Adult Seizures

Seizure in Adults
by Dr. Jason Van Valkenburg
Emergency Medicine/Internal Medicine Combined Conference August 22, 2013

2-5% of people have at least 1 non-febrile seizure during their lifetime
1% of US population with epilepsy — 28% require treatment in ED’s annually

Syncope vs seizure — history (e.g. amnesia, tongue-biting, incontinence, etc.) is critical to try to determine if cause of presentation is syncope or seizure, but even with history this can often be difficult

Epilepsy — < 50% of cases have an identifiable cause
With age, certain causes become more common, e.g. tumor, CVA

Evaluation:
Turnbull et al: Laboratory evaluation: 8% of 136 patients had correctable lab abnormalities, only 2 were unexpected
Glucose is the most common abnormality

ACEP Clinical Practice Guidelines: For an otherwise healthy adult with new onset seizure who has returned to baseline neuro status — check glucose and sodium, pregnancy test if female of child-bearing age, LP if immunocompromised

Neuroimaging:
Indications and timing remain controversial
Henneman et al in retrospective review noted 22% of patients with first time seizure and normal neuro exam had abnormal noncontrast head CT results

Earnest et al evaluated 250 patients with suspected alcohol withdrawal seizures:
58% had an abnormal CT
6% had a clinically significant lesion
7 of the 16 with a clinically significant lesion had a normal neuro exam and no sign of trauma

ACEP: In an adult with a new onset seizure who has returned to baseline neuro status, imaging is recommended, but if desired, it may be deferred if patient has reliable followup.

Admission and initiation of anti-epileptic medication: No good evidence to support any strong recommendations or guidelines
Very individualized
ACEP: normal neuro exam with no significant co-morbidities can be discharged with outpatient followup — these patients do not need admission or anti-epileptics

Risk of seizure recurrence is quite variable: around 15% risk of recurrence

When to get EEG:
Outpatient setting: Predictive of seizure recurrence and allows categorization and optimization of treatment
ED and Inpatient: If any concern for status or prolonged altered mental status with delay in return to baseline
Treiman et al: 518 status epilepticus patients: 25% had EEG evidence of ongoing continued seizure activity even though bedside assessment suggested that seizure had terminated

EM Practice Guideline 2010:
EEG monitoring is indicated to rule out nonconvulsive status epilepticus in patients receiving aggressive anti-epileptic therapy

Pediatric Ovarian Torsion

Critical Case Conference
Discussion by Annalisa Rudser MD

Ovarian torsion

• Affects females of all ages
• 80% of cases < 50 y/o
• 1% of pediatric and adolescent girls — can be pre-menarchal but rare
• Cysts and neoplasms account for 94% of cases
• Vasculature of ovary undergoes excessive rotation — venous outflow obstructed –> congestion –> tissue edema –> arterial compromise/ischemia/necrosis

Doppler is not diagnostically useful in children — not sensitive or specific for torsion
CT/MRI identifies edema which is suggestive of torsion but not as good as US

Linam LE, Darolia R, Naffaa LN, et al. US findings of adnexal torsion in children and adolescents: size really does matter. Pediatric Radiology, 37(10), 2007, pp. 1013-1019.

• Calculate the adnexal volume by US
• No confirmed cases of ovarian torsion had adnexal volume < 20 mL
• Adnexal ratio = volume of affected (painful) ovary/volume of unaffected ovary
• Adnexal ratio > 15 was seen in 40%, controls 0%

Transvaginal is better than transabdominal but done more in menarchal females who use tampons or who are sexually active

Clinically significant features of pediatric torsion:
Duration of pain > 48 hours
Vomiting
HR > 100 bpm
Sensitivities of adnexal volume and adnexal ratio are low but have very good specificity and NPV

 

Helpful tips for interviewing adolescents:
HEADS assessment:

• Home environment
• Education
• Activities
• Drugs/alcohol
• Stressful situations

Reversible Posterior Leukoencephalopathy Syndrome

Critical Case Conference
by Dr. Darcy Rumberger

Reversible Posterior Leukoencephalopathy Syndrome (RPLS)
— Formerly known as Posterior Reversible Encephalopathy Syndrome (PRES)

Can occur in any age group (children to adults)
Slightly more common in women
Use of cytotoxic and immunosuppressant drugs
Seen in hypertensive encephalopathy and eclampsia as well

4 features:
Headache — can be present for days-weeks
Altered level of consciousness
Visual disturbances — e.g. hemianopsia, neglect, cortical blindness
Seizures

Pathogenesis: unclear — multiple theories: disordered cerebral autoregulation vs endothelial dysfunction vs microinfarction

Diagnosis: No specific diagnostic imaging criteria but imaging suggestive
Often seen on CT but better seen on MRI
Symmetrical white matter edema posterior cerebral hemispheres
Cerebellar and brainstem involvement is common
Not confined to single vascular territory
Resolution on neuroimaging takes days to weeks

Treatment: Anti-hypertensive medication (e.g. nicardipine or esmolol)
Diastolic goal DBP < 100-105
No more than 25% drop in BP to avoid iatrogenic cerebral ischemia
Seizure treatment
Eclampsia — usual management (delivery, magnesium)
Cytotoxic drugs — stop or reduce drug
Treat underlying diseases

Prognosis:
Not always reversible — can have permanent deficits or death although most people recover
Recurrence — rare

Pediatric Wheezing

Discussion by Dr. Elizabeth Placzek

Large differential for wheezing — from reactive airway disease to RSV to pneumonia to CHF or other underlying heart or lung problems

Can try standard treatment with bronchodilators (e.g. albuterol)

Don’t forget hypertonic nebulized saline for mucociliary clearance (e.g. 4 mL of 3% saline nebulized).  This can be very useful to facilitate expectoration of mucus in infants or small children. Situations where this may be helpful are bronchiolitis or post-op from chest surgery.

High flow nasal cannula has also been very helpful in children with respiratory distress, preventing intubations. However, this requires special equipment in order to provide high flow humdified oxygen (it’s not just a regular nasal cannula turned up higher).

 

ED Thoracotomy

ED Thoracotomy –Discussion by Dr. Rebecca Gardner at Regions Hospital Critical Case Conference

One suggested approach to blunt traumatic arrest (Dr. Scott Weingart):
Secure airway
Bilateral thoracostomies (finger or needle)
US — if no pericardial tamponade, should just call the code

If they have pericardial tamponade or if vitals are lost in the ER (or CPR < 5 min), consider thoracotomy
If signs of massive head trauma, do not do thoracotomy

Penetrating traumatic arrest:
Better chance of success with thoracotomy than in blunt trauma
Best outcome if stab wound, GSW 2nd best
— loss of vitals signs en route or in ER — do thoracotomy unless CPR > 15 min
If loss of vitals on scene (CPR > 15 min), do not do thoracotomy unless signs of life in ER

Consider exposure to provider as well as chance of meaningful neurologic recovery when making the decision to do the thoracotomy. Avoid the vast consumption of resources for someone who is not going to recover.

Other indications:

Persistent severe post-injury hypotension (SBP<60-70 mmHg) due to:
— Cardiac tamponade
— Hemorrhage — intra-thoracic, intra-abdominal, extremity, cervical
— Air embolism — consider when trauma patient crashes just after intubation — positive pressure introduces air into damaged vasculature

Purpose of ED Thoracotomy:
— Evacuate tamponade
— Control intra-thoracic or cardiac hemorrhage
— Open cardiac massage — 10x the cardiac output than external compressions
— Evacuate massive air embolism
— Occlude descending aorta (can’t be for more than 30 minutes because if longer, release of occlusion releases cytokines which cause patient to crash and die)

Success of ED Thoracotomy:

• Penetrating cardiac trauma — 35%
• All penetrating trauma 15%

Blunt trauma

• 2% success if lose vitals in ED
• 1% success if lose vital signs en route to ED, 0% if lose vitals at scene

Delirium in the ICU

Delirium in the ICU
by Gary Mayeux, MD — Regions Hospital Multidisciplinary Trauma Conference

Delirium leads to

• Increased mortality
• Longer hospital course
• Longer cognitive recovery

Criteria for Diagnosis:

• Occurs over a short time period — hours to days
• Disturbance of consciousness — can be hyperactive or hypoactive
• Change in cognition or perceptual disturbance — may use the Confusion Assessment Method for ICU (CAM-ICU) to assess — (youtube)
• Has a reversible cause

Clinical history and exam is all that you really need

CAM — sensitivity 94%, specificity 89%
Intensive Care Screening Checklist — sensitivity 99%, specificity 64%

Risk Factors

• Being in the ICU — get them out as soon as possible
• Intubation — daily extubation trials
• Advanced age
• Hx of alcohol abuse
• Physiologic stress
• Withdrawal
• Environmental Factors (reduce noise, give them their glasses if they wear them, hearing aids)
• Dehydration
• Polypharmacy — daily evaluation of current meds and stop ones they don’t need to be on or that increase the risk of delirium (e.g. anticholinergics, benzodiazepines)
• Infection
• Malnutrition
• Underlying brain disease (e.g. unrecognized dementia)
• Use of restraints

Pathophysiology is very complex: Acetylcholine appears to have a large role
Cytokine activation also plays a role

Treatment — Prevention is key

• Reorientation to their background
• Cognitive stimulation
• Sleep protocol
• Timely removal of restraints/catheters
• Corrective vision and hearing
• Minimization of noise
• Minimize sedatives/all drugs

Antipsychotics

• Haloperidol
• Atypical antipsychotics have similar efficacy but fewer side effects

Low dose haloperidol with similar efficacy and similar side effects to atypicals

Quetiapine helpful in 1 small study

Prophylaxis with haloperidol showed benefit (January 2013 J of Critical Care)

Benzodiazepines
Associated with worsening of delirium — independent risk factor — 3 fold increase in risk of developing delirium
Less effective
Limited role in delirium (may still need if other clinical circumstances dictate, e.g. etoh withdrawal)

Precedex (dexmedetomidine)
Alpha 2 agonist
Better than benzos
Helpful in etoh withdrawal and benzo withdrawal
Can still extubate while on this medicaton

Take home points:
Recognize it
Prevention is key
Haloperidol (antipsychotics) are still first line of treatment

Beta Blocker Overdose

Dr. Darcy Rumberger Regions Hospital Emergency Medicine Critical Case Conference

Contribution to discussion by Dr. Sam Stellpflug and Dr. Carson Harris

In overdose, beta-blockers lose selectivity
Clinical manifestations: Hypotension, bradycardia, hypoglycemia, hypokalemia

Management — brief version:

• IV Fluids
• Calcium
• High dose Insulin
• Intralipid
• Bicarb

Management in detail:

• Calcium chloride 2-4 amps IV, central route preferred but can give peripherally in a good IV
• Calcium gluconate 0.6 mL/kg (4 amps or 40 mL for 70 kg person) over 10-15 minutes through peripheral IV
• High dose insulin — Bolus 1 unit/kg regular insulin (saturates receptors) + 25 g dextrose (1 am of D50); Drip 1 unit/kg/hr, titrate up to HR and BP goal by doubling dose every 10-15 minutes if no response; Add 0.5 g/kg/hr D10 once blood sugar starts to drop — Monitor blood glucose q 15-20 minutes and monitor K — can give boluses of insulin until you get the drip
• Intralipid — lipid sink to reduce active drug burden on target tissues — 1.5 mL/kg initial bolus followed by infusion 0.25 mL/kg/min for 30-60 minutes (lipidrescue.org)
• Bicarb — consider if any widening of QRS because can see Na channel blockade in some beta-blocker overdoses — also, acidosis may increase drug binding — 3 amps bicarb in 1 L of D5W run at 1-1.5 mL/kg/h
• Glucagon — rapid onset, can rebolus q 3-5 minutes, 50-150 mcg/kg (3-10 mg for 70 kg person)
• Pressors if near dead or at max of all other therapy — increases dysrhythmias and myocardial work — may help but also may harm
• Consider total volume of resuscitation — concentrate drips if possible
• Failure of medical therapy: intra-aortic balloon pump, cardiopulmonary bypass, ECMO

Bedside US — can be used to get some idea of cardiac function in order to follow progress
FloTrac — connected to arterial line — gross estimate of CO — even if arterial line not accurate, can still use it to monitor changes

Goal: get the heart to beat better — having some measure such as ECHO or FloTrac is helpful

Hypertensive Emergency

Regions Emergency Medicine Critical Case Conference — Discussion by Dr. Joe Walter

Hypertensive Emergency — usually BP > 180/110 with signs of end organ damage
Stroke is the most common presentation (24% of cases) followed by pulmonary edema (2nd most common)
Tx: medications based on presentation and hospital/personal preferences — sodium nitroprusside, nicardipine, nitroglycerin, labetalol, esmolol
Goal: lower BP by 25% in 1st 1-2 hours; goal is 160/100 within 12-24 hours, except for in case of aortic dissection with immediate goal of SBP ~ 100

Flash Pulmonary Edema: consider cardiogenic vs non-cardiogenic causes

Burn Pearls — Regions Emergency Medicine Critical Case conference, Discussion led by Dr. Cullen Hegarty with Dr. Frederick Endorf and Dr. William Mohr from Regions Hospital Burn Unit

When deciding to intubate “early” an alert, talking patient: subjective dyspnea is key — heightens suspicion for deeper airway burns. Mechanism of burn also important as well. Textbooks talk about soot in mouth, singed nasal hairs, etc but one can get these findings with flash burns which are not as great  a risk for deeper airway burns and may not require intubation. If in doubt, call burn to discuss (especially if at outside hospital and considering transfer).
Escharotomy:

• Chest — done emergently if any signs of respiratory compromise — push through skin until depth where skin separates on its own
• Extremities — have 6 hours to perform an escharotomy, so should not be done emergently unless long transport — requires specific expertise to perform these appropriately

Rhabdomyolysis in non-electrical burns is a bad sign — Patient is either developing a compartment syndrome quickly or has deep burns to muscle (4th degree), which is also a bad prognosis

Parkland formula is still used for burns: Fluid should be given as a constant infusion, not boluses
LR preferred because large amounts of fluid are required for resuscitation, and NS will cause acidosis.

Burn Consultation:

• Use American Burn Association guidelines
• Scald burns in kids — consult burn because they can put on a long term dressing right away
• Burns to functional areas (hands, joints, face)
• Burns > 10% — consult burn

Wound care:

• Silvadene is very soothing and can reduce amount of analgesia required
• Silvadene can cause a film after 1-2 days of use making it more difficult to examine the wound which is why some burn surgeons do not recommend it from the ED. Regions burn surgeons support the use of Silvadene.
• May use Silvadene even if sulfa allergy. If concerned, you can just do a small test patch, wait 30 minutes. If increased pain, d/c use and use bacitracin instead.
• Silvadene can be used on the face. However, it should be covered with gauze which can be difficult to do on the face so preference may be bacitracin.
• For covering large burn areas in someone you will be transferring, just use a dry sheet — using moist gauze will cause hypothermia
• Small burns — you can use moist gauze for short transport or silvadene for longer transport

 

Respiratory Distress in Infants and Toddlers

Respiratory Distress in Infants and Toddlers — Pearls
By Dr. Kara Seaton

High Risk for respiratory failure with acute respiratory insult:
Younger age (the younger they are, the higher the risk)
H/o prematurity
Neuromuscular compromise/hypotonia
Pulmonary disease
Cardiac disease
Head/airway anatomic abnormalities

Anatomy of an Infant:
Obligate nasal breathers
Large tongue
Positioning of larynx and size/shape of epiglottis can actually result in obstruction when breathing through mouth
Musculature not well developed
Chest wall soft and compliant
Smaller airways

Alveoli don’t open and close like adults

Neurologic: periodic breathing is common because medullary center of brain not fully developed but this can be a problem when pt has difficulty breathing due to underlying illness

Fever increases respiratory rate — 1 degree C can cause RR to go up 3-7 breaths per minute

Bradypnea: results from respiratory muscle faiture, may signal impending respiratory failure — can also be an early sign of bronchiolitis

An infant with respiratory distress with a “normal” respiratory rate may be fatigued and in imminent risk of respiratory failure

Tachycardia — significant insensible losses due to respiratory illness and fever

Significant retractions in more than 1 muscle group is a sign of severe resiratory distress

Be cautious of the child without wheezing. Be sure you hear air movement. Wheezing can only occur when air is moving

Young child, taking deep, sighing, clear breaths may have metabolic acidosis — DKA

Bronchiolitis — often peaks after 3-5 days of illness — gets worse before it gets better — consider hospitalization if high risk or early in course

Consider status asthmaticus

Any anxiety or agitation may be a sign of impending respiratory failure in asthmatics