How to approach a patient with suspected TIA/ Stroke in ED

How to approach a patient with suspected TIA/ Stroke in ED

We know that 10-15% of patient with TIA end up having stroke with up to 50% of these occurring within 48 hours of presentation. 

Time constraint approach

Within 10-15 minutes or less:

• Give Triage Priority with suspected symptoms
• Check vital signs including Bedside glucose determination to rapidly rule out and treat hypoglycemia « 2.8mmoI/L

• Two large caliber(16 gauge or larger) I.V Cannula
• ECG and Cardiac monitoring (look for:::
• A fib (ask about TIA symptoms before thinking to cardiovert patient)
• Crochetage sign (notch in apex of R wave) seen in II, III, aVF is highly specific sign of the presence of a PFO or ASD
• Complete history taking and document time patient last known well 
• Complete neurological examination to exclude other differential
• Complete lab works including CBC, coagulation profile, LFT, U/E & cardiac markers
• NPO

Diagnosis of TIA/Stroke pearls::

• TIA may present with negative symptoms (lack of function), loss of sensory, motor, vision, speech. Common Differentials like Migraine may present with positive symptoms like pain, scotomas, etc.
• Examination of eyes is very important, give regard ti visual field deficits, look for retinal pathology, patients having retinal TIAs need to be worked up same as stroke
• Early signs of stroke on plain CT head (not contraindications to lytic): blurring in basal ganglia, internal capsule or insula; loss of the grey-white junction clarity, sulcal effacement (gyri edema), hyperdense MCA sign has a large differential so exercise caution in ruling in stroke based solely on hyperdense MCA sign 

Within 25 to 30 Min:

• Activate Stoke Team (if available in hospital) and document the time
• Urgent Non Contrast CT Brain
• Chest X ray
• Within 24 hours CT or MRI and vascular imaging (CTA or MRA) from aortic arch to vertex

Within 60min or less:

• Aspirin 324 mg PO (if no hemorrhage in CT brain)
• Labetalol 20mg I.V. 
• If blood pressure above 220/120
• Blood pressure above 185/110 & the patient is eligible for IV tPA (see down)
• Hypertensive Encephalopathy
• Aortic Dissection or MI


• If Hemorrhagic Stroke:
• ED MD secondary survey 
• BP control
• Consider PT/PTT reversal
• Consult Neurosurgery
• NIHSS

• If Ischemic Stroke & within the eligibility: (4.5 hours window) 
• IV tPA (within 60 min) from ERarrival if:
• No contraindications of tPA and within tPA window (4.5 hours) from last well known
• Obtain pre and post tPA NIHSS
• Admit to ICU for 24 hours after tPA infusion.

RISK STRATIFICATION SCORING::

Risk 
stratification 
is 
essential:
 CHADS 
Score 
(CHF,
HTN,
Age>75,
DM,
previous
Stroke)
≥2
 should
 get
 warfarin 
given 
the 
benefits
–
70% 
risk 
reduction 
in 
embolic 
events
–
and 
the 
risks
–
moderate
 bleeds
(10‐12%),
or 
severe
 bleeds
(2‐3%) 
requiring 
hospitalization, 
transfusion, 
or
 causing 
ICH.

Remember
 that 
older 
age 
means 
higher 
risk 
for 
embolic 
event, So older patient will actually get more benefit from warfarin.

INCLUSION & EXCLUSION CRITERIA FOR THROMBOLYTIC THERAPY: 

Administration of Thrombolytic Therapy

Inclusion Criteria: 
Patients presenting within 3 hours of symptoms onset or last seen normal

• Diagnosis of an ischemic stroke causing measurable neurological deficit
• Onset of symptoms is known and is within (3 - 4.5 hours) of the beginning of treatment
• The patient is 18 years age or older

Exclusion Criteria:
Patients presenting within 3 hours

• Significant head trauma or prior stroke within past 3 months
• Symptoms suggest subarachnoid hemorrhage
• Arterial puncture at a non-compressible site in the previous 7 days
• History of previous intracranial hemorrhage
• Intracranial neoplasm, arteriovenous malformation or aneurysm
• Recent intracranial or intraspinal surgery
• Elevated blood pressure that remains higher than 185 mm HG systolic or above 110 diastolic
• Active internal bleeding
• Acute bleeding diathesis, including:
- Platelet count below 100,000/mm3
- Heparin received within last 48 hours that leads to an elevated aPIT
- Current use of Warfarin with INR above 1.7 or PT longer than 15 seconds
- Current use of direct thrombin inhibitors or direct factor with elevated sensitive laboratory tests (such as aPIT)
- INR, platelet count and ecarin clotting time; IT or approximate factor Xa activity assays)
• Blood glucose less than 50 mg/dL
• CT-proven area of multilobar infarct larger than 1/3 total cerebral hemisphere

Relative Exclusion Criteria:
Patients presenting within 3 hours

• Minor or rapidly improving stroke symptoms
• Pregnancy
• Seizure at the onset with postictal residual neurologic impairments
• Major surgery or serious trauma within previous 14 days
• Recent gastrointestinal or urinary tract bleeding in the past 21 days
• Acute MI in the past 3 months.

Inclusion Criteria:
Patients presenting 3 to 4.5 hours from symptoms onset or last seen normal

• Diagnosis of an ischemic stroke causing a measurable neurologic deficit

Relative Exclusion Criteria:
Patients presenting 3 to 4.5 hours from symptoms onset or last seen normal

• Age above 80 years
• Severe stroke with NIHSS score of more than 25
• Patients taking an oral anticoagulant regardless of INR
• Patients with history of both diabetes and prior ischemic stroke

NIH STROKE SCALE SCORING

Disclaimer::
This approach doesn't replace the medical guidelines in any way. Please follow your local guidelines accordingly.

Tricyclic Antidepressants Toxicity

Story goes like this,
A 34 yf has ingested unknown amount of TCA(Tricyclic Antidepressants) ,
The following may be true or false :

1-Pt with prominent anticholinergic toxicity  from TCA poisoning, can benefit  from physostigmine.

False

2-TCAs inhibit the fast sodium channels in the His-Purkinje system and myocardium

True

3-Most seizures are brief and self-limited

True

4-Class IA (eg, procainamide) andClass IC antiarrhythmics (eg, flecainide) can be used for refractory arrhythmias

False

5-ECG changes include R wave in AVR >3 mm; R to S ratio in AVR >0.7 &
Brugada pattern in (15%).

True

6-Consider phenytoin for ventricular dysrhythmias resistant to NaHCO3 and lidocaine and seizures resistant to benzodiazepines.

False

Recommendations:::

●Tricyclic antidepressant (TCA) usage remains common and overdose of TCA medications can be life-threatening. A summary table to facilitate the emergent management of TCA overdose is provided .

●Symptoms and signs of TCA intoxication generally consist of vital sign abnormalities, mental status changes, seizures, and anticholinergic toxicity. Sinus tachycardia and hypotension are common. Sedation is the most typical alteration in mental status, but confusion, delirium, or hallucinations may occur. Anticholinergic toxicity commonly manifests as hyperthermia, flushing, dilated pupils that respond poorly to light, delirium, intestinal ileus, and urinary retention.

●The clinical course of patients with TCA poisoning can be unpredictable, and patients who present immediately after ingestion may initially be well-appearing, only to deteriorate rapidly. Patients must be closely monitored. Maprotiline has been associated with a greater frequency of seizures and arrhythmias than other TCAs.

●Cardiac conduction abnormalities are common in patients with TCA poisoning. These abnormalities can degenerate into ventricular tachycardia and ventricular fibrillation (VT and VF), which occur in approximately 4 percent of TCA overdose cases. The electrocardiogram (ECG) is a most valuable tool in determining the extent of TCA poisoning. The following signs suggest cardiotoxicity:

•Prolongation of the QRS >100 msec

•Abnormal morphology of the QRS (eg, deep, slurred S wave in leads I and AVL)

•Abnormal size and ratio of the R and S waves in lead AVR: R wave in AVR >3 mm; R to S ratio in AVR >0.7

●Although a definitive diagnosis of TCA overdose can be made using serum measurements, such testing is typically not available to clinicians in a timely fashion and seldom plays a role in patient management. Clinically, the diagnosis of TCA poisoning is made based upon a history of ingestion, symptoms and signs consistent with the diagnosis, and characteristic ECG findings.

●Initial treatment of TCA overdose includes assessing and securing the patient’s airway, breathing, and circulation. TCA poisoned patients are frequently moribund and require intubation for airway protection and ventilation. Intravenous boluses of isotonic saline are used to treat hypotension. We recommend sodium bicarbonatetherapy for QRS duration >100 msec or any ventricular arrhythmia caused by TCA poisoning (Grade 1B). The initial dose of sodium bicarbonate is 1 to 2 mEq/kg. In adults, this may be given as two to three 50 mEq (50 mL) vials or prefilled syringes of 8.4 percent sodium bicarbonate given as a rapid IV push through a large bore IV.

●Benzodiazepines remain the treatment of choice for TCA-induced seizures. Reasonable initial treatment options in adults include diazepam 5 mg IV or lorazepam 2 mg IV. Unless bowel obstruction, ileus, or perforation is suspected, we suggest treatment with 1 g/kg of activated charcoal (maximum dose 50 g) in patients who present within two hours of ingestion (Grade 2C). Most patients respond well to standard care; for patients with refractory toxicity, management is reviewed in the text.

●Despite prominent anticholinergic toxicity in some patients, physostigmine is contraindicated as it is associated with cardiac arrest in the setting of TCA toxicity. Class IA (eg, procainamide) andClass IC antiarrhythmics (eg, flecainide) are also contraindicated.

Paracetamol Poisoning: Learning Toxicology

A 42 YF ingested an unknown number of paracetamol tablets,
The following regarding paracetamol toxicity is/are true or false:

1-Histologic recovery lags behind clinical recovery and may take up to three months.

True, fact

2-Acute pancreatitis has been described in Stage 1.

False,
Stage 2

3-It is  suggested to treat with activated charcoal, 1 g/kg (maximum dose 50 g) by mouth for all patients who present within four hours .

True,
From Uptodate

4-Females are probably more protected than males via an increased supply and regeneration of glutathione and greater activity of conjugation enzymes .

False ,

Young children are probably protected via an increased supply and regeneration of glutathione and greater activity of conjugation enzymes 

5-Acute alcohol ingestion is not a risk factor for hepatotoxicity and may even be protective

True, fact
(From Uptodate)

Laceration of Tendons: Orthopedics

Laceration of Tendons

Mallet finger is the injury resulting from laceration or rupture of the extensor tendon over Zone I, the distal phalanx, or distal interphalangeal joint. This injury causes the distal interphalangeal joint to be flexed at 40 degrees. It is the most common tendon injury in athletes.

Swan neck deformity may result from chronic untreated Mallet finger. 

Boutonniere deformity results from an injury in Zone III over the proximal interphalangeal joint. Injury of the central tendon and disruption of the lateral bands allow flexion as well as the flexor digitorum profundus to function unopposed. There is retraction of the extensor hood and resultant extension of the metacarpophalangeal and distal interphalangeal joints. Gamekeeper’s thumb is the rupture of the ulnar collateral ligament. This occurs as the result of radial deviation of the metacarpophalangeal joint.