Why I have chosen Emergency Medicine?

1. I learn to identify ill patient that need to be attend first, and those relatively well patient who can wait. To put it in a simpler way, I learn how to prioritise. To put it in a more professional way, I learn how to triage patients.

2. I learn how to manage different cases, from simple case like soft tissue injury, to severe case like those arrive with GCS 3.

3. I learn Total Quality Management from Dato Abu Hassan. Syndromic interpretation, activation of senses, package of management.

4. I learn how to order necessary investigations that will help in diagnosis or change in management, instead of ordering every single investigation under the sun. This explained why in US they called it "diagnostics" instead of "investigations".

5. I learn about team work in ER. ER is not a stage for one man show. You cannot run the ER yourself. You need your colleagues, your staff nurses, your medical assistants, your seniors, your specialists. There is no hierachy gap between superior and inferior, but at the same time we respect one another, and seek for expert consultation when needed.

6.  In ER or even in pre-hospital setting, we specialised in emergency airway management, we intubate patient in ground zero, with possible on-going CPR. We learn crush intubation. 

7. I learn not to be a diagnostic chaser, even though diagnosis is important. I learn to identify the problems, the syndromes, and carry out investigations and treatments even without a proper diagnosis, this is what Dato Abu Hassan called as "package of management".

8. I learn not to practise bedside medicine. I don't ask one thousand questions and wait for all the possible investigations from the lab before starting the treatment. I don't want to get the right diagnosis but lose the patient.

9. I was given opportunities in hands-on. Bedside ultrasound, neck line, chest tube, RSI, intubation, CPR, TCP.

10. In ER I can forget about visiting the radiologist of the day (ROTD) and beg for a CT scan or ultrasound scan appointment. I scan the patient myself. IVC, FAST, ECHO, lung scan, 2-points-compression test.

11. We are not jack of all trades but master of none. Emergency medicine is a specialisation by itself, which connects all other specialties in a horizontal sense, under the roof of emergency conditions.

12. EDHKL provides teaching opportunities through CME, grand rounds, course (BLS, ACLS, TLS, TQM, airway, FAST).

13. Emergency medicine is not limited to ER or ED with four walls. Emergency medicine covers pre-hospital care (PHC), disasters, retrieving medicine, relieving works.

14. I am learn how to answer some weird questions asked by your relatives, although I might still not be able to arrive to a proper diagnosis or explanation.

15. I can forget about "jaga wad" and do the endless ward round. In the ward, houseman did round x1, then medical officer did round x2, then specialist did round x3, then consultant did round x4. AM round, PM round, oncall round, midnight round. Morning OD blood taking, BD, TDS, QID. When patients going to have a rest in ward?

16. I learn how to take history from patient, and start creating case note from scratch from a piece of paper. I can forget about flipping through the thick case note and read through other people's clerking, and stop reading "case and progress noted" and "continue as planned".

17. I can come to work on time, though I might not be able to go back on time. I don't have to come very early at 5am to review patients in ward, who are sleeping at that odd hour.

18. A senior told me that you can't learn medicine in one day. In a similar way, I learn the fact we can't be staying in the hospital and "jaga" the patient. I learn to passover patient's care to other people, because I am not a robot that can work 24/7. ER is a place where some one will continue the work after your shift or during your off day.

19. In certain environment in the hospital eg. ward, ICU, OT, oncall system might works better than shift system. I also have great respect to those doing 36-hours oncall. But the fact that we work shift and not oncall doesn't mean that we work lesser. We work in a shorter duration of time, but in greater intensity, with patients flowing in non-stop to the ER, regardless whether you still have beds or even chairs for them. Shift system recognises the fact that doctors are humans, and they need rest because they can get exhausted too.

20. I learn how to compromise to improvise, rather than being OCD. I learn how to work in an enviroment with limited resources. I learn how to do ECG without the bulb that connect the lead/wire end to the chest and limbs.

21. I learn to know my limits, when to call for help, when to refer. To put in a more professional way, I learn when to "seek for expert consultation".

22. I learn that effective high quality CPR can actually revive someone.

* * *

Something that I wrote after I finished my posting in emergency as houseman, basically is a list of quotes from emergency physicians and medical officers.

Invaluable lessons from a department that never stop amaze you, from your superiors, from your colleagues, from your staffs, and even from your patients.

"Whether you came to emergency by choice or by force, you came to the right place." - Dr Faisal Salikin

"Don't try to treat the patient alone, we treat the patient together, and share the burden and responsibility together." - Dr Faizal

"It is okay for not knowing, but it is a sin for not learning." - Dr Mawar Ayub

"Triage is an art. The secret is, instead of asking 'which one is right?', you should ask 'which is better for the patient?' " - Dr Alzamani Idrose

"Concordant is bad, discordant is good, but too good is bad." - Dr Umul Khair

"We don't practise bedside medicine. We don't take history for an hour, then examine patient, then take an long list of blood investigations and X-ray, then only start treatment. We start treating before we have an exact diagnosis, this is what we called package of management." - Dato Seri Abu Hassan Asaari

"Patient comes to you will fall into two categories: classic or typical, and atypical presentation. As you see more patients in your practice, more patients with atypical presentation will fall into category of classic presentation. This is what you call experience." - Dato Seri Abu Hassan Asaari

"Learn from the water. They are very humble. They take the shape of the vessel that they are in. They conform to the situation they are in. Even if they lie on the floor, if they want to fly, they can evaporate and become cloud in the sky. If they want to be strong, they can become iceberg and sink a ship. Each of us may be a droplet of water, but if we are united, we can become ocean." - Dr Alzamani Idrose

"Individually, we are a drop of water. Together, we are an ocean." - Dr Alzamani Idrose

* * *

Something that I wrote after I listened to a presentation by Prof Terrence Mulligan in International Clinical Conference on Emergency Medicine (ICCEM) October 2015.

A breathtaking presentation by Prof Terrence Mulligan. He brought us through the rocket science of Ptolemaic geocentrism vs. Corpenican heliocentrism, Newtonian physics & quantum physics, and finally brought us back to emergency medicine.

The explanation of apparent retrograde motion of the planet can be explained in a simpler way after change of perspective.

Many misconceptions of emergency medicine by others is largely due to the lack of understanding the fact that there is a paradigm shift in medicine.

To think that emergency medicine is a jack of all trades but master of none means they have ignored the fact that emergency medicine is a specialty in itself, not in a vertical sense but in a horizontal sense.

CHADS2 + TIMI

1. What is CHADS2 score?

2. What is TIMI score?

3. A male patient presents to you with pyrexia 39'C, nausea/vomiting/diarrhea/abdominal cramp, drowsy. When you assess him, you notice his BP is lowish and pulse rate is irregular, 160/min. CXR showed cardiomegaly. ECG shows atrial fibrillation. He has lid lag sign and proptosis. What is the first line to manage this disease? (hint: this condition is life-threatening).

1. CHADS₂ Score [points]

• C - Congestive heart failure [1]
• H - Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication) [1]
• A - Age ≥75 years [1]
• D - Diabetes mellitus [1]
• S₂ - Pior Stroke or TIA [2]    

CHADS₂ score estimating the risk of stroke in patients with non-rheumatic AF, and it indicates the need of starting anticoagulant therapy with ASA or warfarin.

• Score 0: None or ASA daily
• Score 1: ASA daily or raise INR with warfarin till 2.0-3.0
• Score 2: Raise INR with warfarin till 2.0-3.0 unless contraindicated.

CHA₂DS₂-VASc Score [points]

• C - Congestive heart failure [1]
• H - Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication) [1]
  
• A₂ - Age ≥75 years [2]
  
• D - Diabetes mellitus [1]
  
• S₂ - Pior Stroke or TIA [2]
• V - Vascular disease (eg. peripheral artery disease, MI, aortic plaque) [1]
• A - Age 65-74 years [1]
• Sc - Sex category (i.e. female gender) [1]

CHA₂DS₂-VASc score is a refinement of CHADS₂ score.

2. TIMI (Thrombolysis in MI) Risk Score

History

• Age ≥ 65
• At least 3 risk factors for CAD: HPT or on anti-HPT, smoking, low HDL or high cholesterol, DM, FHx of premature CAD (CAD in male first-degree relative, or father less than 55, or female first-degree relative or mother less than 65).
• Known CAD (stenosis ≥ 50%)
• ASA use in the last 7/7 (patient experiences chest pain despite ASA use in past 7days)

Clinical pictures

• At least 2 angina episodes within the last 24hrs
• ST changes ≥ 0.5mm on admission ECG
• Elevated serum cardiac biomarkers

TIMI risk Score is used in patients with UA/NSTEMI. Every criterion carries 1 point. TIMI score estimates risk at 14 days of all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent revascularization.

Total Score = 7 points

• Low Risk : < 2 point 
• Moderate Risk: 3-4 points 
• High Risk : > 5 points

It is less accurate in predicting events, but is simple and widely accepted. Another scoring system is GRACE prediction score, which estimates all cause mortality from discharge to 6 months, but is a much more extensive scoring system. 

3. Lid lag and proptosis point the diagnosis to hyperthyroid crisis / thyrotoxic storm. The acute abdomen is a bit misleading, at first sight I though is cardiogenic shock or GIT infection.

• Since patient is hypotensive, we should prevent shock by giving IVI NS 500ml/h. Insert a CVL to monitor hydration status to prevent dehydration but at the same time we need to prevent overhydration since patient might have heart failure indicated by cardiomegaly.
• NGT to prevent aspiration since patient is vomiting. 
• Propanolol 1-2mg/6h IV or 40-80mg/6h PO. Contraindication: Pulmonary or peripheral edema, asthma. In these case use atropine 0.4-1mg IV (edema) or diltiazem 60-120mg/6h PO (in asthma)
• Antithyroid: carbimazole 15-25mg/6h PO or via NGT, or propylthiouracil (PTU)  600mg state + 900-1200mg/d in 4-6 divided dose PO or via NGT.
• Block T3/T4 release by: Sodium iodide 1g/d slow IVI or potassium iodide 100mg/6h PO (given 1-4h after antithyroid)
• Hydrocortisone 100mg/6h IV or Dexamethasone 2mg/6h IV (block T3/T4 release and inhibit peripheral conversion of T4 to T3).
• Treat heart failure with diuretic and O2. Treat AF with digoxin.
• Heparin 5000U BD SC to prevent thromboembolism due to AF.
• Infection is the usual cause of thyrotoxic storm. Find source of infection, take blood C+S. Treatment with cephalosporin 3rd-4th generation.
• Treatment fever with fanning, tepid sponging, PCM. Avoid ASA.
• Consider sedation with chlorpromazine in sever agitated patient. 

--- UPDATE ---

There is no doubt that the patient comes with thyroid storm as well as unstable fast atrial fibrillation. First step > emergent cardioversion. AF can be acute or chronic. If AF is prolonged, usually more than 48 hours, then it is chronic. An AF with low BP, low consciousness level should be treated as unstable AF. Unstable AF should be reverted with cardioversion.

Dengue Fever (DF)

1. Patient A is at D3 of DF; his BP is 90/60. Patient B is at D4 of DF; his BP is 90/75. Which patient do you want to pay more attention to and why?
2. What is the difference between DHF and DSS? And what is compensated and decompensated shock of DHF?
3. Please classify DF.
4. A female patient with day 7 of DF is put on IV drip 4 pints NS. Her HCT is 35%. She is completely well now and she can tolerate oral fluid. How many pints of NS you want to give her? Why?
5. What are the complications of DF that you want to avoid?
6. When do you want to admit patient into ICU?

1. Patient B need more attention, because he is in D4 of DF, which is usually in critical period, with risk of shock, hemorrhage, organ impairment. In fact, patient B also has a narrow pulse pressure (15mmHg), which indicated DSS if there is also signs of plasma leakage and hemorrhage.

2. Difference between DHF and DSS

DHF = DF + Hemorrhage + Plasma Leakage
DSS = DHF + Hypovolemia / Profound Shock / Narrow pulse pressure < 20mmHg

Compensated shock

 - Normal SBP

 - Rising DBP

Decompensated shock

 - Hypotension (SBP < 90 mmHg or MAP < 70 mmHg)

 - Narrow pulse pressure (<20 mmHg)

 - Unrecordable BP

In compensated shock, there is compensation of SBP by tachycardia and peripheral vasoconstriction.

 

3. Classification of DF
Aetiology: Dengue virus type 1, 2, 3, and 4

Infection:

• Primary infection : Classical DF
• Secondary infection : DHF, DSS

Clinical:

• DF without warning signs
• DF with warning signs
• Severe DF

4. Since patient is at the end of critical phase (D7), hemodynamically stable with normalisation of HCT after IV 4 pints of NS, IV fluid should be stop and change to oral fluid to prevent fluid overload. HCT 35% is at lower normal limit for female, but can be due to hemodilution after IV fluid.

5. Complications of DF:

• Shock due to hypovolemia (hemorrhage or plasma leakage)
• Organ impairment
• Fluid overload due to excess IV infusion
• Electrolyte imbalance
• Hyper/hypoglycemia

6. Indication for ICU: 

Severe dengue, which is characterised by at least one of the following:

• Severe plasma leakage leading to dengue shock and/or fluid accumulation with respiratory distress.
• Severe haemorrhages.
• Severe organ impairment (hepatic damage, renal impairment, cardiomyopathy, encephalopathy or encephalitis).

--- UPDATE ---

Additional question:

1. Why patient infected by dengue for the second time has a more severe clinical course like DHF and DSS? 

2. Patient with dengue + elevated liver enzymes = ?

3. What is 7-5-3 regime? When is it indicated in patient with dengue?

4. A 5 years old child with DF, in recovery phase, still has subfebrile temperature, but he is not able to swallow paracetamol tablet, what should you do to reduce the fever?

1. Second Dengue fever is more severe and dangerous and it might end up with DHF/DSS. As we know, Dengue virus has 4 serotypes. Second Dengue infection is made up of more than 1 serotype. Second infection tends to be presented with phenomenon of antibody-dependent enhancement (ADE). In ADE, DENV (Dengue virus) will enhance leucocytes to produce non-neutrolizing antibody. These antibodies will bind with DENV and supposedly they are to neutralize the DENV. However, after binding with the DENV, they are not only transfered into wrong compartment of dendritic cells and not being neutralized, they also replicate within the host cells. Thence, after replication, host cell lysis occurs and it is followed by release of virus into the blood stream (viraemia).

2. Dengue+ raised liver enzyme = liver involvement (replication of virus inside the liver cell+ cell lysis and it leads to release of new viruses and liver enzyme)= dengue hepatitis

3. 7-5-3 regime is refered 7cc/kg/h for 1h, 5cc/kg/h for 2h, 3cc/kg/h for 4h. This regime is used in compensated shock of Dengue grade III.

4. We seldom give T. PCM to children but we do give Syr. PCM. If they refuse/unable to tolerate oral PCM, then rectal PCM would be recommended.

There are few cases in which the patients should not die: severe Dengue, bronchial asthma, DKA, malaria. It is because these conditions can be reverted and the patient should live after adequate resuscitation and appropiate management.

Sepsis

1. What is the difference between sepsis, septicaemia and septic shock?

2. What are the criteria to diagnose sepsis?

3. What is early direct goal therapy? (EDGT)

1. Systemic Inflammatory Response Syndrome (SIRS)

• Sepsis: SIRS + infection
• Severe sepsis: Sepsis + organ hypoperfusion e.g. hypoxaemia, oliguria, lactic acidosis, altered mental function
• Septic shock: Severe sepsis + hypotension (SBP < 90mmHg) despite adequate fluid resuscitation, or need vasopressor/inotropes to maintain BP
• Septicaemia: Presence of multiplying bacteria in circulation

2. Diagnosis: SIRS need 2 or more of the below criteria:

• HR >90 bpm
• T° >38°C or <36°C
• RR > 20 breaths/min, or PaCO₂ <32mmHg (4.3kPa)
• WBCC > 12 or <4 x 10⁹/L, or >10% immature band forms

Since sepsis = SIRS + infection, we need 2 or more of the above criteria + culture and sensitivity (C+S) result.

• C+S taken before antibiotic treatment
• > 2 blood C+S taken (each 10ml)
• C+S from percutaneous and vascular device in place

3. Early Goal-Directed Therapy (EGDT) is a more specific form of therapy used for the treatment of severe sepsis and septic shock. This approach involves adjustments of cardiac preload, afterload, and contractility to balance oxygen delivery with an increased oxygen demand before surgery. We need to identify hypotension / serum lactate > 4 mmol/l, if either of them present, administer crystalloid.

Initial goal of resuscitation in < 6hr:

• CVP = 8-12 mmHg (12-15 mmHg if on mechanical ventilation)
• MAP > 65 mmHg
• Urine output > 0.5 ml/kg/hr
• ScvO₂  > 70%

CVP = central venous pressure

MAP = mean arterial pressure

ScvO₂  = central venous oxygen saturation 

MVA

If a patient who has met MVA (motor-vehicle accident) is brought to you, what is the first thing you would do? 

A preliminary survey can be done following ABCDEF.

A: Airway

Protect cervical spine f injure.

Access airway patency, check for any obstruction.

Establish airway if there is obstruction.

B: Breathing

Check RR, bilateral chest movement, precuss and auscultate.

Consider O2, intubation, or manage according to causes, eg. tension pnuemothorax.

C: Circulation

Check PR, BP, and CRT.

If no cardiac output, do CPR.

If shock, use plasma expander or inotropes.

D: Disability

Access level of consciousness by using Glasgow Coma Scale (GCS) or AVPU score.

• A = Alert
• V = responds to Vocal stimuli
• P = responds to Pain
• U = Unresponsive

Check pupils: size, equality, light reaction.

E: Exposure

Undress patient, but cover to avoid hypothermia.

F: Find

Check for all possible trauma site

How do you apply cervical collar? 

To apply the cervical collar,

1. The assistant need to realign the cervical spine by manual stabilisation.
2. The doctor need to measure the length from the horizontal plane that goes through the chin, to the horizontal plane that goes through the shoulder or the clavicle. This is needed to adjust the size or the cervical collar.
3. If necessary cut off any cloth that inhibit the application of the cervical collar, e.g. the hood of a jacket.
4. Slip the posterior piece of the cervical collar behind the neck.
5. Apply the anterior / front piece of the cervical collar over the neck.
6. Check whether the cervical collar fits well to the jaw or whether it is too tight.

--- UPDATE ---

I want to emphasize that if an unconscious patient with MVA comes to you, a cervical collar must be applied because you are not sure whether this patient has cervical fracture or not until it is ruled out. 

LVH, LAD, GCS, RSI

1. How do you diagnose LVH and LAD from ECG?

2. A patient came to you with GCS 7/15(E2V2M3). What is your action? Define GCS.

3. What is RSI? List out the sequence. 

1. Left Ventricle Hypertrophy (LVH)

Romhilt-Estes point score system ("diagnostic" >5 points; "probable" 4 points):
In my opinion it is a rather complex diagnostic criteria.

1. ECG Criteria Points Voltage Criteria (any of):
   
   • R or S in limb leads ≥ 20 mm
   • S in V1 or V2 ≥ 30 mm
   • R in V5 or V6 ≥ 30 mm
2. ST-T Abnormalities: ST-T vector opposite to QRS without digitalis
   ST-T vector opposite to QRS with digitalis
3. Negative terminal P mode in V1 1 mm in depth and 0.04 sec in duration (indicates left atrial enlargement) 3
4. Left axis deviation (QRS of -30° or more) 2
5. QRS duration ≥0.09 sec 1
6. Delayed intrinsicoid deflection in V5 or V6 (>0.05 sec) 1
7. Other voltage-based criteria for LVH include:
   
   • Lead I: R wave > 14 mm
   • Lead aVR: S wave > 15 mm
   • Lead aVL: R wave > 12 mm
   • Lead aVF: R wave > 21 mm
   • Lead V5: R wave > 26 mm
   • Lead V6: R wave > 20 mm

Criteria of LVH on ECG given by my therapy teacher:

• Left axis deviation (LAD)
• R_V5 taller than R_V4
• R_V5/V6 + S_V1 > 35 cm (Sokolow-Lyon index)
• R_I + S_III > 25 cm
• (R_I - S_I) + (S_III - R_III) > 17 cm (Levis index)
• R_aVL > 11 cm
• ST depression in left leads (I, aVL, V5, V6)
• T inversion in left leads (I, aVL, V5, V6)

The most important is the Sokolow-Lyon index, cause it has high specificity, but low sensitivity, e.g. in obese patient the voltage of the ECG waves might be dampen down.

So we should also look for left ventricle strain pattern.

• Left leads (I, aVL, V5, V6) :T-wave inversion + ST-depression
• Right leads (III, aVF, V1, V2) : ST-elevation

NB! T-wave inversion can be sign of ischemic damage to the myocardium, but the pattern is different.

• In LV strain pattern, gradual down-slope of the T-wave + sudden up-slope of the T-wave.
• In LV ischemia, symmetrical downslope + up-slope of the T-wave. 
• Compare with the ECG of the ischemia below.

But it is not absolute, and cardiac enzyme e.g. troponin should always be checked to rule out ischemia.

Left Axis Deviation (LAD)

• R_I > R_II > R_III.
• Upward deflection of QRS-complex in I.
  downward deflection of QRS-complex in III.

2. GSC is Glasgow Coma Scale.

1. Secure ABC of life support.
2. O2, IV access. Consider intubation since GCS < 8.
3. Check vital signs: BP, PR, RR, temperature.
4. Check for any external trauma especially cervical spine trauma.
5. Check for any sign of increased ICP (ophthalmoscopy).
   Check for meningism. (NB! Don't move neck if cervical spine trauma)
6. Investigation: FBC, BUSE, ESR, CRP, LFT, Creatinine, ABG, DXT, toxicology screening.
   CXR, ECG, neuroimaging (CT/MRI), LP (if meningism + no increased ICP)

Management will depend on the cause. 

3. RSI is Rapid Sequence Intubation / Induction

I am not quite sure about this procedure especially the medication and dosage, but I'll try answer with what I read on the Internet. RSI refers to the pharmacologically induced sedation and neuromuscular paralysis prior to intubation of the trachea. RSI is generally used in an emergency setting.

1. Administer 100% oxygen via a nonrebreather mask for 3 minutes for nitrogen washout.
2. Administer a rapidly-acting induction agent IV to produce loss of consciousness.
3. Administer a neuromuscular blocking agent IV immediately after the induction agent.
4. Rapid placement of an endotracheal tube (ETT) between the vocal cords, while the cords are being visualized with the aid of a laryngoscope. 

One important difference between RSI and routine tracheal intubation is that the practitioner does not manually assist the ventilation of the lungs after the onset of general anesthesia and cessation of breathing, until the trachea has been intubated and the cuff has been inflated. 

Another key feature of RSI is the application of manual pressure to the cricoid cartilage, often referred to as the "Sellick maneuver", prior to instrumentation of the airway and intubation of the trachea to prevent regurgitation of gastric contents. However this technique may impede laryngeal view. 

Do share with us more regarding this topic =).

--- UPDATE ---

Answer.

1. LVH: left ventricular hypertrophy. One of the easiest and fastest way is the see V1 and V6. The sum of big box (with 5 small boxes) of R wave in V6 and S wave in V1 must exceed 7 in LVH.

2. GCS: Glascow coma scale. Total number is 15/15(E4V5M6).

E: Eye

• 4= eyes open spontaneously
• 3= eyes open in response to call
• 2= eyes open in response to pain stimuli
• 1= no eye opening

V: Verbal

• 5= oriented
• 4= confused
• 3= inappropriate words
• 2= incomprehensible words
• 1= no voice

M: Motor

• 6= obey commands
• 5= localizes to pain
• 4= withdraw to pain
• 3= abnormal flexion to pain stimuli
• 2= abnormal extension to pain stimuli
• 1= no movement

When the patient comes to us with GCS< 8, theoretically intubation is needed to maintain the airway and also for cerebral protection in case of traumatic brain injury. But first, we must assess the vital sign first. 

Intubation is not needed in case of temporary hypoglycemia. A patient with hypoglycemic attack can have poor GCS. A patient with recurrent massive stroke does not need intubation if GCS is always low all the while. What I want to conclude is that a poor GCS does not necessarily need intubation unless it is indicated and vice versa.

3. RSI: rapid sequence intubation.

It must be done in sequence. (with several "P"s)

1. Preperation

• We must firstly prepare the patient with good position and instruments for intubation. Things to prepare: medications, ambu bag, bag-valve-mask, yankeuer, suction tube, laryngoscope, endotracheal tube (ETT) with appropriate size, K-Y jelly (lubricant gel), oral airway.
• RSI must be done with helps. A team must be formed of a leader and few assistants. A assistant must be selected mainly only to perform cricoid pressure.
• Vital sign monitoring must be ready - you need to observe BP, PR, SPO2, heart beat rhythm during RSI. 

2. Pre-oxygenation

• Bagging can be done with ambu bag and bag-valve-mask. 
• Bagging is not necessarily if there is still spontaneous breathing and we only apply the ambu bag on the mouth without bagging. 
• SPO2 must be maintained at least 99%.

3. Pre-medication

• There are few sedative medications that are mentioned in literature. I only mention common medication. 
• Here, we use Midazolam (0.1-0.3mg/kg/dose). 
• Atropine can be added if there is bradyarrhythmia.

4. Paralysis

• There are mainly 2 types of paralysing medication we use to paralyse the airway for easy intubation. There are Succhynilcholine and Rocuronium. 
• We often use S-choline (1-1.5mg/kg/dose). This medication often would cause muscle fasciculation and it is the main sign that we can see after introduction. The fasciculation will trasmit from head till toe and once it reaches the toe, it is time for intubation. Of cause, each drug has its own side effect and neither the patient can escape from this drug. S-choline can cause raised intracranial pressure, bradycardia and hyperkalemia. Please mind that we must avoid this drug for patient with bradycardia, traumatic brain injury, brain tumor, ESRF (end stage renal failure) and so on.
• In view of S-choline possible adverse effect, Rocuronium would be the substitute. Its usual dosage is 1-1.2mg/kg/dose. After 1 minute of introduction, we are ready to intubate. Of course, due to its prolonged paralysing effect, it is not the first line drug unless it is indicated.

5. Protection

• Once we introduce sedation and followed by paralysing agent, our assistant needs to perform cricoid pressure. Remember that we can only release the cricoid pressure after successful intubation.
• Please find out what is cricoid pressure and how to do it.

6. Positioning

• We need to position the head and the mouth for intubation. 
• Please find out how you would like to place the head in order to visualize the vocal cord.

7. Placement of tube

• Please remember that we always use our left hand to hold the laryngoscope. The blade should face towards the patient. Use our dominant hand to open the patient's mouth. With correct position and cricoid pressure, this step would be possible. 
• The usual size of ETT is 7-7.5mm for adult. ETT with size 8mm is sometimes needed for huge adult patient. ETT is often anchored at 21-22cm at mouth angle. 
• If ETT is inserted too deep, we can create pneumothorax. 
• If ETT is inserted too shallow, it can be dislodged or the patient can have insufficient oxygen supply. 
• After intubation, ETT must be secured. By auscultating the lungs and epigastric region, we can hear the lung breathing sound if the ETT is placed into the airway; otherwise, we can hear sound at epigastric region if the ETT is placed into the esophagus. Esophageal intubation can cause gut perforation and ETT must be taken out and repeated intubation is needed.

8. Post-intubation management

ICU admission must be arranged. CXR must be done. Gauze must be applied over the eyes to avoid eye dryness after intubation. After intubation, 3 things we will see.

• SPO2: SPO2 will remain 100% after intubation. If SPO2 drops, then there is either something not right with the placement of ETT or other causes, e.g pneumothorax.
• Chest expansion with out-in going vapor in ETT: Chest will depress with each out-going vapor from ETT.
• CXR: CXR must be done after intubation to ensure the ETT is in situ.

Doctors must know how to intubate and to perform RSI. It is compulsory!

 

AF, CVA, Orange urine

1. What are the common causes of AF(artrial fibrillation)?
2. What you want to rule out in ECG for patient with CVA(cardiovascular accident= stroke)?
3. A patient with PTB came to you and complaint of passing out urine in orange color after taking anti-TB for 3 days. What would you do? 

1. Common causes of Artrial Fibrillation (AF)

• Ischemic heart disease (IHD)
• Hypertensive heart disease
• Rheumatic heart disease (RHD)
• Thyrotoxicosis
• Post-srugery
• Chronic lung disease
• Atrial septal defects (ASD)
• Acute alcohol intoxication

2. In CVA patient, we need to rule out causes of cardiogenic embolism on ECG

• Artrial fibrillation (AF): Absence of P-wave, irregular base line, irregular RRI.
• Myocardial infarction (MI): Deep Q-wave.
• Left ventrial aneurysm: Residual ST-elevation, deep Q-wave.

3. Orange-coloured urine is SE of Rifampicin. Need to explain that this medication may produce orange coloration of urine, sweat, saliva, or tears, but it is harmless, so reassure patient to continue to take their medication.

Heart rate, Finger clubing, DOTS

1. What is the fastest, most common, efficient way to calculate the heart rate from ECG? (Hint: number 300)

2. How to diagnose finger clubbing and how to stage the finger clubbing? What are the possible cardiovascular causes of finger clubbing? (Hint: one of the test-> diamond window)

3. Once a patient is diagnosed TB, he/she has to follow DOTS. What is DOTS? He/she will given a small recordable TB book and there are 2 kinds of color for it. There will be white and yellow in color. What does the color mean? (Hint: the color has to do with sputum AFB)

1. Calculating heart rate (HR) from ECG

The most common way to calculate HR from ECG is by taking 300 and divide it RR interval (RRI) (represented by number of big boxes).
e.g. The RRI is 4 big boxes, so the HR = 300/4 = 75 beats per min (bpm).

If the patient has very fast HR and the RRI might be less than even 1 big boxes, HR can be calculated by taking 1500 and divide it by RRI (represented by number of small boxes).
e.g. The RRI is 4 small boxes, so HR = 1500/4 = 375 bpm.

However, personally I found out that the fastest and most efficient way to calculate HR is the triplet method. First memorise these 2 triplets:

300-150-100
75-60-50

Then try to find a R wave on a black line, then start counting the black lines after that R wave until u meet the next R wave. When you count, don't count by mentioning "1-2-3-4......", rather you should count by mentioning the triplets that you memorise, i.e. "300-150-100-75.....". So when the number of the black line that you mentioned hit the next R wave, that's the HR. I hope the illustration below helps to understand this concept.

You can make the most out of this triplets method by further memorised the numbers in between those triplets. This become handy when the next R wave falls in between the 2 black lines.

300-200-150-120-100-85
75-65-60-55-50-45

For e.g. when the next R wave falls in between the lines represent 300 and 150, so we can straight away know the HR = 200 bpm.

This method is efficient because it saves the trouble of calculating difficult mathematics, eg 300 divided by1.5 boxes, or 300 divided by 2.5 (either with your mind or with a calculator or the calculator in the handphone).

2. Finger / Digital Clubbing: There are 4 stages of finger clubbing.

1. Increased glossiness and cyanosis at the skin of the root of nail with increased fluctuation at the base of the nail bed. 
2. Lovinbond's sign : loss / reverse of hyponychial angle (angle between nail and nail bed).
3. Hippocratic finger / Parrot beak / Drum-stick: increased anterior-posterior (AP) curvature.
4. Hypertrophic osteoarthopathy (HOA).

• Schamroth's window test: bring the fingers from side together, with the nail facing each other. Loss of the kite-shaped window between the nail indicates finger clubbing.
  
  
  
• Interphalangeal depth ratio: DPD/IPD > 1 indicates finger clubbing.
  DPD : distant phalangeal depth, AP dimension measured at hyponychial angle.
  IPD : interphalangeal depth, AP dimension measured at the distal interphalangeal joint (DIPJ)
  
  
• Elicit fluctuation: I stage of clubbing can be checked by palpating the nail bed with both hands: 2 thumbs below the patient's finger; while 2 index fingers above the patient's finger, near the tip; 2 middle fingers above the patient's finger, at the end of the nail bed. Use your middle fingers to press the nail bed, check whether the distal part of the nail is fluctuating / ballotable.

Summary of the examination for digital clubbing

1. View the fingers from a dorsal and lateral view. Note the width of terminal portion and compare with the proximal part.
2. Look at the angle between the nail and skin (Schamroth's window test)
3. Inspect the periungual skin. Check for cyanosis, shiny, or stretched skin.
4. Elicit fluctuation of the nail bed.
5. Attempt to feel the posterior edge of nail.

Cardiac cause of finger clubbing: infective endocarditis (IE), cyanotic heart disease.

Need to exclude GI and respiratory cause: e.g. liver cirrhosis, bronchial CA.

3. DOTS is Directly Observed Treatment, Short-course. Consists of 5 elements:

1. Government commitment.
2. Detect case with sputum AFB of TB patients.
3. Standard short course of 6/12 TB treatment, with trained supervisor watching patients swallow their anti-TB drugs. DOTS is used with intermittent dosing (thrice weekly). 
4. Regular anti-TB drugs supply.
5. Monitor and report treatment outcome.

Not quite sure about the white and yellow booklet. Anyway this is my guess. Since the patient's sputum AFB need to be checked, so the booklet should be used to record the result of sputum AFB. Since only one booklet is given, and the container for sputum AFB collection is yellow in colour, so the yellow book should be given for patient with smear +ve PTB, while white book should be given to patient with smear -ve PTB. This is just my guess.

--- UPDATE ---

Stage of finger clubbing
I. Fluctuation and softening of finger nail bed
II. Loss of normal angle (Lovinbond's angle)
III. Increased convexity of nailbed
IV. Thickening of whole distal part of finger nail
V. Shiny aspect and striation of nail and skin (HPO)

Causes of FC with CVS origin
1. Artrial myoma
2. Cardiovascular disease with hypoxia
3. Congenital heart disease
4. Infective endocarditis

DOTS is directly observed therapy, short course
What you mentioned about DOTS is right. After a patient is diagnosed TB, he/she needs to come to KK(Klinik Kesihatan) to claim anti-TB medication daily, so that we can make sure the patient is taking medication.
White DOTS book means "smear -ve TB" and yellow one means "smear +ve TB".

Additional question: a senior MO asked me this question.

What are the two types of finger clubbing? (Hint: stage III of clubbing)

Types of finger clubbing:

1. Parrot-beak
2. Drumstick

According to that MO, certain type of clubbing is more common or dominant in certain diseases, due to different pathogenesis or mechanism. He wants me to find the answers myself, but honestly after I searched for few days still can't find the answer. Apparently this information is something that he learnt in India, since he graduated from there, and he asked me to find in Indian website.

2ICS & PTB

1. What is the correct way to identify the second intercostal space? (Hint: sternal angle)

2. What are the criteria to diagnosis PTB (pulmonary tuberculosis)? (Hint: 2/3 criteria)

3. What is TB intensive and maintenance/continuation phase? (hint: type of medication and duration)

1. Second intercostal space:

• The angle of Louis / sternal angle is a useful place to start counting ribs, which helps localize a respiratory finding horizontally. If you find the sternal notch, walk your fingers down the manubrium a few centimeters until you feel a distinct bony ridge. This is the sternal angle. The 2nd rib is continuous with the sternal angle, slide your finger down to localize the 2nd intercostal space.
• The angle of Louis also marks the site of bifurcation of the trachea into the right and left main bronchi and corresponds with the upper border of the atria of the heart.

2. Diagnosis criteria of PTB (2/3):

1. Clinical picture of PTB: cough >2-3/52, fever, LOW, +/- hemoptysis
2. CXR signs of PTB: Upper lobes consolidation / cavitation
3. Sputum AFB (+): 3 x early morning sputum is collected on first day, subsequent 1 x early morning sputum for another 3/7.

However, before diagnosis can be put as PTB, we can consider whether to give anti-TB drugs after collecting the sputum. Signs that suggest PTB (but not enough to diagnose it):

• Clinical picture of PTB
• CXR signs of PTB
• FBC changes: ↑ Monocyte, ↑ Platete, ↑ ESR

If the above signs are fulfilled, it is highly suggestive for PTB, and anti-TB drugs can be given after sputum is collected. Remember to check for serum Na+ to exclude SIADH. 

3. TB treatment:

• Intensive phase of refer to the initial phase of TB treatment, 2/12 duration, on 4 anti-TB drugs. Aims: Eliminate clinical picture of TB, eliminate MTB in sputum, and prevent development of drug resistance.
  
  e.g. 2HRZE or 2HRZS
  
  
• Maintenance/continuation phase refer to the second phase of TB treatment, 4-7/12 duration, on 2 anti-TB drugs. Aims: Suppress MTB in host, and prevent relapse of TB.
  
  e.g. 4HR or 4(HR)3

--- UPDATE ---

 

Answers:

1. The sternal angle is between the manubrium and sternum. Once you identify the location by palpation, the left second rib is just beside it. Your finger moves along the second rib and move down below it. There the second intercostal space is localized. The importance of localization of second intercostal space is to do pleurocentesis, chest tube insertion and etc.

2. The criteria of PTB diagnosis:
a. Clinical symptoms
b. CXR findings
c. Sputum AFB(acid fast bacilli)

• Clinical symptoms: in your clerking, you must ask duration of cough, hemoptysis, evening rising temperature, night sweat, LOA/LOW (loss of appetite and loss of weight), h/o (history of) contact with PTB patients, h/o PTB in the past, risk factor (e.g DM, IVDU/Intravenous drug user, RVD+ve/retroviral disease +ve, so on). The symptoms must be more than 2 weeks duration.
  
• CXR findings: cavitation/haziness over upper zone/apical region of lung field.
  
• Sputum AFB: collection must be done x OD x 3/7

REMEMBER: to diagnose PTB, we need 2 out of 3 criteria.
TB is divided into PTB and EPTB (extrapulmonary PTB). PTB can be smear positive and smear negative.
Even sputum AFB is negative, with 2 other criteria, evidence is enough to label a patient with smear negative PTB. Smear positive PTB is PTB with sputum AFB +ve.
Note: sputum AFB is not sputum MTB.

3. TB intensive phase usually requires 2 months or 56 doses. The initial phase can be extended up to maximum, 84 doses, depending on the patient's condition. During this phase, the standard TB medication would be EHRZ / Ethambuthol + Isoniazid + Rifampicin + Pyrazinamide.
Then the latter phase would be continuation/maintenance phase. During this phase, the standard anti-TB medication would be H (Isoniazid) and R (Rifampicin). It is given at least 6 months.

You must know the common side effect of PTB medication.

• E - 15-25mg/kg/day; max 1200mg
  common SE- optic neuritis
  contraindicated for the patient with advanced age > 70 years old and age < 15 years old, poor vision, renal impairment.
  
• H - 5mg/kg/day; max 300mg
  common SE- liver impairment, skin rash.
  
• R - 10mg/kg/day; max 600mg
  common SE- liver impairment, acute renal failure, thrombocytopenia, drug-induced jaundice
  
• Z - 25mg/kg/day; max 1500mg
  common SE- liver impairment, hyperuricemia

S(Streptomycin)- used when it is indicated. Usually it is given for TAI (treatment after interruption), relapsed TB, reactivation of TB. Common SE- renal impairment, ototoxicity. It is contraindicated in age > 60 and in children, pregnancy.

Another way of TB prescription according to weight. It is used by chest physician in Kedah.

• S - Streptomycin
  0.75mg OD if BW > 30kg;
  0.5mg OD if BW < 30kg
  
• H - Isoniazid
  300mg OD
  
• R - Rifampicin
  600mg OD if BW > 50kg;
  450mg OD if BW 30-50kg and
  300mg OD if BW < 30kg
  
• Z - Pyrazinamide
  1500mg OD if BW >40-50kg;
  1250mg OD if BW 30-40kg and
  1000mg OD if BW < 30kg
  
• E - Ethambutol
  by practise 1400mg OD up to maximum 2600mg OD and we calculate 25mg/kg/day for E

TB medication is mainly prescribed by chest MO; however we need to know the usual dosage.

TB is the second main infectious disease after Dengue fever.

Additional Question:

What are signs of TB of CNS on neuroimaging? (There should be 5)

1. Tuberculoma: non-enhancing and enhancing.
2. Infarct: caused by vasculitis after being insulted by TB granulation tissue
3. Hydrocephalus: communicating and non-communicating
4. Meningeal enhancement, especially basal enhancement

Not sure about the last sign, but might be the following:

1. Cerebral abscess: rare complication
2. Cerebritis with enhancement at cerebral parenchyma
3. Granulation tissue in basal cistern, superficial sulcal spaces, Sylvian fissure
    → Isodense or mildly hyperdense exudate obliterates the basal cistern.
4. Cerebral oedema