generally associated with amnesia during and after the seizure event.
-Can be associated with temporary spike in blood pressure.
-A seizure is UNLIKELY if the following are true: patient was responsive during event or had recall of the experience, lack of post ictal confusion/amnesia, no focal neurologic signs, oral injury, or fecal/urinary soiling.
5. DDX of suspected TIA: Stroke
-Risk factors: heart (irregular rhythm, known a-fib or dilation), hypertension, hypercholesterolemia
-Can be preceded by dizziness or lightheadedness 2/2 mild ischemia to brain
-May presenent as sudden onset of focal neurologic deficit (weakness, changes in sensorium, dysarthria, ataxia) or sudden onset of confusion or severe headache.
-Visual changes can occur if the stroke occurred in an opthalmic/retinal artery, if the stroke affects the visual cortex, or if it grossly affects the R brain (visuo-spatial reasoning)
-+/- LOC
6. DDX of suspected TIA: Cardiac dysfunction
-Anything cardiac that leads to fluctuating CPP will lead to TIA like events.
-MI
-Acute valve failure
-PE
-Arrhythmias
7. DDx of suspected TIA: Medications that cause TIA like symptoms
-Anything that affects electrolyte levels (hypoK can cause numbness, weakness, arrhythmias leading to embolic CVA) - diuretics
-Anything that causes hypoglycemia - sulfonylureas
-Anything that causes hypotension - antihypertensives
-Anything that causes orthostatic hypotension - anything that has a-1 blocking effects, like prazosin, and all drugs that have been used for depression except SSRIs.
8. DDx of suspected TIA: space-occupying lesion
-Generally not associated with dizziness/lightheadedness
-Generally associated with headache, n/v
-25% of patients with brain tumor report weakness in UE, 25% report visual changes
-Gradual changes in behavior and cognition are common, sudden LOC or AMS are less common (unless there is a bleed)
9. DDx of suspected TIA: hypoglcyemia
-Can present with weakness, dizziness, focal neuro findings, ataxia, paresthesias, sweating.
-Treat with glucose immediately to prevent long-term damage.
10. DDx of suspected TIA: Zebras
-Temporal arteritis: amaurosis fugax, jaw claudication, headache, TTP/pain over temporal bone, mostly women in their 70s.
-Hemiplegic migraine: migraine + unilateral weakness or sensory deficits, more common in childhood/adolescence, tends to fade by adulthood.
-Hypokalemic periodic paralysis: periodic events of general or focal paralysis, often occurs in rest period after physical activity. Often begins in childhood.
Tuesday, February 18, 2014
1. Website for intro to radiology modalities:
2. MRI neuroanatomy
3. Gradient Recalled Echo MRI:
-This is the most sensitive test for blood in the brain parenchyma-- it highlights ferromagnetic effects, such as that caused by blood.
-Blood will appear dark on GRE.
-Better than non-contrast CT for detecting intraparenchymal hemorrhage, but worse for detecting SAH.
-DAI will appear as punctate hypodense areas = punctate hemorrhage from axonal injury
4. Contraindications for MRI:
-Spine stimulators (some)... I think I remember the medtronic reps saying the new ones are MRI-safe at the last CNS meeting... but lots of patients complain that they can feel the devices heating up during MRI so who knows? VNS are safe though.
-Old aneurysm clips: ones used in the last 15 years are generally not ferromagnetic, but check the op note to be sure.
-Pacemakers/AICD/LVAD etc, any implanted cardiac devices.
-Breast tissue expanders (before implant surgery)
-Any metallic foreign bodies
-When in doubt, check MRIsafety.com for a full list of specific products and MRI safety.
5. Subarachnoid hemorrhage: (info here)
-Non contrast CT best in first 12 hours, sensitivity decreases after
-If the CT is negative but clinical suspicion is high => LP to look for xanthochromia (looks pink), elevated RBCs, elevated opening pressure.
-Look for blood (hyperdense on non contrast CT) in sulci and cisterns, esp supracellar (aka chiasmatic) and interpeduncular cisterns, as they can show a small amount of blood. (great lecture on cisterns)
From ABC radiology blog:
-Usually due to tearing of subependymal veins.
-Often associated with corpus callosum injury
-Best place to look: occipital horns of lateral ventricles.
-Choroid plexus can calcify and look hyperdense on CT
7. Signs that may indicate herniation on CT:
-Midline shift
-Compression of ipsilateral ventricles
-Loss of supracellar cistern (replacement by herniated brain)
-Cephalad shift of brainstem
-Caudal shift of cerebellum
8. Types of herniation:
-Subfalcine: supratentorial mass forces cingulate gyrus across falx. Shift in septum pellucidum, can compress ACA causing ischemia.
-Descending transtentorial: cerebrum herniates through incisura into posterior fossa. On CT you will see effacement of basal (interpenduncular) and suprasellar cisterns.
-Uncal: uncus of temporal lobe herniates through incisura, effaces suprasellar cistern, may compress PCA.
-Ascending transtentorial: posterior fossa mass/fluid causes anterior displacement of midbrain/brainstem, cerebellar vermis may herniate up as well.
-Cerebellar tonsil: cerebellar tonsils herniate down through foramen magnum, compress brainstem anteriorly.
-Good website on herniation
9. Diffuse Axonal Injury: (good website on DAI)
-Rapid accel/decel forces-- brain decelerates at different rates due to differing densities, leading to shearing force applied to brain parenchyma and axonal injury.
-Most common places to have DAI: grey-white matter junction, basal ganglia, internal capsule, splenium/body of corpus callosum, brainstem.
-Findings on non-contrast CT: punctate hyperintense points, suggestive of microhemorrhage or subtle hypointense regions representing edema
-Findings on gradient echo MRI: punctate hypodense areas corresponding to areas of microhemorrhage where axons were damaged.
-Findings on T2 and T2/FLAIR MRI: oval hyperintense regions = edema
-Findings on Diffusion Weighted MRI: oval hyperintense regions, corresponding to cytotoxic edema
10. Subdurals & CT
-Acute subdural (<3 days): hyperdense on non-contrast CT
-Subacute subdural (3 days to 3 weeks): isodense on non-contrast CT, hard to see-- look for midline shift, increased thickness of grey matter (subdural will look like grey matter), loss of sulci.
-Chronic subdural: hypodense on non-contrast CT
-Acute on chronic subdural: will look heterogenous on CT (mixing of hypodense and hyperdense) or will demonstrate a hematocrit line, where there is a horizontal separation between hyperdense and hypodense.
2. MRI neuroanatomy
3. Gradient Recalled Echo MRI:
-This is the most sensitive test for blood in the brain parenchyma-- it highlights ferromagnetic effects, such as that caused by blood.
-Blood will appear dark on GRE.
-Better than non-contrast CT for detecting intraparenchymal hemorrhage, but worse for detecting SAH.
-DAI will appear as punctate hypodense areas = punctate hemorrhage from axonal injury
4. Contraindications for MRI:
-Spine stimulators (some)... I think I remember the medtronic reps saying the new ones are MRI-safe at the last CNS meeting... but lots of patients complain that they can feel the devices heating up during MRI so who knows? VNS are safe though.
-Old aneurysm clips: ones used in the last 15 years are generally not ferromagnetic, but check the op note to be sure.
-Pacemakers/AICD/LVAD etc, any implanted cardiac devices.
-Breast tissue expanders (before implant surgery)
-Any metallic foreign bodies
-When in doubt, check MRIsafety.com for a full list of specific products and MRI safety.
5. Subarachnoid hemorrhage: (info here)
-Non contrast CT best in first 12 hours, sensitivity decreases after
-If the CT is negative but clinical suspicion is high => LP to look for xanthochromia (looks pink), elevated RBCs, elevated opening pressure.
-Look for blood (hyperdense on non contrast CT) in sulci and cisterns, esp supracellar (aka chiasmatic) and interpeduncular cisterns, as they can show a small amount of blood. (great lecture on cisterns)
From ABC radiology blog:
Supracelllar cistern & interpeduncular cistern separated by Liliequist membrane.
6. Interventricular hemorrhage: -Usually due to tearing of subependymal veins.
-Often associated with corpus callosum injury
-Best place to look: occipital horns of lateral ventricles.
-Choroid plexus can calcify and look hyperdense on CT
7. Signs that may indicate herniation on CT:
-Midline shift
-Compression of ipsilateral ventricles
-Loss of supracellar cistern (replacement by herniated brain)
-Cephalad shift of brainstem
-Caudal shift of cerebellum
8. Types of herniation:
-Subfalcine: supratentorial mass forces cingulate gyrus across falx. Shift in septum pellucidum, can compress ACA causing ischemia.
-Descending transtentorial: cerebrum herniates through incisura into posterior fossa. On CT you will see effacement of basal (interpenduncular) and suprasellar cisterns.
-Uncal: uncus of temporal lobe herniates through incisura, effaces suprasellar cistern, may compress PCA.
-Ascending transtentorial: posterior fossa mass/fluid causes anterior displacement of midbrain/brainstem, cerebellar vermis may herniate up as well.
-Cerebellar tonsil: cerebellar tonsils herniate down through foramen magnum, compress brainstem anteriorly.
-Good website on herniation
9. Diffuse Axonal Injury: (good website on DAI)
-Rapid accel/decel forces-- brain decelerates at different rates due to differing densities, leading to shearing force applied to brain parenchyma and axonal injury.
-Most common places to have DAI: grey-white matter junction, basal ganglia, internal capsule, splenium/body of corpus callosum, brainstem.
-Findings on non-contrast CT: punctate hyperintense points, suggestive of microhemorrhage or subtle hypointense regions representing edema
-Findings on gradient echo MRI: punctate hypodense areas corresponding to areas of microhemorrhage where axons were damaged.
-Findings on T2 and T2/FLAIR MRI: oval hyperintense regions = edema
-Findings on Diffusion Weighted MRI: oval hyperintense regions, corresponding to cytotoxic edema
10. Subdurals & CT
-Acute subdural (<3 days): hyperdense on non-contrast CT
-Subacute subdural (3 days to 3 weeks): isodense on non-contrast CT, hard to see-- look for midline shift, increased thickness of grey matter (subdural will look like grey matter), loss of sulci.
-Chronic subdural: hypodense on non-contrast CT
-Acute on chronic subdural: will look heterogenous on CT (mixing of hypodense and hyperdense) or will demonstrate a hematocrit line, where there is a horizontal separation between hyperdense and hypodense.
Monday, February 17, 2014
1. ADLs--- basic self-care activities done in the home, minimum for being able to live at home independently: bathing, dressing, toileting, continence, transferring from bed to chair, feeding self.
2. Instrumental ADLs-- things that don't need to be done every day, can have hired help to do them: telephone call, managing medications and finances, shopping, cooking, managing transportation.
3. Vitamin E may be helpful in delaying the progression of Alzheimer's but it increases all-cause mortality.
4. Well's criteria for determining risk of PE:
-Clinical signs of DVT - 3 pts
-DVT most likely - 3 pts
-Recent surgery (within 4 weeks) or recent immobilization > 3 days - 1.5 pts
-HR>100 - 1.5 pts
-Previous DVT or PE - 1.5 pts
-Malignancy within last 6 months - 1 pt
-Hemoptysis -1 pt
5 points or more: likely to be PE, go to CT
4 points or less: unlikely PE, d-dimer to r/o
5.Likelihood of CAD by sex, age, chest pain:
-Presyncope- feeling light-headed (cardiac, pulm, blood, vasovagal)
-Dysequilibrium- feeling off balance (cerebellum, DM neuropathy, Tabes dorsalis)
-Vertigo- room spinning (CNS pathology vs peripheral nerve)
7. Common causes of vertigo:
-Vestibular neuritis: common after URI, affects peripheral nerve, may cause horizontal nystagmus that resolves with gaze fixation (bats in the direction of pathology), vertigo doesn't change with position. Inflammation of vestibular nerve.
-Labrynthitis: inflammation of both branches of CN VIII- vestibular and cochlear; causes hearing loss/tinnitus as well as vertigo.
-Benign paroxysmal positional vertigo: Episodic, acute onset episodes of vertigo triggered by position change and resolving minutes after the position change; may cause associated nausea, vomiting, hearing loss. Thought to be due to movement of calcium carbonate in the semicircular canals. (diagnose with dix-hallpike test; turn head 45 degrees to side, lie down fast, extend neck, nystagmus will bat towards the pathological side) (+ dix hallpike)
-Vestibular migraine: causes central vertigo +/- headache, patients usually report history of migraines.
-Menieres: episodes of unilateral tinnitus, hearing loss, vertigo.
-Otitis media: +fever, +findings on ear exam.
8. Central vs peripheral causes of nystagmus:
-More likely peripheral: resolves with gaze fixation worsens with loss of fixation, unidirectional (horizontal or rotational), worsens with Frenzel glasses (prevent fixation)
-More likely central: does not resolve with gaze fixation, lasts longer (much more ominous- TIA/infarct, tumor)
9. Central vs peripheral vertigo:
-Head thrust test: Ask them to look at your nose, then turn their head quickly to the side. Normally, they can still focus on you. If the lesion is peripheral, the vestibular-ocular reflex will fail, and you will see their eyes turn away suddenly, then saccade back when you turn the head to the affected side. A normal head-thrust test in the presence of vertigo suggests CNS pathology.
10. Treatment for peripheral vertigo:
-If its menieres disease, diuretics theoretically reduce endolymph pressure, but unclear evidence
-If its BPPV, epley maneuver (patient sits on table with head turned 45 deg to R. He patient quickly lies back with his head hanging over table. Once the nystagmus stops, turn the head 90 degrees to the left, hold for 30 seconds. Next, the patient rolls onto his left side, with his face at a 45 degree angle to the floor; hold 30 seconds. The patient returns to the sitting position with legs off the left edge of the table. After another 30 seconds, the patient can resume normal head position. Repeat on other side)
-Vestibular rehab (balance exercises)
-Vestibular suppressants- meclizine, diphenhydramine also help with nausea. Nonselective phenothiazine antiemetics (metoclopramide, promethazine) may help. All of these can cause sedation and some are anticholinergics, avoid in elderly.
-Clinical signs of DVT - 3 pts
-DVT most likely - 3 pts
-Recent surgery (within 4 weeks) or recent immobilization > 3 days - 1.5 pts
-HR>100 - 1.5 pts
-Previous DVT or PE - 1.5 pts
-Malignancy within last 6 months - 1 pt
-Hemoptysis -1 pt
5 points or more: likely to be PE, go to CT
4 points or less: unlikely PE, d-dimer to r/o
5.Likelihood of CAD by sex, age, chest pain:
(source)
6. "Dizziness" is usually one of the following:-Presyncope- feeling light-headed (cardiac, pulm, blood, vasovagal)
-Dysequilibrium- feeling off balance (cerebellum, DM neuropathy, Tabes dorsalis)
-Vertigo- room spinning (CNS pathology vs peripheral nerve)
7. Common causes of vertigo:
-Vestibular neuritis: common after URI, affects peripheral nerve, may cause horizontal nystagmus that resolves with gaze fixation (bats in the direction of pathology), vertigo doesn't change with position. Inflammation of vestibular nerve.
-Labrynthitis: inflammation of both branches of CN VIII- vestibular and cochlear; causes hearing loss/tinnitus as well as vertigo.
-Benign paroxysmal positional vertigo: Episodic, acute onset episodes of vertigo triggered by position change and resolving minutes after the position change; may cause associated nausea, vomiting, hearing loss. Thought to be due to movement of calcium carbonate in the semicircular canals. (diagnose with dix-hallpike test; turn head 45 degrees to side, lie down fast, extend neck, nystagmus will bat towards the pathological side) (+ dix hallpike)
-Vestibular migraine: causes central vertigo +/- headache, patients usually report history of migraines.
-Menieres: episodes of unilateral tinnitus, hearing loss, vertigo.
-Otitis media: +fever, +findings on ear exam.
8. Central vs peripheral causes of nystagmus:
-More likely peripheral: resolves with gaze fixation worsens with loss of fixation, unidirectional (horizontal or rotational), worsens with Frenzel glasses (prevent fixation)
-More likely central: does not resolve with gaze fixation, lasts longer (much more ominous- TIA/infarct, tumor)
9. Central vs peripheral vertigo:
-Head thrust test: Ask them to look at your nose, then turn their head quickly to the side. Normally, they can still focus on you. If the lesion is peripheral, the vestibular-ocular reflex will fail, and you will see their eyes turn away suddenly, then saccade back when you turn the head to the affected side. A normal head-thrust test in the presence of vertigo suggests CNS pathology.
10. Treatment for peripheral vertigo:
-If its menieres disease, diuretics theoretically reduce endolymph pressure, but unclear evidence
-If its BPPV, epley maneuver (patient sits on table with head turned 45 deg to R. He patient quickly lies back with his head hanging over table. Once the nystagmus stops, turn the head 90 degrees to the left, hold for 30 seconds. Next, the patient rolls onto his left side, with his face at a 45 degree angle to the floor; hold 30 seconds. The patient returns to the sitting position with legs off the left edge of the table. After another 30 seconds, the patient can resume normal head position. Repeat on other side)
-Vestibular rehab (balance exercises)
-Vestibular suppressants- meclizine, diphenhydramine also help with nausea. Nonselective phenothiazine antiemetics (metoclopramide, promethazine) may help. All of these can cause sedation and some are anticholinergics, avoid in elderly.
Friday, February 14, 2014
1. Cancer screening in adults (USPSTF)
-Lung: screen people aged 55-80 with a >30 pack year smoking history who have smoked within last 15 years. Do not screen if they have been nicotine abstinent for >15 years, if they could not tolerate lung resection surgery, or if they are going to die of something else first (USPSTF grade B)
-Colon: screen people 50-74. Choice of high-sensitivity stool card every year, or sigmoidoscopy q5 years + stool card q3 years, or colonoscopy q10 years. (USPSTF grade A) You probably shouldn't screen people aged 75-85 (grade C), definitely for the love of jesus do not screen people older than 85 (grade D)
-Prostate: do not screen using PSA, and since we have no better test, that means don't screen at all. Screening doesn't change the rate of discovery of malignant prostate cancers, only increases discovery of benign cancers that wouldn't have killed anyone. The risk of the follow up biopsy (which requires 30 different samples) leading to incontinence or impotence are high. (USPSTF grade D)
-Breast: mammograms every 2 years for women aged 50-75 (USPSTF Grade B), younger 50 if the patient really wants it (grade C), unclear if there is benefit after age 75. Sidenote: In a young woman with a significant family history of breast cancer, don't do mammograms, just go straight to genetic testing. If she's BRCA+, she'll need to start tamoxifen for life.
2. Non-cancer screening tests:
-Bone density: Women should get a DEXA at 65. You only need to do it once if it's normal, as the data shows that if its normal at 65 it'll always be normal. Screen at 60 if the woman has risk factors (white or asian race, skinny, smoker)
-AAA: Men aged 65-75 who have ever smoked should get one abdominal u/s to look for AAA.
-Hyperlipidemia (men): Screen all men >35 (USPSTF grade A), screen men >20 if they have risk factors for CAD (USPSTF Grade A)
-Hyperlipidemia (women): Screen women >45 ONLY IF they have risk factors (USPSTF grade A), screen women >20 if they have risk factors (USPSTF grade B).
-Depression: all adolescents aged 12-18 and all adults should be screened for depression, if you have the ability to follow up with treatment. (USPSTF B) PHQ 9: 70-80% sens, 95%+ spec using 10 as cutoff score, compared to gold standard psych interview. ~10% prevalence
3. Vaccinations:
-Zoster vaccine at 60
-Colon: screen people 50-74. Choice of high-sensitivity stool card every year, or sigmoidoscopy q5 years + stool card q3 years, or colonoscopy q10 years. (USPSTF grade A) You probably shouldn't screen people aged 75-85 (grade C), definitely for the love of jesus do not screen people older than 85 (grade D)
-Prostate: do not screen using PSA, and since we have no better test, that means don't screen at all. Screening doesn't change the rate of discovery of malignant prostate cancers, only increases discovery of benign cancers that wouldn't have killed anyone. The risk of the follow up biopsy (which requires 30 different samples) leading to incontinence or impotence are high. (USPSTF grade D)
-Breast: mammograms every 2 years for women aged 50-75 (USPSTF Grade B), younger 50 if the patient really wants it (grade C), unclear if there is benefit after age 75. Sidenote: In a young woman with a significant family history of breast cancer, don't do mammograms, just go straight to genetic testing. If she's BRCA+, she'll need to start tamoxifen for life.
2. Non-cancer screening tests:
-Bone density: Women should get a DEXA at 65. You only need to do it once if it's normal, as the data shows that if its normal at 65 it'll always be normal. Screen at 60 if the woman has risk factors (white or asian race, skinny, smoker)
-AAA: Men aged 65-75 who have ever smoked should get one abdominal u/s to look for AAA.
-Hyperlipidemia (men): Screen all men >35 (USPSTF grade A), screen men >20 if they have risk factors for CAD (USPSTF Grade A)
-Hyperlipidemia (women): Screen women >45 ONLY IF they have risk factors (USPSTF grade A), screen women >20 if they have risk factors (USPSTF grade B).
-Depression: all adolescents aged 12-18 and all adults should be screened for depression, if you have the ability to follow up with treatment. (USPSTF B) PHQ 9: 70-80% sens, 95%+ spec using 10 as cutoff score, compared to gold standard psych interview. ~10% prevalence
3. Vaccinations:
-Zoster vaccine at 60
-Pneumovax: for healthy adults, one after 65 (if you got one before 65, then you'll need a booster 5 years later if you are over 65 at that point)
-Pneumovax: for adults who are immunocompromised or have diabetes, chronic lung dx, chronic kidney dx, chronic heart disease, no spleen, sickle cell, history of cancer, history of bone marrow/solid organ transplant, they should get their first pneumovax shot anytime, and a booster 5 years later.
-Prevnar: for adults that have no spleen, sickle cell, CSF leak, cochlear implant, or are immunocompromised should get prevnar first, then pneumovax 8 weeks later. If they already got pneumovax, wait 1 year to give prevnar.
-Pneumovax: for adults who are immunocompromised or have diabetes, chronic lung dx, chronic kidney dx, chronic heart disease, no spleen, sickle cell, history of cancer, history of bone marrow/solid organ transplant, they should get their first pneumovax shot anytime, and a booster 5 years later.
-Prevnar: for adults that have no spleen, sickle cell, CSF leak, cochlear implant, or are immunocompromised should get prevnar first, then pneumovax 8 weeks later. If they already got pneumovax, wait 1 year to give prevnar.
-Flu shot every year
-Meningitis vaccine first shot from age 11-13, second booster at 16.
4. Chemoprophylaxis:
-Meningitis vaccine first shot from age 11-13, second booster at 16.
4. Chemoprophylaxis:
-All women should take baby aspirin and vitamin D from age 55 to age 80 to prevent strokes
-All men should take baby aspirin from age 45 on to prevent MI.
-Initiate aspirin at younger age if the person has risk factors for MI/CVA and no risks for GI bleed
5. In an adult presenting with fatigue/insomnia/depressive like symptoms, do the following workup:
-Comprehensive metabolic panel: Screen for electrolyte, renal, and hepatic problems.
-TSH: Rule out hypothyroidism (affects 5% of the US population)
-CBC: Check for anemia and vitamin deficiencies.
-Erythrocyte sedimentation rate: Test for rheumatologic disease.
-EKG: Should be done if the patient is using drugs that might alter cardiac conductivity
-TSH: Rule out hypothyroidism (affects 5% of the US population)
-CBC: Check for anemia and vitamin deficiencies.
-Erythrocyte sedimentation rate: Test for rheumatologic disease.
-EKG: Should be done if the patient is using drugs that might alter cardiac conductivity
-Testing to r/o parkinsons (depression can precede motor presentation)
-Testing to r/o dementia (mini-cog has sens 99%, spec 93%, better than MMSE; do 3 words, clockface to recall those 3 words)
6. Ankle tendonitis: usually posterior tibial tendon. At first, it's just pain with aggravation, then it progresses to pain all the time, worse with exercise/during the day. It's a chronic disesae
7. Tarsal tunnel syndrome: pain, tingling, numbness in bottom of feet or on medial side of ankle, pain is often shooting in quality, due to entrapment of tibial nerve.
8. DDx of cough:
-Post-nasal drip (now called upper airway cough syndrome)
-Asthma
-Acute/Chronic Bronchitis
-Vocal cord dysfunction
-GERD
-ACE-I
-Tobacco-related
-Post-infectious
-Non asthma eosinophilic bronchitis
Rarer, more serious causes: structural lung findings (lung CA, sarcoid, TB), CHF
9. DDx palpitations:
-Heart: arrhythmias, valve disease, congenital heart defects, coronary disease (atypical presentation)
-Things that make it more likely cardiac: lasting > 5 minutes, irregular rhythm, history of heart dx, accompanied by pleuritic/positional chest pain.
-Endo: hyperthyroid, vasomotor (menopause)
-Psych: panic attack, anxiety
-Anemia
-Drugs: stimulants, alcohol, tobacco, caffeine, street drugs, sympathomimetics, vasodilators, anticholinergics, w/d from b-blockers
In a prospective cohort study of 190 patients at a university medical center who complained of palpitations:
31% was anxiety or panic
43% was cardiac
(40% dysrhythmias and 3% other cardiac causes)
6% due to drugs
10. MIs in women are much more likely to be atypical--McSweeny et al noted that 95% of women reported prodromal symptoms, but only 29.7% reported chest discomfort.
Prodromal symptoms may include: fatigue, dyspnea, neck and jaw pain, palpitations, cough, nausea and vomiting, indigestion, back pain, dizziness, numbness
40% of initial cardiac events in women are fatal.
Thursday, February 13, 2014
1. Diagnosing shoulder injuries:
-People over 40 are more likely to have rotator cuff tears, under 40 are more likely to have nstability/dislocation
-Pain that travels past the elbow is more likely c-spine in origin
-People who are diabetic or have thyroid pathology are more likely to get frozen shoulder (adhesive capsulitis), which is a dramatic, dramatic loss of ROM.
-Pain with abduction past the shoulder may be rotator cuff, or bursitis, or tendinitis in rotator cuff
-Pain with weight lifting may be an AC joint pathology, as weight lifting loads the AC joint.
2. ROM test:
-Neers test: flex arm up, "near the ear", test impingement of rotator cuff
-Hawkins test, start with nears test, then bend elbow and advance towards opposite shoulder, also test of impingement.
-Speed's test: they hold hand palm up, elbow bent, you push down on their hand to test biceps & biceps tendon
-Yergesons' test: they try to supinate and flex, you try to prevent them. again tests biceps/biceps tendon.
-Obrien's test: hold arm straight out, across midline, thumb up and thumb down you press on it. More pain on thumb down = labrum injury
3. Ankle tests:
-If you squeeze their tib and fib together near the knee, it opens up the tib and fib by the ankle; if this is painful it may indicate syndesmotic/high ankle sprain
-Thomas test: have them lie prone, squeeze the calf muscle, pulls on achilles, if their foot fails to plantar flex, it indicates possible achilles injury.
4. Integrative medicine learning modules available online through the university of Arizona.
5. Diagnosis of hypertension:
-2 blood pressure measurements, >1 week apart. A good real world approach is if you find one elevated (not severe) have them attempt diet and exercise control, and to measure their BP at home (i.e. at walgreens) 3-4 times, and then follow up with you 1-2 months later. If it is still high, then you can start treatment.
-JNC 7:
<120/80 is target.
>140 sys or >90 diastolic was treated with starting 1 drug (thiazide)
>160 sys or >100 diastolic you start two drugs, thiazide + ACE/ARB or CCB or BB
-JNC 8:
definition of hypertension for everyone under 60 is >140/90 and for everyone over 60 is >150/100 should get treated.
6. DDx hypertension
-Smoking, caffeine, NSAIDs, cold medicines, cocaine. (To keep in mind when you are diagnosing essential hypertension)
-Vascular: renal artery stenosis, fibromuscular dysplasia, aortic coarctation (depending on location, may cause htn in brachial aa)
-Endocrine: hyper or hypothyroidism, hyperparathyroidism, cushing's disease, addison's disease
-Renal: ESRD, AKI, obstructive uropathy, nephritic or nephrotic syndrome, PCKD
-Other: sleep apnea, chronic alcoholism.
7. Initial workup of hypertension
-EKG for baseline
-Urine- microalbuminuria
-Lipids, A1C
8. Treatment & CI to drugs (JNC 8)
-You can start anything as first line- diuretic, ACE/ARB, or CCB.
-If the person is black, then prefer diuretic or CCB because of better response.
-ACEI: CI in pregnancy or in any woman of reproductive age who is not using reliable contraception and is sexually active, angioedema patients.
-B-blocker: severe heart failure, severe COPD
-Thiazide diuretic: gout, taking lithium
9. Treating hyperlipidemia: Old guidelines (ATP III)
-Old guidelines (ATP III): target LDL varies depending on cardiac equivalents, treat to target.
-Cardiac equivalents: DM, CVA, renal failure, symptomatic carotid disease, PAD, AAA
-Cardiac risk factors: smoking, hypertension (taking any antihypertensives or BP > 140/90), HDL<40, early CAD in first-degree family member (early =<55 males, <65 females), advanced age (women > 55, men >45)
10-year risk factor calculator here
If someone higher than target LDL but not high enough to start a statin, then they should start diet and exercise.
(image from NHLBI ATP III guidelines)
10. Treating hyperlipidemia: New guidelines (ATP 4)
-Now there are 4 groups of people that should definitely be on statins, of varying intensity-
(1) Everyone with clinically significant cardiovascular disease (start high intensity statin)
(2) everyone with an LDL>190 (start high intensity statin)
(3) every diabetic with an LDL>70 (start medium intensity statin)
(4) everyone with an LDL > 70 and a 10-year cardiac risk > 7.5%. (start medium intensity statin)
-If someone comes in with terrible numbers on their lipid labs, generally you will start by treating LDLs first (i.e. starting a statin) and then if their triglycerides are still high after that, you can add a fibrate or niacin. Unless their triglycerides are >500, then you treat that first to avoid pancreatitis.
-If you start a statin, get baseline LFTs and follow them every year-- you need to see a 3x elevation to be adequately sure that the statin is causing a meaningful change to the liver.
-Don't start a statin in someone with either acute or chronic liver disease.
-People over 40 are more likely to have rotator cuff tears, under 40 are more likely to have nstability/dislocation
-Pain that travels past the elbow is more likely c-spine in origin
-People who are diabetic or have thyroid pathology are more likely to get frozen shoulder (adhesive capsulitis), which is a dramatic, dramatic loss of ROM.
-Pain with abduction past the shoulder may be rotator cuff, or bursitis, or tendinitis in rotator cuff
-Pain with weight lifting may be an AC joint pathology, as weight lifting loads the AC joint.
2. ROM test:
-Neers test: flex arm up, "near the ear", test impingement of rotator cuff
-Hawkins test, start with nears test, then bend elbow and advance towards opposite shoulder, also test of impingement.
-Speed's test: they hold hand palm up, elbow bent, you push down on their hand to test biceps & biceps tendon
-Yergesons' test: they try to supinate and flex, you try to prevent them. again tests biceps/biceps tendon.
-Obrien's test: hold arm straight out, across midline, thumb up and thumb down you press on it. More pain on thumb down = labrum injury
3. Ankle tests:
-If you squeeze their tib and fib together near the knee, it opens up the tib and fib by the ankle; if this is painful it may indicate syndesmotic/high ankle sprain
-Thomas test: have them lie prone, squeeze the calf muscle, pulls on achilles, if their foot fails to plantar flex, it indicates possible achilles injury.
4. Integrative medicine learning modules available online through the university of Arizona.
5. Diagnosis of hypertension:
-2 blood pressure measurements, >1 week apart. A good real world approach is if you find one elevated (not severe) have them attempt diet and exercise control, and to measure their BP at home (i.e. at walgreens) 3-4 times, and then follow up with you 1-2 months later. If it is still high, then you can start treatment.
-JNC 7:
<120/80 is target.
>140 sys or >90 diastolic was treated with starting 1 drug (thiazide)
>160 sys or >100 diastolic you start two drugs, thiazide + ACE/ARB or CCB or BB
-JNC 8:
definition of hypertension for everyone under 60 is >140/90 and for everyone over 60 is >150/100 should get treated.
6. DDx hypertension
-Smoking, caffeine, NSAIDs, cold medicines, cocaine. (To keep in mind when you are diagnosing essential hypertension)
-Vascular: renal artery stenosis, fibromuscular dysplasia, aortic coarctation (depending on location, may cause htn in brachial aa)
-Endocrine: hyper or hypothyroidism, hyperparathyroidism, cushing's disease, addison's disease
-Renal: ESRD, AKI, obstructive uropathy, nephritic or nephrotic syndrome, PCKD
-Other: sleep apnea, chronic alcoholism.
7. Initial workup of hypertension
-EKG for baseline
-Urine- microalbuminuria
-Lipids, A1C
8. Treatment & CI to drugs (JNC 8)
-You can start anything as first line- diuretic, ACE/ARB, or CCB.
-If the person is black, then prefer diuretic or CCB because of better response.
-ACEI: CI in pregnancy or in any woman of reproductive age who is not using reliable contraception and is sexually active, angioedema patients.
-B-blocker: severe heart failure, severe COPD
-Thiazide diuretic: gout, taking lithium
9. Treating hyperlipidemia: Old guidelines (ATP III)
-Old guidelines (ATP III): target LDL varies depending on cardiac equivalents, treat to target.
-Cardiac equivalents: DM, CVA, renal failure, symptomatic carotid disease, PAD, AAA
-Cardiac risk factors: smoking, hypertension (taking any antihypertensives or BP > 140/90), HDL<40, early CAD in first-degree family member (early =<55 males, <65 females), advanced age (women > 55, men >45)
Risk Factors
|
Target LDL
|
LDL to start statin:
|
1+ cardiac equivalents or 10 year risk >20%
|
100 (70 optimal)
|
130
|
2+ risk factors & 10 year risk 10-20%
|
130
|
130
|
2+ risk factors & 10 year risk <20%
|
130
|
160
|
0-1 risk factors
|
160
|
190
|
If someone higher than target LDL but not high enough to start a statin, then they should start diet and exercise.
(image from NHLBI ATP III guidelines)
10. Treating hyperlipidemia: New guidelines (ATP 4)
-Now there are 4 groups of people that should definitely be on statins, of varying intensity-
(1) Everyone with clinically significant cardiovascular disease (start high intensity statin)
(2) everyone with an LDL>190 (start high intensity statin)
(3) every diabetic with an LDL>70 (start medium intensity statin)
(4) everyone with an LDL > 70 and a 10-year cardiac risk > 7.5%. (start medium intensity statin)
-If someone comes in with terrible numbers on their lipid labs, generally you will start by treating LDLs first (i.e. starting a statin) and then if their triglycerides are still high after that, you can add a fibrate or niacin. Unless their triglycerides are >500, then you treat that first to avoid pancreatitis.
-If you start a statin, get baseline LFTs and follow them every year-- you need to see a 3x elevation to be adequately sure that the statin is causing a meaningful change to the liver.
-Don't start a statin in someone with either acute or chronic liver disease.
Wednesday, February 12, 2014
1. Rhogam
-Given to all Rh neg women at 28 weeks, and and again immediately after delivery if baby is Rh positive (draw the baby's blood).
-Give earlier than 28 weeks if there is blood-blood mixing (i.e. miscarriage)
2. Vaginal bleeding through a closed cervix happens in 20-40% of pregnancies, leads to spontaenous Ab half the time.
-Worry about an ectopic.
-Do u/s to look for viable fetus, check cervix-- if its open, abortion is inevitable, B-hcg to trend to follow progress.
-For the next pregnancy, they can get a cerclage if incompetent cervix is the problem (no contractions before loss)
3. EC effectiveness (in descending order)
-Copper iud
-Ella (ulipristal)
-Plan b (1.5 mg levonorgestrel)
-Yuzpe method - 100 ug estrogen, 0.5 mg levonorgestrel, then another dose of the same 12 hours later. If you give the estrogen all at once, it can cause bad nausea and then the method fails.
4. Contraindications for estrogen:
-Smoking 10-15 cigarettes per day or more
-Personal hx of breast cancer within last 5 years is an absolute CI. Family history of breast cancer is not.
-Within 6 weeks of delivery, increased risk of DVT 2/2 increased estrogen. Wait 3 weeks in low risk women, 4 weeks if the woman is breast-feeding, 6 weeks in high risk women.
-Hypertension (>160/100)
-Migraine with true aura (seeing things, Neuro sx)
Highly useful chart for determining relative and absolute CI to various methods of birth control by comborbidity
5. Soft contraindications for contraception:
-Patch isn't effective in obese women, as the transdermal absorption is ineffective at some point
-Depo-provera shot can cause weight gain, so
5. Soft contraindications for contraception:
-Patch isn't effective in obese women, as the transdermal absorption is ineffective at some point
-Depo-provera shot can cause weight gain, so
6. Pregnancy termination:
-Chronic systemic corticosteroid use is a CI to mifepristone as the latter has some effect on adrenal cortex receptor and can interfere with steroid effects.
-For d&c, you need to be N mm dilated for a pregnancy that is N weeks.
7. Screening tests in sexually active teen female
-Hiv, gc/chlamydia, syphillis in high prevalence locations or high risk populations (men who have sex with men, ppl who have sex for drugs or $)
-Depression
-Intimate partner violence
-Ask them if they wear a seat belt-- Wearing a seat belt is the single most predictive factor of risky behavior
8. Screening tests in sexually active teen male:
8. Screening tests in sexually active teen male:
-Males have the same tests as above, except they don't get gc/chlamydia because they are usually symptomatic and because the long-term consequences are not as severe for them.
9. Easy pap generalization:
-21 to 30 q3
-30 to 65 q5/hpv
10. Drinking something bitter (ex dandelion root tea) 30 minutes before a meal may improve digestion
10. Drinking something bitter (ex dandelion root tea) 30 minutes before a meal may improve digestion
Tuesday, February 11, 2014
1. ADA guidelines for screening for diabetes
-Screen everyone over age 45
-Screen people under age 25 if they have a BMI>25 and one risk factor-- CAD, family history of diabetes, non Caucasian race.
2. Diagnosis of diabetes:
-Clinical symptoms of diabetes + a random glucose over 200 is immediately diagnostic of type II DM.
-All other tests for DM (fasting glucose, random glucose, Hb A1C, etc) need to be done twice on two separate occasions.
3. Workup after first diagnosis of diabetes:
-ADA recommends getting an ekg at diagnosis to look for old MIs (q waves), and to set a baseline.
-Look at protein in urine with urine microalbuinuria to cr ratio. Treat microalbuinuria with ACE.
4. Following severity of DM:
-An A1C of 6 is an avg sugar of 120, every one point higher on A1C is 30 points higher on glucose
-Goal A1C <7 for most people, <8 for people with lots of comorbidities because its more dangerous to drop their sugars.
-There is some evidence that attempting to get A1C below 6.5 or 6 may lead to increased hospitalizations
-Goal sugars: 80-100 fasting, 100-140 postprandial (2 hrs after meals). For people with really badly controlled DM or people who you really don't want to be hypoglyclemic, you can have a goal of 100-120 fasting.
5. Treating Diabetes:
-Diet and exercise usually can drop A1C at most by 1-1.5 points, so it's not indicated in people with severe disease. Aim for 45-60 grams of carbs per meal.
-Metformin is first line, causes weight loss (good for PCOS girls to lose weight), diarrhea/nausea
-If that's not enough, then you add a sulfonylurea (need to have glucometer to check because it can push you into hypoglycemia) glipizide is more commonly used than glyburide.
-If that's not enough, third line is DPP4 inhibitor if they can afford it, if they can't afford it then you go straight to insulin.
-If that's not enough, then you start on basal Insulin: 0.2 units/kg/day basal (glargine aka lantus $15 for one month supply)
-If that's not enough, then you add prandial Insulin: 0.2 U/kg/day per day split between their meals. One good point to add prandial insulin is if their fasting sugar is normal but their overall glucose control is poor. You can also have an insulin sliding scale that depends on carb consumption
-How to titrate insulin: have them start at their usual dose at night, and measure the fasting glucose the next morning. If glucose is 120-200, add 1 unit the next night. If glucose is 200-300, add 2 units the next night. If glucose is >300, add 3 units the next night.
6. Diabetes in older people & people with ESRD:
-Diabetes tends to get worse with age
-Older people have poorer renal function, and insulin is renally cleared, so whatever insulin you give them will have a longer-lasting, stronger effect than in a young person. Same for ESRD.
-Metformin is also renally cleared, so it's contraindicated in anyone with a Cr > 2.5
7. Diabetes and blood pressure:
-ADA says aim for 130/80, or 140/90 if you can't get lower safely
-JNC 8 says 140/90 for everyone under 60, regardless of whether they are diabetic or not.
8. Preventative care in someone with well controlled DM:
-See PCP q6 months for diabetes checks.
-Opthomology visit with dilated eye exam every year.
-Pneumovax once before 65 and once after, 5 years apart (non-diabetics only need one after 65) people who are immunocompromised or have chronic lung dx need the same as diabetics.
-Tdap once, then Td booster every 10 years
9. Refer to endocrine if someone is a really brittle diabetic, i.e. A1C is high but they have frequent significant hypoglycemic episodes.
10. End of life care:
-Executive PoA- finances, estate
-Healthcare PoA- healthcare decisions
-Surrogate act of IL ranking of who gets to be the decision maker:
Guardian > spouse > adult children > parents > adult siblings > adult grandchildren > close friend of patient > guardian of estate > courts
Monday, February 10, 2014
1. Dysmenorrhea + menorrhagia:
-Likely DDx: fibroids vs endometriosis (esp if +dysparenuria) vs adenomyosis vs chronic PID.
-In an adolescent who has severe menorrhagia at onset of menses, test for vWB disease-- but do so before you start OCPs, as it can compromise the results.
-OCPs treat menorrhagia, but not dysmenorrhea.
-Mirena IUD is very effective at treating menorrhagia associated with fibroids, and threating pain (via endometrial atrophy, uterine size shrinking-- fibroids don't get smaller, but uterus overall does)
2. Treatments for PMS:
-Danazol: androgenic, with progesterone effects. Lowers estrogen, prevents ovulation-- but has pro-androgenic effects (hirsuitism, lowers HDLs, weight gain)
-GnRH agonists: like leupron/leuprolide lower estrogen and prevent ovulation, but have menopause-like side effects (hot flashes, vaginal dryness)
-Continuous or intermittent SSRIs: intermittent can take from start of luteal phase to beginning of menses (14 days), or from start of symptoms to beginning of menses or 3 days. Intermittent SSRIs at low doses are effective, compared to continuous, and have fewer side effects. Both fluoxetine and sertraline have been well studied; venlafaxine probably works too.
-Likely DDx: fibroids vs endometriosis (esp if +dysparenuria) vs adenomyosis vs chronic PID.
-In an adolescent who has severe menorrhagia at onset of menses, test for vWB disease-- but do so before you start OCPs, as it can compromise the results.
-OCPs treat menorrhagia, but not dysmenorrhea.
-Mirena IUD is very effective at treating menorrhagia associated with fibroids, and threating pain (via endometrial atrophy, uterine size shrinking-- fibroids don't get smaller, but uterus overall does)
2. Treatments for PMS:
-Danazol: androgenic, with progesterone effects. Lowers estrogen, prevents ovulation-- but has pro-androgenic effects (hirsuitism, lowers HDLs, weight gain)
-GnRH agonists: like leupron/leuprolide lower estrogen and prevent ovulation, but have menopause-like side effects (hot flashes, vaginal dryness)
-Continuous or intermittent SSRIs: intermittent can take from start of luteal phase to beginning of menses (14 days), or from start of symptoms to beginning of menses or 3 days. Intermittent SSRIs at low doses are effective, compared to continuous, and have fewer side effects. Both fluoxetine and sertraline have been well studied; venlafaxine probably works too.
3. Folic acid supplements in pregnancy:
-400ug/day if low risk
-1mg/day if mom has diabetes (interferes w folate uptake)
-4mg/day if there is high risk (family history of neural tube defect)
4. Prenatal & early pregnancy labs:
-H&H to check for anemia
-T&S, check for Rh antibodies if Rh-
-U/S is indicated only for dating if the patient isn't certain of her LMP
-Infectious disease screen: hiv, hep b, syphilis, gc/chlamydia, varicella/rubella titers
-1st trimester screen is offered to everyone, at 10-13 weeks
-Quad screen - done to everyone 15-20 weeks
5. GBS & pregnancy:
-If mom is GBS positive: give IV penicillin during labor, 2 doses, 4 hours apart
-If a first trimester urine screen comes + for GBS, you should treat it because there is so much GBS that it's getting into the urine
-If you do not know if a woman has GBS or not and she comes in in labor, do not presumably treat with penicillin unless the following risk factors are present: premature <37 weeks, prolonged ROM, fever in mom.
6. Treat asymptomatic bacteriuria in pregnant ladies because there is a much higher risk of urinary reflux and pyelonephritis. The baby sitting on the bladder pushing pressure up, sitting on ureters causing obstruction and promoting reflux.
-After treating you test to cure.
-If someone has recurrent UTI or pyelo, they get prophylaxis for the rest of the pregnancy.
-Tx with macrobid (bid) or Keflex (tid). CIPRO IS CONTRAINDICATED IN PREGNANCY
7. Nausea and pregnacy:
-Progesterone is the hormone that causes hormone-driven nausea. It causes smooth muslce relaxation, which slows gut motility (evolutionary hypothesis: increase absorption of nutrients?). Additionally, progesterone relaxes the smooth muscles of uterus, preventing premature labor. It can also relax muscles in blood vessels, leading to syncope and dizziness.
-Nausea will usually go away by second trimester.
-Non pharmacologic treatments for early nausea: sea bands, smell of lemon, taste of ginger. Acupuncture and guided imagery are very effective as well. Naturalstandard.com is a good database of herbal remedies.
-Pharmacotherapy for severe nausea: vitamin B6 TID, hydroxyzine, Reglan, zofran.
-Everyone is nauseous in the third trimester, because the baby is pressing on the stomach and causing reflux. Treat this as you would treat GERD-- tums first, then H2 blockers, then PPIs.
8. URI and pregnancy:
-Prolonged fever in pregnancy is bad, as it leads to preterm labor
-No NSAIDs as they could close the ductus
-Tylenol is safe
-No sudafed or other OTC cold medicines with vasoconstrictive effects
-If a pregnant woman has a viral URI, she is at increased risk of bacterial superinfection as pregnancy is an immunosuppressed state.
9. Gestational Diabetes:
-USPSTF recommends screening in everyone after 24 weeks, earlier
-If someone has gestational DM, they should check their sugars 4x day, fasting and 2h postprandial, aiming for less than 95 fasting less than 120 post prand.
-Tx with glyburide, regular/NPH insulin. Metformin is OK in pregnancy.
-If diet is really poor, can try diet changes, but diabetes is dangerous in pregnancy so don't give someone too much time, especially if it's late in the pregnancy.
Statins and ace inhibitors are teratogens. Metformin/glyburide is ok. Get a1c under 7 with insulin.
10. Pre Eclampsia
-Dx with 24 hr urine P-Cr ratio, and 2 BP measurements 6 hours apart, need to be systolic >160 or diastolic > 110
-There is some evidence that spot p-cr ratio may be effective in diagnosing if it is positive, but a negative spot p-cr does not rule out pre-eclampsia and you have to do the 24 hour.
-CBC to look at platelets, LFTs to r/o HELLP syndrome. BMP to look at renal function.
-Give mag to prevent seizures.
-If she is seizing, give mag to break the seizure, as no other antiepileptics work in eclampsia
-If you need to deliver, give mom IM or IV steroids to speed up fetal lung maturation; oral or inhaled steroids will not help. Be careful if there is a possible history of psychosis
-In general, in hypertension in pregnancy, the threshold to treat is 160/100. She won't stroke out with anything less, and won't have long term effects of HTN in 8 months. Labetalol, methyl dopa first line.
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