Showing posts with label CPG. Show all posts
Showing posts with label CPG. Show all posts

Wednesday, June 13, 2012

Dengue: The New WHO 2010 Severity Classification

WHO, in its recent dengue guidelines 2009, has alluded to the fact that its existing classification into dengue fever and dengue hemorrhagic fever (further divided into 4 grades) have a number of limitations due to the rigidity of its criteria.  Download also the Malaysian guidelines on dengue management.

For example,  in a number of cases, patients can present with dengue and shock but without fulfilling all the 4 criteria for DHF These patients would have been classified as dengue fever if the WHO criteria were strictly applied.

The requirement of 20% increase in HCT as one of the evidence of plasma leakage is difficult to fulfill due to several issues:
  • Baseline hematocrit may not be easily available unless blood sampling for full blood count has been recently obtained in the same hospital or healthcare center where the patient presents himself to.
  • Early fluid administration in a health clinic may have changed the hematocrit reading prior to referral to hospital.
  • Bleeding itself will lower the HCT level
(* Previously, the following must ALL be present in order to classify the patients as having dengue hemorrhagic fever:
  • Fever, or history of acute fever, lasting 2–7 days, occasionally biphasic.
  • Haemorrhagic tendencies, evidenced by at least one of the following :
  1. a positive tourniquet test
  2. petechiae, ecchymoses or purpura
  3. bleeding from the mucosa, gastrointestinal tract, injection sites or other locations
  4. haematemesis or melaena.
  • Thrombocytopenia (100,000 cells per mm3 or less).
  • Evidence of plasma leakage due to increased vascular permeability, manifested by at least one of the following:
  1. a rise in the HCT equal to or greater than 20% above average for age, sex and population
  2. a drop in the HCT following volume-replacement treatment equal to or greater than 20% or baseline
  3. signs of plasma leakage such as pleural effusion, ascites and hypoproteinaemia.)
As such, since 2009-2010, WHO and Malaysia has adopted a new classification that is more pragmatic. The whole idea is to capture early the group of patients that may potentially deteriorate due to the following pathogenetic processes:
Plasma leakage
Hemorrhage
Organ impairment
Under this classification, the patients would be classified into either
  • Dengue fever (either probable or laboratory-confirmed)
  • Dengue fever WITH warning signs
  • Severe dengue (under which may have manifestations of severe plasma leakage, severe hemorrhage, severe organ impairment

For patients to be classified as dengue fever (probable), the pre-criteria is that any patients living in or travelling ENDEMIC AREA for dengue (including Malaysia) AND with FEVER and with 2 out of the following criteria:
  • Nausea, vomiting
  • Rash
  • Aches and pains 
  • Tourniquet test positive 
  • Leukopenia 
  • Any warning sign

These can be remembered with the following mnemonic:
AEEGYPTI (AEGYPTI)
A = Area endemic
E = Emesis
E = Exanthem (rash)
G = groan and ache
Y = yes to warning signs
P = Positive tourniquet test
T = total white cell low
I = increased temperature

Patients with dengue with warning signs need to be admitted.  These warning signs are:

Abdominal pain or tenderness 
Persistent vomiting
Clinical fluid accumulation 
Mucosal bleed
Lethargy, restlessness 
Liver enlargment >2 cm 
Laboratory: increase in HCT concurrent with rapid decrease in platelet count
The warning signs can be remembered by:
FLLLAVI (“Flavivirus”)
F = fluid accumulation
LLL = Liver, Lab, Lethargy
A = Abd pain
V = vomiting
I = “insignificant” bleed (“insignificant” does not mean “not important” but minor)
Other pointers in the diagnosis and management of dengue and severe dengue fever that should be kept in mind:

1. The earliest abnormality in the full blood count is a progressive decrease in total white cell count; not thrombocytopenia or increased hematocrit.

2. A relative bradycardia may be noted despite the fever, especially in the recovery phase. It is not always tachycardia in dengue.

3. Do not give acetylsalicylic acid (aspirin), ibuprofen or other non-steroidal anti-inflammatory agents (NSAIDs) as these drugs may aggravate the bleeding in dengue due to capillary fragility. Acetylsalicylic acid (aspirin) may be associated with Reye’s Syndrome.

4. Fresh whole blood or fresh red cells should be given whenever possible. This is because oxygen delivery at tissue level is optimal with high levels of 2,3 di-phosphoglycerate (2,3 DPG). Stored blood loses 2,3 DPG, low levels which may impede the oxygen-releasing capacity of hemoglobin.

5. If the haematocrit was low (<40% in children and adult females, <45% in adult males), this indicates bleeding and the need to cross- match and transfuse blood as soon as possible (see treatment for haemorrhagic complications).

The criteria in Surviving Sepsis Campaign Guideline for blood transfusion, i.e., hematocrit of <30% is not applicable to severe dengue. In fact, blood transfusion is life-saving and should be given as soon as severe bleeding is suspected or recognized. Do not wait for the haematocrit to drop too low before deciding on blood transfusion. This is because, in dengue, bleeding usually occurs AFTER a period of prolonged shock that is preceded by plasma leakage. During the plasma leakage the hematocrit IN FACT, increases to relatively high values before the onset of severe bleeding. As a result, when bleeding occurs in the later stage, hematocrit will then drop from this higher level; and therefore, it may not be as low as in the absence of plasma leakage.

6. A patient with normal SBP and normal mentation does not mean that he is not in shock. Patients in dengue shock often remain conscious and lucid. Look for narrowed pulse pressure despite normal SBP.

Once decompensation occurs, the BP may drop abruptly. Such prolonged hypotensive shock and hypoxia may in turn lead to multi-organ failure and an extremely difficult clinical course.

Differentiating chikungunya from dengue.
The key distinguishing feature for chikungunya is JOINT PAIN.

In fact, some clinicians came out with the aphorism “dengue + arthritis = chikungunya”!

The classical triad of clinical features for chikungunya infection are
•    fever,
•    arthralgia and
•    skin rash
(Ref: Robinson, M.C., 1955. An epidemic of virus disease in Southern Province, Tanganyika territory, in 1952-1953. Trans. R. Soc. Trop. Med. Hyg., 49 :28-32)
The arthralgia in chikungunya is usually symmetrical and involved more than one joint. The pain can be excruciating and involved fingers, wrist, elbows, toes, ankles and knees.

On the other hand, dengue presents with myalgia compared to chikungunya. The rash in chikungunya appears earlier (even in day 1 or 2 itself), as compared to dengue (around day 4). Furthermore, the rash in chikungunya starts with face and chest; those in dengue, the legs and trunks.

Sunday, July 04, 2010

The 2009 COPD Malaysian Guidelines - What's Important From Emergency Medicine Perspective?


The new 2009 Malaysian CPG on Chronic Obstructive Pulmonary Disease is out.

Download the guideline here at the Malaysian Thoracic Society Website here or here at the Academy of Medicine Malaysia website (scroll to the Respiratory Medicine section).

I have also given a talk on COPD last week.

Here's my five points summary of the importance of this guideline from Emergency Medicine perspective:

  1. COPD is no longer just considered a lung parenchymal pathology, but one with significant systemic effects
  2. Spirometry is required for both diagnosis and assessment of severity. Every effort should be made to refer patient for spirometry.
  3. Smoking cessation is the single most cost effective - intervention to reduce the risk of developing COPD and stop its progression. Even a brief 3-min of counseling may result in smoking cessation rates of 5-10%.
  4. The combination of LABA/ICS has been shown to improve lung function, quality of life and reduce exacerbation compared with placebo in COPD patients with FEV1 <>
  5. Consider NIV in patients with persistent hypercapnoeic respiratory failure despite optimal medical therapy.


Creative Commons License
The 2009 COPD Malaysian Guidelines - What's Important From Emergency Medicine Perspective? by Dr. Chew Keng Sheng is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.


Conflict of Interest:
This set of slide was prepared for my talk during lunch time in the department I am working in. The lunch was sponsored by Astra-Zeneca (M) Sdn Bhd ["AZ"] and I have received educational grant from AZ to attend MTS scientific meeting on Asthma and COPD.

Wednesday, September 23, 2009

Pediatric Protocols For Malaysian Hospitals FREE download in MPA website



The Pediatric Protocols for Malaysian Hospitals is available for FREE download at the Malaysian Pediatric Association Website. I am awaiting to purchase a printed copy because eventually I find reading from a laptop screen is very tiring and straining the eyes.

Anyway, you may click here to download the protocol in pdf. Click here to access the website of Malaysian Pediatric Association.

Sunday, October 14, 2007

Q&A based on Malaysian MOH CPG Management of Acute STEMI


I have compiled a series of Q&A notes based on the latest CPG on STEMI. If there is any mistake, please email me at cksheng74@yahoo.com. Cheers,
K.S. Chew



Management of Acute Myocardial Infarction



  1. In some cases of early MI, the ECG can be normal or equivocal. In such cases, serial ECG is advocated. What is the time interval recommended for the repeat ECG?

  1. Which cardiac biomarkers are most specific for MI?

  1. For the diagnosis of STEMI, what is the value of CK-MB should be as compared to its normal range?

  1. Why is CKMB useful for diagnosis of reinfarction?

  1. In a patient with a known diagnosis of coronary heart disease, how often can sublingual GTN be given while en route to emergency department?

  1. What is the time interval for

    1. Door to ECG?
    2. Door to needle?
    3. Door to balloon?

  1. Generally which is better – primary PCI or fibrinolytic therapy?

  1. So, how effective is fibrinolytic therapy?

  1. How would you decide which therapy (primary PCI or fibrinolytic therapy) to be given? What are factors of consideration?

  1. In people considered high risk, primary PCI is generally preferred. Who are considered high risk?

  1. In selected groups of people presented very late (>12 hours), reperfusion therapy would still be beneficial. Who are they?

  1. What are the available choices of fibrinolytic therapy?

  1. What are the regimens of giving streptokinase?

  1. Can fibrinolytic therapy still be given in a patient with hypotension (systolic BP<90>

  1. Can fibrinolytic therapy be given in NSTEMI?

  1. What are the definitions of

1. Primary PCI

2. Facilitated PCI

3. Delayed PCI

4. Rescue PCI

5. Emergency PCI

  1. How long should complete bed rest be advocated in a patient with acute myocardial infarction in the cardiac care unit?

  1. What is concomitant therapy that should be given in ED and CCU?

  1. What are the roles of nitrates in the management of acute myocardial infarction?

  1. What are the contraindications of giving nitrates?

  1. What are the differences between unfractionated heparin and low molecular weight heparin?

  1. What is the different between early ventricular fibrillation and late ventricular fibrillation that complicates AMI?

  1. Does all 2nd degree Mobitz 2 and 3rd degree heart block that complicates AMI require treatment?

  1. What is the treatment modality for AMI patient complicated with cardiogenic shock?

  1. How do you suspect the diagnosis of mechanical complications in AMI?

  1. What is clinical triad of right ventricular infarction?

  1. Which lead would you look for in the diagnosis of right ventricular infarction?

  1. How would you manage a patient complicated with right ventricular infarction? What would you suspect if the patient does not respond to the standard measures?

  1. How would you suspect the diagnosis of reinfarction?

  1. What is post infarct angina?

  1. List the medications that have been shown to reduce the incidence of sudden death.

  1. What should be the target

    1. blood pressure
    2. lipids level
    3. glycemic control in a post MI patient?

  1. What are medications that should be continued on in a post MI patient as secondary prevention?

  1. How long should a patient with AMI be hospitalized?


Management of Acute Myocardial Infarction

  1. At least 15 min. Comparison with previous ECGs may also be useful.

  1. Cardiac troponins and CKMB. However they only start to rise after around 3 hours. So, early measurement may lead to a false negative results. Free fatty acid binding proteins and myoglobin rise earlier (around 1.5 hours)

  1. At least twice that of upper limit of normal.

  1. CK-MB rises and falls early (falls by 48 hours; CK falls by 72 hours). Persistently elevated values of CK-MB are almost never due to myocardial necrosis. Therefore CK-MB is useful for diagnosis of reinfarction. By contrast, troponins fall only by 7 – 14 days (Troponin I remain elevated up to 7 – 10 days and Troponin T remains elevated up to 10 – 14 days)

  1. That depends whether the pain is suggestive of STEMI. If the patient is severe, patient should take one tab of S/L GTN and be rapidly transported to hospital. If pain is not severe, take one tablet of GTN and repeat every 5 minutes, for a maximum of 3 tablets. If pain still persist after three tablets, patient should go to hospital.

  1. Time interval for
    1. Door to ECG? Within 10 minutes
    2. Door to needle? Within 30 minutes
    3. Door to balloon? Within 90 minutes
    4. Therefore the PCI time delay (which is (door to balloon) – (door to needle) time difference should be less than 60 minutes

  1. Most studies indicate that primary PCI is superior to fibrinolytic therapy

  1. Fibrinolytic therapy has been shown to be effective when given early. If given within 1 hour from time of osnet of symptoms, able to reduce mortality by up to 50%.

  1. Depends of

Time from onset of symptoms

Facilities available

Transport time

More than 12 hours

Generally both not given especially if patient already stable and asymptomatic except for certain groups of patients (see next question).

Less than 12 hours

If more than 3 hours but less than 12 hours

PPCI is preferred. But if can’t transfer within 2 hours, then fibrinolytic

If less than 3 hours

PPPCI and fibrinolytic shown to be equally effective

Unless if PCI facilities nearby (acceptable PCI time delay)

If patients is considred high risk, then PPCI preferred (see next question)

  1. High risks include:

- large infarcts

- anterior infarcts

- cardiogenic shock

- elderly patient

- post revascularization (post PCI and post CABG)

- post infarct angina

  1. Reperfusion therapy would still be beneficial even though patient presented very late (> 12 hours), if
    1. Still with persistent symptoms
    2. Hemodynamic instability
    3. Electrical instability

  1. Fibrinolytic can be divided into

I Fibrin selective

Ia Older generation

Alteplase

Higher achievement of reperfusion

But higher rate of reocclusion also

So, need heparin (post administration of ) for at least 48 hours (Level of evidence I, Grades of recommendation A; as compared to usage of heparin in post streptokinase, Level of evidence of IIa, class of recommendation B)

Ib Newer second generation

Tenecteplase

As efficacious as alteplase but

a. Slightly lower bleeding rate

b. Easier to administer (main advantage) – can give as single or double boluses

Again, need heparin for at least 48 hours

Non fibrin selective

Classically streptokinase

Less efficacious as compared with fibrin selective

Lower risk of intracranial hemorrhage

Overall, reduction of mortality is less than fibrin selective type

Antigenic, therefore less effective if given again after 5 days of the first administration in cases of reinfarction

  1. Streptokinase can be given as
    1. 1.5 mega units in 100 cc normal saline or D5% over 1 hour
    2. 1.5 mega units over 20 minutes (faster infusion)
    3. 0.75 mega units (half of it) as a bolus then the rest over the next 50 minutes IF there is no clinical reperfusion

  1. Can. But support with inotrope prior to administration.

  1. No. May even be detrimental if given in NSTEMI

  1. Definitions of

Primary PCI – PCI performed promptly when patient having symptoms

Facilitated PCI – Combining PCI and fibrinolytic to achieve reperfusion rates

Delayed PCI – PCI after >72 hours post fibrinolytic – not for routine

Rescue PCI – PCI when failed fibrinolytics (no clinical evidence of reperfusion)

Emergency PCI – PCI when patient in cardiogenic shock

  1. At least 12 hours; stool softeners is encouraged also because Valsalva maneuver has been shown to precipitate dangerous hemodynamic and ECG changes particularly in the youngs.

  1. In ED – MONA Morphine, Oxygen, Nitrates, Aspirin (+/- clopidogrel); in CCU, MONA + ABC – ACEI, Beta Blocker, Clopidogrel

  1. Nitrates actually has not been shown to improve survival but is used for:

- continuing chest pain

- heart failure

- hypertension

  1. Beware of nitrates in

- SBP <>

- RV infarction

- History of PDEI usage (like Viagra)

  1. LMWH actually was associated with better clinical outcomes as compared to UFH following fibrinolytics; however higher risk of bleeding; therefore, in patients over 75 years old and with renal impairment (serum creatinine > 200 ÎĽmol/l) – UFH is preferred.

  1. Early VF (<48>

  1. No – if hemodynamically stable

  1. Emergency PCI

  1. Sudden clinical deterioration and new onset murmurs

  1. Hypotension, clear lung base, elevated JVP

  1. rV4 – look for ST elevation – however this maybe transient, resolving by 8 – 10 hours

  1. Re-fill the RV (optimize with IV fluid) and inotropes. If doesn’t respond, think of both LV and RV dysfunctions

  1. Recurrence of chest pain; recurrence of STE at least 0.1 mV in contiguous leads; re-elevation of CKMB

  1. Early recurrent angina after successful reperfusion.

  1. ACEI, Aldosterone antagonists, eplerenone, B-blocker, statins

  1. Target

    1. blood pressure <130/80
    2. lipids level LDL<2.0>
    3. glycemic control in a post MI patient: FBS <6.0>

  1. Medications

Aspirin – indefinitely

Clopidogrel – at least 1 month

B-blocker – indefinitely

ACEI – indefinitely

Statins – indefinitely

Warfarin- if persistent AF; for LV thombus 3 – 6/12 of warfarin

  1. If asymptomatic and uncomplicated, can discharge after 3-5 days.

Reference:

Clinical Practice Guidelines on Management of Acute ST Segment Elevation Myocardial Infarction (STEMI) 2007. Ministry of Health, Malaysia, National Heart Association Malaysia and Academy of Medicine, Malaysia; 2007.

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