winter edition
SEASONAL MAGAZINE CPS’
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O Hello Hello CPSolvers, this New Year marked the transitions for many across the world. From the astronomical event of, ‘planetary parade’ to prolonged fires on the West Coast, and ongoing interesting conversations about the future of vaccines! - Being a child who benefited from the pulse polio drive in my home country, I am constantly reminded of Sara Ban Breathnach’s famous quote, “Take a leap of faith and begin this wondrous new year by believing!” - All of us from the CPSolvers Magazine are excited to share this winter edition. This edition includes amazing stories of patients who ‘believed’ and healthcare professionals who upheld their patients by taking the effort to sharpen their diagnostic skills. In this edition we have included an opportunity for you to read or listen to the content. Let us know what you think, and feel free to share your thoughts on these amazing stories in the comments. And once again, Happy New Year, 2025!! A special thanks to the outstanding Academy members for making this edition possible! Aye, Lera, Minahil, Vijay, and Vinicius have poured their creativity and talent into crafting these beautiful case summaries. We would also like to extend our gratitude to Seeme Kh and Rainiel Reyes for contributing to this edition and sharing their thoughtful summary of a podcast episode and an interesting case they saw respectively.
~Kuchal & Sawsan
Case reflection and Recap by CPS’ Audience: Seeme Rukh
VMR Recap:1
VMR Recap:2
SUBSPECIALTY VMR: NEUROLOGY
RLR PODCAST EPISODE
Crack the Code: Decipher This ECG with Us!
case reflection by:Rainiel Reyes
Book Review:Every Patient tells a story Medical mysteries and the art of diagnosis -Lisa Sanders, MD
Case reflection and Recap by CPS’ Audience and participant: Seeme Rukh
A BRIEF INTRODUCTION ABOUT THE CASE REVIEWER: My name is Seeme Rukh, a medical graduate from Pakistan. In my spare time, I enjoy creating candles. I am passionate about illuminating my patients’ lives, just as candles illuminate a room.
VMR RECAP 1: January 16th
“A zebra that anyone can catch”
Case presenter: Leul Yosef Case discussants: Rabih Geha & Youssef Saklawi Highlighted by Lera Novotnaia
A 20-year-old male with a history of ear discharge for 8 years presented with a fever of 40.5°C lasting for the past 2 weeks. He also reported a severe persistent headache and a productive cough with bloody sputum. DIAGNOSTIC JOURNEY
Now, it’s time to ask two questions:
-Where does the disease live? We have two localizing signs: cough and headache. -What is the true time course—2 weeks or 8 years? The problem can be truly subacute or chronic with recent complication.
Let’s dig deeper into this case!
Patient lives in the malaria-endemic area. On exam, he has nuchal rigidity. There’s also active discharge from right ear, and a perforated tympanic membrane. CBC revealed a WBC of 4K with 81% neutrophils, hemoglobin of 16.7, and platelets of 51K. Blood smear showed toxic granulation of neutrophils and platelet aggregation.
There’s a high chance that we are dealing with pyogenic bacterial infection.
So where’s the source?
Ear?
Brain MRI: findings consistent with right ear otomastoiditis complicated by meningitis.
Blood?
Aerobic blood cultures: negative. Smears: positive for Plasmodium vivax.
Lungs?
Chest CT: multiple randomly distributed bilateral lung nodules with cavitations. Highly suggestive of septic pulmonary emboli.
In endemic settings, a partial immunity to malaria can result in asymptomatic infection. Also, non-Falciparum malaria is unlikely to be the cause of neurological manifestations seen in this case. Case closed, right? But there’s a twist.
The story doesn’t end here.
During hospitalization patient developed painful neck and right arm swelling. US revealed extensive thrombosis of internal jugular, axillary and subclavian veins.
1° infection (chronic suppurative
Otogenic Lemierre syndrome
otitis media, mastoiditis)
Here are a few more clues: -Thrombocytopenia—a common finding in invasive infections with Fusobacterium necrophorum. -Subacute presentation. That means there’s a hidden abscess. At the same time, septic pulmonary emboli point to an endovascular infection.
Septic pulmonary embolism
Septic IJV thrombophlebitis
Tap HERE to explore the full story behind the case!
One-and-a-half Syndrome
Clinical Presentation 73 years old male with sudden onset of horizontal diplopia for 1 day PMH - hypertension, hyperlipidemia no history of headache, facial/eye pain, seizure, weakness, or sensory abnormality.
What to consider first when a patient comes with horizontal diplopia? Neuro or Eye problem?
Ask the patient to cover each eye and see whether diplopia goes away or not!
If diplopia goes away ( diplopia occurs only when both eyes are open ) ( binocular diplopia ) - it’s due to misalignment of the eyes - likely Neurological problems Brainstem CN 3,4,6 palsies Extraocular muscles Neuromuscular junction Central coordination
If diplopia does not go away and persists when the other eye is closed ( monocular diplopia ) - it’s due to ocular problem in that opened eye Refractive error Lens abnormalities Corneal issues Retinal problems
Neurologic examination diplopia goes away when one eye is covered CN 3,4,6 examination - extraocular movement right lateral gaze - left eye stay in the middle, right eye can do abduction but not adduction and nystagmus on abduction left lateral gaze - no movement, both eyes stay in the middle convergence - normal, other CN - normal, motor 5/5 all limbs, reflexes +2, plantars - flexor, sensory, cerebellar, gait - all normal
Where is the lesion? Localization
Lesion in Dorsal Pons affecting ipsilateral PPRF and ipsilateral MLF ipsilateral PPRF controls CN6 nuclei + contralateral CN3 via MLF ipsilateral MLF - ipsilateral CN3 (INO) PPRF - parapontine reticular formation MLF - medial longitudinal faciculus INO - internuclear ophthalmoplegia MRI shows small infarct in left dorsal pons
Watch Neuro VMR episode of One-and-a-half syndrome with Dr. Aaron Berkowitz, Aye, Vale
Watch teaching point recap showcasting One-and-a-half syndrome by Aye
Do you know? One-and-a-half syndrome is first described and named by Dr. Charles Miller Fisher who described a lot of neuro- ophthalmologic signs He is also the one to be named after Miller Fisher Syndrome! Let’s play a little fun game!
As CN 7 wrap around CN 6 and if it involed in one-and-a-half syndrome
7 + 1 & 1/2 = 8 & 1/2 eight-and-a-half syndrome
If CN 7 + 1 & 1/2 + corticospinal tract or cerebellar tract involved and presents with ipsilateral/contralateral weakness/ataxia - it involved half of body 1/2 weakness or 1/2 ataxia
7 + 1 & 1/2 + 1/2 = 9 nine syndrome
7 + 1 & 1/2 + 5 = 13 & 1/2 thirteen-and-a-half syndrome
If 7 + 1 & 1/2 + CN 5
If CN 7 + 1 & 1/2 + CN 7 bilateral CN 7 + 1 & 1/2
7 + 7 + 1 & 1/2 = 15 & 1/2 fifteen-and-a-half syndrome
7 + 8 + 1 & 1/2 = 16 & 1/2 sixteen-and-a-half syndrome
If CN 7 + CN 8 + 1 & 1/2
All regards to my mentors - Aaron, Rabih, Prof Rez and to everyone who has come across during this journey!
Best wishes, Aye
Please reach out to me for anything related with Neurology ayechanmoethant@outlook.com
VMR RECAP 2
December 17th
Case presenter : Vinicius Case Discussants: Ravi Singh & John Black Highlighted by: Vinicius
A 82 yo man was brought to the ED after outpatient labs revealing a Hb of 6.6
Questions Urgent transfusion necessary? Hemolytic process? Decreased Haptoglobin? LDH level? Indirect Bilirubin level? Schistocytes
HPI: Fatigue
Dyspnea on moderate exertion Resting angina that relieves with isossorbide - irradiation to the back No orthopnea or PND
Mismatch between supply and demand
PE: BP: 110/60 mmHg, HR: 80 bpm, SO2: 95%. on RA Mild pallor CV: Distant heart sounds,harsh systolic ejection murmur 4+/6 at the aortic focus, irradiating to the carotids, the carotid pulse were weak and delayed (pulsus parvus et tardus). No JVD or HJR.
PMHx: 2 MIs
Aortic stenosis Stent in the LCx HTN COPD CKD 3a Former smoker
LABS: Hb - Baseline: 8,5 Ht: 21.7% Plat: 159 x 10³ WBC: 3.74 x 10³ Cr: 2.1 - baseline 2.1 BUN: 20 LDH, Vitamin B12, and Folic Acid: Normal Iron Studies: Serum Iron 25 Ferritin: 20 TIBC: 400 Transferrin Sat: 6% Ret. Count: 1% Coagulation profile normal Fecal occult blood positive
IMAGING: EKG: LVH, low voltage, enlarged left atrium Echo: 62% Left ventricle: eccentric hypertrophy with segmental wall motion abnormalities Aortic valve thickening with severe stenosis and moderate insufficiency.
COLONOSCOPY: Angiodysplasia in the cecum and ascending colon Colonic diverticula
Aortic Stenosis SAD: Syncope Angina Dyspnea
Diagnosis: Heyde Syndrome Aortic stenosis → Shear stress → Loss of HMW vWF multimers → Acquired von Willebrand disease.
Tx: TAVI preferred for symptomatic patients > 80 yo or younger patients or any age with high prohibited surgical risk or with age expectancy <10 y vs SAVI
Podcast Episode Recap Episode 373 A sudden problem,but where is it?
Case presenter: Reza Manesh Case discussants: Rabih Geha Highlighted by: Minahil Ramzan
A 30-year-old male presents with sudden abdominal pain accompanied by nausea and vomiting. His past medical history includes ESRD, HTN, Crohn’s disease, ITP, and a history of splenectomy. He is on dialysis and multiple medications.
Causes of fever : neutropenia , infection , ischemia
Vitals and Examination Temp : 38.1 C , BP : 190/128 , HR:101 , O2 saturation : 96% Abdomen : Diffuse periumbilical tenderness , soft abdomen,bowel sounds positive
Hb:7.7 , platelet : 51k ,WBC : 15k(predominant neutrophils) , Chem 7:nl, lactate:nl , LFT:nl ,BNP: 3k , Trop:506
His saturation dropped to 84% on room air. Physical examination revealed crackles in the lungs. He was on 40 L of oxygen via high-flow nasal cannula with 50% FiO2. EKG: ST elevation in V1-V6.
The patient's abdominal pain and systemic symptoms could be secondary to: Aspiration pneumonitis: Esophageal pathology causing reflux or aspiration. 1. Ascites: Compression of the diaphragm leading to shortness of breath (SOB). 2. Intra-abdominal vascular compromise: Could have triggered severe hypertension (HTN), resulting in acute heart strain and flash pulmonary edema 3.
CXR: B/L lung field opacification CT chest(without contrast): Nodular confluent consolidations Lower extremeties ultrasound : Negative for DVT
Reperfusion in the coronary arteries following acute occlusion leads to myocardial edema, which creates the Wellens pattern on the EKG
Troponin increased to 1380 EKG:Wellens pattern Echo: Moderate concenteric LVH, akinetic apex , LVEF:55-60%
Troponin X EF
What preparations will you make for the patient?
Troponin
EF
Patient underwent cardiac cathetrization revealed diffuse stenotic coronary artery disease.
relatively low
relatively low
Takotsubo
low
ACS
very high low maintained
Acute Coronary Syndrome
Take-Home Point: Always perform an EKG in patients presenting with upper abdominal pain, regardless of age, as it can be a referred symptom of cardiac ischemia.
Crack the Code: Decipher This ECG with Us! BEYOND THE INNOCUOUS - The Tale of Masquerading RBBB By: Vijay
A 59 year gentleman with PMH of DM presented with progressive dyspnea and syncope since 6 months BEYOND THE INNOCUOUS - The Tale of Masquerading RBBB
What is the likely Diagnosis??? ECG shows a Normal sinus rhythm, Left Axis deviation, R in aVL > 10mm, rSR’ in V1, absent S in lead I, Initially appears RBBB with LAD likely Bifascicular block (RBBB + LAHB/LVH) Looking Beyond?? RBBB: rSR’ in V1, Wide S in lead I, V6 Masquerading RBBB = RBBB and LBBB morphologies in the ECG Standard Type: RBBB in Limb leads, LBBB in precordial leads Precordial Type: LBBB in Limb leads, RBBB in precordial leads Why is recognition Essential? High risk of progression to complete Heart Block Early recognition ensures close monitoring and PPM in symptomatic cases. Associated with poor prognosis even in asymptomatic patients Wide S in I Normal ECG
Absent S in I Masquerading RBBB
ECG of the same patient 1 week later showing progression to High grade AV Block
Case Reflection 2 by: Rainiel Reyes
A Brief introduction about our case presenter: Hi, My name is Rainiel Reyes, I am a 3rd year podiatry student at Rosalind Franklin University currently on my Internal Medicine rotation. Hope to subspecialize in wound care. Shortness of breath Case Presentation: History of Present Illness: Patient was an 88 year old female with a past medical history of hypertension, type II diabetes mellitus, hyperlipidemia, and a stroke 10 years prior with residual right sided weakness. She presented to the ED with shortness of breath that began one day prior. She stated that the shortness of breath began the night before and she felt it continue through the morning. Patient also described her heart beat to be racing and does not know if it is considered irregular. Patient denied chest pain, fever, chills, swelling in extremities, or urinary discomfort, but noted that she had been urinating less than normal.
Review of Systems: A review of systems was otherwise negative.
Vitals: Her vital signs at initial presentation included a BP 206/117, HR 101, and RR 30.
Physical Exam Findings: She was fully alert and oriented to who she was, place, time, and reason. She did not display any signs of acute distress upon examination and was saturating well on 6L of oxygen provided through NC. She displayed normal breath sounds without wheezing, rales but she did display an elevated breathing rate. During the examination, her heart rate was within normal limits, displaying a regular rhythm, S1/S2 without murmur, and absence of gallop or rub. Patient did not display any pitting edema and had palpable pedal pulses. Patient demonstrated right sided weakness as well. Lab Findings: Patient’s CBC and CMP displayed WBC 13.4, Hb 10.7, Glucose 257, BUN 27, Cr 1.35. Patient’s roponin was also noted to have elevated from 0.05>0.87 and BNP had increased from 1000>1544. Diagnostic Test Findings: Chest x-ray showed bilateral pulmonary edema and small effusions. An echocardiogram showed EF 40%. Apico-antero-septal akinesis, moderate to severe AS, LA mild dilation, and an RVSP of 46. V/Q scan was negative for pulmonary embolism.
Final Diagnosis: Acute hypoxic respiratory failure due to acute CHF exacerbation.
Teaching Pearls:
Acute hypoxic respiratory failure involves an inability to maintain adequate oxygenation for tissues or an inadequate removal of carbon dioxide from tissues. It may result from V/Q mismatch, shunt, hypoventilation, diffusion limitation, or low inspired oxygen tension.
It is more common among men than women but is more likely in individuals with pre-existing pulmonary or cardiac conditions such as COPD, pneumonia, PE, or CHF.
It most commonly presents as shortness of breath and is oftentimes associated with tachycardia, fatigue, or heart palpitations.
From a diagnostic standpoint, acute hypoxemic respiratory failure is defined by PaO2 less than 60 mm Hg or SaO2 less than 88%.
A common treatment involves cardiac catheterization and the placement of stents, which was the case in terms of this patient. Following treatment, patients are recommended to undergo cardiac rehabilitation two to three times a week for 12 to 18 weeks beginning about a month after surgery or a cardiac event. The treatment consists of light aerobic exercises, nutrition changes, and other lifestyle recommendations.
Book Review
-by Kuchal Agadi
Book :
The Review
“The eyes cannot see what the mind doesn’t know.” But what makes the medical diagnosis even more mysterious, “even if you know about an illness, you may not think of it if a patient presents with an unusual version of the disease.” This book starts with the story of a patient with Cannabis hyperemesis syndrome; Dr.Sanders skillfully weaves the art of diagnosis, including the art of history taking, physical examination and how teaching these skills to the budding doctors have evolved overtime. She also crafts the limitations of medical management, patient’s compliance; and ingenious storytelling tools to overcome it. Dr.Sanders goes on to explain, “the doctors ability to give the patient’s story back to the patient, in a form that will allow them to understand what their illness, and what it means” helps patients gain control, and enhances their compliance. To take this weaving analogy further, the warp of the book is the art of diagnosis, available technology, including google, limitations of the tests, costs, bias and the controls in our healthcare system to keep the hospitals accountable. The Weft are the various stories including one on Hodgkin’s lymphoma to chronic lyme’s disease, to surgical checklists which have been pivotal to decreased medical errors, to last but not the least Gregory House’s famous line, “Everybody Lies.” Dr.Sanders reminds us that “a story that helps the patient makes sense of even a devastating illness is a story that heals.”
Know Your Author
Art of Diagnosis:
Medical Journalism
6*4 is not always 24, it could be something else
Doctors are caring, thoughtful people. It's a venue for them to share their expertise with the world
Invaluable skill to be a good Doctor: Being comfortable with the uncertainties which is integral to practising medicine
I love my patients, and love working with them to figure out what the problem is, and how to take care of it. It’s always humane. What keeps you going?
Long Covid Clinic: A space within our healthcare system for patients with unusual symptoms, complex health issues due to COVID. This space helps to improve lives, save money and keeps doctors interested. IT’s exciting to be on the frontier, trying to figure things out. Excited about the possibilities.
Share Your Story: Contribute to Our Next Issue!
Every case is educational and a unique learning opportunity. We want to hear your cases and get to know you! As we look ahead to future seasons of our magazine, we invite our readers to share their educational cases and reflections that highlight valuable lessons learned.
Link to google forms
“ One Life, So many Dreams”
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