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121-140 of 226 results by Aisha Liferidge
- Indications and timing of head CT scans in patients with a first-time seizure (FTS), who have returned to a normal baseline, are controversial.
- The range of such patients with abnormal head CT's is broad, at 3 to 41%.
- A retrospective study found that 22% of patients with a FTS and normal neurologic exams, had an abnormal head CT (Hennemen, et al).
- Another study found that in patients with suspected alcohol withdrawal seizures, 58% had an abnormal head CT, 16% of which were clinically significant findings (Earnest, et al).
- When feasible, neuroimaging of the brains of patients presenting with a FTS should be performed in the emergency department. Deferred outpatient neuroimaging may be used when reliable follow-up is ensured. (Level B Recommendation).
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- The classic triad of fever, meningismus (stiff neck), and altered mental status only occurs in 44% of cases of acute bacterial meningitis (ABM).
- Headache is a much more common presenting complaint with ABM.
- The sensitivity and specificity of Kernig and Brudzinski signs are suboptimal, making their presence or absence of little diagnostic value.
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The following symptoms of phenytoin toxicity typically present initially, once plasma concentrations reach the listed levels below:
- Nystagmus (on lateral gaze, at 20 mcg/mL)
- Ataxia (at 30 mcg/mL)
- Dysarthria and lethargy (at over 40 mcg/mL)
Other associated symptoms include tremor, hyper-reflexia, nausea, and vomiting.
- The therapeutic ranges for phenytoin (dilantin) and phenobarbital in adults are 10 to 20 mcg/mL and 10 to 30 mcg/mL, respectively.
- Phenytoin plasma levels rise more rapidly than phenobarbital levels; therefore, an acute overdose of the two together will likely manifest as phenytoin toxicity before phenobarbital toxicity.
- Phenytoin has a more narrow margin between therapeutic and toxic levels than does phenobarbital.
- Glucose abnormalities and hyponatremia are the two laboratory findings most frequently associated with triggering first-time seizures in adult patients.
- Always check an HCG in women who present with their first seizure, as this may reveal the source (i.e. eclampsia) and/or may affect testing, disposition, and initiation of an anti-epileptic drug (AED).
- Drug abuse screens should be considered in patients with their first seizure, but no prospective studies have demonstrated benefit from routine use.
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- To be conscious, one must be both awake and alert.
- Patients who sustain severe anoxic cortical damage, with brainstem sparing, exhibit wakefulness and sleep, but are not aware, and thus, are unconscious.
- This description is the hallmark of a "vegetative state."
- A coma is a deep depression in the state of altered level of consciousness, which is characterized by the patient's response to verbal or painful stimuli.
Depending on the location of infarct, stroke patients with dysarthria (a motor speech disorder) may exhibit the following signs and symptoms:
- "Slurred" speech
- Speaking softly or barely able to whisper
- Slow rate of speech
- Rapid rate of speech with a "mumbling" quality
- Limited tongue, lip, and jaw movement
- Abnormal intonation (rhythm) when speaking
- Changes in vocal quality ("nasal" speech or sounding "stuffy")
- Hoarseness
- Breathiness
- Drooling or poor control of saliva
- Chewing and swallowing difficulty
- Progressive Multifocal Leukoencephalopathy (PML) is a life-threatening demyelinating condition that results from the reactivation of the polyomavirus JC. It primarily affects the immunocompromised (most commonly individuals with CD4 counts of < 200).
- Prior to the advent and widespread use of anti-retroviral therapy, 1 to 5% of those with AIDS developed PML. HAART is now considered a mainstay of treatment, along with cessation of immunosupressant therapies.
- PML lesions typically occur bilaterally in the peri-ventricular white matter portions of the brain and do not conform to specific cerebrovascular territories.
- Non-contrast CT and MRI may reveal PML lesions, but definitive diagnosis is made via brain biopsy.
- Symptoms of PML include subacute neurologic deficits such as: mental status abnormality, gait ataxia, limb ataxia, hemiparesis, monoparesis, and visual abnormalities such as diplopia and hemianopia. Seizure occurs in up to 18% of cases.
- Lidocaine toxicity typically manifests as central nervous system symptoms such as tongue numbness, tinnitus, visual disturbances, seizure, and cardiovascular depression.
- The maximum dose of lidocaine without epinephrine is 5 mg/kg (4.5 mg/kg, to be exact) and 7 mg/kg for lidocaine with epinephrine. The total maxiumum dose is 300 mg.
- During the emergency department management of all stroke patients, an NPO (nothing by mouth) status should be maintained until a formal swallow study can be performed to determine whether there is dysphagia.
- The best predictor of dysphagia (swallowing difficulty) in a stroke patient is the presence of dysarthria (motor speech abnormality).
- While the absence of a gag reflex, may suggest some degree of dysphagia, remember that about 10 to 15% of people lack a gag reflex.
- Dysarthria is a motor speech abnormality that commonly results from stroke and is related to focal muscular deficits in the face.
- One of the most challenging aspects of recognizing dysarthria relates to distinguishing it from apraxia.
- Apraxia has nothing to do with a focal motor deficit, but rather a cortical deficit which results in an inability to optimally execute the function of the facial musculature.
- Isolated dysarthria without other neurologic deficit, termed pure dysarthria, is rare and thought to result from multiple lacunar infarcts causing hypoperfusion of the frontal cortex.
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- While most typically only test and document that "cranial nerves II - XII are intact" when examining a patient, I would argue that cranial nerve I should also be tested in all head injury cases wherein there was significant facial/nasal trauma
- Direct blows to the face, by way of airbag deployment, dash board trauma, or assault, for example, can easily cause the ethmoid bone (see image below) to fracture leaving the olfactory nerve exposed to potential trauma as it crosses the cribiform plate.
- Shearing of this nerve can cause irreversible anosmia or hyposmia (inability or decreased ability to smell, respectively).
- The easiest, most effective way to test cranial nerve I is one nostril at a time (occlude the one not being tested), using items such as coffee, peppermint oil, or cloves. More annoying smells like that of an alcohol prep or benzoin, can also be used and would likely be more readily accessible in an emergency department.
- Xanthochromia is the yellowish discoloration of the supernatant from centrifuged cerebrospinal fluid (CSF).
- Xanthochromia is an abnormal finding and results from the lysis of red blood cells.
- Xanthochromia is present is CSF in > 90% of patients within 12 hours of subarachnoid hemorrhage (SAH) onset.
- Several conditions cause increased intracranial pressure (ICP), requiring lumbar puncture (LP) with opening pressure (OP) measurement for diagnostic and therapeutic management.
- Examples of such include: pseudotumor cerebri, (cryptococcal) meningitis, intracranial mass, and intracranial hemorrhage.
- In order to ensure an accurate measurement, OP should be assessed while the patient is in the lateral decubitus position with the neck and legs in a neutral position.
- Normal OP ranges from 10 to 100 mm H20 in children, 60 to 200 mm H20 after age 8, and up to 250 mm H20 in the obese. OP > 250 = intracranial hypertension.
- OP (the meniscus level) can fluctuate by 2 to 5 mm H20 with patient's pulse and by 4 to 10 mm H20 with patient's respirations.
- A patient's symptoms of headache and/or neurologic deficit is often relieved by lowering the ICP through slow removal of CSF during LP. The pressure level should not be lowered by any more than 50% of the initial OP.
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- 5 to 10% of TIA victims go on to have a complete stroke within 7 days.
- The following validated ABCD clinical prediction rule can be used to risk stratify your next TIA patient in determining who requires an expedited in-patient work-up:
Risk Factor Score
- Age > or = 60 1
- Blood Pressure (SBP > 140 and/or DBP > or = 90) 1
- Clinical Features (choose one)
-- Unilateral weakness 2
-- Speech impairment w/o weakness 1
-- Other 0
- Duration of Symptoms (minutes)
-- > 60 2
-- 10 to 59 1
-- < 10 0
Total 0-6
Seven-day risk of stroke (stroke/no. of patients; %) | ||
| Point total | Possible TIA* | Probable or definite TIA |
| 0 or 1 | 0/28 (0) | 0/2 (0) |
| 2 | 0/74 (0) | 0/28 (0) |
| 3 | 0/82 (0) | 0/32 (0) |
| 4 | 1/90 (1; 95% CI, 0 to 3) | 1/46 (2; 95% CI, 0 to 6) |
| 5 | 8/66 (12; 95% CI, 4 to 20) | 8/49 (16; 95% CI, 6 to 27) |
| 6 | 11/35 (31; 95% CI, 16 to 47) | 11/31 (35; 95% CI, 19 to 52) |
| Total | 20/375 (5.3; 95% CI, 3 to 7.5) | 20/188 (10.6; 95% CI, 6 to 15) |
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- Patients who have recently undergone aneurysmal coiling commonly present to the ED with complaints of new or worsened focal neurologic deficits that may be suggestive of stroke.
- Aneurysms can be stabilized by clipping or coiling them. Coiling is performed in a minimally invasive manner, wherein platinum (a material that can be visualized radiographically and is flexible) coils are deployed into the bulb of the aneurysm, via femoral artery cannulation.
- The relative risk of mortality or morbidity at one year post-coiling was found to be 22.6% less than that associated with clipping. The latter is an older, more invasive technique requiring craniotomy and direct manipulation of the brain.
- Hemorrhage is a less likely complication related to aneurysm coiling, thus your indication for a non-contrast Head CT in these patients would most appropriately be "rule out infarct" rather than "rule out bleed."
- Brain infarct is the more common complication of this treatment, and results from the accidental embolization of plaque during the coiling procedure.
- Here are a couple of great links with illustrated overviews of the process of coiling, including a real time You Tube clip:
http://www.brainaneurysm.com/aneurysm-treatment.html
http://www.youtube.com/watch?v=Mvy8g_oDbbk
- Syncope is defined as a transient loss of consciousness and accounts for an estimated 1% to 3% of emergency department (ED) visits.
- While syncope typically is of benign origin, it occasionally signals significant mortality and morbidity, which can make determining the disposition of syncope patients a challenge.
- The San Francisco Syncope Rule (96% sensitivity, 62% specificity) is a clinical tool used to determine which syncope patients are at low risk for a short-term (7-day) serious outcome (i.e. MI, arrhythmia, PE, stroke, SAH, significant hemorrhage, any condition causing or likely to cause a return ED visit or hospitalization).
Specifically, absence of all of the following 5 findings (acronym CHESS) were associated with no serious outcome within 7 days of the syncopal episode according to this rule:- Congestive heart failure
- Hematocrit less than 30
- EKG Abnormalities
- Systolic BP less than 90
- Shortness of breath
- While this decision rule, in addition to one's clinical skill, may be used as a guide in caring for and dispositioning syncopal patients, know that its ability to be extrapolated to a general population of ED patients has yet to be validated.
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- The majority of those afflicted with bell palsy experience neurapraxia or a local nerve conduction block, which usually predicts a prompt and full recovery. 80% to 90% of Bell Palsy patients experience recovery without any noticeable disfigurement within 6 weeks to 3 months.
- Some Bell Palsy patients experience axonotmesis, disruption of the axons, which increases their risk of an incomplete recovery.
- One is at higher risk of developing sequelae in the following scenarios:
-- Age greater than 60 years
-- Diabetes
-- Decreased taste or salivary flow on the affected side
-- Complete paralysis
- Common post-Bell Palsy sequelae that you may see clinically include:
-- Synkinesis - abnormal contracture of facial muscles with smiling or
closing eyes; may cause slight chin movement with blinking, eye closure
with smiling, contracture around mouth with blinking.
-- Crocodile tears - lacrimation while eating.
-- Hemifacial muscle spasms - tonic contractures of affected side of face,
rare, often seen during times of fatigue, stress, or while sleeping.
- Bell Palsy is the most common cause of unilateral facial weakness.
- It is caused by edema and ischemia causing compression of the facial nerve (cranial nerve seven).
- While Bell Palsy is by definition an idiopathic facial palsy, the etiology is often infact discovered and attributed to conditions such as Lyme Disease, Herpes Simplex Virus, and HIV.
- Classic symptoms of Bell Palsy include:
-- acute onset of unilateral upper and lower facial paralysis (over 48 hr. period)
-- posterior auricular pain
-- decreased tearing
-- hyperacusis (due to stapedius muscle weakness)
-- taste disturbances
- Bell Palsy is a diagnosis of exclusion. If the facial paralysis is isolated to the lower face, if there is associated contralateral weakness, and/or if there is diplopia, a central cause for the symptoms, rather than Bell Palsy, must be strongly considered.
- Neurologic complications affect 30 to 60% of allograft organ transplant recipients.
- Many of these complications are related to immunosuppresant medication neurotoxicity.
- Calcineurin inhibitors such as tacrolimus (FK-506 or Fujimycin) and cyclosporin are classically associated with the following neurologic disorders:
- Cranial Nerve Palsy: Tacrolimus toxicity can cause reversible internuclear ophthalmoplegia.
- Movement Disorders: Tacrolimus and cyclosporin often cause tremor, which can be further compounded by the development of asterixis should the patient also have significant renal or hepatic insufficiency.
- Visual Abnormalities: Cortical blindness, visual disturbances, hallucinations, retinal toxicity, and optic neuropathies have all been attributed to calcineurin inhibitor toxicity. Opsoclonus (rapid, involuntary, uncontrolled, multivectorial eye movements) has specifically been associated with cyclosporin neurotoxicity.
- Neurotoxicity related to immunosuppresant drug therapy is most likely to occur early after transplantation and during a rejection episodes, times at which medication doses are typically at their highest. Dose adjustment often results in resolution of symptoms.
- Be sure to check drug levels of immunosuppresant medications, particularly when a transplant patient presents with a neurologic disorders.