Ryan O'Keefe

Daily Pearl(s): Drug-Induced Acute Pancreatitis (DIAP) Lisinopril is a known but rare cause of pancreatitis, with a proposed mechanism involving an idiosyncratic reaction or angioedema of the pancreatic duct. Drug-induced acute pancreatitis is a diagnosis of exclusion, often suspected when there is a close temporal relationship between starting a medication and the onset of symptoms. Biliary sludge seen on ultrasound, while not a definitive obstructing stone, can still be a risk factor for pancreatitis and should be considered in the differential diagnosis. Source: CPS - March 16, 2026 Mainstream Mondays VMR with Youssef & Magnus - acute abdominal pain

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The hematologists I work with shared that a rough way to tell if a patient has been regularly taking (and absorbing) prescribed hydrea is to check the MCV. It causes macrocytosis due to interference with ribonucleotide reductase and DNA synthesis. Guidelines generally look for MCV >100 as a signal of adequate effect.

what is your best pearl, or most useful reference, about interpreting a complete blood count with differential? The blood count is one of the most commonly ordered tests in clinical medicine, but its subtleties are woefully overlooked.

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Daily Pearl(s): Lithium Toxicity Chronic lithium toxicity is a state of lithium accumulation that occurs in patients on long-term therapy, typically precipitated by a decrease in renal clearance. Common medications that reduce lithium clearance and precipitate toxicity include NSAIDs, ACE/ARBs, and thiazides. Unlike acute overdose which presents with prominent GI symptoms, chronic toxicity manifests primarily with neurologic dysfunction. Common presentations include ataxia, dysarthria (slurred speech), tremor, confusion, and encephalopathy, which can progress to seizures and coma. An elevated serum lithium level confirms the diagnosis, though the absolute level correlates poorly with the severity of chronic neurologic symptoms. Lithium can also independently cause a neutrophilic leukocytosis, which can confound the clinical picture when an infection is also present. Management involves holding Lithium, providing aggressive IV hydration to enhance renal clearance and treating the underlying cause of AKI. Source: March 13, 2026 VMR with Rabih & Anmolpreet - dysuria, cloudy urine, and urinary incontinence

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Daily Pearl(s): Signs of a Pulmonary Hypertensive Crisis and RV Failure The physical exam triad of an elevated JVP, a left parasternal heave, and a loud P2 is highly suggestive of severe pulmonary hypertension and significant RV strain. A left parasternal heave is a palpable, sustained lifting of the chest wall along the left sternal border (the patient's left). A loud P2 (pulmonic component of the second heart sound, S2) is an accentuated sound from the pulmonary valve closing ("slamming shut") at the end of ventricular systole, and is heard best at the upper left sternal border. D-shaped left ventricular septum on echocardiography is a classic sign of severe RV pressure overload. Acute RV failure can trigger a vicious "spiral of death" where hypoxemia and acidosis worsen pulmonary vascular resistance, which further strains the RV, decreases cardiac output, and perpetuates the cycle. Breaking the RV "death spiral" involves supporting systemic blood pressure which helps perfuse the RV, optimizing preload (often with diuretics), and reducing RV afterload with pulmonary vasodilators such as inhaled nitric oxide or IV prostacyclines. Of course, treating any inciting cause (PE, infection) is also critical. Intubation is extremely high-risk in patients with acute RV failure, as positive pressure ventilation and sedative agents can precipitate hemodynamic collapse by reducing preload and increasing afterload. Source: March 11, 2026 VMR with Sharmin & Kirtan - SOB and fever and 1 day of chest pain

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Daily Pearl(s): Abdominal Pain in Patients with a VP Shunt In patients with new VP shunt presenting with fever or altered mental status, shunt-associated meningitis should be a primary consideration even with any typical presentation. Classic meningeal signs, like nuchal rigidity, are frequently absent in device-related CNS infections. In such cases, fever and confusion might be the only clues. Abdominal pain can be a red herring in VP shunt infections, representing irritation or infection of the distal catheter tip rather than a primary intra-abdominal process. Source: March 9, 2026 Mainstream Mondays VMR with Maddy & Zakariyya G - 3 days of weakness and RUQ pain

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Daily Pearl(s): Hypotension vs Shock Hypotension is a measurement, whereas shock is a clinical syndrome of end-organ hypoperfusion. The primary goal is to determine if hypotension is causing shock by assessing vital organs, primarily the brain (mental status) and kidneys (urine output). The central venous pressure (CVP) is the most important diagnostic branch point. Low CVP points to hypovolemic or distributive shock. Hypovolemic shock is caused by a "hole" in the cardiovascular system leading to intravascular volume loss (via hemorrhage, GI losses, severe dehydration). Management is volume repletion and controlling the source of loss. In hypovolemic shock with no obvious source of bleeding, remember the hidden spaces: the retroperitoneum, thigh, and GI tract. Distributive shock is a hunt for a "substance" causing vasodilation. Think sepsis, anaphylaxis, drugs, or a critical hormone deficiency like cortisol. High CVP indicates an "arrest of flow" problem (cardiogenic or obstructive). "Arrest of Flow" (cardiogenic/obstructive) is uniquely morbid because it reduces organ perfusion from two sides: low arterial inflow and high venous outflow pressure. The difference between obstructive and cardiogenic shock is myocardial health. Obstructive shock features a healthy pump facing a mechanical block and may transiently benefit from fluids. Examples include massive pulmonary embolism, cardiac tamponade, tension pneumothorax, dynamic LV outflow tract obstruction. Management involves temporizing with fluids to help the healthy heart push against the obstruction while urgently addressing the mechanical cause via needle decompression, pericardial synthesis, or thrombolysis/thrombectomy. Cardiogenic shock is primary pump failure where fluids are more likely detrimental. It can be caused by myocardial infarction or end-stage cardiomyopathy. It's often a slower progressive process. Management involves inotropes, vasopressors, and mechanical circulatory support, as well as addressing the cause of cardiac dysfunction. Source: Academy w/ Rabih - Hypotension - March 8, 2026

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Daily Pearl(s): Diagnosing ALS Progressive, asymmetric weakness with preserved sensation should always raise concern for a motor neuron disease like ALS. Electrodiagnostics (EMG/NCS) are the cornerstone of diagnosis. NCS should show normal sensory nerve function. EMG confirms widespread lower motor nerve (LMN) damage, revealing evidence of active denervation (fibrillations, positive sharp waves) and chronic reinnervation (large, polyphasic motor unit potentials) in multiple body regions, often demonstrating subclinical involvement. The Progressive Muscular Atrophy (PMA) subtype of ALS presents with predominantly lower motor neuron signs, making it a key mimic of myopathy or neuropathy and a frequent diagnostic challenge. In the setting of profound weakness, reflexes will be diminished or absent regardless of etiology; therefore, hyporeflexia loses its specific localizing value for neuropathy versus advanced myopathy. The "split-hand" sign (preferential atrophy of the thenar/first dorsal interosseous muscles) and its "split-leg" analogue are specific physical signs of ALS. A low serum creatinine is a powerful indicator of significant muscle atrophy and should not be dismissed as simply "good renal function" in a patient with weakness. MRI of the brain and spine is crucial to exclude structural mimics like spinal cord compression or myelopathy, but is typically unremarkable in ALS itself. A muscle biopsy may be performed to exclude myositis; in ALS it shows features of neurogenic atrophy (grouped fiber atrophy), not primary inflammation or necrosis. Source: March 6, 2026 VMR with Rabih & Rahul - progressive lower extremity weakness

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Daily Pearl(s): Bleeding on DOACs Bleeding on a renally-cleared anticoagulant (like apixaban) can create a vicious cycle: hemorrhage causes pre-renal AKI, which impairs drug clearance, leading to supratherapeutic anticoagulation and worsening hemorrhage. Source: March 5, 2026 VMR with Rabih & Mohammed - acute epistaxis

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Daily Pearl(s): Strep Pneumo Meningitis The classic triad of meningitis (fever, nuchal rigidity, altered mental status) is often absent in elderly or immunocompromised hosts, requiring a high index of suspicion. In patients with meningitis 2/2 strep pneumo, BCx are often positive and inflammatory markers like procalcitonin are usually elevated. Empiric treatment for suspected bacterial meningitis must include coverage for drug-resistant strep pneumo (vancomycin plus a third-generation cephalosporin like ceftriaxone), as resistance can lead to clinical failure with monotherapy. The benefit of adjunctive dexamethasone in bacterial meningitis is greatest when given just before or with the first dose of antibiotics; its utility is diminished in delayed presentations. Source: March 4, 2026 VMR with Steph & Zaven - altered mental status & fever

@samarthrawal Sam keeps cooking!

I’ve been using Pearls regularly, and feel it’s now ready for a broader release, so I made a small video :) 🔵 Pearls is an app for clinicians I built for capturing clinical pearls while rounding or studying. Some useful features: - Automatically fetch context: after you add a concept or phrase, an AI agent will (optionally) fetch additional information and augment your note. I like pasting clinical trials, and letting Pearls update my note by fetching more details in the background. - Auto generate Anki cards: you can convert any Pearl into an Anki card and directly import to your deck. - Sync across mobile/web devices, auto-tagging, search and filtering Pearls I’ve been using it quite regularly and have found it valuable in helping me capture and remember my own clinical knowledge. Available for free: contextualmed.com/pearls/