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Marking
CCS
CBS
CCS - EPIC Part II SET I - Marking
Step
1
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56
1%
Name of Candidate
Name of Examiner
CCS 1-Vignette 1
1) What is your differential diagnosis ?
Pregnancy-induced hypertension (gestational hypertension without proteinuria) / Preeclampsia (gestational hypertension with proteinuria)
Essential hypertension
Pheochromocytoma
Primary aldosteronism (Conn’s Syndrome)
Cushing’s syndrome
CCS 1-Vignette 1
2) What is diagnostic criteria for preeclampsia?
SBP > 140 mm Hg and DBP > 90 mm Hg, after 20 weeks of gestation.
Proteinuria - ≥300 mg in a 24-hour collection Protein/creatinine ratio ≥30 mg/mmol spot urine or positive dipstick 1+
Any maternal organ dysfunction – renal , hepatic, neurological, hematological, cardiorespiratory
Uteroplacental dysfunction
CCS 1-Vignette 1
3) What investigations will you send?
Complete blood count
renal function and electrolytes
Liver function test
Clotting profile
Blood group matching
Urinalysis
CCS 1-Vignette 1
4) What is your further management
Antihypertensives
Magnesium Sulphate
Urgent delivery
CCS 1-Vignette 1
5) How will you control the BP?
Antihypertensives
Magnesium Sulphate
Urgent delivery
CCS 1-Vignette 1
6) What monitoring will you consider in this patient
Intra-arterial blood pressure monitoring
urine output, intake-output chart
central venous catheter
Continuous foetal heart monitoring
CCS 1-Vignette 1
7) What are the principles of fluid management?
Have a reduced circulating intravascular volume – risk of hypotension plus risk of pulmonary edema - Restrictive management recommended
Unless oliguria – give fluid challenge
CCS 1-Vignette 2
8) What is your Immediate management
ABC
Adequate maternal oxygenation
optimize utero-placental perfusion – reposition mother on side.
Administer anticonvulsants
CCS 1-Vignette 2
9) What is the anticonvulsant of choice in eclampsia with dose
Magnesium Sulphate
Loading dose 4–6 g over 10–15 min IV
Maintenance 1-2gm IV /hour Or 4gm IM every 4 hours
CCS 1-Vignette 2
10) What are the risks of airway management in this patient?
Risk for sudden hypoxemia – as oxygen consumption increases and functional residual capacity decreases during pregnancy
increased rates of failed intubation
Difficult laryngoscopy – Smaller size of ETT as Increasing edema of the airway structures
RSI
Wedge with left tilt to prevent IVC compression
CCS 1-Vignette 2
11) What monitoring should be consider with the use of Magnesium sulphate
Urine output
DTR
Serum magnesium concentration
CCS 1-Vignette 2
12) What is the target serum magnesium concentration
4-7 mEq/L
CCS 1-Vignette 2
13) What are the signs of magnesium toxicity ?
Muscle weakness and may lead to respira- tory paralysis (>7.5 mmol/L)
increased PR and QT intervals and QRS duration - sinoatrial and atrioventricular block (>7.5 mmol/L)
CCS 1-Vignette 2
14) What is the treatment of Magnesium sulphate toxicity
IV calcium gluconate
RRT
CCS 1-Vignette 3
15) What is the cause for excessive bleeding
DIC
HELLP syndrome
CCS 1-Vignette 3
16) How investigations will you send ?
PT INR, aPTT
Platelet count
Plasma fibrinogen
D dimer
CCS 1-Vignette 3
17) Scoring system for DIC?
International Society for Thrombosis & Hemostasis (ISTH)
Pregnancy‐modified scoring system by Erez
CCS 1-Vignette 3
18) How will you manage ?
1:1:1:1 PRBC: Platelet: FFP: Cryo
Treat the cause
Maintain organ perfusion
Tranexamic acid
CCS 1-Vignette 3
19) What is the evidence of using Tranexamic acid ?
WOMAN trial of 10000 patients
Multicentre, RCT
Maternal death due to bleeding was significantly reduced in women given tranexamic acid
CCS 1-Vignette 4
20) What are the complications of PIH/ eclampsia?
Cardiac – Pulm edema,
Renal - AKI
Liver- Subcapsular liver hematoma, Liver rupture,
Neuro – Cerebral hgge, cerebral edema, temporary blindness
CCS 1-Vignette 4
21) Her Husband complains that he was told she would become all right after the operation. She appears to be sinking. How would you explain the situation to him?
Discuss the expected maternal risks and possibility of complications and treatment options available
Documentation
CCS 2-Vignette 1
1) What is your differential diagnosis ?
poisoning- beta blocker,
CCB poisoning
Opioid poisoning
Cardiac event
CCS 2-Vignette 1
2) How will you approach this case?
ABC,
BP support,
sugar correct
temp correction
CCS 2-Vignette 1
3) What investigations will you order?
CBC,
RFT, Elec,
Coag, LFT
ECG, ABG, urine analysis
Toxicology analysis
Gastric lavage
Brain imaging
CCS 2-Vignette 1
4) What empiric treatment would you like to initiate
Dextrose
Naloxone
Thiamine
CCS 2-Vignette 1
5) Is there a role of gastric decontamination? How will u do ?
Since the patient presents within 1 hour – yes
Use of activated charcoal
CCS 2-Vignette 1
6) what precautions will you take before giving gastric lavage ?
Not recommended these days
Protect the airway prior
C/I in corrosive substance or a hydrocarbon poisoning.
CCS 2-Vignette 2
7) Is there anything else you would want to do now ?
Multiple-dose activated charcoal
whole bowel irrigation
CCS 2-Vignette 2
8) Explain the dosing in multiple-dose activated charcoal
The initial dose of charcoal is 50 to 100 g,
Repeated every 1, 2, or 4 hours by a dose equivalent to 12.5 g/h.
CCS 2-Vignette 2
9) Why explains the altered sensorium on arrival?
Hypoglycemia
Cerebral hypoperfusion
Metoprolol has high lipid solubility and crosses the BBB – causes CNS symptoms.
CCS 2-Vignette 2
10) What ECG abnormalities can be seen in beta blocker toxicity
AV conduction delays - Prolonged PR, AV blocks
Non specific ST-T seg changes
Prolonged QTc
Asystole
Multifocal ventricular extrasystoles
Vent tachycardia/fibrillation
Torsades de pointes
CCS 2-Vignette 2
11) How will you manage the hemodynamics?
judicious intravenous crystalloid fluids
inotropic drugs such as dopamine, dobutamine, epinephrine, norepinephrine, or phenylephrine
Atropine (poor response usually)
CCS 2-Vignette 2
12) What is the specific antidote ?
Glucagon
CCS 2-Vignette 2
13) What monitoring will you consider?
ECG monitoring
Invasive HD monitoring
Glucose monitoring
Neuro monitoring - watch for seizures
CCS 2-Vignette 3
14) What will you consider next?
Administer Calcium gluconate.
high-dose insulin, euglycemia (HIE)
Lipid emulsion
Pacing
CCS 2-Vignette 3
15) what are the possible side effects of Glucagon?
Hypocalcemia,
hyperglycemia
, induces vomiting
CCS 2-Vignette 3
16) Is there a role of dialysis in this patient?? Why ?
No role
Metoprolol is lipophilic – not removed by dialysis
CCS 2-Vignette 3
17) Which are the water-soluble and renally excreted beta-blockers ?
acebutolol,
atenolol,
nadolol,
Sotalol
CCS 2-Vignette 3
18) What precautions will you take in view of medicolegal aspect
Documentation,
preservation of samples.
Notify police
CCS 3-Vignette 1
1) What is the percentage of burns? what formulas are available to calculate the same
Approx 65%
The rule of nines
Lund–Browder Diagram
CCS 3-Vignette 1
2) Does this patient need immediate intubation? Why ?
Yes
Facial involvement
Inhalational injury -possibility
CCS 3-Vignette 1
3) What precautions will you take for securing her airway?
Anticipate difficult airway
Risk of airway edema
Avoid Succinyl choline – risk of hyperkalemia due to tissue damage
CCS 3-Vignette 1
4) What other respiratory complications should be considered after looking at the history
CO poisoning
Cyanide poisoning
CCS 3-Vignette 1
5) How will you resuscitate her ?
Secure wide bore access/ Central line
Parkland formula – 4ml/kg in 24 hours – 50% in first 8 hours, rest in next 16 hours
Crystalloids isotonic
CCS 3-Vignette 2
6) Why are patients with burns at a higher risk for infection/ sepsis?
mechanical disruption of the skin, thus allowing microbes to penetrate in deeper tissues
Colonisation of wound with bacteria (gram-negative and gram-positive) and yeast from the hosts’ GI and URT, and /or from hands of HCWs or hospital environment.
percentage of burns is an independent risk factor for early colonisation
Over-resuscitation
CCS 3-Vignette 2
7) Based on the parameters given on day 3, do you think the patient is in sepsis??
NO
CCS 3-Vignette 2
8) What are the criteria for diagnosis of sepsis in burns patients?
AHA -presence of three or more of the following six criteria : i. Temperature >39 °C or <36.5 °C
ii. Progressive tachycardia >110 beats per minute
iii. Progressive tachypnea >25 breaths per minute or minute ventilation >12 L/min
iv. Thrombocytopenia <100,000/mcl (does not apply until 3 days after burn)
v. Hyperglycemia in the absence of pre-existing diabetes mellitus (Untreated plasma glucose >200 mg/dl or intravenous insulin >7 units/hr IV, significant resistance to insulin [>25% increase in insulin requirements over 24 h])
vi. Inability to continue enteral feedings >24 h (Abdominal distension, enteral feeding intolerance [two times feeding rate], uncontrollable diarrhea [>2500 ml/day])
documented infection is identified defined as: • Culture positive infection, or
• Pathologic tissue source identified, or
• Clinical response to antimicrobial
CCS 3-Vignette 2
9) How are drug pharmacokinetics and pharmacodynamics altered in a patient of burns?
During the first 24 hours, cardiac output is depressed and capillary leak is present - distribution and clear- ance of administered drugs are delayed.
After 24 hours, increased cardiac output leads to accelerated drug absorption and distribution,
hypoalbuminaemia - increases free fractions of drug - rapid clearance of protein bound drugs
increased α1-glycoprotein levels
diffusion in the edematous tissue- third space
CCS 3-Vignette 2
10) Pain management in burns?
Incremental doses of an IV opioid.
Use of Ketamine – esp for procedural pain during dressing etc
Use of patient controlled analgesia
CCS 3-Vignette 3
11) Does this indicate invasive infection ?? How to confirm?
No
indicates colonization (< 105 bacteria / gm of tissue)
Quantitative cultures to be done to diagnose wound infection (> 105 per gm of tissue)
CCS 3-Vignette 3
12) How do you define invasive infection in a burns patient?
Invasive infection should be considered only if there are purple-black and punched out areas of the wound
Pathogens in burn wound at a sufficient concentration, depth and surface area to cause suppurative separation of eschar or graft loss, invasive of surrounding unburned tissue, or sepsis syndrome.
CCS 3-Vignette 3
13) How will you treat this patient now?
localised colonisation with pseudomonas – topical antibiotics
wound care
IV antibiotic prophylaxis at the time of wound manipulation
Close watch - for evidence of invasive infection or evidence of sepsis.
CCS 3-Vignette 3
14) What are the common organisms seen in burn wound infection?
MRSA
Pseudomonas,
Klebsiella
Acinetobacter
CCS 3-Vignette 4
15) How will you manage further?
is in sepsis with septic shock.
Send cultures – 2 sets (one set from central line and other from peripheral collection), wound tissue culture.
Start higher antibiotics
Invasive line access will be changed to a new site
early wound debridements
CCS 3-Vignette 4
16) Choice of antibiotics?
high possibility of drug resistant pseudomonas
IV Meropenem
IV Colistin
Teicoplanin IV for MRSA
CCS 3-Vignette 5
17) What is the further plan on antibiotics, based on culture report? What is the evidence for the same?
Teicoplanin needs to be stopped
Continue with Meropenem and Colistin combination
Patient is in shock, with bacteremia - combination of colistin with meropenem has shown a reduction in mortality, higher clinical and microbiological response.
CCS 3-Vignette 5
18) What is the place of antibiotic stewardship in a burns unit ?
Avoid Prophylactic antibiotics
perioperative antibiotics - in patients with severe burns with aggressive debridements or in patients undergoing skin grafting.
no role of selective gut decontamination
CCS 3-Vignette 5
19) What are the strategies of Infection prevention in a burns patient?
Contact precautions (single use masks, gowns, and gloves
Hand washing before and after contact
Cohort nursing
Decreased use of invasive devices, and improved aseptic technique when inserting devices.
Timely closure of the burn wound - the use of a dedicated operating theatre for burn surgeries
Installation of Laminar airflow techniques in burn units.
AllEscort
