Saturday, March 24, 2012

Stroke

Now at the stroke ward... which seems interesting! Am glad that I managed to get that for my SSC!


TIA v Stroke

1) TIA: Focal neurological deficity that resolves <24 hours
  • Transient ischaemic attack: a sign of impending stroke


2) Stroke: A focal neurological deficit of acute onset that persists >24 hours
The term CVA (cerebrovascular accident) is not a recommended term as it is avoidable.

To describe stroke, it is best to describe it as follows:
Side of stroke + Disability
(e.g. L. sided ischemic stroke with right hemiparesis, right homonymous hemianopia and expressive dysphasia

Stroke Classification (Bamford): TACS, PACS, LACS (lacuns) and POCS

  • Total Anterior Circulation Stroke (TACS): 3 of the following: New higher cerebral dysfunction (eg dysphasia,  NOT dysarthria), homonymous visual field defect and ipsilateral motor and/or sensory deficit of at least two areas of face, arm and leg 
 (relating to the GCS: E - hemianopia V - dysphasia/higher cerebral M - hemiplegia)

  • Partial Anterior Circulation Stroke (PACS): 2 of the above

  • Posterior Circulation Stroke (POCS): Basically cerebellar dysfunction
  1. D: Dysdiadokinesia
  2. A: Ataxia
  3. N: Nystagmus
  4. I: Intentional tremor
  5. S: Slurred speech
  6. H: Heel shin test

Others worth mentioning...
Ipsilateral cranial nerve palsy
isolated homonymous visual field defect
  • Lacunar Circulation Stroke (LACS): Internal capsule

  1. Pure motor > 2/3 face, arm, leg 
  2. Pure sensory > 2/3 face, arm, leg 
  3. Mixed (motor and sensory) > 2/3 face, arm, leg 
  4. Ataxic hemiparesis
  5. No higher dysphasia or visuospatial or hemianopia or vertebrobasilar problems
Investigations

U&E and LFTs and Glucose
FBC (polycythemia)
Cholesterol levels
TFT (just to rule out reversible causes)
CXR and ECG
Coagulation screen – young and cryptogenic strokes
ESR, CRP - r/o temporal arteritis

Imaging:
CT Head / MRI - more detailed
Cardiac echo
Carotid ultrasound: Stenosis
ECG: rule out AF
 

Acute Stroke Management

• Aspirin 300 mg initially and then 75 mg od
• Consider Thrombolysis within 3 hours of witnessed symptom onset (ie. if you wake up with a stroke, you won't get it) using alteplase

Thrombolysis - Inclusion Criteria
  • Clinical signs and symptoms of acute stroke
  • Clear time of onset
  • Presentation within 3 hours
  • Hemorrhage excluded by CT
  • NIHSS<25
  • Consent to treat (every effort made to contact next of kin)

Thrombolysis – Exclusion Criteria

  • Rapidly improving neurological signs
  • Systolic blood pressure (SBP) greater than 185 or diastolic blood pressure (DBP) greater than 110
  • Seizure at stroke onset
  • Symptoms suggestive of subarachnoid haemorrhage
  • Suspected acute pericarditis
  • Stroke or serious head trauma within 3 months
  • Major surgery or serious bodily trauma within 2 weeks
  • History of a prior ICH
  • Intracranial neoplasm
  • Arteriovenous malformation or aneurysm
  • GI or urinary tract hemorrhage within 21 days
  • Arterial puncture at a noncompressible site or lumbar puncture within 1 week
  • Concomitant oral anticoagulant (INR>1.7)
  • Platelet count <100 x 109/L
  • Prothrombin time (PT) >15 (INR >1.7)
  • Activated partial thromboplastin time (aPTT) elevated beyond reference range
  • Glucose <50 mg/dL or >400 mg/dL
  • Positive pregnancy test (in woman of childbearing age)
  • Blood should be sent for type and screen in case transfusions are required
Thrombolysis - Scanning

• Non contrast head CT scan
• An immediate head CT scan is imperative.
• Any Haemorrhage is an absolute contraindication to thrombolysis.
• Early signs of major infarction on initial CT scan (eg, mass effect, oedema, hypodensity
involving more than one third of the middle cerebral artery territory) are a reason for caution in the use of thrombolytic therapy, because the risk of haemorrhage is increased.

Thrombolysis – Practical Aspects

  1. Arrange for an emergency head CT scan and laboratory studies.
  2. Monitor BP at least every 15 minutes before tPA. If high, intravenous labetalol bolus (or other suitable agent). BP must be under these parameters to administer tPA.
  3. Establish intravenous access for hydration and thrombolytic therapy.
  4. Mix tPA as soon as the patient is deemed to be a potential candidate for treatment
  5. Monitor for improvement of neurological deficits.
  6. Place a Foley indwelling catheter and nasogastric tube, if necessary, prior to starting tPA.
  7. During and after tPA infusion, monitor BP at least every 15 minutes for 2 hours.
Complications – Intracerebral Haemorrhage

ICH may be signaled by acute hypertension, headache, neurological deterioration, and
nausea or vomiting.

If ICH is suspected, obtain an emergent head CT scan and obtain PT, aPTT, platelet count, and fibrinogen.

If ICH is present on CT scan, evaluate lab studies and administer, if needed, 6-8 units of
cryoprecipitate containing fibrinogen and factor VIII, 6-8 units of platelets, and/or fresh frozen plasma.

Swallowing

– Nil orally initially
– SALT assessment + IV fluids
– Temporary NG feed if appropriate
– PEG placement if appropriate
– Try to ensure nutrition in all patients


Secondary prevention
Medications: Aspirin (300mg for two weeks, then 75mg for life) (/clopidogrel if allergy) and dipyridimole, statin
Lifestyle advice: exercise, stop smoking, lose weight, don't drive for at least one month.
Endarterectomy if carotid dopplers show stenosis (the stenosis is cleaned out by vascular surgeons)

Virtually all patients with atrial fibrillation who have a history of stroke or TIA should be
treated with warfarin in the absence of contraindications


Source: MedRevise.co.uk, DOK.org.uk

Friday, March 16, 2012

Pediatrics -> Geriatrics

Now in my final unit of the academic year, I finally finish with the geriatrics block (big change from the pediatrics as I was about to find!). Although just 2 weeks into it, I am beginning to think that geriatrics is not as intriguing as I had hoped. When I worked as a volunteer, I loved chatting with the elderly. You had all the time in the world to speak to them.

But now as a medical student, it becomes a bit different. Your role is to gather a history, give some differential diagnosis, leaving you little time for a chat (if you want to get your work done)

I liked interacting with pediatric patients more... or maybe I just think too much about the few not-so-good experiences with dementia/delirious patients I met. However I think the pathology/diseases that present in the geriatrics ward are more interesting than the pedatric ones. There were tons more murmurs to hear (predominantly MR). It has also given me more opportunity to look out for abnormalities therefore systems examination become more relevant.

A patient with lung CA (maybe small cell?) had paraneoplastic syndrome. One of it being SIADH.
The syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH) is characterized by excessive release of antidiuretic hormone (ADH or vasopressin) from the posterior pituitary gland or another source. The result is hyponatremia and sometimes fluid overload. It is usually found in patients diagnosed with pneumonia, brain tumors, head trauma, strokes, meningitis, encephalitis, or small-cell carcinoma of the lung.

Suspect SIADH if all of the following diagnostic criteria are met:
  • Hyponatraemia (serum sodium concentration less than 135 mmol/L).
  • Decreased plasma osmolality (less than 280 mOsmol/kg).
  • Increased urine osmolality (greater than 100 mOsmol/kg).
  • Increased urinary sodium concentration (greater than 30mmol/L).
  • No clinical or biochemical features of adrenal and thyroid dysfunction.
  • No dehydration on clinical examination.
  • No use or recent use of diuretic medication.
  • Most people with hyponatraemia are asymptomatic, particularly if hyponatraemia is mild (serum sodium concentration of 130–135 mmol/L) and has developed slowly.
  • When symptoms of hyponatraemia are present, they are often non-specific and are related to both the severity of the hyponatraemia and its rate of onset.
  • Early symptoms
    • Anorexia.
    • Nausea.
    • Lethargy and apathy (associated with slow-onset hyponatraemia).
  • Late symptoms (associated with severe or rapid-onset hyponatraemia).
    • Disorientation.
    • Agitation.
    • Seizures.
    • Coma.

Treatment: Fluid restriction, hypertonic saline, demeclocycline (to induce DI)

With saline infusion: A rapid rise in the sodium level may cause central pontine myelinolysis.[6] Avoid correction by more than 12 mEq/L/day

I hope to spend more time on this unit examining patients!

Source: Wikipedia and CKS NICE