Symptom-Based DDx & Plans — Renal

111. Acute Kidney Injury

/AcuteKidneyInjury · differentiate prerenal vs intrinsic vs postrenal first, then treat the cause · dehydration (prerenal) · sepsis · ATN · obstruction · medication-related · Super Compact

Approach — frame AKI as prerenal vs intrinsic vs postrenal, then treat that cause. A rise in creatinine or fall in urine output is sorted into prerenal (hypoperfusion — dehydration, sepsis, cardiorenal), intrinsic (ATN, AIN, glomerular), or postrenal (obstruction). The discriminating workup is fast and cheap: volume assessment, urinalysis + microscopy, urine electrolytes (FENa), a renal ultrasound to exclude obstruction, and a medication review. Always check for the immediately reversible — obstruction and hypovolemia — and the dangerous complications (hyperkalemia, acidosis, volume overload, uremia).

Key discriminators: poor intake/orthostasis/FENa <1%/bland sediment → prerenal (dehydration) · sepsis/hypotension/shock → septic/ischemic ATN · muddy-brown granular casts/FENa >2%/ischemic or nephrotoxic insult → ATN · hydronephrosis on US/distended bladder/anuria-or-fluctuating output → obstruction (postrenal) · temporal link to a nephrotoxin (NSAIDs, contrast, aminoglycosides) or AIN drug (± eosinophils/WBC casts) → medication-related

Initial Sx/Data (all comers): volume status exam, bladder/obstruction assessment, full medication review; BMP (creatinine trend, K, bicarb), urinalysis + microscopy (casts, blood, protein), urine electrolytes/FENa (or FEUrea if on diuretics), renal ultrasound (hydronephrosis), CBC; review nephrotoxins/contrast; bladder scan/catheter if retention suspected · (the two fastest reversible causes are obstruction — relieve it — and hypovolemia — replete it; and always check a potassium urgently because hyperkalemia is the AKI complication that kills first)

Neg (don't-miss): denies missed obstruction (US/bladder scan — fully reversible if relieved early) · denies missed life-threatening hyperkalemia/severe acidosis/volume overload (treat emergently) · denies missed rapidly progressive glomerulonephritis (hematuria + red cell casts + rising Cr → urgent nephrology) · denies ongoing nephrotoxin exposure · denies missed uremic emergency needing dialysis

DDx: dehydration (prerenal) · sepsis · ATN · obstruction (postrenal) · medication-related · (also: cardiorenal/hepatorenal, AIN, glomerulonephritis, contrast nephropathy, rhabdomyolysis, TLS, abdominal compartment syndrome)

Plan — by Diagnosis

CONSULT (as relevant): Nephrology (intrinsic AKI, unclear cause, dialysis need, RPGN) · Urology (obstruction) · ICU (refractory hyperkalemia, severe acidosis, emergent dialysis)

Dehydration (prerenal)

– Confirm: poor intake/volume loss, orthostasis, FENa <1%, bland urine, BUN:Cr >20
– Plan: IV isotonic fluid resuscitation (e.g. balanced crystalloid), treat the source of losses, hold diuretics/nephrotoxins, monitor creatinine + urine output response (prerenal should improve with volume)
– True prerenal AKI corrects with volume; if creatinine doesn't respond, reconsider ATN or another intrinsic cause.

Sepsis

– Confirm: infection + hypoperfusion/shock driving renal injury
– Plan: treat sepsis (source control + antibiotics + fluid resuscitation + vasopressors to MAP ≥65), restore renal perfusion, avoid/adjust nephrotoxins, renally dose drugs; supportive renal care
– Septic AKI is treated by treating the sepsis and restoring perfusion — there's no renal-specific magic bullet.

ATN

– Confirm: ischemic (prolonged hypoperfusion) or nephrotoxic insult, muddy-brown granular casts, FENa >2%
– Plan: supportive — remove the insult, optimize perfusion/avoid further injury, manage volume + electrolytes + acid-base, renally dose meds, await recovery; dialysis for refractory complications
– ATN is supportive and time — protect the kidney from a second hit while it recovers; watch for the diuretic recovery phase.

Obstruction (postrenal)

– Confirm: hydronephrosis on ultrasound, distended bladder, fluctuating/anuric output
– Plan: relieve the obstruction promptly — bladder catheter for outlet obstruction; urology/IR (ureteral stent or nephrostomy) for upper-tract; watch for post-obstructive diuresis (replace losses, monitor electrolytes)
– Obstruction is fully reversible if relieved early — and post-obstructive diuresis can be dramatic; replace the volume.

Medication-related

– Confirm: temporal link to a nephrotoxin (NSAIDs, contrast, aminoglycosides, ACEi/ARB) or AIN drug (PPIs, antibiotics — ± eosinophils/WBC casts/rash)
– Plan: STOP the offending agent; supportive care; for suspected AIN consider steroids per nephrology; avoid re-exposure; renally dose remaining meds
– Deprescribing is the treatment — and AIN is easy to miss without checking the urine for eosinophils/WBC casts.

Cross-cutting

– Manage complications (all comers): hyperkalemia (calcium for membrane stabilization, insulin+dextrose/albuterol to shift, then remove with diuresis/binders/dialysis), metabolic acidosis, volume overload (diuresis or dialysis), uremia; renally dose all drugs; avoid nephrotoxins/contrast
– Trend: creatinine, urine output, potassium, bicarb, volume status, response to the targeted therapy
– Escalation triggers (dialysis — "AEIOU"): refractory Acidosis, refractory Electrolytes (hyperkalemia), Intoxication (dialyzable), Overload (refractory), Uremia (pericarditis, encephalopathy) → urgent nephrology + dialysis ± ICU
– Discharge checklist: cause identified + reversible factors corrected + creatinine trending down/stable; nephrotoxins addressed + medication list renally adjusted; obstruction relieved if present; nephrology follow-up if indicated; return precautions (decreased urine, swelling, confusion, weakness)

111. Acute Kidney Injury

/AcuteKidneyInjury · complete reference · prerenal vs intrinsic vs postrenal, relieve obstruction and replete volume, manage hyperkalemia, treat the cause · Full Card

Approach — Prerenal vs Intrinsic vs Postrenal, Then Treat the Cause

• A rise in creatinine or a fall in urine output is sorted into prerenal (hypoperfusion — dehydration, sepsis, cardiorenal), intrinsic (ATN, AIN, glomerular disease), or postrenal (obstruction).

• The discriminating workup is fast and cheap: a volume assessment, urinalysis with microscopy, urine electrolytes (FENa), a renal ultrasound to exclude obstruction, and a medication review.

• Always check for the immediately reversible — obstruction and hypovolemia — and the dangerous complications (hyperkalemia, acidosis, volume overload, uremia).

• Key discriminators: poor intake, orthostasis, a FENa under 1%, and a bland sediment → prerenal (dehydration); sepsis, hypotension, or shock → septic or ischemic ATN; muddy-brown granular casts, a FENa over 2%, and an ischemic or nephrotoxic insult → ATN; hydronephrosis on ultrasound, a distended bladder, or anuric or fluctuating output → obstruction (postrenal); a temporal link to a nephrotoxin (NSAIDs, contrast, aminoglycosides) or an AIN drug (with eosinophils or WBC casts) → medication-related.

Initial Symptoms / Data (all comers)

• A volume status exam, a bladder and obstruction assessment, and a full medication review.

• BMP (creatinine trend, potassium, bicarbonate), urinalysis with microscopy (casts, blood, protein), urine electrolytes and FENa (or FEUrea if on diuretics), a renal ultrasound (hydronephrosis), and CBC; review nephrotoxins and contrast; a bladder scan or catheter if retention is suspected.

• The two fastest reversible causes are obstruction — relieve it — and hypovolemia — replete it; and always check a potassium urgently because hyperkalemia is the AKI complication that kills first.

Neg (don't-miss)

• Pt denies a missed obstruction (ultrasound or bladder scan — fully reversible if relieved early) and a missed life-threatening hyperkalemia, severe acidosis, or volume overload (treat emergently).

• Pt denies a missed rapidly progressive glomerulonephritis (hematuria with red cell casts and a rising creatinine → urgent nephrology) and ongoing nephrotoxin exposure.

• Pt denies a missed uremic emergency needing dialysis.

DDx

Dehydration (prerenal) · sepsis · ATN · obstruction (postrenal) · medication-related · (also: cardiorenal or hepatorenal syndrome, AIN, glomerulonephritis, contrast nephropathy, rhabdomyolysis, tumor lysis syndrome, abdominal compartment syndrome)

Plan — by Diagnosis

CONSULT (as relevant): Nephrology (intrinsic AKI, unclear cause, dialysis need, RPGN) · Urology (obstruction) · ICU (refractory hyperkalemia, severe acidosis, emergent dialysis)

• Dehydration (prerenal) — confirm: poor intake or volume loss, orthostasis, a FENa under 1%, bland urine, and a BUN-to-creatinine ratio over 20. Plan: IV isotonic fluid resuscitation (e.g. a balanced crystalloid), treat the source of losses, hold diuretics and nephrotoxins, and monitor the creatinine and urine output response (prerenal should improve with volume).

• Sepsis — confirm: infection with hypoperfusion or shock driving the renal injury. Plan: treat the sepsis (source control, antibiotics, fluid resuscitation, and vasopressors to a MAP of at least 65), restore renal perfusion, avoid or adjust nephrotoxins, and renally dose drugs; supportive renal care.

• ATN — confirm: an ischemic (prolonged hypoperfusion) or nephrotoxic insult, with muddy-brown granular casts and a FENa over 2%. Plan: supportive — remove the insult, optimize perfusion and avoid further injury, manage volume, electrolytes, and acid-base, renally dose medications, and await recovery; dialysis for refractory complications.

• Obstruction (postrenal) — confirm: hydronephrosis on ultrasound, a distended bladder, and fluctuating or anuric output. Plan: relieve the obstruction promptly — a bladder catheter for outlet obstruction; urology or IR (a ureteral stent or nephrostomy) for upper-tract obstruction; watch for post-obstructive diuresis (replace losses, monitor electrolytes).

• Medication-related — confirm: a temporal link to a nephrotoxin (NSAIDs, contrast, aminoglycosides, ACEi or ARB) or an AIN drug (PPIs, antibiotics — with eosinophils, WBC casts, or rash). Plan: stop the offending agent; supportive care; for suspected AIN consider steroids per nephrology; avoid re-exposure; renally dose the remaining medications.

• Cross-cutting — manage complications (all comers): hyperkalemia (calcium for membrane stabilization, insulin and dextrose or albuterol to shift, then remove with diuresis, binders, or dialysis), metabolic acidosis, volume overload (diuresis or dialysis), and uremia; renally dose all drugs; avoid nephrotoxins and contrast.

• Trend: creatinine, urine output, potassium, bicarbonate, volume status, and the response to the targeted therapy.

• Escalation triggers (dialysis — "AEIOU"): refractory Acidosis, refractory Electrolytes (hyperkalemia), Intoxication (a dialyzable agent), Overload (refractory), and Uremia (pericarditis, encephalopathy) → urgent nephrology and dialysis, with possible ICU.

• Discharge checklist: the cause identified, reversible factors corrected, and the creatinine trending down or stable; nephrotoxins addressed and the medication list renally adjusted; obstruction relieved if present; nephrology follow-up if indicated; return precautions for decreased urine, swelling, confusion, or weakness.

Red Flags

• A high or rising potassium → hyperkalemia is the AKI complication that kills first; treat emergently and get an ECG.

• Hydronephrosis or a distended bladder → obstruction; relieve it, because it's fully reversible early.

• Hematuria with red cell casts and a rapidly rising creatinine → rapidly progressive glomerulonephritis; urgent nephrology.

• Refractory acidosis, volume overload, or uremic symptoms → emergent dialysis evaluation.

• An ongoing nephrotoxin or repeated contrast → a preventable second hit to a recovering kidney.

Senior IM Resident Pearls

• Three buckets, fast. Prerenal, intrinsic, postrenal — the volume exam, urine microscopy, FENa, and a renal ultrasound sort almost every case.

• Check the potassium first. Hyperkalemia is the complication that arrests the heart before the creatinine ever matters.

• Relieve obstruction early. A bladder scan and a catheter can reverse an AKI in minutes — never skip it.

• Prerenal responds to volume. If the creatinine doesn't improve with adequate repletion, you're dealing with ATN or another intrinsic cause.

• Deprescribe the nephrotoxin. NSAIDs, contrast, aminoglycosides, and AIN-causing drugs are common and modifiable — stop them.

• Watch the recovery phase. Post-ATN and post-obstructive diuresis can dump volume and electrolytes — replace them.

• Common mistake: diuresing or scanning with contrast an AKI patient before excluding obstruction and hypovolemia — protect the kidney instead of hitting it again.

Symptom-Based DDx & Plans — Neurologic

112. Dizziness / Vertigo

/DizzinessVertigo · differentiate peripheral from central (the can't-miss is stroke), and don't forget systemic causes · BPPV · stroke (central) · orthostasis · medication effect · Super Compact

Approach — the critical split is peripheral vs central vertigo, and "dizziness" vs true vertigo. First clarify what the patient means (spinning vertigo vs lightheadedness/presyncope vs disequilibrium). For true vertigo, the high-stakes job is separating benign peripheral (BPPV, vestibular) from a central cause (posterior-circulation stroke) — and the timing/triggers plus the HINTS exam do this better than imaging early. Lightheadedness points instead to orthostasis, medication effect, or a cardiac/systemic cause.

Key discriminators: brief, positional, triggered by head movement, fatigable + Dix-Hallpike-positional nystagmus → BPPV · sudden, sustained vertigo + central HINTS (normal head-impulse, direction-changing nystagmus, skew) / other neuro signs / vascular risk → stroke (central — don't miss) · lightheadedness on standing + orthostatic BP drop → orthostasis · temporal link to a new/culprit drug (antihypertensives, sedatives, aminoglycosides, anticonvulsants) → medication effect

Initial Sx/Data (all comers): characterize the symptom + timing + triggers, orthostatic vitals, full neuro exam (gait, cerebellar, cranial nerves); HINTS exam for acute continuous vertigo (Head-Impulse, Nystagmus, Test-of-Skew), Dix-Hallpike for positional; ECG (arrhythmia/presyncope), glucose, CBC (anemia), medication review; MRI brain (not CT) if central features (CT misses posterior fossa) · (a central, dangerous cause can have a deceptively normal exam except for the HINTS findings — and a normal CT does not exclude a posterior-circulation stroke)

Neg (don't-miss): denies missed posterior-circulation stroke (central HINTS, neuro signs, vascular risk, new gait instability, inability to walk → MRI/stroke pathway) · denies missed cardiac/arrhythmic presyncope (ECG/telemetry) · denies missed severe anemia/GI bleed as cause of lightheadedness · denies relying on a normal CT to exclude stroke · denies missed vertebral artery dissection (neck pain + vertigo)

DDx: BPPV · stroke (central vertigo) · orthostatic hypotension · medication effect · (also: vestibular neuritis/labyrinthitis, Ménière, cardiac arrhythmia, anemia, hypoglycemia, vestibular migraine, vertebral artery dissection)

Plan — by Diagnosis

CONSULT (as relevant): Neurology (central vertigo/stroke, unclear) · Cardiology (arrhythmic presyncope) · ENT (recurrent peripheral vertigo, Ménière)

BPPV

– Confirm: brief positional vertigo, positive Dix-Hallpike with characteristic nystagmus
– Plan: canalith repositioning (Epley maneuver) — first-line and often curative; vestibular suppressants only briefly if needed; reassurance + home exercises
– The Epley maneuver treats BPPV directly — don't just hand out meclizine, reposition the otoliths.

Stroke (central vertigo)

– Confirm: sudden sustained vertigo + central HINTS / neuro signs / vascular risk / inability to walk; MRI brain
– Plan: activate stroke pathway/neurology; MRI (not CT) to confirm posterior-circulation infarct; ischemic in window → reperfusion eligibility; manage risk factors; consider vertebral artery dissection
– A central HINTS pattern or the inability to stand/walk is a stroke until MRI proves otherwise — CT will miss it.

Orthostatic hypotension

– Confirm: lightheadedness on standing + documented orthostatic BP drop; assess volume/meds
– Plan: rehydrate/treat hypovolemia, reduce offending meds (antihypertensives/diuretics), slow position changes, compression stockings; find why (bleeding, dehydration, autonomic)
– Orthostatic "dizziness" is presyncope, not vertigo — and the underlying cause (e.g. a bleed) still needs explaining.

Medication effect

– Confirm: temporal link to a culprit (antihypertensives, sedatives, anticonvulsants, aminoglycosides — vestibulotoxic)
– Plan: adjust/stop the offending agent, review polypharmacy, renal dosing; monitor for resolution
– Aminoglycosides are vestibulotoxic; many common drugs cause dizziness — review the list before extensive workup.

Cross-cutting

– Trend: symptom resolution, gait/neuro exam, orthostatics, ECG/telemetry as relevant
– Escalation triggers: central/posterior-circulation stroke → emergent neuro/MRI/reperfusion; vertebral artery dissection → neurology/imaging; arrhythmic presyncope → cardiology/telemetry; severe anemia/bleed → resuscitation + source control
– Discharge checklist: central cause excluded + diagnosis established + safe gait/ambulation; cause-specific treatment (Epley, deprescribing, hydration); follow-up (neuro/ENT/cardiology as relevant); return precautions (new neuro signs, inability to walk, severe headache/neck pain, syncope, worsening symptoms)

112. Dizziness / Vertigo

/DizzinessVertigo · complete reference · clarify the symptom, separate peripheral from central with HINTS, exclude stroke, treat the cause · Full Card

Approach — Peripheral vs Central, and True Vertigo vs Lightheadedness

• First clarify what the patient means (spinning vertigo versus lightheadedness or presyncope versus disequilibrium).

• For true vertigo, the high-stakes job is separating a benign peripheral cause (BPPV, vestibular neuritis) from a central cause (posterior-circulation stroke) — and the timing and triggers plus the HINTS exam do this better than imaging early.

• Lightheadedness points instead to orthostasis, medication effect, or a cardiac or systemic cause.

• Key discriminators: brief, positional vertigo triggered by head movement and fatigable with a positive Dix-Hallpike → BPPV; sudden, sustained vertigo with a central HINTS pattern (a normal head-impulse test, direction-changing nystagmus, skew deviation), other neuro signs, or vascular risk → stroke (central — don't miss); lightheadedness on standing with an orthostatic BP drop → orthostasis; a temporal link to a new or culprit drug (antihypertensives, sedatives, aminoglycosides, anticonvulsants) → medication effect.

Initial Symptoms / Data (all comers)

• Characterize the symptom, timing, and triggers; orthostatic vitals; and a full neuro exam (gait, cerebellar testing, cranial nerves).

• A HINTS exam for acute continuous vertigo (Head-Impulse, Nystagmus, Test-of-Skew), a Dix-Hallpike for positional vertigo; ECG (arrhythmia or presyncope), glucose, CBC (anemia), and a medication review; an MRI brain (not CT) if there are central features (CT misses the posterior fossa).

• A central, dangerous cause can have a deceptively normal exam except for the HINTS findings — and a normal CT does not exclude a posterior-circulation stroke.

Neg (don't-miss)

• Pt denies a missed posterior-circulation stroke (a central HINTS pattern, neuro signs, vascular risk, new gait instability, or inability to walk → MRI and the stroke pathway) and a missed cardiac or arrhythmic presyncope (ECG, telemetry).

• Pt denies a missed severe anemia or GI bleed as a cause of lightheadedness and relying on a normal CT to exclude a stroke.

• Pt denies a missed vertebral artery dissection (neck pain with vertigo).

DDx

BPPV · stroke (central vertigo) · orthostatic hypotension · medication effect · (also: vestibular neuritis or labyrinthitis, Ménière disease, cardiac arrhythmia, anemia, hypoglycemia, vestibular migraine, vertebral artery dissection)

Plan — by Diagnosis

CONSULT (as relevant): Neurology (central vertigo or stroke, unclear cases) · Cardiology (arrhythmic presyncope) · ENT (recurrent peripheral vertigo, Ménière disease)

• BPPV — confirm: brief positional vertigo with a positive Dix-Hallpike and characteristic nystagmus. Plan: canalith repositioning (the Epley maneuver) — first-line and often curative; vestibular suppressants only briefly if needed; reassurance and home exercises.

• Stroke (central vertigo) — confirm: sudden sustained vertigo with a central HINTS pattern, neuro signs, vascular risk, or inability to walk; an MRI brain. Plan: activate the stroke pathway and neurology; an MRI (not CT) to confirm a posterior-circulation infarct; ischemic stroke within the window → reperfusion eligibility; manage risk factors; consider vertebral artery dissection.

• Orthostatic hypotension — confirm: lightheadedness on standing with a documented orthostatic BP drop; assess volume and medications. Plan: rehydrate and treat hypovolemia, reduce offending medications (antihypertensives, diuretics), slow position changes, compression stockings; find why (bleeding, dehydration, autonomic dysfunction).

• Medication effect — confirm: a temporal link to a culprit (antihypertensives, sedatives, anticonvulsants, aminoglycosides — vestibulotoxic). Plan: adjust or stop the offending agent, review polypharmacy, renal dosing; monitor for resolution.

• Cross-cutting — trend: symptom resolution, the gait and neuro exam, orthostatics, and ECG or telemetry as relevant.

• Escalation triggers: a central or posterior-circulation stroke → emergent neurology, MRI, and reperfusion; vertebral artery dissection → neurology and imaging; arrhythmic presyncope → cardiology and telemetry; severe anemia or a bleed → resuscitation and source control.

• Discharge checklist: the central cause excluded, the diagnosis established, and a safe gait and ambulation; cause-specific treatment (the Epley maneuver, deprescribing, hydration); follow-up (neurology, ENT, or cardiology as relevant); return precautions for new neuro signs, inability to walk, a severe headache or neck pain, syncope, or worsening symptoms.

Red Flags

• A central HINTS pattern (normal head-impulse, direction-changing nystagmus, skew) → posterior-circulation stroke; MRI and the stroke pathway.

• Inability to stand or walk unassisted → a central cause; benign peripheral vertigo rarely does this.

• Neck pain with vertigo → vertebral artery dissection; imaging and neurology.

• A normal head CT → does not exclude a posterior-circulation stroke; get an MRI if central features are present.

• Dizziness with chest pain, palpitations, or syncope → an arrhythmic or cardiac cause; ECG and telemetry.

Senior IM Resident Pearls

• Ask what "dizzy" means. Spinning vertigo, lightheadedness, and imbalance are three different workups — clarify before you chase one.

• HINTS beats CT early. In acute continuous vertigo, the HINTS exam is more sensitive for stroke than an early CT.

• CT misses the posterior fossa. A normal CT is falsely reassuring — get an MRI when central features are present.

• The Epley maneuver is the treatment for BPPV. Reposition the otoliths instead of relying on meclizine.

• Can't walk means central. Inability to ambulate unassisted is a strong pointer away from a benign peripheral cause.

• Don't forget systemic causes. Anemia, hypoglycemia, arrhythmia, and medications cause "dizziness" without any vertigo.

• Common mistake: labeling acute vertigo as "BPPV" or "labyrinthitis" and missing a posterior-circulation stroke that the HINTS exam would have caught.

Symptom-Based DDx & Plans — Cardiovascular / General

113. Leg Swelling

/LegSwelling · differentiate unilateral (think DVT) from bilateral (think systemic), then treat the cause · CHF · DVT · venous insufficiency · cirrhosis · nephrotic syndrome · Super Compact

Approach — the first fork is unilateral vs bilateral. Unilateral leg swelling is a DVT until excluded (also cellulitis, lymphedema, Baker cyst); bilateral swelling points to a systemic cause — cardiac (CHF), hepatic (cirrhosis), renal (nephrotic), or venous (chronic insufficiency), distinguished by the associated findings (JVD, ascites, proteinuria, skin changes). The acute, dangerous miss is a DVT (with its risk of PE); the rest is sorting the systemic edema by organ.

Key discriminators: UNILATERAL, acute, calf pain/warmth, VTE risk → DVT (don't miss) · bilateral + JVD/orthopnea/crackles/elevated BNP → CHF · bilateral + ascites/stigmata of liver disease/low albumin → cirrhosis · bilateral + heavy proteinuria/low albumin/periorbital edema → nephrotic syndrome · bilateral/chronic, brawny skin changes/varicosities, worse with standing → venous insufficiency

Initial Sx/Data (all comers): distribution (uni vs bilateral), exam (JVD, ascites, skin, varicosities, calf), VTE risk (Wells); compression ultrasound for unilateral/suspected DVT (D-dimer if low pretest), BNP + echo (cardiac), LFTs/albumin/coags (hepatic), urinalysis + spot protein:creatinine + albumin (renal), BMP, TSH · (bilateral edema can still hide a unilateral DVT on one side — examine and image asymmetry; and new bilateral edema deserves a cause, not just a diuretic)

Neg (don't-miss): denies missed DVT (unilateral, VTE risk → ultrasound; PE risk) · denies missed phlegmasia/limb-threatening DVT · denies missed cellulitis vs DVT confusion · denies missed new heart failure / nephrotic syndrome / cirrhosis as the unexplained cause · denies treating edema with a diuretic without diagnosing the driver · denies missed medication-induced edema (CCBs)

DDx: CHF · DVT · venous insufficiency · cirrhosis · nephrotic syndrome · (also: lymphedema, medication-induced — amlodipine/NSAIDs, cellulitis, hypoalbuminemia/malnutrition, Baker cyst, hypothyroidism)

Plan — by Diagnosis

CONSULT (as relevant): Cardiology (heart failure) · Nephrology (nephrotic syndrome) · Hepatology (cirrhosis) · Vascular (DVT complications, venous disease)

CHF

– Confirm: bilateral, JVD/orthopnea/crackles, elevated BNP, echo
– Plan: IV loop diuretic (furosemide), Na/fluid restriction, daily weights + strict I/O, optimize GDMT, identify trigger; see the dyspnea card's CHF approach
– Diurese, but find the trigger and optimize chronic therapy — edema is the tip of a decompensation.

DVT

– Confirm: unilateral, calf pain/warmth, VTE risk, positive compression ultrasound
– Plan: anticoagulation (LMWH/DOAC; UFH if procedure likely/unstable) unless contraindicated; assess for PE if symptoms; limb-threatening phlegmasia → vascular/thrombolysis; provoked vs unprovoked guides duration
– A DVT is a PE waiting to happen — anticoagulate promptly, and screen for PE symptoms.

Venous insufficiency

– Confirm: chronic, bilateral, brawny skin changes/varicosities/hyperpigmentation, worse with standing
– Plan: compression therapy (stockings), leg elevation, skin care; treat venous ulcers; address weight/mobility; not primarily a diuretic problem
– Compression, not diuretics, is the mainstay — and over-diuresing chronic venous edema causes prerenal AKI.

Cirrhosis

– Confirm: bilateral + ascites, stigmata of liver disease, low albumin, abnormal LFTs/coags
– Plan: sodium restriction + diuretics (spironolactone ± furosemide in combination), manage ascites (paracentesis for tense/symptomatic + albumin for large-volume), treat the liver disease/complications
– Spironolactone-based diuresis with sodium restriction is the cirrhotic edema strategy — different from the CHF loop-first approach.

Nephrotic syndrome

– Confirm: heavy proteinuria, low albumin, edema (± hyperlipidemia); quantify protein, nephrology workup
– Plan: sodium restriction + loop diuretics for edema, treat the underlying glomerular disease (nephrology — often needs biopsy/immunosuppression), manage complications (thromboembolism risk, hyperlipidemia), ACEi/ARB for proteinuria
– Nephrotic patients are hypercoagulable — keep VTE on the radar while you treat the proteinuria.

Cross-cutting

– Trend: weight/edema, the organ-specific markers (BNP, albumin, proteinuria), renal function during diuresis, response to therapy
– Escalation triggers: PE from DVT → anticoagulation/thrombolysis per severity; phlegmasia/limb-threatening DVT → vascular; decompensated heart failure → see dyspnea card; tense ascites/SBP → paracentesis/treatment; severe nephrotic complications → nephrology
– Discharge checklist: cause diagnosed (not just edema treated) + appropriate therapy started; DVT anticoagulation plan + duration if applicable; organ-specific follow-up (cardiology/nephrology/hepatology/vascular); medication review (edema-causing drugs); return precautions (unilateral swelling/calf pain, dyspnea/chest pain, rapid weight gain, decreased urine)

113. Leg Swelling

/LegSwelling · complete reference · unilateral means DVT until excluded, bilateral means a systemic cause, diagnose the driver before diuresing · Full Card

Approach — Unilateral (DVT) vs Bilateral (Systemic)

• The first fork is unilateral versus bilateral. Unilateral leg swelling is a DVT until excluded (also cellulitis, lymphedema, Baker cyst).

• Bilateral swelling points to a systemic cause — cardiac (CHF), hepatic (cirrhosis), renal (nephrotic syndrome), or venous (chronic insufficiency), distinguished by the associated findings (JVD, ascites, proteinuria, skin changes).

• The acute, dangerous miss is a DVT (with its risk of PE); the rest is sorting the systemic edema by organ.

• Key discriminators: unilateral, acute swelling with calf pain or warmth and VTE risk → DVT (don't miss); bilateral swelling with JVD, orthopnea, crackles, or an elevated BNP → CHF; bilateral swelling with ascites, stigmata of liver disease, or a low albumin → cirrhosis; bilateral swelling with heavy proteinuria, a low albumin, or periorbital edema → nephrotic syndrome; bilateral or chronic swelling with brawny skin changes or varicosities, worse with standing → venous insufficiency.

Initial Symptoms / Data (all comers)

• The distribution (unilateral versus bilateral), exam (JVD, ascites, skin changes, varicosities, calf exam), and VTE risk (Wells score).

• A compression ultrasound for unilateral or suspected DVT (a D-dimer if low pretest probability), BNP and echo (cardiac), LFTs, albumin, and coagulation studies (hepatic), urinalysis with a spot protein-to-creatinine ratio and albumin (renal), BMP, and TSH.

• Bilateral edema can still hide a unilateral DVT on one side — examine and image asymmetry; and new bilateral edema deserves a cause, not just a diuretic.

Neg (don't-miss)

• Pt denies a missed DVT (unilateral swelling with VTE risk → ultrasound; PE risk) and a missed phlegmasia or limb-threatening DVT.

• Pt denies confusing cellulitis with a DVT and a missed new heart failure, nephrotic syndrome, or cirrhosis as the unexplained cause.

• Pt denies treating edema with a diuretic without diagnosing the driver and a missed medication-induced edema (calcium channel blockers).

DDx

CHF · DVT · venous insufficiency · cirrhosis · nephrotic syndrome · (also: lymphedema, medication-induced edema — amlodipine, NSAIDs, cellulitis, hypoalbuminemia or malnutrition, a Baker cyst, hypothyroidism)

Plan — by Diagnosis

CONSULT (as relevant): Cardiology (heart failure) · Nephrology (nephrotic syndrome) · Hepatology (cirrhosis) · Vascular (DVT complications, venous disease)

• CHF — confirm: bilateral swelling with JVD, orthopnea, or crackles, an elevated BNP, and an echo. Plan: an IV loop diuretic (furosemide), sodium and fluid restriction, daily weights with strict I/O, optimize guideline-directed medical therapy, and identify the trigger (see the dyspnea card's CHF approach).

• DVT — confirm: unilateral swelling with calf pain or warmth and VTE risk, and a positive compression ultrasound. Plan: anticoagulation (LMWH or a DOAC; UFH if a procedure is likely or unstable) unless contraindicated; assess for PE if there are symptoms; limb-threatening phlegmasia → vascular service and thrombolysis; provoked versus unprovoked status guides the duration.

• Venous insufficiency — confirm: chronic bilateral swelling with brawny skin changes, varicosities, or hyperpigmentation, worse with standing. Plan: compression therapy (stockings), leg elevation, and skin care; treat venous ulcers; address weight and mobility; not primarily a diuretic problem.

• Cirrhosis — confirm: bilateral swelling with ascites and stigmata of liver disease, a low albumin, and abnormal LFTs and coagulation studies. Plan: sodium restriction with diuretics (spironolactone with or without furosemide in combination), manage ascites (paracentesis for tense or symptomatic ascites, with albumin for large-volume removal), and treat the liver disease and its complications.

• Nephrotic syndrome — confirm: heavy proteinuria, a low albumin, and edema (with possible hyperlipidemia); quantify protein, a nephrology workup. Plan: sodium restriction with loop diuretics for edema, treat the underlying glomerular disease (nephrology — often needs a biopsy and immunosuppression), manage complications (thromboembolism risk, hyperlipidemia), and an ACEi or ARB for proteinuria.

• Cross-cutting — trend: weight and edema, the organ-specific markers (BNP, albumin, proteinuria), renal function during diuresis, and the response to therapy.

• Escalation triggers: a PE from a DVT → anticoagulation or thrombolysis per severity; phlegmasia or a limb-threatening DVT → vascular; decompensated heart failure → see the dyspnea card; tense ascites or SBP → paracentesis and treatment; severe nephrotic complications → nephrology.

• Discharge checklist: the cause diagnosed (not just the edema treated) with appropriate therapy started; a DVT anticoagulation plan and duration if applicable; organ-specific follow-up (cardiology, nephrology, hepatology, or vascular); a medication review (edema-causing drugs); return precautions for unilateral swelling or calf pain, dyspnea or chest pain, rapid weight gain, or decreased urine.

Red Flags

• Acute unilateral swelling with VTE risk → a DVT; ultrasound and anticoagulation, with attention to PE.

• A markedly swollen, painful, dusky limb → phlegmasia or a limb-threatening DVT; vascular emergency.

• New bilateral edema with dyspnea, JVD, or orthopnea → decompensated heart failure.

• Bilateral edema with heavy proteinuria → nephrotic syndrome, which is also a prothrombotic state.

• Edema treated with escalating diuretics and no diagnosis → a missed driver and iatrogenic prerenal AKI.

Senior IM Resident Pearls

• Unilateral is a DVT until proven otherwise. The asymmetry is the clue — image it before chasing systemic causes.

• Bilateral edema has an organ. Heart, liver, or kidney — find which before reaching for a diuretic.

• Compression beats diuretics in venous disease. Over-diuresing chronic venous edema just causes prerenal AKI.

• Cirrhotic edema isn't CHF edema. Spironolactone-based diuresis with sodium restriction, not a loop-first strategy.

• Nephrotic patients clot. Keep VTE in mind while treating the proteinuria and albumin.

• Check the medication list. Amlodipine and NSAIDs are common, reversible causes of bilateral edema.

• Common mistake: reflexively diuresing new edema without distinguishing unilateral from bilateral or diagnosing the systemic driver behind it.

Symptom-Based DDx & Plans — Endocrine / Metabolic

114. Hyperglycemia

/Hyperglycemia · differentiate DKA vs HHS vs uncomplicated, then treat by acuity · DKA · HHS · poor diabetic control · Super Compact

Approach — first decide: is this a hyperglycemic emergency (DKA or HHS) or uncomplicated hyperglycemia? The dividing test is checking for an anion-gap metabolic acidosis with ketones (DKA) versus profound hyperglycemia with hyperosmolality and minimal ketosis (HHS) versus simple elevated glucose without acidosis/osmolar derangement (poor control). The emergencies share a treatment skeleton — fluids, potassium before/with insulin, insulin infusion, find the trigger — but differ in emphasis. Always hunt the precipitant (infection, missed insulin, new diagnosis, MI).

Key discriminators: high glucose + anion-gap acidosis + ketones (β-hydroxybutyrate) + often type 1/younger → DKA · very high glucose (often >600) + high serum osmolality + minimal ketones/acidosis + often type 2/elderly + profound dehydration/AMS → HHS · elevated glucose, no acidosis, no osmolar emergency → poor diabetic control (chronic/subacute)

Initial Sx/Data (all comers): volume + mental status, identify precipitant; glucose, BMP (anion gap, K, bicarb, BUN/Cr), serum/urine ketones (β-hydroxybutyrate), VBG (pH), serum osmolality (HHS), CBC + infection workup, ECG/troponin (precipitant), HbA1c; phosphate/magnesium · (potassium is the number that matters most early — total-body potassium is depleted even when serum looks normal/high, and insulin will drop it fast; replete before insulin if K is low)

Neg (don't-miss): denies missed DKA (check a gap + ketones in any sick hyperglycemic, including euglycemic DKA on SGLT2 inhibitors) · denies dangerous hypokalemia from insulin (replete K first if low) · denies missed precipitant (infection/MI/missed insulin) · denies cerebral edema from over-rapid correction (esp pediatric/HHS) · denies missed HHS hyperosmolar emergency

DDx: DKA · HHS · poor diabetic control · (also: euglycemic DKA — SGLT2 inhibitors, stress/steroid-induced hyperglycemia, new-onset diabetes, mixed DKA-HHS)

Plan — by Diagnosis

CONSULT (as relevant): Endocrinology (complex DKA/HHS, brittle diabetes, transition planning) · ICU (severe DKA/HHS, hemodynamic/mental status compromise) · Diabetes education (discharge)

DKA

– Confirm: hyperglycemia + anion-gap metabolic acidosis + ketonemia; identify trigger
– Plan: (1) IV fluids first (isotonic crystalloid); (2) potassium — if K <3.3 hold insulin + replete first; if 3.3–5.2 add K to fluids; if >5.2 monitor; (3) IV insulin infusion; (4) add dextrose to fluids when glucose ~200 to keep insulin running until the gap closes; (5) monitor glucose/gap/K closely; (6) treat the precipitant; transition to subcutaneous insulin with overlap once gap closed + eating
– Treat DKA by closing the gap, not just the glucose — keep insulin running with dextrose until ketosis resolves, and never let insulin drive the potassium down.

HHS

– Confirm: profound hyperglycemia + high serum osmolality + minimal ketosis/acidosis + severe dehydration ± AMS
– Plan: aggressive IV fluid resuscitation (the cornerstone — fluid deficits are larger than DKA), careful potassium repletion, IV insulin infusion (after fluids underway), correct osmolality/glucose GRADUALLY to avoid cerebral edema, treat the precipitant, monitor neuro status
– HHS is a fluid problem first — the deficit is huge; correct glucose and osmolality slowly to protect the brain.

Poor diabetic control

– Confirm: elevated glucose, no acidosis, no hyperosmolar emergency; review regimen/adherence/HbA1c
– Plan: adjust the home regimen (basal-bolus or oral agents per type), correct reversible drivers (infection, steroids, nonadherence, diet), diabetes education, arrange follow-up; inpatient sliding-scale/basal-bolus as appropriate — avoid sliding-scale-only
– Don't manage inpatient hyperglycemia with sliding-scale insulin alone — use scheduled basal-bolus and fix the driver.

Cross-cutting

– Shared skeleton (emergencies): fluids → potassium (before/with insulin) → insulin infusion → dextrose when glucose ~200 → treat trigger → transition to subcutaneous with overlap
– Trend: glucose hourly, anion gap (DKA) / osmolality (HHS), potassium, mental/volume status, precipitant resolution
– Escalation triggers: severe DKA/HHS, hemodynamic instability, altered mental status, refractory electrolytes → ICU; cerebral edema (neuro deterioration during correction) → emergent management; the precipitant (sepsis, MI) per its own pathway
– Discharge checklist: resolution of the emergency (gap closed/osmolality corrected) + stable on subcutaneous regimen + eating; precipitant treated; diabetes education + glucometer/insulin teaching + sick-day rules; endocrine/PCP follow-up; return precautions (vomiting, inability to eat/drink, very high glucose, confusion)

114. Hyperglycemia

/Hyperglycemia · complete reference · separate DKA from HHS from uncomplicated, fluids and potassium before insulin, close the gap, find the trigger · Full Card

Approach — Emergency (DKA / HHS) vs Uncomplicated

• First decide: is this a hyperglycemic emergency (DKA or HHS) or uncomplicated hyperglycemia?

• The dividing test is checking for an anion-gap metabolic acidosis with ketones (DKA) versus profound hyperglycemia with hyperosmolality and minimal ketosis (HHS) versus a simple elevated glucose without acidosis or osmolar derangement (poor control).

• The emergencies share a treatment skeleton — fluids, potassium before or with insulin, an insulin infusion, find the trigger — but differ in emphasis.

• Always hunt the precipitant (infection, missed insulin, new diagnosis, MI). Key discriminators: a high glucose with an anion-gap acidosis and ketones (β-hydroxybutyrate), often in type 1 or younger patients → DKA; a very high glucose (often over 600) with a high serum osmolality and minimal ketones or acidosis, often in type 2 or elderly patients with profound dehydration and AMS → HHS; an elevated glucose with no acidosis and no osmolar emergency → poor diabetic control.

Initial Symptoms / Data (all comers)

• Volume and mental status, and identify the precipitant.

• Glucose, BMP (anion gap, potassium, bicarbonate, BUN and creatinine), serum and urine ketones (β-hydroxybutyrate), VBG (pH), serum osmolality (HHS), CBC with an infection workup, ECG and troponin (precipitant), and HbA1c; phosphate and magnesium.

• Potassium is the number that matters most early — total-body potassium is depleted even when the serum looks normal or high, and insulin will drop it fast; replete before insulin if the potassium is low.

Neg (don't-miss)

• Pt denies a missed DKA (check a gap and ketones in any sick hyperglycemic patient, including euglycemic DKA on SGLT2 inhibitors) and dangerous hypokalemia from insulin (replete potassium first if it's low).

• Pt denies a missed precipitant (infection, MI, missed insulin) and cerebral edema from over-rapid correction (especially pediatric patients and HHS).

• Pt denies a missed HHS hyperosmolar emergency.

DDx

DKA · HHS · poor diabetic control · (also: euglycemic DKA — SGLT2 inhibitors, stress or steroid-induced hyperglycemia, new-onset diabetes, mixed DKA-HHS)

Plan — by Diagnosis

CONSULT (as relevant): Endocrinology (complex DKA or HHS, brittle diabetes, transition planning) · ICU (severe DKA or HHS, hemodynamic or mental status compromise) · Diabetes education (discharge)

• DKA — confirm: hyperglycemia with an anion-gap metabolic acidosis and ketonemia; identify the trigger. Plan: (1) IV fluids first (isotonic crystalloid); (2) potassium — if it's under 3.3, hold insulin and replete first; if it's 3.3 to 5.2, add potassium to the fluids; if it's over 5.2, monitor; (3) an IV insulin infusion; (4) add dextrose to the fluids when the glucose reaches around 200 to keep insulin running until the gap closes; (5) monitor glucose, gap, and potassium closely; (6) treat the precipitant; transition to subcutaneous insulin with overlap once the gap has closed and the patient is eating.

• HHS — confirm: profound hyperglycemia with a high serum osmolality, minimal ketosis or acidosis, severe dehydration, and possible AMS. Plan: aggressive IV fluid resuscitation (the cornerstone — fluid deficits are larger than in DKA), careful potassium repletion, an IV insulin infusion (after fluids are underway), correct the osmolality and glucose gradually to avoid cerebral edema, treat the precipitant, and monitor neuro status.

• Poor diabetic control — confirm: an elevated glucose with no acidosis and no hyperosmolar emergency; review the regimen, adherence, and HbA1c. Plan: adjust the home regimen (basal-bolus or oral agents per type), correct reversible drivers (infection, steroids, nonadherence, diet), diabetes education, and arrange follow-up; inpatient scheduled basal-bolus as appropriate — avoid sliding-scale-only management.

• Cross-cutting — shared skeleton (emergencies): fluids → potassium (before or with insulin) → an insulin infusion → dextrose when the glucose reaches around 200 → treat the trigger → transition to subcutaneous insulin with overlap.

• Trend: glucose hourly, the anion gap (DKA) or osmolality (HHS), potassium, mental and volume status, and precipitant resolution.

• Escalation triggers: severe DKA or HHS, hemodynamic instability, altered mental status, or refractory electrolytes → ICU; cerebral edema (neuro deterioration during correction) → emergent management; the precipitant (sepsis, MI) per its own pathway.

• Discharge checklist: resolution of the emergency (gap closed, osmolality corrected), stable on a subcutaneous regimen, and eating; the precipitant treated; diabetes education with glucometer and insulin teaching and sick-day rules; endocrine or PCP follow-up; return precautions for vomiting, inability to eat or drink, a very high glucose, or confusion.

Red Flags

• An anion-gap acidosis with ketones → DKA; a normal or near-normal glucose doesn't exclude it on SGLT2 inhibitors (euglycemic DKA).

• A low potassium → hold insulin and replete first; insulin will drop it further and can cause arrhythmia.

• Profound hyperglycemia with a high osmolality and AMS → HHS; the fluid deficit is enormous.

• Neurologic deterioration during correction → cerebral edema; correct glucose and osmolality gradually.

• A sick hyperglycemic patient → always look for the precipitant (infection, MI, missed insulin).

Senior IM Resident Pearls

• Fluids and potassium before insulin. The order matters — insulin into a hypokalemic patient is dangerous.

• Close the gap, not the glucose. Keep insulin running with added dextrose until the ketoacidosis resolves, even as the glucose normalizes.

• HHS is a fluid emergency. The deficit dwarfs DKA — resuscitate volume aggressively and correct osmolality slowly.

• Euglycemic DKA is real. On SGLT2 inhibitors the glucose can be near-normal — check the gap and ketones in a sick patient.

• Always find the trigger. Infection, MI, and missed insulin precipitate most emergencies — treat them in parallel.

• Don't run sliding-scale alone. Scheduled basal-bolus controls inpatient hyperglycemia far better than reactive sliding scale.

• Common mistake: stopping the insulin infusion when the glucose normalizes but before the gap closes — the ketoacidosis rebounds.

Symptom-Based DDx & Plans — Endocrine / Metabolic

115. Hypoglycemia

/Hypoglycemia · treat the glucose immediately, then differentiate the cause by its duration · insulin · sulfonylureas · poor PO intake · Super Compact

Approach — treat first, then differentiate by how long the hypoglycemia will last. Low glucose is an immediate threat — treat at once (oral fast carbs if able, IV dextrose / D50 or glucagon if not), then recheck. The differentiation that matters is the expected duration and recurrence risk: a short-acting insulin overshoot resolves quickly, whereas sulfonylurea (and long-acting insulin) hypoglycemia is prolonged and relapsing and needs extended monitoring (and octreotide for sulfonylureas). Poor PO intake on glucose-lowering therapy is the common inpatient setup.

Key discriminators: recent insulin dose (esp rapid/short-acting) + mismatch with intake → insulin (often shorter, but long-acting/large doses persist) · on a sulfonylurea (glipizide/glyburide), esp elderly/renal impairment → sulfonylurea (PROLONGED, recurrent — needs extended obs ± octreotide) · reduced/held meals while continuing glucose-lowering meds, NPO, poor appetite → poor PO intake

Initial Sx/Data (all comers): recheck/confirm glucose, symptoms (adrenergic — tremor/sweating/palpitations; neuroglycopenic — confusion/seizure), medication + insulin + meal review, renal/hepatic function (drug clearance); fingerstick + serial glucose monitoring; in non-diabetics or unclear cases, the hypoglycemia workup (insulin, C-peptide, sulfonylurea screen, cortisol) drawn at the time of hypoglycemia · (the key safety question is not just "treat it" but "how long will it keep happening" — sulfonylureas and long-acting insulin cause delayed, recurrent hypoglycemia that outlasts a single dextrose push)

Neg (don't-miss): denies premature discharge of prolonged hypoglycemia (sulfonylurea/long-acting insulin — monitor longer) · denies recurrent/relapsing hypoglycemia after initial correction · denies missed neuroglycopenia/seizure as the presentation · denies missed non-diabetic cause (adrenal insufficiency, insulinoma, sepsis, liver failure) · denies missed factitious/medication-error hypoglycemia

DDx: insulin · sulfonylureas · poor PO intake (on glucose-lowering therapy) · (also: long-acting insulin, renal/hepatic impairment reducing drug clearance, adrenal insufficiency, sepsis, insulinoma, alcohol, factitious)

Plan — by Diagnosis

CONSULT (as relevant): Endocrinology (recurrent/unexplained hypoglycemia, insulinoma workup, brittle diabetes) · Toxicology/Poison control (sulfonylurea overdose) · ICU (refractory/severe)

Insulin

– Confirm: recent insulin dose mismatched with intake; review type (rapid vs long-acting)
– Plan: treat the glucose (oral carbs or IV dextrose/D50; glucagon if no access), recheck; hold/adjust the insulin; for long-acting insulin or large doses → extended monitoring (effect outlasts a single correction); identify the dosing/intake mismatch
– Short-acting insulin hypoglycemia resolves quickly; long-acting or large doses keep dropping the glucose — monitor accordingly.

Sulfonylureas

– Confirm: on a sulfonylurea (glipizide/glyburide), esp elderly/renal impairment — prolonged, recurrent
– Plan: treat the glucose; AVOID over-relying on dextrose boluses alone (can stimulate more insulin); octreotide suppresses sulfonylurea-driven insulin release for refractory/recurrent cases; PROLONGED observation/monitoring (often 24+ hours) because it relapses; hold the agent
– Sulfonylurea hypoglycemia is the classic trap — it recurs for many hours; octreotide and extended monitoring, not a single D50 and discharge.

Poor PO intake

– Confirm: reduced/held meals while continuing glucose-lowering meds, NPO, poor appetite
– Plan: treat the glucose, adjust/hold glucose-lowering meds to match intake, ensure carbohydrate intake or dextrose-containing IV fluids while NPO, reconcile the regimen to the patient's actual eating
– The fix is matching the medication to the intake — don't keep full diabetic dosing on a patient who isn't eating.

Cross-cutting

– Immediate treatment (all comers): conscious/able → 15–20 g fast oral carbohydrate, recheck in 15 min, repeat; unable/altered → IV dextrose (D50) or glucagon if no IV; then a longer-acting carbohydrate/meal to prevent relapse
– Trend: serial glucose, recurrence (the central concern), mental status, the causative drug's expected duration
– Escalation triggers: refractory/recurrent hypoglycemia → continuous dextrose infusion + octreotide (sulfonylurea) + ICU/endocrine; neuroglycopenic seizure/coma → emergent treatment; unexplained → hypoglycemia workup
– Discharge checklist: sustained euglycemia off active correction for an appropriate observation period (LONGER for sulfonylurea/long-acting insulin); regimen adjusted to prevent recurrence; cause + contributing factors addressed (renal function, intake, dosing); education (recognition/treatment, sick-day rules); follow-up; return precautions (recurrent lows, confusion, inability to eat)

115. Hypoglycemia

/Hypoglycemia · complete reference · treat immediately, then judge duration and recurrence risk, monitor sulfonylureas long, match meds to intake · Full Card

Approach — Treat First, Then Differentiate by Duration

• Low glucose is an immediate threat — treat at once (oral fast carbohydrates if able, IV dextrose or D50 or glucagon if not), then recheck.

• The differentiation that matters is the expected duration and recurrence risk: a short-acting insulin overshoot resolves quickly, whereas sulfonylurea (and long-acting insulin) hypoglycemia is prolonged and relapsing and needs extended monitoring (and octreotide for sulfonylureas).

• Poor PO intake on glucose-lowering therapy is the common inpatient setup.

• Key discriminators: a recent insulin dose (especially rapid or short-acting) mismatched with intake → insulin (often shorter, but long-acting or large doses persist); on a sulfonylurea (glipizide, glyburide), especially in elderly or renally impaired patients → sulfonylurea (prolonged, recurrent — needs extended observation and possibly octreotide); reduced or held meals while continuing glucose-lowering medications, NPO status, or poor appetite → poor PO intake.

Initial Symptoms / Data (all comers)

• Recheck and confirm the glucose; the symptoms (adrenergic — tremor, sweating, palpitations; neuroglycopenic — confusion, seizure); a medication, insulin, and meal review; and renal and hepatic function (drug clearance).

• Fingerstick and serial glucose monitoring; in non-diabetics or unclear cases, the hypoglycemia workup (insulin, C-peptide, sulfonylurea screen, cortisol) drawn at the time of hypoglycemia.

• The key safety question is not just "treat it" but "how long will it keep happening" — sulfonylureas and long-acting insulin cause delayed, recurrent hypoglycemia that outlasts a single dextrose push.

Neg (don't-miss)

• Pt denies premature discharge of prolonged hypoglycemia (sulfonylurea or long-acting insulin — monitor longer) and recurrent or relapsing hypoglycemia after initial correction.

• Pt denies a missed neuroglycopenia or seizure as the presentation and a missed non-diabetic cause (adrenal insufficiency, insulinoma, sepsis, liver failure).

• Pt denies a missed factitious or medication-error hypoglycemia.

DDx

Insulin · sulfonylureas · poor PO intake (on glucose-lowering therapy) · (also: long-acting insulin, renal or hepatic impairment reducing drug clearance, adrenal insufficiency, sepsis, insulinoma, alcohol, factitious hypoglycemia)

Plan — by Diagnosis

CONSULT (as relevant): Endocrinology (recurrent or unexplained hypoglycemia, insulinoma workup, brittle diabetes) · Toxicology or Poison control (sulfonylurea overdose) · ICU (refractory or severe cases)

• Insulin — confirm: a recent insulin dose mismatched with intake; review the type (rapid versus long-acting). Plan: treat the glucose (oral carbohydrates or IV dextrose or D50; glucagon if no access), recheck; hold or adjust the insulin; for long-acting insulin or large doses → extended monitoring (the effect outlasts a single correction); identify the dosing or intake mismatch.

• Sulfonylureas — confirm: on a sulfonylurea (glipizide, glyburide), especially in elderly or renally impaired patients — prolonged and recurrent. Plan: treat the glucose; avoid over-relying on dextrose boluses alone (they can stimulate more insulin release); octreotide suppresses sulfonylurea-driven insulin release for refractory or recurrent cases; prolonged observation and monitoring (often 24 or more hours) because it relapses; hold the agent.

• Poor PO intake — confirm: reduced or held meals while continuing glucose-lowering medications, NPO status, or poor appetite. Plan: treat the glucose, adjust or hold glucose-lowering medications to match intake, ensure carbohydrate intake or dextrose-containing IV fluids while NPO, and reconcile the regimen to the patient's actual eating.

• Cross-cutting — immediate treatment (all comers): conscious and able → 15 to 20 g of fast oral carbohydrate, recheck in 15 minutes, repeat; unable or altered → IV dextrose (D50) or glucagon if there's no IV; then a longer-acting carbohydrate or meal to prevent relapse.

• Trend: serial glucose, recurrence (the central concern), mental status, and the causative drug's expected duration.

• Escalation triggers: refractory or recurrent hypoglycemia → a continuous dextrose infusion, octreotide (sulfonylurea), and ICU or endocrine involvement; a neuroglycopenic seizure or coma → emergent treatment; unexplained hypoglycemia → the hypoglycemia workup.

• Discharge checklist: sustained euglycemia off active correction for an appropriate observation period (longer for sulfonylurea or long-acting insulin); the regimen adjusted to prevent recurrence; the cause and contributing factors addressed (renal function, intake, dosing); education (recognition and treatment, sick-day rules); follow-up; return precautions for recurrent lows, confusion, or inability to eat.

Red Flags

• A sulfonylurea (especially in an elderly or renally impaired patient) → prolonged, recurrent hypoglycemia; monitor long and consider octreotide.

• Long-acting insulin or a large dose → the effect outlasts a single dextrose correction; extended monitoring.

• Neuroglycopenic symptoms (confusion, seizure, coma) → severe hypoglycemia; treat emergently.

• Recurrence after initial correction → the underlying driver is still active; don't discharge yet.

• Hypoglycemia in a non-diabetic → work it up (adrenal insufficiency, insulinoma, sepsis, liver failure).

Senior IM Resident Pearls

• Treat first, ask second. Glucose goes in immediately; the differential and workup come after the patient is safe.

• Sulfonylureas are the classic trap. They relapse for many hours — octreotide and extended monitoring, not one D50 and a discharge.

• Match the drug's duration to the monitoring. The real question is how long the hypoglycemia will keep recurring.

• Don't keep full dosing on a patient who isn't eating. Poor PO intake plus unchanged glucose-lowering meds is the commonest inpatient cause.

• Draw the workup at the moment of hypoglycemia. In unexplained cases, insulin, C-peptide, and the sulfonylurea screen are only useful when drawn low.

• Follow correction with a real meal. A longer-acting carbohydrate prevents the rebound after the fast carbs wear off.

• Common mistake: correcting a sulfonylurea hypoglycemia with a single dextrose push and discharging — it recurs hours later, sometimes fatally.

Symptom-Based DDx & Plans — Gastrointestinal / Infectious

116. Diarrhea

/Diarrhea · differentiate infectious vs inflammatory vs drug-induced, flag C. diff and IBD, support volume · C. difficile · viral gastroenteritis · medication-induced · IBD flare · Super Compact

Approach — sort the cause (infectious vs inflammatory vs drug-induced) while supporting volume and electrolytes. Most acute diarrhea is self-limited viral, but the inpatient priorities are identifying C. difficile (recent antibiotics/healthcare exposure), recognizing an IBD flare, catching medication culprits, and flagging the dangerous (bloody diarrhea, systemic toxicity, severe dehydration, toxic megacolon). The discriminators are the setting, the stool character (watery vs bloody/inflammatory), and a focused stool/lab workup.

Key discriminators: recent antibiotics/hospitalization + watery diarrhea ± leukocytosis → C. difficile (test + treat) · acute, watery, self-limited, sick contacts → viral gastroenteritis · temporal link to a new/culprit drug (antibiotics, PPIs, metformin, chemo, laxatives, Mg) → medication-induced · bloody diarrhea + abdominal pain + known/young IBD + systemic features → IBD flare · (red flags: bloody stool, high fever, severe dehydration, distension/toxicity → toxic megacolon, ischemic colitis, invasive infection)

Initial Sx/Data (all comers): volume/electrolyte status, stool character (watery vs bloody), exposures + medications + antibiotic history; BMP (electrolytes, renal), CBC; C. difficile testing if risk; stool studies (culture, pathogens, WBC/lactoferrin) for severe/bloody/prolonged/immunocompromised; lactate + imaging (CT) if ischemia/toxic megacolon suspected; flexible sigmoidoscopy/colonoscopy per GI for IBD · (do NOT give antimotility agents — loperamide — in possible C. difficile, inflammatory/bloody, or toxic colitis, because they can precipitate toxic megacolon; treat the consequences — dehydration, hypokalemia — in everyone)

Neg (don't-miss): denies missed C. difficile (antibiotic/healthcare exposure → test + treat) · denies toxic megacolon / fulminant colitis (distension, systemic toxicity, dilated colon → surgery, no antimotility) · denies missed ischemic colitis · denies missed severe dehydration/electrolyte derangement · denies missed invasive/bloody bacterial infection · denies giving antimotility in inflammatory/infectious colitis

DDx: C. difficile · viral gastroenteritis · medication-induced · IBD flare · (also: bacterial enteritis — Salmonella/Shigella/Campylobacter/E. coli, ischemic colitis, microscopic colitis, malabsorption, overflow from impaction)

Plan — by Diagnosis

CONSULT (as relevant): GI (IBD flare, severe/refractory, scope) · Infectious Disease (severe/recurrent C. diff, complex infection) · Surgery (toxic megacolon, fulminant colitis, ischemia)

C. difficile

– Confirm: antibiotic/healthcare exposure, watery diarrhea, positive C. difficile testing; assess severity
– Plan: stop the inciting antibiotic if possible; oral vancomycin or fidaxomicin (first-line; oral vancomycin ± IV metronidazole for fulminant); contact precautions; NO antimotility agents; surgery for fulminant/toxic megacolon
– Oral vancomycin or fidaxomicin is first-line now (not metronidazole) — and never give loperamide in C. diff.

Viral gastroenteritis

– Confirm: acute watery, self-limited, sick contacts, benign exam
– Plan: supportive — oral/IV rehydration, electrolyte correction, usually self-limited; stool studies only if severe/bloody/prolonged/immunocompromised; avoid unnecessary antibiotics
– The mainstay is rehydration; most viral diarrhea needs no testing or antibiotics.

Medication-induced

– Confirm: temporal link to a culprit (antibiotics, PPIs, metformin, chemo, magnesium, laxatives)
– Plan: identify + stop/adjust the offending agent; supportive rehydration; rule out C. difficile if antibiotic-associated
– Antibiotic-associated diarrhea is a fork: medication effect vs C. difficile — test before assuming it's benign.

IBD flare

– Confirm: bloody diarrhea, abdominal pain, known/new IBD, systemic features; endoscopy/imaging, inflammatory markers, exclude superimposed infection (incl C. diff)
– Plan: per GI — corticosteroids for the acute flare, optimize/escalate IBD therapy (biologics/immunomodulators), exclude + treat infection first, VTE prophylaxis (IBD flares are prothrombotic), watch for toxic megacolon/perforation
– Always exclude superimposed C. difficile before escalating immunosuppression in an IBD flare — and remember IBD flares are prothrombotic.

Cross-cutting

– Support (all comers): rehydration (oral or IV), aggressive electrolyte correction (hypokalemia common), monitor renal function; avoid antimotility agents in inflammatory/infectious/toxic colitis
– Trend: stool frequency/character, volume/electrolytes, inflammatory markers, abdominal exam (distension/toxicity)
– Escalation triggers: toxic megacolon/fulminant colitis → surgery + ICU; severe dehydration/shock → resuscitation ± ICU; ischemic colitis with necrosis → surgery; severe/recurrent C. diff → ID/surgery
– Discharge checklist: cause identified + treated + hydration/electrolytes restored + diarrhea improving; C. diff precautions/treatment course if applicable; offending meds addressed; GI follow-up for IBD; return precautions (bloody stool, high fever, severe abdominal pain/distension, inability to maintain hydration, lightheadedness)

116. Diarrhea

/Diarrhea · complete reference · infectious vs inflammatory vs drug-induced, flag C. diff and toxic colitis, never antimotility a colitis · Full Card

Approach — Infectious vs Inflammatory vs Drug-Induced, While Supporting Volume

• Most acute diarrhea is self-limited viral, but the inpatient priorities are identifying C. difficile (recent antibiotics or healthcare exposure), recognizing an IBD flare, catching medication culprits, and flagging the dangerous (bloody diarrhea, systemic toxicity, severe dehydration, toxic megacolon).

• The discriminators are the setting, the stool character (watery versus bloody or inflammatory), and a focused stool and lab workup.

• Key discriminators: recent antibiotics or hospitalization with watery diarrhea and possible leukocytosis → C. difficile (test and treat); acute, watery, self-limited diarrhea with sick contacts → viral gastroenteritis; a temporal link to a new or culprit drug (antibiotics, PPIs, metformin, chemotherapy, laxatives, magnesium) → medication-induced; bloody diarrhea with abdominal pain in a known or young IBD patient with systemic features → IBD flare; and red flags — bloody stool, a high fever, severe dehydration, or distension and toxicity → toxic megacolon, ischemic colitis, or invasive infection.

Initial Symptoms / Data (all comers)

• Volume and electrolyte status, stool character (watery versus bloody), and exposures, medications, and antibiotic history.

• BMP (electrolytes, renal function), CBC; C. difficile testing if at risk; stool studies (culture, pathogens, WBC or lactoferrin) for severe, bloody, prolonged, or immunocompromised cases; lactate and imaging (CT) if ischemia or toxic megacolon is suspected; flexible sigmoidoscopy or colonoscopy per GI for IBD.

• Do not give antimotility agents (loperamide) in possible C. difficile, inflammatory or bloody diarrhea, or toxic colitis, because they can precipitate toxic megacolon; treat the consequences — dehydration, hypokalemia — in everyone.

Neg (don't-miss)

• Pt denies a missed C. difficile (antibiotic or healthcare exposure → test and treat) and a toxic megacolon or fulminant colitis (distension, systemic toxicity, a dilated colon → surgery, no antimotility).

• Pt denies a missed ischemic colitis and a missed severe dehydration or electrolyte derangement.

• Pt denies a missed invasive or bloody bacterial infection and giving antimotility agents in inflammatory or infectious colitis.

DDx

C. difficile · viral gastroenteritis · medication-induced · IBD flare · (also: bacterial enteritis — Salmonella, Shigella, Campylobacter, E. coli, ischemic colitis, microscopic colitis, malabsorption, overflow diarrhea from impaction)

Plan — by Diagnosis

CONSULT (as relevant): GI (IBD flare, severe or refractory disease, endoscopy) · Infectious Disease (severe or recurrent C. difficile, complex infection) · Surgery (toxic megacolon, fulminant colitis, ischemia)

• C. difficile — confirm: antibiotic or healthcare exposure, watery diarrhea, and positive C. difficile testing; assess severity. Plan: stop the inciting antibiotic if possible; oral vancomycin or fidaxomicin (first-line; oral vancomycin with IV metronidazole for fulminant disease); contact precautions; no antimotility agents; surgery for fulminant disease or toxic megacolon.

• Viral gastroenteritis — confirm: acute watery diarrhea, self-limited, with sick contacts and a benign exam. Plan: supportive — oral or IV rehydration, electrolyte correction, usually self-limited; stool studies only if severe, bloody, prolonged, or immunocompromised; avoid unnecessary antibiotics.

• Medication-induced — confirm: a temporal link to a culprit (antibiotics, PPIs, metformin, chemotherapy, magnesium, laxatives). Plan: identify and stop or adjust the offending agent; supportive rehydration; rule out C. difficile if it's antibiotic-associated.

• IBD flare — confirm: bloody diarrhea, abdominal pain, known or new IBD, and systemic features; endoscopy or imaging, inflammatory markers, exclude superimposed infection (including C. difficile). Plan: per GI — corticosteroids for the acute flare, optimize or escalate IBD therapy (biologics, immunomodulators), exclude and treat infection first, VTE prophylaxis (IBD flares are prothrombotic), and watch for toxic megacolon or perforation.

• Cross-cutting — support (all comers): rehydration (oral or IV), aggressive electrolyte correction (hypokalemia is common), and monitor renal function; avoid antimotility agents in inflammatory, infectious, or toxic colitis.

• Trend: stool frequency and character, volume and electrolytes, inflammatory markers, and the abdominal exam (distension, toxicity).

• Escalation triggers: toxic megacolon or fulminant colitis → surgery and ICU; severe dehydration or shock → resuscitation with possible ICU; ischemic colitis with necrosis → surgery; severe or recurrent C. difficile → ID and surgery.

• Discharge checklist: the cause identified and treated, hydration and electrolytes restored, and the diarrhea improving; C. difficile precautions and treatment course if applicable; offending medications addressed; GI follow-up for IBD; return precautions for bloody stool, a high fever, severe abdominal pain or distension, inability to maintain hydration, or lightheadedness.

Red Flags

• Abdominal distension with systemic toxicity and a dilated colon → toxic megacolon; surgery, and never antimotility agents.

• Recent antibiotics with watery diarrhea → C. difficile; test and treat with oral vancomycin or fidaxomicin.

• Bloody diarrhea with severe pain out of proportion or vascular risk → ischemic colitis.

• An IBD flare → exclude superimposed C. difficile before escalating immunosuppression, and remember it's prothrombotic.

• Severe dehydration with hypokalemia → correct aggressively; it's the common dangerous consequence.

Senior IM Resident Pearls

• Never antimotility a colitis. Loperamide in C. difficile, inflammatory, or toxic colitis can precipitate toxic megacolon.

• Antibiotic-associated diarrhea is a fork. It's either a benign medication effect or C. difficile — test before assuming.

• Oral vancomycin or fidaxomicin is first-line for C. diff. Metronidazole has been displaced except as an adjunct in fulminant disease.

• Exclude infection before escalating IBD therapy. A superimposed C. difficile masquerading as a flare changes everything.

• Most diarrhea is supportive. Rehydration and electrolytes carry the day; testing is for the severe, bloody, or prolonged.

• IBD flares clot. Give VTE prophylaxis even amid bloody diarrhea — the prothrombotic risk outweighs it.

• Common mistake: reaching for loperamide to "settle" a bloody or antibiotic-associated diarrhea and tipping a colitis into toxic megacolon.

Symptom-Based DDx & Plans — Musculoskeletal / Neurologic

117. Back Pain

/BackPain · screen red flags first (the emergency is epidural abscess/cord compression), then differentiate · degenerative · compression fracture · osteomyelitis · epidural abscess · Super Compact

Approach — most back pain is benign, so the job is to screen for the dangerous minority first. Before treating presumed mechanical pain, actively screen RED FLAGS — fever, IV drug use, immunosuppression, neuro deficit, bowel/bladder dysfunction, saddle anesthesia, cancer history, trauma, anticoagulation. The can't-miss emergencies are spinal epidural abscess and cord compression / cauda equina (and unstable fracture, malignancy). With red flags → urgent MRI. Without them → differentiate degenerative vs fracture and manage conservatively.

Key discriminators: chronic/mechanical, worse with activity, no red flags → degenerative · sudden pain after minor trauma in osteoporosis/steroids/elderly, focal tenderness → compression fracture · fever + focal spinal tenderness + IVDU/bacteremia → osteomyelitis · fever + back pain + neuro deficit + IVDU/immunosuppression → epidural abscess (EMERGENCY) · saddle anesthesia/bilateral leg weakness/urinary retention or incontinence → cauda equina/cord compression (EMERGENCY)

Initial Sx/Data (all comers): red-flag screen, focused neuro exam (strength, sensation including perineal/saddle, reflexes, post-void residual), spine palpation; if red flags: urgent MRI of the spine, ESR/CRP + CBC, blood cultures (infection); X-ray (fracture); cancer workup if suspected; type/screen if surgical · (neuro deficits, bowel/bladder dysfunction, saddle anesthesia, or fever with back pain change this from a benign complaint into a time-critical emergency — image urgently and consult, don't discharge with analgesics)

Neg (don't-miss): denies missed spinal epidural abscess (fever + neuro deficit + IVDU/immunocompromise → emergent MRI/neurosurgery) · denies missed cauda equina / cord compression (saddle anesthesia, retention, bilateral deficits → emergent MRI/decompression) · denies missed vertebral osteomyelitis/discitis · denies missed malignancy/pathologic fracture · denies missed AAA/visceral referred pain

DDx: degenerative disease · compression fracture · osteomyelitis · epidural abscess · (also: cauda equina syndrome, cord compression, malignancy/metastasis, herniated disc with radiculopathy, AAA, pyelonephritis/renal, referred visceral pain)

Plan — by Diagnosis

CONSULT (as relevant): Neurosurgery/Spine surgery (epidural abscess, cord compression, cauda equina, unstable fracture) · Infectious Disease (osteomyelitis, abscess) · Oncology (malignancy) · PT (mechanical)

Degenerative disease

– Confirm: chronic/mechanical pain, worse with activity, no red flags, normal neuro exam
– Plan: conservative — analgesia (acetaminophen/NSAIDs), stay active, PT, avoid early/routine imaging in the absence of red flags; muscle relaxants short-term if needed
– Uncomplicated mechanical back pain needs no early imaging — reassurance, activity, and analgesia are the treatment.

Compression fracture

– Confirm: sudden pain after minor trauma, osteoporosis/steroid/elderly, focal tenderness, X-ray/CT (± MRI for age/cord)
– Plan: analgesia, mobilization as tolerated, treat osteoporosis (calcium/vitamin D + bone-protective therapy), evaluate for pathologic/malignant cause; vertebroplasty/kyphoplasty in selected refractory cases
– A new compression fracture is also a cue to work up and treat the underlying osteoporosis (or malignancy).

Osteomyelitis

– Confirm: fever + focal spinal tenderness, IVDU/bacteremia, elevated ESR/CRP, MRI, blood cultures (± biopsy)
– Plan: blood cultures + identify organism (image-guided biopsy if needed) THEN targeted IV antibiotics (prolonged course), ID involvement, monitor for abscess/neuro progression, surgery for instability/abscess/deficit
– Get the organism before antibiotics where possible — vertebral osteomyelitis needs a prolonged, targeted course, not empiric guessing.

Epidural abscess

– Confirm: fever + back pain + neuro deficit + risk (IVDU/immunocompromise/bacteremia), elevated inflammatory markers, EMERGENT MRI
– Plan: EMERGENT MRI + neurosurgery — surgical decompression/drainage for deficit or progression; broad empiric then targeted IV antibiotics (cover S. aureus incl MRSA); blood cultures; this is a neurosurgical emergency — neuro outcome depends on time to decompression
– The classic triad (fever, back pain, neuro deficit) is often incomplete — a low threshold for MRI saves the cord; delay causes permanent paralysis.

Cross-cutting

– Cauda equina / cord compression (EMERGENCY): saddle anesthesia, bilateral leg weakness, urinary retention/incontinence → EMERGENT MRI + neurosurgical decompression (± steroids for malignant compression) — do not delay
– Trend: neuro exam (serial), pain, inflammatory markers/cultures (infection), post-void residual
– Escalation triggers: epidural abscess / cauda equina / cord compression / unstable fracture with deficit → emergent MRI + neurosurgery; sepsis from osteomyelitis → sepsis pathway; new/progressing neuro deficit → emergent imaging
– Discharge checklist: dangerous causes excluded + cause treated + neuro exam stable/improving; antibiotic course + ID follow-up (infection); osteoporosis/malignancy workup (fracture); PT + analgesia plan (mechanical); return precautions (fever, leg weakness/numbness, saddle numbness, bowel/bladder changes, worsening pain)

117. Back Pain

/BackPain · complete reference · screen red flags, image urgently for epidural abscess and cauda equina, manage the benign majority conservatively · Full Card

Approach — Screen the Dangerous Minority First

• Most back pain is benign, so the job is to screen for the dangerous minority first. Before treating presumed mechanical pain, actively screen red flags — fever, IV drug use, immunosuppression, a neuro deficit, bowel or bladder dysfunction, saddle anesthesia, a cancer history, trauma, and anticoagulation.

• The can't-miss emergencies are a spinal epidural abscess and cord compression or cauda equina (and an unstable fracture, malignancy). With red flags → an urgent MRI. Without them → differentiate degenerative disease versus fracture and manage conservatively.

• Key discriminators: chronic or mechanical pain, worse with activity, with no red flags → degenerative; sudden pain after minor trauma in an osteoporotic, steroid-using, or elderly patient with focal tenderness → compression fracture; fever with focal spinal tenderness and IV drug use or bacteremia → osteomyelitis; fever, back pain, and a neuro deficit with IV drug use or immunosuppression → epidural abscess (emergency); saddle anesthesia, bilateral leg weakness, or urinary retention or incontinence → cauda equina or cord compression (emergency).

Initial Symptoms / Data (all comers)

• A red-flag screen, a focused neuro exam (strength, sensation including perineal and saddle, reflexes, post-void residual), and spine palpation.

• If red flags are present: an urgent MRI of the spine, ESR and CRP with CBC, blood cultures (infection); X-ray (fracture); a cancer workup if suspected; type and screen if surgical.

• Neuro deficits, bowel or bladder dysfunction, saddle anesthesia, or fever with back pain change this from a benign complaint into a time-critical emergency — image urgently and consult, don't discharge with analgesics.

Neg (don't-miss)

• Pt denies a missed spinal epidural abscess (fever with a neuro deficit and IV drug use or immunocompromise → emergent MRI and neurosurgery) and a missed cauda equina or cord compression (saddle anesthesia, retention, bilateral deficits → emergent MRI and decompression).

• Pt denies a missed vertebral osteomyelitis or discitis and a missed malignancy or pathologic fracture.

• Pt denies a missed AAA or visceral referred pain.

DDx

Degenerative disease · compression fracture · osteomyelitis · epidural abscess · (also: cauda equina syndrome, cord compression, malignancy or metastasis, a herniated disc with radiculopathy, AAA, pyelonephritis or renal causes, referred visceral pain)

Plan — by Diagnosis

CONSULT (as relevant): Neurosurgery or Spine surgery (epidural abscess, cord compression, cauda equina, unstable fracture) · Infectious Disease (osteomyelitis, abscess) · Oncology (malignancy) · PT (mechanical pain)

• Degenerative disease — confirm: chronic or mechanical pain, worse with activity, with no red flags and a normal neuro exam. Plan: conservative — analgesia (acetaminophen, NSAIDs), stay active, PT, avoid early or routine imaging in the absence of red flags; muscle relaxants short-term if needed.

• Compression fracture — confirm: sudden pain after minor trauma in an osteoporotic, steroid-using, or elderly patient with focal tenderness, on X-ray or CT (with MRI for indeterminate age or cord involvement). Plan: analgesia, mobilization as tolerated, treat osteoporosis (calcium and vitamin D with bone-protective therapy), evaluate for a pathologic or malignant cause; vertebroplasty or kyphoplasty in selected refractory cases.

• Osteomyelitis — confirm: fever with focal spinal tenderness, IV drug use or bacteremia, an elevated ESR and CRP, an MRI, and blood cultures (with possible biopsy). Plan: blood cultures and identify the organism (image-guided biopsy if needed) then targeted IV antibiotics (a prolonged course), ID involvement, monitor for abscess or neuro progression, and surgery for instability, abscess, or a deficit.

• Epidural abscess — confirm: fever with back pain and a neuro deficit and risk factors (IV drug use, immunocompromise, bacteremia), elevated inflammatory markers, and an emergent MRI. Plan: an emergent MRI and neurosurgery — surgical decompression or drainage for a deficit or progression; broad empiric then targeted IV antibiotics (cover S. aureus including MRSA); blood cultures; this is a neurosurgical emergency — the neuro outcome depends on the time to decompression.

• Cross-cutting — cauda equina or cord compression (emergency): saddle anesthesia, bilateral leg weakness, and urinary retention or incontinence → an emergent MRI and neurosurgical decompression (with steroids for malignant compression) — do not delay.

• Trend: the neuro exam (serial), pain, inflammatory markers and cultures (infection), and post-void residual.

• Escalation triggers: an epidural abscess, cauda equina, cord compression, or an unstable fracture with a deficit → emergent MRI and neurosurgery; sepsis from osteomyelitis → the sepsis pathway; a new or progressing neuro deficit → emergent imaging.

• Discharge checklist: dangerous causes excluded, the cause treated, and the neuro exam stable or improving; an antibiotic course with ID follow-up (infection); an osteoporosis or malignancy workup (fracture); a PT and analgesia plan (mechanical); return precautions for fever, leg weakness or numbness, saddle numbness, bowel or bladder changes, or worsening pain.

Red Flags

• Saddle anesthesia, urinary retention, or bilateral leg weakness → cauda equina; emergent MRI and decompression.

• Fever with back pain and a neuro deficit, especially with IV drug use → epidural abscess; the outcome is time-dependent.

• Fever with focal spinal tenderness and bacteremia → vertebral osteomyelitis or discitis.

• A cancer history with new or progressive back pain → metastatic cord compression until proven otherwise.

• Sudden severe pain with minor trauma in an osteoporotic patient → a compression fracture, possibly pathologic.

Senior IM Resident Pearls

• Screen red flags every time. Back pain is usually benign, but the screen is what catches the cord-threatening minority.

• The epidural abscess triad is often incomplete. Don't wait for fever, pain, and a deficit together — a low MRI threshold saves the cord.

• Cauda equina is a clock. Saddle anesthesia and retention mandate emergent imaging and decompression, not analgesia and discharge.

• Get the organism in osteomyelitis. Culture or biopsy before antibiotics where possible — the course is long and targeted.

• No early imaging for benign pain. Uncomplicated mechanical back pain doesn't need an MRI; activity and analgesia do the work.

• A compression fracture is a bone-health flag. Work up and treat the osteoporosis or malignancy behind it.

• Common mistake: treating febrile back pain or a new neuro deficit as "muscle strain" and missing the epidural abscess or cord compression that needed emergent surgery.

Symptom-Based DDx & Plans — Rheumatologic / Infectious

118. Joint Pain / Swollen Joint

/JointPainSwollenJoint · tap the joint — septic arthritis is the can't-miss, then crystals vs inflammatory · gout · septic arthritis · CPPD · RA flare · Super Compact

Approach — every acutely hot, swollen joint gets arthrocentesis, because the can't-miss is septic arthritis. The single decisive test is synovial fluid analysis (cell count, Gram stain + culture, crystals). A monoarticular hot joint is septic arthritis until the tap says otherwise; the same fluid distinguishes crystal disease (gout — negatively birefringent urate; CPPD — positively birefringent calcium pyrophosphate) and points to inflammatory (RA flare) vs other. Crystals do NOT exclude infection — a joint can have both.

Key discriminators (after the tap): very high WBC (often >50k, neutrophilic), positive Gram stain/culture, fever, ill → septic arthritis (EMERGENCY) · negatively birefringent needle-shaped urate crystals, first MTP/podagra, hyperuricemia → gout · positively birefringent rhomboid calcium pyrophosphate crystals, knee/wrist, elderly/chondrocalcinosis → CPPD (pseudogout) · known RA, polyarticular/symmetric flare, elevated inflammatory markers → RA flare

Initial Sx/Data (all comers): joint exam (mono vs poly, effusion, warmth, range), fever/systemic features; ARTHROCENTESIS with synovial fluid cell count + differential, Gram stain + culture, crystal analysis (the decisive test); blood cultures + CBC/ESR/CRP (infection), uric acid (limited acute value), X-ray (chondrocalcinosis/erosions/fracture) · (do not let a history of gout or the finding of crystals talk you out of tapping and culturing — septic arthritis and crystal arthritis coexist, and a missed septic joint destroys cartilage within days)

Neg (don't-miss): denies missed septic arthritis (hot joint not tapped/cultured → joint destruction; tap EVERY acute hot joint) · denies crystals used to exclude infection (they coexist) · denies missed disseminated gonococcal arthritis · denies missed prosthetic joint infection · denies missed systemic disease presenting as arthritis (consider beyond the four)

DDx: gout · septic arthritis · CPPD (pseudogout) · RA flare · (also: reactive arthritis, gonococcal arthritis, osteoarthritis flare, hemarthrosis, Lyme, viral arthritis, prosthetic joint infection)

Plan — by Diagnosis

CONSULT (as relevant): Rheumatology (crystal/inflammatory diagnosis, refractory, RA) · Orthopedics (septic arthritis — drainage, prosthetic joint) · Infectious Disease (septic/gonococcal/prosthetic)

Gout

– Confirm: negatively birefringent needle-shaped urate crystals, podagra/first MTP, hyperuricemia
– Plan: acute: NSAIDs, colchicine, or corticosteroids (intra-articular or systemic) — choose by comorbidity/renal function; do NOT start or stop urate-lowering therapy during the acute flare (continue if already on it); after resolution, urate-lowering (allopurinol) with prophylaxis for at-risk patients
– Treat the acute flare with anti-inflammatories; don't start allopurinol mid-flare, but don't stop it if they're already taking it.

Septic arthritis

– Confirm: high synovial WBC, positive Gram stain/culture, fever, monoarticular, ill-appearing
– Plan: EMERGENCY — urgent joint drainage (arthrocentesis/arthroscopic/surgical washout) + prompt empiric IV antibiotics (cover S. aureus incl MRSA; add gram-negative/gonococcal coverage per risk) after cultures; orthopedics; serial drainage; tailor by culture
– Drainage + IV antibiotics, urgently — a septic joint is a surgical emergency that destroys cartilage in days. Don't wait for blood cultures to start.

CPPD (pseudogout)

– Confirm: positively birefringent rhomboid calcium pyrophosphate crystals, knee/wrist, chondrocalcinosis on X-ray
– Plan: acute: NSAIDs, colchicine, or corticosteroids (intra-articular often effective for a single joint); evaluate for associated metabolic conditions (hyperparathyroidism, hemochromatosis) in younger/recurrent
– Managed like gout acutely; recurrent/young CPPD warrants a metabolic workup (hyperparathyroidism, hemochromatosis).

RA flare

– Confirm: known RA, polyarticular/symmetric, elevated inflammatory markers — after excluding infection
– Plan: per rheumatology — corticosteroids for the acute flare, optimize/escalate DMARD/biologic therapy, NSAIDs for symptoms; exclude superimposed septic joint first if a single joint is disproportionately involved
– A single hot joint in an RA patient on biologics can be septic — don't reflexively call it "just a flare," tap it.

Cross-cutting

– The tap is the pivot (all comers): send cell count/differential, Gram stain + culture, crystals on every acute effusion; start empiric antibiotics promptly if septic is suspected; crystals + infection can coexist
– Trend: joint exam/effusion, synovial + blood culture results, inflammatory markers, response to therapy
– Escalation triggers: septic arthritis → urgent drainage + IV antibiotics + orthopedics; prosthetic joint infection → orthopedics/ID; disseminated gonococcal/systemic sepsis → ID + sepsis pathway; rapidly destructive course → urgent intervention
– Discharge checklist: septic arthritis excluded or treated (drainage + antibiotic course) + diagnosis established + joint improving; crystal disease: acute therapy + outpatient urate-lowering plan (gout); RA: rheumatology follow-up + therapy optimization; return precautions (increasing joint pain/swelling/redness, fever, inability to use the joint)

118. Joint Pain / Swollen Joint

/JointPainSwollenJoint · complete reference · tap every acute hot joint, septic until the fluid says otherwise, crystals don't exclude infection · Full Card

Approach — Tap the Joint; Septic Arthritis Is the Can't-Miss

• Every acutely hot, swollen joint gets arthrocentesis, because the can't-miss is septic arthritis. The single decisive test is synovial fluid analysis (cell count, Gram stain and culture, crystals).

• A monoarticular hot joint is septic arthritis until the tap says otherwise; the same fluid distinguishes crystal disease (gout — negatively birefringent urate crystals; CPPD — positively birefringent calcium pyrophosphate crystals) and points to inflammatory disease (RA flare) versus other causes.

• Crystals do not exclude infection — a joint can have both.

• Key discriminators after the tap: a very high WBC (often over 50,000, neutrophilic), a positive Gram stain or culture, fever, and an ill patient → septic arthritis (emergency); negatively birefringent needle-shaped urate crystals, first MTP involvement or podagra, and hyperuricemia → gout; positively birefringent rhomboid calcium pyrophosphate crystals, knee or wrist involvement, and chondrocalcinosis in an elderly patient → CPPD (pseudogout); known RA with a polyarticular symmetric flare and elevated inflammatory markers → RA flare.

Initial Symptoms / Data (all comers)

• A joint exam (monoarticular versus polyarticular, effusion, warmth, range of motion) and fever or systemic features.

• Arthrocentesis with synovial fluid cell count and differential, Gram stain and culture, and crystal analysis (the decisive test); blood cultures with CBC, ESR, and CRP (infection), uric acid (limited acute value), and X-ray (chondrocalcinosis, erosions, fracture).

• Do not let a history of gout or the finding of crystals talk you out of tapping and culturing — septic arthritis and crystal arthritis coexist, and a missed septic joint destroys cartilage within days.

Neg (don't-miss)

• Pt denies a missed septic arthritis (a hot joint not tapped or cultured → joint destruction; tap every acute hot joint) and crystals being used to exclude infection (they coexist).

• Pt denies a missed disseminated gonococcal arthritis and a missed prosthetic joint infection.

• Pt denies a missed systemic disease presenting as arthritis (consider beyond the four common causes).

DDx

Gout · septic arthritis · CPPD (pseudogout) · RA flare · (also: reactive arthritis, gonococcal arthritis, an osteoarthritis flare, hemarthrosis, Lyme arthritis, viral arthritis, prosthetic joint infection)

Plan — by Diagnosis

CONSULT (as relevant): Rheumatology (crystal or inflammatory diagnosis, refractory disease, RA) · Orthopedics (septic arthritis — drainage, prosthetic joint) · Infectious Disease (septic, gonococcal, or prosthetic joint infection)

• Gout — confirm: negatively birefringent needle-shaped urate crystals, podagra or first MTP involvement, and hyperuricemia. Plan: acute — NSAIDs, colchicine, or corticosteroids (intra-articular or systemic) — choose by comorbidity and renal function; do not start or stop urate-lowering therapy during the acute flare (continue it if already on it); after resolution, urate-lowering therapy (allopurinol) with prophylaxis for at-risk patients.

• Septic arthritis — confirm: a high synovial WBC, a positive Gram stain or culture, fever, monoarticular involvement, and an ill-appearing patient. Plan: an emergency — urgent joint drainage (arthrocentesis, arthroscopic, or surgical washout) with prompt empiric IV antibiotics (cover S. aureus including MRSA; add gram-negative or gonococcal coverage per risk) after cultures; orthopedics; serial drainage; tailor by culture.

• CPPD (pseudogout) — confirm: positively birefringent rhomboid calcium pyrophosphate crystals, knee or wrist involvement, and chondrocalcinosis on X-ray. Plan: acute — NSAIDs, colchicine, or corticosteroids (intra-articular injection is often effective for a single joint); evaluate for associated metabolic conditions (hyperparathyroidism, hemochromatosis) in younger or recurrent cases.

• RA flare — confirm: known RA, polyarticular or symmetric involvement, and elevated inflammatory markers — after excluding infection. Plan: per rheumatology — corticosteroids for the acute flare, optimize or escalate DMARD or biologic therapy, NSAIDs for symptoms; exclude a superimposed septic joint first if a single joint is disproportionately involved.

• Cross-cutting — the tap is the pivot (all comers): send cell count and differential, Gram stain and culture, and crystals on every acute effusion; start empiric antibiotics promptly if septic arthritis is suspected; crystals and infection can coexist.

• Trend: the joint exam and effusion, synovial and blood culture results, inflammatory markers, and the response to therapy.

• Escalation triggers: septic arthritis → urgent drainage, IV antibiotics, and orthopedics; a prosthetic joint infection → orthopedics and ID; disseminated gonococcal infection or systemic sepsis → ID and the sepsis pathway; a rapidly destructive course → urgent intervention.

• Discharge checklist: septic arthritis excluded or treated (drainage and an antibiotic course), the diagnosis established, and the joint improving; crystal disease — acute therapy and an outpatient urate-lowering plan (gout); RA — rheumatology follow-up and therapy optimization; return precautions for increasing joint pain, swelling, or redness, fever, or inability to use the joint.

Red Flags

• An acutely hot, swollen monoarticular joint → septic arthritis until the tap says otherwise; tap and culture, don't assume gout.

• Crystals in the fluid → do not exclude infection; a joint can harbor both, so culture anyway.

• A hot joint in an RA patient on biologics → could be septic; don't dismiss it as a flare.

• A prosthetic joint that becomes painful and swollen → prosthetic joint infection; orthopedics and ID.

• Fever, migratory arthritis, and a rash in a young sexually active patient → disseminated gonococcal arthritis.

Senior IM Resident Pearls

• Tap every acute hot joint. The synovial fluid is the one test that separates a treatable crisis from a chronic nuisance.

• Crystals don't rule out sepsis. Gout and a septic joint coexist — always send a culture even when you see urate.

• A septic joint is a surgical emergency. Drainage plus IV antibiotics, urgently — cartilage is destroyed within days.

• Don't start allopurinol mid-flare. But don't stop it either if the patient is already taking it — stopping prolongs the attack.

• Steroids are an option in crystal disease. When NSAIDs and colchicine are contraindicated (renal disease), intra-articular or systemic steroids work well.

• Young or recurrent CPPD earns a metabolic workup. Look for hyperparathyroidism and hemochromatosis.

• Common mistake: calling a hot joint "gout" or "an RA flare" on history alone and missing the septic arthritis that the tap would have revealed.

Symptom-Based DDx & Plans — Geriatric / General

119. Weight Loss / Failure to Thrive

/WeightLossFTT · differentiate organic vs psychiatric/functional vs decreased intake, target the workup · malignancy · dementia · depression · malnutrition · Super Compact

Approach — quantify the loss, then sort organic vs psychiatric/functional vs decreased intake. Unintentional weight loss / failure to thrive is differentiated into organic disease (malignancy, chronic illness, malabsorption, hyperthyroidism), psychiatric/functional (depression, dementia, social/financial), and simple decreased intake. The workup is broad but directed — basic labs + age-appropriate cancer screening + a targeted search led by associated clues, not a shotgun of every test. Don't over-investigate without directed findings, but don't under-investigate a significant documented loss.

Key discriminators: documented significant loss + anemia/localizing symptoms/abnormal screen/age → malignancy (age-appropriate cancer workup) · cognitive decline + impaired feeding/swallowing + caregiver context → dementia · low mood/anhedonia/positive depression screen, often reversible → depression · low intake + low albumin/cachexia, repletion needed → malnutrition · (also hyperthyroid, malabsorption, chronic disease, medication anorexia)

Initial Sx/Data (all comers): quantify weight loss (degree + timeframe), functional/cognitive/mood/social assessment, swallow + intake history, medication review; CBC, CMP, TSH, HbA1c, inflammatory markers, age-appropriate cancer screening (and CT/directed imaging only if clues), nutrition assessment (albumin/prealbumin), depression screen (PHQ), cognitive screen · (let the directed clues drive imaging — a careful history and basic labs plus age-appropriate screening find most causes; indiscriminate whole-body scanning is low-yield without a localizing finding)

Neg (don't-miss): denies missed occult malignancy (significant loss + clues → age-appropriate/targeted workup) · denies missed treatable depression (a common, reversible cause — screen and treat) · denies missed reversible decreased intake (dentition, dysphagia, social/financial, medication anorexia, depression) · denies refeeding syndrome when repleting (low phosphate/K/Mg) · denies missed hyperthyroidism/chronic infection (TB/HIV)

DDx: malignancy · dementia · depression · malnutrition · (also: hyperthyroidism, malabsorption — celiac/pancreatic, chronic infection — TB/HIV, chronic organ disease — CHF/COPD/CKD, medication-induced anorexia, social/financial — food insecurity)

Plan — by Diagnosis

CONSULT (as relevant): Oncology (malignancy) · Psychiatry (depression) · Nutrition/Dietitian (malnutrition — essential) · Geriatrics (multifactorial FTT) · Social work (food insecurity/caregiver support) · Speech (swallow evaluation)

Malignancy

– Confirm: significant documented loss + anemia/localizing symptoms/abnormal screen, age-appropriate cancer screening + directed imaging/endoscopy by clues
– Plan: complete the targeted cancer workup (imaging/endoscopy/biopsy as directed), oncology referral, manage symptoms + nutrition; pursue tissue diagnosis + staging
– Significant unintentional loss with anemia or localizing symptoms is a cancer workup — let the clues direct it rather than scanning blindly.

Dementia

– Confirm: cognitive decline + impaired feeding/swallowing, baseline-confirmed; swallow evaluation, cognitive assessment
– Plan: swallow eval + feeding strategies/diet modification, optimize intake (assistance, supplements, appetite support), caregiver support + safety, goals-of-care discussion; exclude superimposed reversible causes (depression, infection)
– Address feeding mechanics and caregiver support; weigh goals of care before aggressive nutritional interventions in advanced dementia.

Depression

– Confirm: low mood/anhedonia, positive depression screen (PHQ) — a common, treatable cause of weight loss in the elderly
– Plan: treat depression (antidepressant — consider appetite/side-effect profile, e.g. mirtazapine for poor appetite; psychotherapy), psychiatry referral, monitor mood + weight response, address contributing social factors
– Depression is one of the most common reversible causes of weight loss in older adults — screen and treat it.

Malnutrition

– Confirm: low intake, low albumin/prealbumin, cachexia; nutrition assessment; identify the driver of poor intake
– Plan: nutritional support (oral supplements, dietitian, address dysphagia/dentition/access, enteral nutrition if indicated), treat reversible causes of poor intake; when repleting, START LOW + monitor for refeeding syndrome (low phosphate/K/Mg — replete electrolytes, advance calories gradually, thiamine)
– Refeeding syndrome is the danger of repletion — go slow, replace phosphate/K/Mg and thiamine, and advance calories gradually.

Cross-cutting

– Multifactorial in the elderly — assess all domains (medical, psychiatric, functional, social); nutrition + PT/OT central; reconcile appetite-suppressing medications
– Trend: weight, intake/nutrition markers, the corrected driver, mood/cognition/function, screening/workup results
– Escalation triggers: refeeding syndrome (severe electrolyte shifts) → close monitoring ± ICU; newly diagnosed malignancy → oncology pathway; severe malnutrition with complications → admit + careful repletion; failure to thrive with safety concerns → disposition planning
– Discharge checklist: reversible causes addressed + cause identified or workup in motion + nutrition plan in place; depression treated/referred; safe disposition + caregiver/social support; nutrition + PCP/specialty follow-up; medication review; return precautions (continued weight loss, inability to eat/swallow, new localizing symptoms, mood deterioration)

119. Weight Loss / Failure to Thrive

/WeightLossFTT · complete reference · quantify the loss, sort organic vs functional vs intake, direct the workup by clues, replete carefully · Full Card

Approach — Organic vs Psychiatric/Functional vs Decreased Intake

• Unintentional weight loss and failure to thrive is differentiated into organic disease (malignancy, chronic illness, malabsorption, hyperthyroidism), psychiatric or functional causes (depression, dementia, social or financial factors), and simple decreased intake.

• The workup is broad but directed — basic labs plus age-appropriate cancer screening plus a targeted search led by associated clues — not a shotgun of every test.

• Don't over-investigate without directed findings, but don't under-investigate a significant documented loss.

• Key discriminators: a documented significant loss with anemia, localizing symptoms, an abnormal screen, or older age → malignancy (an age-appropriate cancer workup); cognitive decline with impaired feeding or swallowing and a caregiver context → dementia; low mood, anhedonia, or a positive depression screen, often reversible → depression; low intake with a low albumin or cachexia requiring repletion → malnutrition; and also hyperthyroidism, malabsorption, chronic disease, and medication-induced anorexia.

Initial Symptoms / Data (all comers)

• Quantify the weight loss (degree and timeframe), and assess function, cognition, mood, and social context, along with a swallow and intake history and a medication review.

• CBC, CMP, TSH, HbA1c, inflammatory markers, age-appropriate cancer screening (and CT or directed imaging only if there are clues), a nutrition assessment (albumin, prealbumin), a depression screen (PHQ), and a cognitive screen.

• Let the directed clues drive imaging — a careful history and basic labs plus age-appropriate screening find most causes; indiscriminate whole-body scanning is low-yield without a localizing finding.

Neg (don't-miss)

• Pt denies a missed occult malignancy (a significant loss with clues → an age-appropriate or targeted workup) and a missed treatable depression (a common, reversible cause — screen and treat).

• Pt denies a missed reversible decreased intake (dentition, dysphagia, social or financial factors, medication-induced anorexia, depression) and refeeding syndrome when repleting (low phosphate, potassium, magnesium).

• Pt denies a missed hyperthyroidism or chronic infection (TB, HIV).

DDx

Malignancy · dementia · depression · malnutrition · (also: hyperthyroidism, malabsorption — celiac or pancreatic, chronic infection — TB or HIV, chronic organ disease — CHF, COPD, CKD, medication-induced anorexia, social or financial causes — food insecurity)

Plan — by Diagnosis

CONSULT (as relevant): Oncology (malignancy) · Psychiatry (depression) · Nutrition or Dietitian (malnutrition — essential) · Geriatrics (multifactorial FTT) · Social work (food insecurity, caregiver support) · Speech (swallow evaluation)

• Malignancy — confirm: a significant documented loss with anemia, localizing symptoms, or an abnormal screen, with age-appropriate cancer screening and directed imaging or endoscopy by clues. Plan: complete the targeted cancer workup (imaging, endoscopy, biopsy as directed), an oncology referral, and manage symptoms and nutrition; pursue a tissue diagnosis and staging.

• Dementia — confirm: cognitive decline with impaired feeding or swallowing, confirmed against baseline; a swallow evaluation and cognitive assessment. Plan: a swallow evaluation with feeding strategies and diet modification, optimize intake (assistance, supplements, appetite support), caregiver support and safety, and a goals-of-care discussion; exclude superimposed reversible causes (depression, infection).

• Depression — confirm: low mood or anhedonia with a positive depression screen (PHQ) — a common, treatable cause of weight loss in the elderly. Plan: treat the depression (an antidepressant — consider the appetite and side-effect profile, e.g. mirtazapine for poor appetite; psychotherapy), a psychiatry referral, monitor mood and weight response, and address contributing social factors.

• Malnutrition — confirm: low intake with a low albumin or prealbumin and cachexia; a nutrition assessment; identify the driver of poor intake. Plan: nutritional support (oral supplements, a dietitian, address dysphagia, dentition, and access, enteral nutrition if indicated), treat reversible causes of poor intake; when repleting, start low and monitor for refeeding syndrome (low phosphate, potassium, magnesium — replete electrolytes, advance calories gradually, give thiamine).

• Cross-cutting: failure to thrive is multifactorial in the elderly — assess all domains (medical, psychiatric, functional, social); nutrition and PT/OT are central; reconcile appetite-suppressing medications.

• Trend: weight, intake and nutrition markers, the corrected driver, mood, cognition, and function, and the screening and workup results.

• Escalation triggers: refeeding syndrome (severe electrolyte shifts) → close monitoring with possible ICU; a newly diagnosed malignancy → the oncology pathway; severe malnutrition with complications → admit and careful repletion; failure to thrive with safety concerns → disposition planning.

• Discharge checklist: reversible causes addressed, the cause identified or the workup in motion, and a nutrition plan in place; depression treated or referred; a safe disposition with caregiver and social support; nutrition and PCP or specialty follow-up; a medication review; return precautions for continued weight loss, inability to eat or swallow, new localizing symptoms, or mood deterioration.

Red Flags

• A significant documented loss with anemia or localizing symptoms → occult malignancy; direct the workup by the clues.

• A positive depression screen → a common, reversible cause; treat it before assuming an ominous diagnosis.

• Refeeding a severely malnourished patient → watch phosphate, potassium, and magnesium for refeeding syndrome.

• Weight loss with heat intolerance, tremor, or tachycardia → hyperthyroidism; check the TSH.

• Weight loss with night sweats, fever, or risk factors → chronic infection such as TB or HIV.

Senior IM Resident Pearls

• Quantify before you investigate. Confirm a real, significant loss — much "weight loss" is unmeasured and shapes how hard you look.

• Let clues drive imaging. History, basic labs, and age-appropriate screening outperform indiscriminate whole-body scanning.

• Depression is the reversible one. It's among the commonest causes in older adults and responds to treatment — screen for it.

• Repletion has a danger. Refeeding syndrome drops phosphate, potassium, and magnesium — go slow and give thiamine.

• FTT is multifactorial. Medical, psychiatric, functional, and social domains all contribute — assess each rather than fixating on one.

• Reconcile the medication list. Many drugs suppress appetite or cause nausea — a reversible contributor that's easy to miss.

• Common mistake: either pan-scanning every patient without a localizing clue, or missing the treatable depression and reversible intake problems behind the loss.

Symptom-Based DDx & Plans — Cardiovascular

120. Palpitations

/Palpitations · capture the rhythm during the event, then differentiate arrhythmia vs systemic vs anxiety · atrial fibrillation · SVT · electrolyte abnormality · anxiety · Super Compact

Approach — the symptom IS the rhythm, so the central task is to capture it. Palpitations are only diagnostic when you record the heart rhythm during an episode — ECG during symptoms, telemetry, or ambulatory monitoring. The differentiation is cardiac arrhythmia (AFib, SVT, VT) vs systemic driver (thyroid, anemia, electrolytes, fever, stimulants) vs anxiety (a diagnosis of exclusion). Flag the unstable arrhythmia (→ cardioversion) and the dangerous substrates (WPW, long QT, VT) immediately.

Key discriminators: irregularly irregular, no P waves → atrial fibrillation · sudden-onset regular narrow-complex tachycardia, abrupt termination → SVT · K/Mg/Ca derangement with ectopy/QT changes → electrolyte abnormality · situational, with anxiety/panic features, normal cardiac workup → anxiety (exclusion) · (red flags: syncope, chest pain, structural heart disease, wide-complex tachycardia/VT, delta wave/WPW, prolonged QT, family history sudden death)

Initial Sx/Data (all comers): characterize (regular vs irregular, onset/offset, associated syncope/chest pain), 12-lead ECG (capture during symptoms if possible) + telemetry/ambulatory monitor; electrolytes (K/Mg/Ca), TSH, CBC (anemia), glucose; troponin if ischemia suspected; medication/stimulant/substance review; echo if structural disease suspected · (the whole game is documenting the rhythm during an episode — a normal resting ECG between events doesn't exclude a paroxysmal arrhythmia; arrange monitoring to catch it)

Neg (don't-miss): denies missed unstable arrhythmia (hypotension/chest pain/AMS/heart failure → synchronized cardioversion) · denies missed ventricular tachycardia / wide-complex tachycardia · denies missed WPW (delta wave) or long QT (drug interactions/sudden death risk) · denies missed dangerous electrolyte derangement (QT-prolonging, arrhythmogenic) · denies anchoring on "anxiety" before excluding cardiac/systemic causes

DDx: atrial fibrillation · SVT · electrolyte abnormality · anxiety · (also: ventricular tachycardia, atrial flutter, sinus tachycardia from a driver — fever/anemia/hypovolemia, hyperthyroidism, premature beats, WPW, stimulant/medication effect)

Plan — by Diagnosis

CONSULT (as relevant): Cardiology/Electrophysiology (arrhythmia, WPW, VT, ablation) · ICU (unstable arrhythmia) · Endocrine (thyroid) · Psychiatry (anxiety after cardiac exclusion)

Atrial fibrillation

– Confirm: irregularly irregular, no discrete P waves on ECG
– Plan: UNSTABLE → synchronized cardioversion; STABLE → rate control (beta-blocker or non-dihydropyridine CCB — diltiazem) vs rhythm control per patient; anticoagulation decision by CHA₂DS₂-VASc (stroke prevention); treat reversible triggers (thyroid, sepsis, electrolytes); address onset timing for cardioversion safety (clot risk if >48 h)
– Three parallel questions: rate vs rhythm, anticoagulate by CHA₂DS₂-VASc, and is the patient unstable (→ cardiovert). Mind the 48-hour clot window before cardioversion.

SVT

– Confirm: sudden-onset regular narrow-complex tachycardia, abrupt termination
– Plan: UNSTABLE → synchronized cardioversion; STABLE → vagal maneuvers first, then adenosine (rapid IV push); if recurrent → rate-controlling agents, cardiology/EP for ablation; identify/treat triggers
– Vagal maneuvers, then adenosine for stable SVT; cardiovert if unstable. Recurrent SVT is an EP/ablation referral.

Electrolyte abnormality

– Confirm: K/Mg/Ca derangement with ectopy/arrhythmia/QT changes on ECG
– Plan: correct the specific abnormality (replete potassium + magnesium — magnesium is key for arrhythmia and torsades; correct calcium), continuous monitoring during correction, watch the QT, identify the cause of the derangement
– Repletion of magnesium along with potassium is essential — hypomagnesemia drives refractory hypokalemia and torsades.

Anxiety

– Confirm: situational, panic/anxiety features, normal cardiac + systemic workup — a diagnosis of exclusion
– Plan: reassurance after cardiac/systemic causes excluded; treat anxiety/panic (therapy, SSRIs), reduce stimulants (caffeine, etc.), psychiatry referral if indicated
– Anxiety is a legitimate cause but only after the arrhythmic and systemic causes are off the table — not a default for a young patient.

Cross-cutting

– Capture the rhythm (all comers): ECG during symptoms + telemetry/ambulatory monitoring; correct electrolytes; screen systemic drivers (thyroid, anemia, fever, hypovolemia, stimulants)
– Trend: rhythm/telemetry, electrolytes (during correction), symptom-rhythm correlation, response to therapy
– Escalation triggers: hemodynamically unstable arrhythmia → synchronized cardioversion (ACLS) + ICU; ventricular tachycardia → ACLS/cardiology + ICU; WPW with AFib (avoid AV-nodal blockers) → EP/cardiology; torsades/long QT → magnesium + remove offending agents + ICU
– Discharge checklist: rhythm documented + dangerous arrhythmia/substrate excluded + cause treated; AFib anticoagulation + rate/rhythm plan if applicable; electrolytes corrected; monitoring arranged for paroxysmal cases; cardiology/EP follow-up as relevant; return precautions (syncope, chest pain, sustained palpitations, dyspnea)

120. Palpitations

/Palpitations · complete reference · capture the rhythm during the event, separate arrhythmia from systemic and anxiety, flag the unstable and dangerous substrates · Full Card

Approach — The Symptom Is the Rhythm; Capture It

• Palpitations are only diagnostic when you record the heart rhythm during an episode — an ECG during symptoms, telemetry, or ambulatory monitoring.

• The differentiation is cardiac arrhythmia (atrial fibrillation, SVT, VT) versus a systemic driver (thyroid disease, anemia, electrolytes, fever, stimulants) versus anxiety (a diagnosis of exclusion).

• Flag the unstable arrhythmia (→ cardioversion) and the dangerous substrates (WPW, long QT, VT) immediately.

• Key discriminators: an irregularly irregular rhythm with no P waves → atrial fibrillation; a sudden-onset regular narrow-complex tachycardia with abrupt termination → SVT; a potassium, magnesium, or calcium derangement with ectopy or QT changes → electrolyte abnormality; situational episodes with anxiety or panic features and a normal cardiac workup → anxiety (exclusion); and red flags — syncope, chest pain, structural heart disease, a wide-complex tachycardia or VT, a delta wave or WPW, a prolonged QT, or a family history of sudden death.

Initial Symptoms / Data (all comers)

• Characterize the palpitations (regular versus irregular, onset and offset, associated syncope or chest pain).

• A 12-lead ECG (capture during symptoms if possible) with telemetry or an ambulatory monitor; electrolytes (potassium, magnesium, calcium), TSH, CBC (anemia), and glucose; troponin if ischemia is suspected; a medication, stimulant, and substance review; an echo if structural disease is suspected.

• The whole game is documenting the rhythm during an episode — a normal resting ECG between events doesn't exclude a paroxysmal arrhythmia; arrange monitoring to catch it.

Neg (don't-miss)

• Pt denies a missed unstable arrhythmia (hypotension, chest pain, AMS, or heart failure → synchronized cardioversion) and a missed ventricular tachycardia or wide-complex tachycardia.

• Pt denies a missed WPW (delta wave) or long QT (drug interactions, sudden death risk) and a missed dangerous electrolyte derangement (QT-prolonging, arrhythmogenic).

• Pt denies anchoring on "anxiety" before excluding cardiac and systemic causes.

DDx

Atrial fibrillation · SVT · electrolyte abnormality · anxiety · (also: ventricular tachycardia, atrial flutter, sinus tachycardia from a driver — fever, anemia, hypovolemia, hyperthyroidism, premature beats, WPW, stimulant or medication effect)

Plan — by Diagnosis

CONSULT (as relevant): Cardiology or Electrophysiology (arrhythmia, WPW, VT, ablation) · ICU (unstable arrhythmia) · Endocrine (thyroid disease) · Psychiatry (anxiety after cardiac exclusion)

• Atrial fibrillation — confirm: an irregularly irregular rhythm with no discrete P waves on ECG. Plan: unstable → synchronized cardioversion; stable → rate control (a beta-blocker or a non-dihydropyridine calcium channel blocker — diltiazem) versus rhythm control per patient; an anticoagulation decision by CHA₂DS₂-VASc score (stroke prevention); treat reversible triggers (thyroid, sepsis, electrolytes); address the onset timing for cardioversion safety (clot risk if over 48 hours).

• SVT — confirm: a sudden-onset regular narrow-complex tachycardia with abrupt termination. Plan: unstable → synchronized cardioversion; stable → vagal maneuvers first, then adenosine (a rapid IV push); if recurrent → rate-controlling agents and cardiology or EP for ablation; identify and treat triggers.

• Electrolyte abnormality — confirm: a potassium, magnesium, or calcium derangement with ectopy, arrhythmia, or QT changes on ECG. Plan: correct the specific abnormality (replete potassium and magnesium — magnesium is key for arrhythmia and torsades; correct calcium), continuous monitoring during correction, watch the QT, and identify the cause of the derangement.

• Anxiety — confirm: situational episodes with panic or anxiety features and a normal cardiac and systemic workup — a diagnosis of exclusion. Plan: reassurance after cardiac and systemic causes are excluded; treat the anxiety or panic (therapy, SSRIs), reduce stimulants (caffeine), and a psychiatry referral if indicated.

• Cross-cutting — capture the rhythm (all comers): an ECG during symptoms with telemetry or ambulatory monitoring; correct electrolytes; screen for systemic drivers (thyroid disease, anemia, fever, hypovolemia, stimulants).

• Trend: rhythm and telemetry, electrolytes (during correction), the symptom-rhythm correlation, and the response to therapy.

• Escalation triggers: a hemodynamically unstable arrhythmia → synchronized cardioversion (ACLS) and ICU; ventricular tachycardia → ACLS, cardiology, and ICU; WPW with atrial fibrillation (avoid AV-nodal blockers) → EP and cardiology; torsades or long QT → magnesium, remove offending agents, and ICU.

• Discharge checklist: the rhythm documented, a dangerous arrhythmia or substrate excluded, and the cause treated; an atrial fibrillation anticoagulation and rate or rhythm plan if applicable; electrolytes corrected; monitoring arranged for paroxysmal cases; cardiology or EP follow-up as relevant; return precautions for syncope, chest pain, sustained palpitations, or dyspnea.

Red Flags

• Palpitations with hypotension, chest pain, altered mental status, or heart failure → an unstable arrhythmia; synchronized cardioversion.

• A wide-complex tachycardia → ventricular tachycardia until proven otherwise; treat as VT.

• A delta wave (WPW) with atrial fibrillation → avoid AV-nodal blocking agents, which can accelerate conduction.

• A prolonged QT → risk of torsades; replete magnesium and remove QT-prolonging drugs.

• Palpitations with syncope or a family history of sudden death → an inherited arrhythmia or structural disease; cardiology.

Senior IM Resident Pearls

• Capture the rhythm or you have nothing. The diagnosis lives in an ECG or monitor strip taken during symptoms — a normal resting tracing doesn't exclude a paroxysmal arrhythmia.

• AFib is three questions at once. Rate versus rhythm, anticoagulate by CHA₂DS₂-VASc, and is the patient unstable — answer all three.

• Mind the 48-hour window. Cardioverting AFib of uncertain or prolonged duration risks an embolic stroke without anticoagulation or a TEE.

• Vagal then adenosine for stable SVT. Cardiovert only if unstable; recurrent SVT is an ablation referral.

• Give magnesium with potassium. Hypomagnesemia causes refractory hypokalemia and torsades — replete both.

• Don't blame anxiety first. It's a real cause but only after the arrhythmic and systemic causes are genuinely excluded.

• Common mistake: reassuring a young patient with "anxiety" or treating an unstable rhythm with drugs when the hemodynamics called for immediate synchronized cardioversion.