Archive for October, 2010

TB guidelines from malaysia thoracic society

Posted: October 27, 2010 by chao85 in Medicine, Paediatrics


Menstrual disorders


–          Divided into

a)      Primary

–  Absence of menstruation by 16 years old with present of secondary sexual characteristic or absence of menstruation by 14 years old without present of secondary sexual characteristic

b)      Secondary

–   > 6 months absence of menstruation with regular menses previously or > 12 months absence of menstruation without regular menses previously (oligomenorrhea)

–          Causes

Level Primary Secondary
CNS Functionala)      Anorexic 

b)      Excessive sport

c)       Malnourished


Kallman’s syndrome



Peter-Pan’s syndrome

HyperprolactinemiaSheehans syndrome 




Periphery Testicular feminization syndrome (androgen insenxitivity syndrome) 46, XYConstitutional delay 

Chronic systemic diseases (renal, heart, TB)

Thyroid, adrenal disorders

Chemo- or radio-therapy


Thyroid dysfunction (hypothyroidism)Drugs 

a)      Post pill (COC)

b)      Progesterone

c)       Implants

Ovary POFa)      Idiopathic 

b)      Radiation

c)       Surgery

d)      Cytotoxicity

e)      Karyotype abnormal (45, XO)


Gonadal dysgenesis

a)      Turner’s (45, XO)

b)      Swyers (46, XY or 46, XX)


Premature menopause

Mosaic-Turner (46, XX or 45, XO)

Uterus Meyer-Rokitansky-Kuster-Hauzes syndrome Ashermann’s syndrome
Outflow tract Imperforate hymenVaginal atresia 

Transverse vaginal septum

Cervical / vaginal agenesis

–          Diagnosis

a)      Primary

–  Secondary sexual characteristic ?

–   Sexual infantilism ?

–   US, anatomy ?

–   Virilism ? PCOS

b)      Secondary

–  Pregnancy test !

–   Breast feeding ?

–   Virilism ? PCOS + US

–   Hysteroscopy

–   Colposcopy

–   Progesterone challenge

–          Treatment

a)      FSH & LH

b)      Prolactin (norm till 20ug/L)

c)       TFT (prolactin increase, due to increase TRH)

d)      Serum testosterone (+ / -) : DHEAS

Pelvic pain


– divided into 3 groups

1)      Cyclical – dysmenorrheal

2)      Associated with intercourse – dyspareuria – superficial

– Deep

3)      Chronic ( more than 6 months)

– divided into:

a) gynecological – endometriosis, Uterine fibroids, adenomyosis, Uterovaginal prolapsed, ovarian mass ( especially if twisted) chronic PID, maglinancy, pelvic congestion syndrome, residual ovary syndrome ( trapped ovary syndrome), ovarian remnant syndrome

b) non-gynecological:

– urological – UTI, cystitis, malignancy, etc.

– GIT – IBS, IBD, malignancy, chronic appendicitis, adhesions in abdomen / pelvis due to    infection, perforation and surgery.

– Muscularskeletal – trauma, prolapsed iv disc, osteoarthritis, spondylodisthesis

– Psychological –  physical / sexual / emotional abuse


– Imaging importance! Ultrasound, CT, MRI, diagnostic laparascopy, hysteroscopy, saline infusion sonohysterography.( for intrauterine mass)

* by invasive procedure for diagnostic, may try medical therapy 1st

Eg. Suspect dysmenorrheal – COC, GnRH agonist.

IBS – antispasmodic, diet changes

* but if chronic pain – directly diagnostic laparascopy.


– lower abdomen / pelvic pain associated with menstruation. Onset may be prior, during or continue after cessation of menses.

– may be headache, nausea, vomiting, backache, diarrhea

a) Primary

– no obvious cause

– onset < 20% usually. Decreased with age.

– begins within a day of onset of flow, lasts 24-72hours, crampy

– Improves after childbirth.

b) secondary

– associated with pelvic pathology.

– onset > 20%. Increased with age.

– begins several days by menses, gradually increase in severity as menses approach.

– endometriosis, adenomyosis, polyps, fibroids, PID, IUD, obstructions, ovarian cysts, cancer.

– may be other symptoms associated with primary disease

history: past menstrual history


– ultrasound, MRI pelvis, diagnostic laparascopy( gold standard), diagnostic hysteroscopy, saline infusion sonohysterography.

– Final diagnostic: laparascopic uterine nerve ablation (LUNA)


– Medical – paracetamol, NSAIDs, COX-2 inhibitor (mefenemic acid 0.5 TDS, naproxen 0.55 BD, ibuprofen 0.4 BD/TDS, diclofenac natrium 0.05 BD), buscopan 10mg TDS.

– COCs

– Depot MPA ( Depo Provera 3 mths)

– Laparoscopy

– presacral neurectomy, LUNA

– hysterectomy may be with BSO


– presence of ectopic endometrial tissue outside the uterus.

History: chronic pelvic pain


Dyspareunia (due to rectovaginal / uterosacral involvement)

Intermenstrual bleeding may be premenstrual spotting


Abdominal swelling(endometrioma)

If invasion GIT/ urology –present symptom of them

Common sites: ovaries, pelvic peritoneum, uterosacral ligaments, fallopian tubes, rectovaginal septum( can cause rectal/ vaginal bleeding cyclically), vagina(etc- urinary tract( ureter, bladder), GIT, abdomen, abdomen/ episotomy scar, abdominal organs, lungs.

Physical exam: pelvic mass & tenderness on bimanual & rectoveginal exam.

Lab test not helpful!

Gold standard – direct visualization via laparatomy/ laparascopy

US, MRI only useful in presence of mass. Ovary “ chocolate cyst”



– induce pseudopregnancy/ pseudomenopause – progesterone

– surgery – destroy foci

Radical TAH +/ – BSO

* High recurrence rates

classification of endometriosis

Stage I (score 1-5) minimal

– isolated implants & no significant adhesions

Stage II (score 6 -15) mild

– shallow implants on the pelvic lining & 1 ovary; with filmy adhesion in the other ovary

Stage III (score 16-40) moderate

– deep implants on the pelvic lining & 1 ovary; dense adhesions in the other ovary

Stage IV ( score >40) severe

– deep implants on the ovaries, fallopian tube & pelvic lining

* stage – poor correlation with degree of symptom & fertility prognosis


Posted: October 19, 2010 by chao85 in Medicine



These guidelines are intended to provide awareness and education in

  • Early recognition of STEMI
  • Evidence-based practice for the management of STEMI
  • Secondary prevention following STEMI with the intention of reducing the morbidity and mortality associated with


Clinical Questions

• Diagnosis

• Treatment strategy

• Risk reduction

• Special group

– Elderly

– Diabetics

– Women



Acute coronary syndrome (ACS) is a clinical syndrome of IHD ranging from unstable angina, NSTEMI to STEMI depending upon the degree and acuteness of coronary occlusion.

STEMI: Myocardial infarction due to acute TOTAL occlusion of the coronary artery

NSTEMI: Myocardial infarction due to acute SUB-TOTAL occlusion of the coronary artery

Pathogenesis of STEMI

STEMI is necrosis of heart muscle due to inadequate blood supply following an acute total coronary occlusion. This occlusion is usually due to atherosclerotic plaque rupture, fissuring or ulceration with superimposed thrombosis and coronary vasospasm. Rarely, it may result from nonatherosclerotic arterial disease such as coronary vasospasm alone, coronary embolism or vasculitis.


Diagnostic approach of STEMI

1)      Clinical hx of ischaemic type chest pain

2)    ECG

3)       Serum cardiac biomarkers (myocardial injury or necrosis)


1)      Chest pain – retrosternal, severe, crushing, squeezing or pressing in nature, pain may radiate to the jaw or down the left upper limb (pain may be burning in nature and of lesser severity.)

2)      Lasting > 30 min,

3)      Associated with profuse sweating, nausea, vomiting and SOB. It is sometimes described as chest tightness only.

4)      It may be in the epigastric region and be misinterpreted as indigestion or heart burn.

5)      Rarely may it be localized to the back in the interscapular region only resulting in a misdiagnosis.

6)      Other – unexplained nausea and vomiting, weakness, dizziness, light-headedness and syncope, which may occur in the presence or absence of chest pain.

7)      Diabetics, the elderly and females may not present with typical chest pains

  • dyspnoea and atypical chest pains.

8)      PMH:

  • Previous history of IHD, PCI or CABG
  • Risk factors for atherosclerosis
  • Symptoms suggestive of previous TIA or other forms of CVS disease
  • Symptoms suggestive of peripheral vascular disease


1)      Hyperacute changes of a tall peaked T-wave, ST segment elevation followed by the development of Q-wave, return of the ST segment to isoelectric and T-wave inversion.

2)      The cut off points for new or presumed new ST segment elevation ≥ 0.2mV in V1/V2/V3 and ≥ 0.1mV in other leads. This should be present in ≥2 contiguous leads.

3)      The presence of new onset or presumably new LBBB in a patient with typical type chest pain indicates an INFARCT.

Inferior STEMI

**However in early MI, the ECG may be normal or equivocal. Patients with continuous chest pain and in whom the clinical index of suspicion of STEMI is high, 12 lead ECG tracings repeated at close intervals of at least 15 min might show evolving changes.

Comparison with previous ECG’s may also be helpful in such situations. In patients with an inferior infarct, one should look for associated posterior, lateral and RV infarct. The latter requires right sided chest leads for diagnosis.

Serum Cardiac Biomarkers

  • Confirm the diagnosis of STEMI.
  • One should not, however, wait for the results of these biomarkers before initiating reperfusion therapy.
  • Cardiac biomarkers:

a)      Cardiac troponins (cTnT and cTnI)

b)      Creatine kinase-Myocardial Band (CK-MB)

c)      Creatine kinase (CK)

d)     Myoglobin

e)      Fatty Acid Binding Proteins

  • CT and CK-MB are the most specific cardiac biomarkers. It takes about 3-8 hrs after STEMI for them to rise. Thus, too early a measurement may result in a misleadingly low level.
  • Diagnosis STEMI – CK-MB should be 2X the upper limit of normal. Persistently elevated values of CK-MB are almost never due to myocardial necrosis.
    • CK-MB rises early and falls early. Hence, CKMB measurements are useful for the diagnosis of reinfarction.
    • CK is not as sensitive or as specific as CK-MB. Nevertheless, it is also useful for the diagnosis of STEMI and reinfarction.
    • CTnT / CTnI – sufficient to indicate myocardial necrosis. They are useful in detecting MI in patients presenting with atypical histories and non-diagnostic ECG’s.
    • Troponin levels are more important for the diagnosis of NSTEMI than STEMI.
    • Troponins may remain elevated for up to 14 days.
      • Not useful for the diagnosis of reinfarction.

It is recommended that measurement of cardiac biomarkers be done at periodic intervals, at hospital admission and again at 12-24 hours. This would help to establish or exclude the diagnosis and may be useful for an estimation of infarct size.

AST and LDH levels are not sensitive or specific for AMI with frequent false positive elevations.


Other Diagnostic Modalities

  1. CXR,
  2. Echocardiography – useful bedside imaging technique in difficult diagnostic situations.
  3. multislice computed tomography (MSCT) and
  4. radionuclide techniques
  • TRO or confirm the presence of acute infarction or ischaemia.
  • Identify non-ischaemic conditions causing chest pain such as valvular heart disease, pulmonary embolism, aortic dissection and pneumothorax.
  • Identify mechanical complications of acute infarction.
  • Provide prognostic information.

Difficult Diagnosis??

≈2-8% of patients presenting with chest pains to the ED have been misdiagnosed and sent home. The morbidity and mortality in these patients is high. To reduce this misdiagnosis, we suggest the following measures be taken in all patients presenting with chest pains:

  • They should be given priority in the emergency department and attended to urgently.
  • Myocardial ischemia or infarction should be excluded in all these patients.
  • Clinical suspicion should be high in all patients with predisposing risk factors for atherosclerosis.
  • A careful history will often help in making the diagnosis.
  • An ECG should be done as soon as possible in all patients with chest pains especially when the clinical suspicion of AMI is high. The threshold for doing an ECG in a patient presenting with chest pain should be low.
  • Where the initial ECG is non-diagnostic, it should be repeated and compared with old ECG’s.
  • Cardiac biomarkers especially the troponins, are helpful in ruling in or ruling out a MI.
  • Where the diagnosis is unclear but the clinical suspicion is high, these patients should be observed in the ED for a few hours and the resting ECG and cardiac biomarkers repeated to look for serial changes. If these remain stable, then the patient may be sent home but asked to return for an early review in the outpatient clinic.
  • In addition, the hospital needs to:
    • Educate all medical staff on the importance of early detection and treatment of AMI because this results in myocardial salvage and improved patient outcomes.
    • Have regular refresher courses on ECG interpretation.
    • Implement critical pathways for patients presenting with chest pains to the ED




Immediate measures to be taken in suspected cases of STEMI

For the general public:

  • Seek immediate medical attention at the nearest hospital.
  • Call for an ambulance (dial 991 or hospital direct line if known) or get someone to take you immediately to the nearest hospital.
  • Do not drive yourself.
  • If not on regular aspirin and with no history of allergy, chew and swallow one 300mg tablet of aspirin immediately.

For Patients with known CHD:

If the pain is suggestive of STEMI, take one dose of SL GTN and be rapidly transported to the hospital.

  • If the pain is not severe, take one tablet of GTN and repeat q 5 min for a max of 3 doses.
  • If the pain still persists after 15 min, go to the hospital.

For the general practitioner / family physician:

  • Ask patient to chew and swallow one 300mg tablet of aspirin.
  • Give SL GTN.
  • If the ECG shows ischemic changes, give clopidogrel 300mg of if available.
  • Wherever possible, set up IV access.
  • Pain relief with IV opiates (morphine 3-5mg slowly).
  • Avoid IM injections since this could result in intramuscular hematomas if fibrinolytic agents are subsequently administered.
  • Call an ambulance or ask the patient’s relative or friend to send the patient immediately to the nearest hospital.
  • Wherever possible, contact the doctor at the hospital so that the patient can be treated promptly on arrival.

For Allied Health Care Personnel:

Immediate measures to be taken when there is an ambulance call:-

  • Note nature of complaint.
  • Obtain name of caller, address and telephone number.
  • If possible, request that a relative or friend wait at a strategic place to help locate the patient.
  • Dispatch an adequately equipped ambulance with trained paramedics immediately.
  • Patient should be given O2 & aspirin (if he has not taken) and transported to hospital.
  • Upon reaching the hospital, the patient should be taken directly to the ED
    • An ECG should be done as soon as possible.
    • In hospitals where networking facilities are available, allied health care personnel in the ambulance should relay/transmit the ECG to the call centre for review by the Specialist, for consideration of pre-hospital fibrinolysis or primary PCI.
    • Allied Health care personnel should be trained:-
      • to identify patients at high risk of developing CHD.
      • to identify patients presenting with AMI.
      • on the importance of early referral and treatment.
      • In basic and advanced CPR.




Early management of STEMI is directed at:

  1. Pain relief
  2. Establishing early reperfusion
  3. Treatment of complications – arrhythmias

Initial Recognition and Management

When the patient with suspected STEMI reaches ED, evaluation and initial management should take place promptly (FAST TRACK – RED ZONE) because the benefits of reperfusion therapy is greater the earlier it is initiated.

A quick targeted hx should be taken and vital signs noted. The diagnosis should be confirmed with an ECG, which should be done ASAP, preferably within 10 min of the patient’s arrival in the ED.

It is important to relieve pain and quickly assess the patient’s suitability for reperfusion by either fibrinolytic therapy or primary PCI.

The following should be done immediately and concomitantly in the ED

* When clinically indicated

** Preferred option in

  • High rish patients,
  • Presence of C/I to fibrinolytic therapy &/or
  • PCI time delay [(door to balloon time) – (door to needle time)] of < 60 min

*** If door to balloon is within 90 min

  • Assessment and stabilization of the patient’s haemodynamics.
  • SL GTN if chest pain persists (unless SBP < 90 mmHg).
  • Continuous ECG monitoring.
  • 300mg of aspirin chewed and swallowed if not given earlier.
  • Clopidogrel at a dose of 300mg should be given if not given earlier.
  • O2 by nasal prongs / facemask.
  • Venous access established and blood taken for cardiac biomarkers, FBC, RP, glucose and lipid profile.

Preferably 2 IV lines should be set up.

  • Pain relief – morphine should be administered IV at 2-5mg q 5-15 min until pain is relieved. Watch for evidence of toxicity – hypotension and respiratory depression.
  • Anti-emetics ( IV metoclopromide 10mg or promethazine 25mg ) should be given.
  • IM should be avoided.
  • Assessment for reperfusion strategy.


I. Reperfusion Strategies

ü  Early and prompt reperfusion is crucial as TIME LOST MYOCARDIUM LOST.

ü  Despite overwhelming data showing that prompt reperfusion therapy improves survival it is still widely underutilized and delayed.

ü  Most studies indicate that primary PCI is superior to fibrinolytic therapy as a reperfusion strategy.

ü  However in patients who present within 3 hrs of symptom onset and are at low risk, both treatment strategies appear to have similarmbenefits.

ü  In the majority of our hospitals, fibrinolytic therapy is more readily available and constitutes the main reperfusion strategy.

ü  If both choices are available, the following factors help guide the choice of reperfusion strategies:

a)      Time from symptom onset to first medical contact

b)      Time delay to PCI (time from hospital arrival to balloon dilatation – door to balloon time)

c)      Time to hospital fibrinolysis (time from hospital arrival to administration of fibrinolytic therapy – door to needle time)

d)     C/I to fibrinolytic therapy

e)      High risk patients

The best reperfusion strategy will depend upon:

A) Time from onset of symptoms

• Early presentation (within 3 hrs)

If both treatment options are readily available, they have been shown to be equally effective except for the following situations where primary PCI is the preferred strategy:

– fibrinolytic therapy is contraindicated

– in high-risk patients

– PCI time delay [(door-to-balloon time) – (door-to-needle time)] is < 60 min.

• Late presentation (3 to 12 hrs)

Primary PCI is preferred. The door to balloon time should be within 90 min if the patient presents at a PCI capable facility.

If transferred from a center with no PCI facilities, it should be < 2 hrs. (including transfer delay)

If the time delay to primary PCI is longer than as mentioned, then fibrinolytic therapy should be given.

• Very late presentation (> 12 hrs)

Both primary PCI and fibrinolytic therapy are not routinely recommended in patients who are asymptomatic and haemodynamically stable.MYOCARDIAL IN FAR CTI ON (STE MI)

However, reperfusion therapy would still be beneficial in patients with persistent ischaemic symptoms, haemodynamic or electrical instability. In this subgroup, primary PCI is the preferred strategy.

B) Contraindications to fibrinolytic therapy

C) High risk patients

These include patients with:

• Large infarcts

• Anterior infarcts

• Cardiogenic shock

• Elderly patients

• Post revascularization (post CABG and post PCI)

• Post infarct angina

Primary PCI is the preferred strategy in these patients.

The goals of time to reperfusion therapy should be within:

• 30 minutes door to needle time

• 90 minutes door to balloon time

II. Fibrinolytic Therapy

When given within 1 hr from time of onset of symptoms, it is most beneficial and has been shown to be able to abort the infarction and reduce mortality by up to 50%.

The door-to-needle time should be within 30 mins.

Strategies should be put in place to achieve this target.

Fibrinolytic therapy should be made available in all hospitals and there should be protocols to initiate it in the ED.

Pre-hospital fibrinolytic therapy has been shown to achieve faster reperfusion.

Patients presenting with a low SBP < 90mm Hg should receive inotropic support prior to fibrinolytic therapy.


ü  Patients with STEMI. It has no role and may even be detrimental in patients with NSTEM.


  1. 1. Absolute
  • Risk of Intracranial haemorrhage
    • Any hx of intracranial haemorrhage
    • Ischaemic stroke within 3 months
    • Known structural cerebral vascular lesion (e.g. arteriovenous malformation)
    • Known intracranial neoplasm

  • Risk of bleeding
    • Active bleeding or bleeding diathesis (excluding menses)
    • Significant head trauma within 3 months
    • Suspected aortic dissection
  1. 2. Relative
  • Risk of intracranial haemorrhage
    • Severe uncontrolled hypertension on presentation (BP > 180/110 mm Hg)*
    • Ischaemic stroke > 3 months ago
    • History of chronic, severe uncontrolled hypertension
  • Risk of Bleeding
    • Current use of anticoagulation in therapeutic doses (INR > 2)
    • Recent major surgery < 3 weeks
    • Traumatic or prolonged CPR >10 minutes
    • Recent internal bleeding (e.g. GIT/UT haemorrhage) within 4 weeks
    • Non-compressible vascular puncture
    • Active peptic ulcer
  • Others
  • Pregnancy
  • Prior exposure (>5 days and within 12 months of first usage) to streptokinase (if planning to use same agent)

* The bp should be reduced prior to institution of fibrinolytic therapy.

Choice of Fibrinolytic Agent

  1. 1. Streptokinase

It is not fibrin specific and is less efficacious than fibrin selective agents.

Despite having a lower risk of intracranial haemorrhage, the reduction in mortality is less than with fibrin specific agents.

Streptokinase is antigenic and promotes the production of  antibodies. Thus the utilization of this agent for re-infarction is less effective if given again 5 days after the first administration .

PCI or fibrin specific agents should then be considered.


– 1.5 mega units in 100 ml NS or 5% dextrose over 1 hr.

Other regimens are:

– 1.5 mega units over 20 min, or

– 0.75 mega unit bolus and then repeated at the same dose after an interval of 50 min if there is no clinical reperfusion.


The last 2 regimens achieve a higher coronary artery patency rate and are associated with lower in-hospital mortality. However they are associated with a higher incidence of hypotension.

  1. 2. Alteplase

This agent is fibrin specific and achieves better reperfusion at 90 min as compared to streptokinase.

However there is a higher rate of reocclusion. Thus heparin needs to be given for 48 hours.

Regimen: For patients > 65 kg

15 mg bolus; then 50 mg over 30 min and 35 mg over the next 60min

For patients < 65 kg

15 mg bolus; then 0.75 mg/kg over 30 min and 0.5 mg/kg over the next 60min

  1. 3. Second generation fibrin specific agents: Tenecteplase, Reteplase

These second generation fibrin specific agents are as efficacious as alteplase .

Tenecteplase has been shown to have a slightly lower bleeding risk as compared to alteplase

The main advantage of using these agents is that they are easier to administer. They are given as single or double bolus injections and also do not induce antibody production.

Regimen: Tenecteplase (TNK-tPA) single IV bolus

30mg if < 60kg

35mg if 60 to < 70kg

40mg if 70 to < 80kg

45mg if 80 to < 90kg

50mg if >90kg

Heparin needs to be given for 48 hours

Indicators of Successful Reperfusion

There is no sensitive bedside clinical method to reliably detect successful reperfusion. Some useful guides are:

• Resolution of chest pain (may be confounded by the use of narcotic analgesics).

• Early return of ST segment elevation to isoelectric line or a decrease in the height of the ST elevation by 50% in the lead that records the highest ST elevation therapy within 60-90mins of initiation of fibrinolytic therapy.

• Early peaking of CK and CK-MB levels.

• Restoration and/or maintenance of haemodynamic and/or electrical stability

The occurrence of ‘reperfusion arrhythmias’ is not a reliable indicator of successful reperfusion. An exception is accelerated idioventricular rhythm and sudden sinus bradycardia which have been correlated with a patent infarct related coronary artery after fibrinolytic therapy or primary PCI.

Failed Fibrinolysis

Failure of fibrinolytic agents to open up the occluded infarct related artery is manifested as continuing chest pain, persistent ST segment elevation and hemodynamic instability. These patients are more likely to develop complications such as heart failure and arrhythmias.

The treatment of choice for these patients is rescue PCI. They should not be given a second dose of a fibrinolytic agent. This is because there has been no difference in event free survival demonstrated if these patients are given a repeat dose of a fibrinolytic agent or if they are treated conservatively.

III. Percutaneous Coronary Intervention (PCI)

Primary PCI

Primary PCI is the reperfusion strategy of choice as indicated earlier. It should be performed promptly by experienced operators and in centers performing a sufficient number of primary PCI procedures.

Facilitated PCI

Current evidence indicates that strategies combining fibrinolytic therapy are associated with higher reperfusion rates and TIMI flow.

However, it is associated with higher mortality and bleeding rates. It is therefore not recommended.

Rescue PCI

Rescue PCI may be considered in patients who have failed fibrinolytic therapy or have recurrent chest pain and/or ischaemic complications. Those who may benefit are patients with:

• ongoing chest pains

• haemodynamic and electrical instability

• cardiogenic shock in patient < 75 years old, within 36 hours of STEMI and <18 hours of shock whose coronary anatomy is suitable for revascularization

• heart failure and onset of chest pain within 12 hours

• cardiogenic shock – In these high risk patients, those who are <75 years of age and who present within 36 hours of STEMI and <18 hours of shock may be considered for rescue PCI if their coronary anatomy is suitable for revascularization. This strategy is associated with high mortality and morbidity rates. As such, patients should be individually evaluated.

Delayed PCI (> 72 hours after fibrinolytic therapy)

Routine angiography and PCI in asymptomatic and stable patients post fibrinolytic therapy is controversial.


1) General Measures

  • A period of at least 12 hrs of complete bed rest is recommended following admission to CCU. Patients with uncomplicated infarcts are encouraged to ambulate early. Those with  aemodynamic instability will need a longer period of monitoring.
  • Sedatives may be useful.
  • Use of bedside commodes and assisted bedside washing should be safe in most patients.
  • The Valsalva maneuver has been shown to precipitate dangerous haemodynamic and ECG changes particularly in the young and thus prevention of constipation with stool softeners is encouraged.

2) Monitoring

The general condition of the patient, vital signs, pulse oximetry and the ECG should be continuously monitored following STEMI, looking for complications.

3) Concomitant Therapy

a) Oxygen

  • Oxygen is indicated in the presence of hypoxemia. In uncomplicated cases, its use should probably be limited to the first 24 hours.
  • Oxygen, via nasal prongs, at 2 – 4 litres/min is usually adequate. One should aim to maintain the oxygen saturation above 95%.

b) Antiplatelet Agents

  • Aspirin

Aspirin is indicated in all patients at diagnosis and should be continued indefinitely unless contraindicated. The initial dose of 100-300mg should be followed by a maintenance dose of 75 – 150mg daily

  • Clopidogrel

Clopidogrel, when given together with aspirin and fibrinolytic therapy in STEMI, has been shown to reduce the odds of an occluded infarct related artery, death or reinfarction without increasing the risk of bleeding or cerebrovascular accidents. A loading dose of 300 mg should be given followed by a maintenance dose of 75 mg daily. We recommend treatment for at least 1 month after fibrinolytic therapy. Following PCI, a longer period of dual antiplatelet therapy

(up to 12 months) is necessary particularly when drug-eluting stents are used.


c)  β-blockers

Current recommendations are to use oral β-blockers early in all patients without specific contraindications. In patients with asymptomatic LV dysfunction (LV ejection fraction on echocardiogram < 40%) and not in overt heart failure, carvedilol has been shown to reduce the frequency of death and recurrent AMI. When indicated, it should be started in patients who are

hemodynamically stable after 48 hours.

Contraindications to β – blockers:

1) Bradycardia < 60/minute

2) SBP < 100mmHg

3) Pulmonary congestion with crepitations beyond the lung bases

4) Signs of peripheral hypoperfusion

5) Second or third degree atrio-ventricular (AV) block

6) Asthma or chronic obstructive airway disease ( COAD)

7) Severe peripheral vascular disease

c) ACEI and Angiotensin Receptor Blockers (ARB)

Early use of ACEI (within 24 hours) following STEMI has been shown to improve survival. ACEI should be started when the bp is stable and SBP remains above 100mmHg.

The benefits of ACEI are greatest in patients with:

• Heart failure

• Anterior infarcts

• Asymptomatic left ventricular dysfunction ( LV ejection fraction < 40% on echocardiography)

In patients who cannot tolerate ACEI, the ARB, valsartan, has been shown to have a similar survival benefit.

C/I to ACEI and ARB therapy:

1) Systolic BP < 100mmHg

2) Established contraindications e.g. bilateral renal artery stenosis, worsening renal function.

Type Initiation dose Target dose

Metoprolol 25mg bd 100mg bd

Atenolol 25mg od 100mg od

Propranolol 5mg tds 80mg tds

Carvedilol 3.125mg bd 25mg bd



d) Nitrates

The routine use of nitrates has not been shown to have a survival


Nitrates can be considered in patients with:

• Continuing chest pain and / or ischemia

• Heart failure

• Hypertension

In the acute stage, IV nitrates are recommended because of their rapid onset of action, ease of titration and potential for prompt termination in the event of side effects. After the first 48 hours, oral or topical nitrates may be continued in patients with persisting ischemia and/or heart failure.

C/I to nitrate therapy:

1) Hypotension (SBP< 90mmHg)

2) RV infarction

3) History of phospho-diesterase 5 inhibitors ingestion depending upon the half-life of the agent.

e) Calcium Channel Blockers (CCB)

There is no data to support the routine use of CCB post STEMI.

However they may be used as adjunctive therapy in patients with hypertension and/or on-going ischaemia despite β-blockers and nitrates.

In patients who cannot tolerate β-blockers, verapamil or diltiazem may be used for secondary prevention.

Calcium channel blockers should be avoided in patients with LV dysfunction, pulmonary congestion, bradycardia and AV block.

Type Initiation dose Target dose

Captopril 6.25mg bd –tds 25 – 50mg tds

Ramipril 2.5mg bd 10mg od

Enalapril 2.5 – 5mg od 10mg od

Lisinopril 5mg od 10mg od

Perindopril 2mg od 4mg od

Valsartan 80mg od 160mg bd


f)  Antithrombotics

The antithrombotics that have been studied in STEMI are:

• Unfractionated heparin

• Low molecular weight heparin

• Synthetic pentasaccharide – fondaparinux

Heparin is indicated in patients with :

– post infarct angina

– atrial fibrillation

– mural thrombus

– extensive anterior infarction

– post fibrin-specific fibrinolytic agent 31,32,33

– post non fibrin-specific fibrinolytic agent 31

A) Unfractionated heparin (UFH)

Unfractionated heparin is administered as a bolus of 60units/kg (maximum 4000units) followed by an infusion rate of 12units/kg/hour (maximum 1000units/hour) adjusting the dose to maintain the aPTT of 1.5 to 2.5 times control.

B) Low molecular weight heparin (LMWH)

Low molecular weight heparin is given subcutaneously twice a day. LMWH was associated with better clinical outcomes as compared to UFH when given following fibrinolytic therapy in STEMI. This benefit was seen with both fibrin-specific and non-fibrin specific agents, but at an increased risk of bleeding. These studies however, were done prior to the usage of clopidogrel in STEMI. In patients >75 years of age and with renal impairment (serum creatinine > 200umol/L in women and >250umol/L in men), UFH is preferable to LMWH.

Patients given aspirin, clopidogrel, fibrinolytic therapy and LMWH have been found to have a higher rate of patency of the infarct related artery without an increase in the risk of bleeding complications in one substudy.

We caution the use of all 4 agents (aspirin, clopidogrel, fibrinolytic therapy and UFH/LMWH) together until the efficacy and safety of the combination is established in future trials.

C) Synthetic pentasaccharide

A trial on fondaparinux at a dose of 2.5mg/kg per day, given for 8 days, or the duration of index hospitalization to patients who were given fibrinolytic agents or who were not reperfused, was shown to reduce death or reinfarction at 30 days when compared to UFH. The risk of bleeding was not increased.

g)  Glycoprotein IIb/IIIa Receptor Inhibitors

Glycoprotein IIb/IIIa receptor inhibitors are used mainly in the setting of primary PCI. In primary PCI, the glycoprotein IIb/IIIa receptor inhibitor, abciximab, has been shown to improve patient outcomes.

h)  Statins

Recent data has shown that statins started within 24 hours of admission or continued after admission leads to a reduction in major adverse cardiac events.


i)  Aldosterone Antagonists

Eplerenone, a selective aldosterone receptor antagonist, when added to β-blockers and ACE-I, has been shown to reduce mortality and hospitalizations when given to patients post myocardial infarction with impaired LV function and mild HF.

j) Others – Mg, Lignocaine, Glucose – Insulin K Infusions

Mg and Lignocaine are not recommended for routine use in patients with STEMI.

Although earlier studies and meta-analysis seem to indicate that Glucose-Insulin–K infusions are beneficial, more recent studies have not shown reduction in mortality or infarct size.


• All patients should receive 100 – 300 mg aspirin and 300 mg clopidogrel followed by a maintenance dose of 75-150 mg of aspirin long term and 75 mg of clopidogrel daily for at least a month.

• All patients should be on β blockers if there are no specific contraindications.

• Other medications that have been shown to improve survival if given early are ACE inhibitors (or ARB if ACE intolerant) and statins.


Posted: October 17, 2010 by chao85 in Medicine

Definition of Stroke

“Stroke is a clinical syndrome characterized by rapidly developing clinical symptoms and/or signs

of focal, and at times global, loss of cerebral function, with symptoms lasting > 24 hours

or leading to death, with no apparent cause other than that of vascular origin”.

Definition of Transient Ischaemic Attack (TIA)

“A Clinical syndrome characterized by an acute loss of focal cerebral or monocular function with

symptoms lasting <  24 hours and which is thought to be due to inadequate cerebral or

ocular blood supply as a result of arterial thrombosis or embolism”.

Cause & Pathophysiology

3 main causes of ischemic stroke:

  1. Atherothromboembolism (50%)
  2. Intracranial small vessel disease (penetrating artery disease) (25%)
  3. Cardiogenic embolism (20%)
  4. Others ( arterial dissection, trauma, vasculitis (primary/secondary), metabolic disorders, congenital disorders and other less common causes such as migraine, pregnancy, oral contraceptives, etc.)


Atheroma affects mainly the large and medium sized arteries at places of confluence, branching or tortuosity of vessels.

The process begins in childhood as fatty streaks and progresses over years with gradual buildup of fibrolipid plaque and infiltration of inflammatory cells, eventually narrowing the vessel lumen. The final step occurs with ulceration and platelet-fibrin thrombus formation on the plaque surface.

The atherothrombotic plaque can grow to obstruct a vessel, with intraluminal propagation of the thrombus proximally or distally to cause occlusion, or embolism occurs from the plaque surface to occlude smaller distant vessel(s).

Intracranial small vessel disease is thought to be due to lipohyalinosis but other causes may include microatheroma and angionecrosis, or thromboembolism from a larger artery. The clinical syndrome caused by this is lacunar infarction due to occlusion of small perforating arteries.

Vascular risk factors associated with increased risk of stroke: (primary prevention therapy)

AGE – after 55 yo 

  • Aspirin 50mg q other day (>65yo women)

  • Treat medically if bp sys>140mmHg &/or dia >90mmHg
  • Lifestyle changes if bp sys 130-139mmHg &/or dia 80-90mmHg
  • Target bp for DM sys<130mmHg &/or dia <80mmHg
  • Hypertension should be treated in the very elderly (>70yo) to reduce the risk
SEX – male>female 

  • Post menopausal Hormone replacement therapy for female

  • Cessation of smoking

  • Strict bp control
  • Maintain tight glycemic control



  • High risk grp – keep LDL<2.6mmol/L
  • ≥1 risk factors: keep LDL<3.4mmol/L
  • No risk factor: keep LDL<4.2mmol/L

  • Avoid heavy alcohol consumption

Embolism from the heart causes approximately 20% of all ischaemic strokes. The most common causes are atrial fibrillation (AF) and valvular heart disease. Not all cardiac sources pose similar threat in causing stroke.

The steps to a diagnosis of ischaemic stroke and the various causes which need investigation to identify the underlying cause for the stroke:


Based on Oxfordshire Community Stroke Project (OCSP)

Total Anterior Circulation Stroke (TAC) All of 

  • Hemiplegia contralateral to the cerebral lesion, usually with ipsilateral hemisensory loss
  • Hemianopia contralateral to cerebral lesion
  • New disturbance of higher cerebral function (dysphasia, visuospatial)
Lacunar Stroke (LAC) Pathological definition 

  • Occlusion of a single deep (LS) perforating artery
  • 5% can be due to haemorrhage
  • Occurs at strategic sites
  • More likely seen on MRI than CT scan
  • Classical lacunar syndromes correlated with relevant lacunes at autopsy
Partial Anterior Circulation Stroke (PAC) Any of 

  • Motor / sensory deficit + hemianopia
  • Motor/sensory deficit + new higher cerebral dysfunction
  • New higher cerebral dysfunction + hemianopia
  • New higher cerebral dysfunction alone
  • A pure motor/sensory deficit less extensive than for LAC (eg. confined to one limb, or to face and hand but not to whole arm)
Posterior Circulation Stroke (POC) Any of 

  • Ipsilateral cranial nerve palsy (single / multiple) with contralateral motor and/or sensory deficit
  • Bilateral motor and/or sensory deficit
  • Disorder of conjugate eye movement (horizontal/vertical)
  • Cerebellar dysfunction without ipsilateral long tract sign
  • Isolated hemianopia or cortical blindness
  • Other signs include Horner’s sign, nystagmus, dysarthria, hearing loss, etc
Code last letter as follows:



Syndrome: Indeterminate pathogenesis, prior to imaging (e.g. TACS) 

Infarct (e.g., TACI)

Haemorrhage (e.g., TACH)


  1. History – from family members, witness, patient
  2. Physical examination (Full Neurological examination +  conscious level + higher mental function test)
  3. Supplemented with selected diagnostic tests

The diagnosis should provide answers to the following questions: ( 3 what, 1 where, 1 why)

1. What is the neurological deficit?

2. Where is the lesion?

3. What is the lesion?

4. Why has the lesion occurred?

5. What are the potential complications and prognosis?

Clinical features of stroke:

The areas of the brain affected by the stroke depend on the particular artery that is affected: middle cerebral artery (pink); posterior cerebral artery (green); and anterior cerebral artery (blue).

  1. Anterior artery circulation (carotid artery)
    1. Middle cerebral artery
      1. i.      Aphasia (dominant hemisphere)
      2. ii.      Hemiparesis / plegia
      3. iii.      Hemisensory loss/disturbance
      4. iv.      Homonymous hemianopia
      5. v.      Parietal lobe dysfunction, e.g. astereognosis, agraphaesthesia, impaired two-point discrimination, sensory and visual inattention, left-right dissociation and acalculia
  2. Anterior cerebral artery
    1. i.      Weakness of lower limb more than upper limb
  3. Posterior (vertebrobasilar) artery circulation

  1. i.      Homonymous hemianopia
  2. ii.      Cortical blindness
  3. iii.      Ataxia
  4. iv.      Dizziness or vertigo
  5. v.      Dysarthria
  6. vi.      Diplopia
  7. vii.      Dysphagia
  8. viii.      Horner’s syndrome
  9. ix.      Hemiparesis or hemisensory loss contralateral to the cranial nerves palsy
  10. x.      Cerebellar signs



  1. Confirm the diagnosis
  2. Determine the stroke mechanism
  3. Risk stratification and prognostication
  4. Identify potentially treatable large obstructive lesions of the cerebrovascular circulation

Blood investigations

FBC Exclude anemia, polycythaemia, thrombocytosis, thrombocytopenia, etc
Random Blood Glucose Exclude hypoglycaemia, new diagnosis of DM
Urea & Electrolyte Hydration status, excludes electrolyte imbalances
Clotting profile ( if thrombolysis is considered) Baseline
Lipid profile (fasting)
Glucose (fasting)
OPTIONAL TESTS (in selected patients)
Autoimmune screen ESR, ANA, RF, anti ds-DNA antibody, C3-C4 levels, etc
Thrombophilia screen & Lupus anticoagulants Serum fibrinogen, anti-thrombin III, Protein C, Protein S, factor IV leyden, Antiphospholipid Ab,
Homocysteine (fasting)

Other investigations

12 lead ECG Mandatory
Ambulatory ECG For suspected arrhythmias or SAN diease


CXR Mandatory
CT brain
  • The emergency neuroimaging scan of choice for all patients
  • Differentiates haemorrhage from infarction
  • Confirms site of lesion, cause of lesion, extent of brain affected
ECHO cardiography For suspected cardioembolism, assess cardiac function
MRI (magnetic resonance imaging)
  • Sensitive
  • Not available in emergency setting, limited by expense
  • Useful tool to select patients for thrombolysis where available
Carotid duplex Ultrasound Allows identification of extracranial vessel disease
Transcranial Doppler Ultrasound Identifies intracranial vessel disease with prognostic and therapeutic implications
MR angiography (MRA)
  • Non invasive tool to assess intra- and extra-cerebral circulation
  • Objective assessment of vessel stenosis
CT angiography (multislice CT scan)
  • Non invasive tool to assess intra- and extra-cerebral circulation.
  • Involves intravenous contrast injection
MR venography In suspected cerebral venous thrombosis
Contrast angiogram
  • Gold standard assessment of cerebral vasculature
  • Reserved for patients planned for intervention


  • Metabolic/toxic encephalopathy (hypoglycaemia, non-ketotic hyperglycaemia,
  • Wernicke-Korsakoff syndrome, drug intoxication)
  • Epileptic seizures (postictal Todd’s paresis)
  • Hemiplegic migraine
  • Structural intracranial lesions ( e.g. subdural haematoma, brain tumour, arteriovenous malformation)
  • Encephalitis (e.g. herpes simplex virus), brain abscess, tuberculoma
  • Head injury
  • Hypertensive encephalopathy
  • Relapsing Multiple Sclerosis
  • Conversion disorders
  • Hyperviscosity syndrome
  • Peripheral nerve lesions (e.g. Guillain-Barre Syndrome)



Aim: to save the adjacent dysfunctional tissue by restoration of circulation and normalization of the metabolism.


  • In selected patients presenting within 3 hours:
  • IV bolus 10% rt-pa (0.9mg/kg, maximum 90mg) followed by an infusion over 1hr.
  • Start aspirin within 48 hrs of stroke onset.
  • Use of aspirin within 24 hours of rt-PA is not recommended
  • The use of heparins (unfractionated heparin, LMW heparin or heparinoids) is not routinely recommended as it does not reduce the mortality in patients with acute ischaemic stroke.


  • A large number of clinical trials testing a variety of neuroprotective agents have been completed.
  • These trials have thus far produced negative results.
  • To date, no agent with neuroprotective effects can be recommended for the treatment of patient with acute ischaemic stroke at this time.

Regime for treatment of Acute Ischemic Stroke with Intravenous Thrombolysis rt-PA (recombinant tissue PA – alteplase)

  • IV bolus over 1 min rt-PA 10% (0.9mg/kg, maximum 90mg);
  • Followed by an infusion over 1hr is recommended for carefully selected patients within 3hrs of the acute onset of ischaemic stroke.
  • Admit the patient to an ICU or a **stroke unit for monitoring.
  • Perform neurological assessments q 15 min during the infusion of rt-PA (1 hr) and q 30 min for the next 6 hrs and then q hr until 24 hr from Rx.
  • If the patient develops severe headache, acute hypertension, nausea or vomiting discontinue the infusion if agent is still being administered and obtain a CT scan of brain.
  • Measure bp q 15 min for the 1st 2 hrs, q 30 min for the next 6 hrs and then q hr until 24 hrs from Rx.
  • If B.p systolic > 180mm Hg or diastolic >105mm Hg, administer anti-hypertensive medications to maintain bp at or below these levels.
  • Delay placement of nasogastric tubes, indwelling bladder catheters or intra-arterial pressure catheters.
  • Avoid antiplatelet drugs for the first 24 hrs after administration of rt-PA.

* C/I of streptokinase in acute ischemic stroke because of poor clinical outcome*

**STROKE UNIT – unit in the hospital only managing stroke patients. The core disciplines of the stroke team are: medical (neurologist, geriatrician or general physicians with interest in stroke), nursing, physiotherapy, occupational therapy and speech therapy. In bigger centres, it may include neurosurgeon, social worker and dietitian.

IV rt-PA can be given ONLY if the following is available:

1. A physician with expertise in the diagnosis and management of stroke.

2. Appropriate neuroimaging tests are available 24 hours a day

3. Capability to manage the complications of thrombolysis, particularly intracranial


Characteristics of Patients with Ischaemic Stroke Who Could Be Treated With rt-PA

1. Diagnosis of ischaemic stroke causing measurable neurological deficit

2. The neurological signs should not be clearing spontaneously, minor and isolated

3. Caution should be exercised in treating a patient with major deficits

4. Onset of symptoms ❤ hours before beginning treatment

5. No contraindication for thrombolytic therapy

6. Sys Bp < 185mm Hg and/or dia. Bp < 110mm Hg

7. Brain CT is normal

8. The patient or family understand the potential risks and benefits from treatment

Contraindications for intravenous thrombolytic therapy

1. Current use of oral anticoagulant or PT > 15sec (INR > 1.7)

2. Use of heparin in the previous 48 hrs and a prolonged aPTT

3. A platelet count < 100,000/mm3

4. Another stroke or any serious head injury in the previous 3/12

5. Major surgery within the preceding 14 days

6. Arterial puncture at noncompressible site within the last 21 days

7. Pre-treatment sys. bp > 185mmHg or dia. bp > 110mmHg

8. Neurological signs that are improving rapidly

9. Isolated mild neurological deficits, such as ataxia alone, sensory loss alone, dysarthria alone or minimal weakness

10. Prior intracranial haemorrhage

11. A blood glucose < 2.7mmol/l or > 22.2mmol/l

12. Seizure at the onset of stroke

13. GIT or UT bleeding within the preceding 24 days

14. Recent MI


  • Supportive care
  • Treatment of acute complications.

This is important to improve mortality and functional disability.

  1. Oxygen and Airway Support
  • To prevent hypoxia and potential worsening of the neurological injury.

  1. Regular Observation
  • To recognise impaired pulmonary function (pulse oxymeter), circulatory function (PR, bp) and to recognise complications from mass effect.
  1. Mobilisation
  • First treated with bed rest, but mobilisation should begin as soon as the patient’s condition is judged to be stable.
  • This involves passive and full-range-of-motion exercises, frequent turning, the use of alternating pressure mattresses (ripple mattress), and close surveillance of the skin. Measures to avoid falls are an important part of mobilisation.
  1. Blood Pressure
  • Hypertension following stroke is quite common.
  • However, its optimal management has not been established.
  • Very high blood pressure should be reduced gradually.
  • Proposed drugs: Labetolol 10-20 mg boluses at 10 min intervals up to 150-300 mg or 1 mg/ml infusion, 1-3 mg/min or Captopril 6.25-12.5 mg orally.
  • Sublingual use of a calcium antagonist, such as nifedipine, should be avoided because of rapid decline in blood pressure.

  1. Blood Glucose
  • Hyperglycaemia following acute stroke is strongly associated with subsequent mortality and impaired neurological recovery.
  • This applies to diabetics and non-diabetics.
  1. Nutrition
  • Sustaining nutrition is important as malnutrition after a stroke might interfere with recovery.
  • Persons with infarctions of the brain stem, multiple strokes, large hemispheric lesions, or depressed consciousness are at the greatest risk for aspiration.
  • Swallowing impairments are associated with an increased mortality.
  • Early initiation of PEG feeding has not been shown to improve long-term outcome.
  • A water swallow test should be performed before the patient is allowed to eat or drink.
  • A wet voice after swallowing, incomplete oral-labial closure, or coughing reflex on swallowing indicates high risk of developing aspiration.
  • A videofluoroscopic modified barium swallow examination can be performed later if indicated.
  • If the patient fails the swallowing test, a nasogastric tube should be inserted to prevent aspiration.
  • Percutaneous placement of an endogastric (PEG) tube is superior to nasogastric tube feeding if a prolonged need for devices is anticipated.
  1. Infection
  • The commonest complication = pneumonia and UTI.
  • The appearance of fever should prompt a search for infection and appropriate antibiotic therapy should be administered early. Bladder catheters should be avoided if possible.

  1. Fever
  • A meta-analysis suggested that fever after stroke onset is associated with marked increase in mortality and morbidity.
  • Anti-pyretics should be used to control elevated temperatures in acute stroke patients.

  1. Raised Intracranial Pressure
  • Cerebral oedema and increased intracranial pressure largely occur with large cerebral infarctions.
  • The head of the bed can be elevated by 20 to 30 degrees in an attempt to help venous drainage.
  • Hyperventilation is an emergency measure that acts almost immediately; a reduction of the PCO2 by 5 to 10 mm Hg can lower intracranial pressure by 25% to 30%.
  • Mannitol (0.25 to 0.5 g/kg) IV administered over 20 minutes lowers intracranial pressure and can be given 1 6 hrs.
  • The usual max daily dose is 2 g/kg.
  • If hydrocephalus is present, drainage of CSF via an intraventricular catheter can rapidly lower intracranial pressure.
  • Hemicraniectomy and temporal lobe resection have been used to control intracranial pressure and prevent herniation among those patients with very large infarctions of the cerebral hemisphere.
  • Ventriculostomy and suboccipital craniectomy is effective in relieving hydrocephalus and brain stem compression caused by large cerebellar infarctions


  • Haemorrhagic transformation should be considered as a cause of neurological deterioration following the use of a thrombolytic agent.
  • If an urgent brain CT confirms a haemorrhage, stop the rt-Pa infusion.
  • Obtain blood samples for coagulation tests, infuse fresh frozen plasma and cryoprecipitate, and seek immediate neurosurgical opinion.


  • Depends on the stroke type, size and location.
  • Haemorrhagic stroke has a higher mortality than ischaemic stroke. However patients with haemorrhagic stroke show a better neurological and functional recovery.
  • Brainstem infarct, large hemispheric infarct and cardio embolic stroke also carry a poor prognosis.
  • Lacunar infarct has the lowest mortality rate.