A 24 years old lady with a history of HbH thallasemia with post splenectomy 8 years ago on frequent blood transfusion presented to ED with a history of shortness of breath. This patient frequently defaulted treatment and had been non compliant to medication. A month prior, she was admitted into medical ward for decompensated cardiac failure due to cardiomyopathy as a result of iron deposition.

She was seen gasping and was able to speak in few words at best. What was noticeable was her leg swelling was worsening and was tender on palpation. Her jugular venous pulse was strong and reaching her earlobe. She was put on high flow mask and a baseline ECG was recorded as below.

Do you recognize any particular pattern in this 12-lead ECG?

Answer:
The 12-leads ECG showed a variant of the SI QIII TIII of pulmonary embolism.  Noted that there is right axis deviation with a prominent S wave in lead I (hence SI), and T wave in lead III. (TIII). There is no Q wave though in lead III (QIII). Another distinctive pattern seen was T wave inversion of V1 - V3 as well as P pulmonale (tall tented P waves) seen esp in lead II.

The patient had been having DVT from prolonged immobilization and US Doppler revealed significant DVT over the right lower limb. CT Pulmonary Angiography confirmed the diagnosis with multiple scattered areas of embolization in the lungs. The patient was started on unfractionated heparin infusion and overlapped with warfarin. Her condition improved after 1 week of admission. She was discharged with warfarin, however, knowing that her prognosis is guarded in view of her condition and prolonged non-conpliance to medical therapy.

A week after discharge, the patient was readmitted into ED red zone with another spell of shortness of breath. It was another episode of pulmonary embolism with pulmonary hypertension with biventricular failure and the patient was intubated and admitted into CCU but did not make it through after 2 days there. The parents were counselled of the prognosis and they did not wish for active resuscitation in view of her deteriorating condition thereafter.

A 68 years old lady presented to the ED with productive cough for the past 3 days. She was brought today in view of her complains of generalized lethargy and weakness. Prior to further investigations, a baseline ECG was done. She was initially sent for green zone fast track, but was subsequently uptriage to yellow. What are your findings?

Answer:
This is a rare pattern of atrial bigeminy. While most are familiar with the easy-to-spot ventricular bigeminy with a wide QRS complex, this can be rather confusing as one may thought of Mobitz type II or 2:1 block. However, a closer look will reveal a few things:
1) The QRS complex exhibits grouped beating, being regularly irregular
2) There are presence of P waves prior to each QRS complexes
3) All P wave have an associated QRS complexes
4) The 2nd P wave have slightly different morphology than the 1st P wave, suggestive of 1st P wave originated from the sinus focus whilst the 2nd P (premature atrial contraction) may originate from another focus.

Atrial bigeminy, as a manifestation of premature atrial contraction, is a harmless rhythm in the proper clinical context. Most people with atrial bigeminy do not have organic heart disease, albeit the fact that it is more common in people with heart disease than those without. There are certain factors linked to the occurence of atrial bigeminy, such as caffein intake, emotional stress, smoking, alcohol use and fatigue. One things is of concern is that patioent with atrial bigeminy may not have the 2nd QRS wave transmitted into a pulse, which had caused this patient to have a pulse rate of 50-60 despite a heart rate of 100-110.

In this patient, no identifiable cause was found despite the alert and uptriage to Red Zone initially. Repeated ECG 1 hour later showed resolution to sinus rhythm and her pulse rate returned to 80-90 beats per minute. Nevertheless, the patient was admitted for community acquired pneumonia with a high CURB-65 score.

A 53 years old Malay gentleman with no known medical illness came to ED complaining of worsening epigastric pain for the past 3 days.He had earlier seek treatment from a GP 2 days ago and was treated as gastritis. He was discharged with syrup MMT and oral ranitidine. He claimed that the symptoms improved after taking the medication, albeit not completely.

However, today, the pain worsened and became rather severe, hence the reason he made a trip down to the ED. He was given syrup MMT and ranitidine and a baseline ECG was done. Routine blood investigations was done and it was noted that cardiac enzymes were normal as well.

2 hours later, the patient was noted to be sweating. He looked lethargic and pale. He still complained of epigastric pain. A repeat ECG was done in view of the patient's discomfort.

Normal 12-lead ECG 

Posterior lead ECG

Inferior ECG

What would be your intepretation? Is there any bedside test to confirm your diagnosis? Any further blood investigations that can be taken?

Answer:

The 12-lead ECG showed significant ST - elevation over the inferior leads II, III, aVF whilst the lead V1-V3 showed ST depression. In a case of inferior MI, it is prudent to do a right sided ECG and posterior lead ECG The reason being is that inferior segment of the heart is supplied by the right coronary artery, which also supplies the right and posterior aspect of the heart. An occlusion at the right coronary artery that affects the inferior aspect may affect the other 2 as well. Of coursem other signs may include bradycardia and subsequent hypotension, as a result of sinuatrial node involvement, which is also supplied by the right coronary artery.

The right sided ECG showed no ischemic changes over the right aspect of the heart, but a quick look at the posterior leads showed significant ST-elevation as well.

Hence, this is an acute inferoposterior myocardial infarct. A bedside ECHO can be done and for this patient, there is hypokinesia over the inferoposterior region, correlating with the ECG findings. Cardiac triple test (bedside rapid test) was done for this patient. Myoglobin and CKMB was positive whilst TnI was negative, suggestive of recent onset basis. (Kindly refer to Malaysian CPG for acute coronary syndrome to have a quick review of the peak and through of the cardiac enzymes).

The patient was started on streptokinase fibrinolytic therapy in view of no PCI in the center. 1.5mU Streptokinase was given in 100cc normal saline over 1 hour (there are 2 other recommended regime). The streptokinase was witheld once midway as patient developed hypotension (side effects of streptokinase therapy) and restarted slowly once BP picked up after 1 pint of NS was given. Repeated ECG showed good resolution of the ST elevation and the patient was sent to CCU for close monitoring and management.

Case submitted by Dr Jefrrey Lee on 15th Nov 2011

This is an extremely rare case. just would like to share it for academic purpose.

A 38 year old primigravida at 22 weeks POA was referred from MCH for stabilisation of severe hypertension in pregnancy 

(BP=220/120 on 2 separate occasions). 

No previous known history of hypertension but there is a family history of hypertension. 
She is asymptomatic for preeclampsia, urine protein trace. 
Routine PET workup taken shows that she is extremely hyperkalaemic (serum potassium =8.9). 
Creatinine and other PET workup was normal and ECG does not show any changes suggestive of hyperkalaemia. 
She was given cocktail, serum potassium improved to 4.5 but again increase to 7.8 a day later. - Sample was not lysed. 
ABG was taken shows a compensating metabolic acidosis. She was otherwise asymptomatic with normal urine output.

The diagnosis is beyond our level as it is made by the Physician. But it is worthwhile to consider this when we cannot explain why a patient remain hypertensive, with asymptomatic hyperkalaemia and metabolic acidosis. 

Ready for the diagnosis? --> Gordon's syndrome or type II pseudohypoaldosteronism. Nice to know, nice to forget too : )

An elderly bed bound lady in her early 70's, was found to have urine as of such in her CBD bag.

Given that this is the first time the patient developed this condition,
1) What would your differential diagnoses be?

• Purple Urine Bag Syndrome - Although the name suggests more of urine discoloration, most of the time, the catheter and the bag are more markedly stained by the pigment.
• Porphyria - less likely, but still possible

2) What do you think are the risk factors for such condition?

•  Before we identify the risk factors, it is prudent to know how it is formed. Tryptophan in the food gets metabolized in the intestines into indoles. Enterohepatic circulation converts it into indoxyl suplhate which is then detoxified by the liver into indoxyl. These are excreted into the urine, which would be metabolized by colonizing bacteria(in alkaline environment) in the CBD into indigo (blue) and indirubin (red). The blue and red pigments when mixed, of course, gives you the purple hue from where the name originated from.  

 

•  Risk factors, of course are bedridden female elderly, alkaline urine, chronic constipation(to allow tryptophan metabolism and enterohepatic circulation metabolism to occur), long standing indwelling catheter(for colonization of bacteria in the CBD).

3) How do you treat this condition, should there be a need?

•  There are many advocates for different treatment, including:
  i) Urinary sanitization - by replacing the indwelling urine catheter and ensuring proper catheter hygiene, the urine condition will slowly but surely to improve
  ii) Constipation management - Since constipation is a risk factor, it is prudent to help the patients to move their bowels, hence preventing or reducing the formation of indoxyl.
  iii) A short course of antibiotics - Treatment of the UTI can be done, although it should not be the sole treatment. The above mentioned methods should also be practiced, otherwise there would still be recurrent infection!

Case Submission by Dr Jeffrey Lee (July 1st, 2011)

A 17 years old teenage boy was admitted to the wards after allegedly ingested 2 cups of Paraquat. Upon admission, he was vomiting profusely and multiple oral ulcers were seen upon inspection.

On investigation, his creatinine levels were raised from 168 μmol/ L on admission to 694 μmol/ L and >1000 μmol/ L over a week. The chest radiograph shows progressive changes suggestive of massive fibrosis.


Some questions to ponder:

1. What is your immediate management of this patient should you be the House Officer attending to this patient?
2. Give your full medical diagnosis of this patient from the information given.
3. What are the other signs and symptoms you should look out for?
4. What are the other complications you should be cautious of?
5. What are the investigations need to be done, particularly for monitoring purpose?

Upon admission, a nasogastric tube was inserted and NG Fuller's earth and Mist Alba was administered STAT with adequate hydration till diarrhea. Activated charcoal was also administered and the boy was being considered for peritoneal dialysis should his blood urea raises to a critical level.

A new protocol from the Sarawak General Hospital advocates the use of immunosuppressive agents. The agent recommended was IV Cyclophosphamide and pulse therapy of Dexamethasone. These agents presumably modulate the immunoresponse and have a reno-protective effect. These therapy was commenced on this patient. While the renal function improved with 2 or 3 cycles of immunosuppresion, the lung could not be saved as fibrosis has started to set in.

Further questions:

1. What are the dosage of the treatment given?
2. What are the indications for the use of immunosuppresive agents? Should we use them for all paraquat poisoning?

Well, this is a case file from some site (will be revealed with the answers). Maybe you would want to try to test your Peds ability if you've gone through the posting. Link to answer page is located at the bottom of the post.

An 18-month-old girl presents was presented with 2 days of fever and irritability. On the day of arrival to the A&E, her mother reported that the child has developed new onset of drooling and decreased oral intake. Her past medical history is unremarkable. On physical examination, she is febrile, ill appearing, and has neck stiffness.
The following soft tissue lateral of the neck X-ray is obtained.

Question:

1. What is the next most appropriate management strategy at this time?
   a. Discharge to home with supportive care
   b. Discharge to home with oral antibiotics
   c. Admit for intravenous antibiotics and surgical consultation
   d. Emergent intubation
   e. Cricothyroidotomy
   
   
2. What is your diagnosis?
   
   
3. What do you expect to see during your physical examination?
   
   
4. Give at least 3 differentials, that would make use of radiographic evaluation to differentiate between them.

Here is a case from Med Case Reports with some addition of questions, and we'll include our discussions here before revealing the answer. Try cracking your rusty head. :P

A 26-year-old female student presents with a 5-day history of cough, low-grade fever (temperature 37.6 C), sore throat, and coryza.
On exam, there is mild conjunctivitis and pharyngitis. Tympanic membranes are inflamed, and one bullous lesion is seen. Chest exam shows few basilar rales.

Laboratory findings are as follows:
Hct: 38
WBC: 12,000/μL
Lymphocytes: 50%
Mean corpuscular volume (MCV): 83 nL
Reticulocytes: 3% of red cells
CXR: bilateral patchy lower lobe infiltrates

1.The sputum Gram stain is likely to show

a. Gram-positive diplococci
b. Tiny gram-negative coccobacilli
c. White blood cells without organisms
d. Acid-fast bacilli

and what is your reason?


2. This patient is likely to have

a. High titers of adenovirus
b. High titers of IgM cold agglutinins
c. A positive silver methenamine stain
d. A positive blood culture for Streptococcus pneumoniae

And the reason being? What are the other diagnostic tests?

3. Treatment of choice is

a. Erythromycin
b. Supportive therapy
c. Trimethoprim-sulfamethoxazole
d. Cefuroxime

Dosage, mechanism of action, side effects?

4. Further Management and possible complications?

5. Last but not least, what are the general investigations done for patients with suspected pneumonia, and its indications.


Now, take a deep breath, and only check the answers once you've given this a try.

Source: Med Case Reports

Q:A 29-year-old female of African descent presents to your hospital with symptoms of
cough, difficulty in breathing, lethargy, and felt some bumpy nodules on her neck. Physical exam shows cervical adenopathy and hepatomegaly. A chest X-Ray was done and the image was shown as below.


1. How should you further investigate for a confirmatory diagnosis?
a. Bronchoscopy and transbronchial lung biopsy
b. Serum angiotensin converting enzyme (ACE) level
c. Scalene node biopsy
d. Liver biopsy
e. Open lung biopsy

2. What would your diagnosis be?

Try and take your time to ponder, the solution is only if you can't find a satisfactory answer.