An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
Obstructive Uropathy
Obstruction can rapidly cause sepsis, electrolyte emergencies, and irreversible renal injury. The key is to recognize who needs urgent drainage, not just identify a blocked system.
Also known asurinary tract obstruction · urinary obstruction · hydronephrosis
A 68-year-old man sits forward on the stretcher, shifting every few seconds as waves of pain cross his right flank. He says he has barely passed urine since yesterday, and his daughter noticed he has been unusually foggy this morning. The monitor shows a regular rhythm, but his creatinine is more than twice its recorded baseline. The bedside scan is ready, and the next move has not yet been made.
— What’s your move? Read on.
Before you read
What finding makes a urinary obstruction an infected emergency?
When does a catheter solve the problem—and when does it miss the obstruction?
When to Think of It
Consider obstruction with acute urinary retention, flank pain or renal colic, oliguria/anuria, unexplained acute kidney injury, or recurrent UTI with hydronephrosis. Check for lower-tract retention with bladder scan; renal ultrasound or CT helps identify upper-tract obstruction and its cause.
Sick or Not Sick
The pivotal call is whether obstruction is infected or causing threatened renal function. Fever or sepsis with an obstructed collecting system, bilateral obstruction, obstruction of a solitary functioning kidney, anuria, or significant AKI calls for urgent urology involvement and decompression—not antibiotics or observation alone.
The First Fifteen Minutes
If hypotensive, confused, or poorly perfused: establish IV access, monitor, send CBC, metabolic panel, urinalysis/culture, and lactate as indicated; give balanced crystalloid in 500–1,000 mL IV boluses with reassessment if hypovolemic, particularly cautiously in heart or renal failure.
If severe pain: fentanyl 0.5–1 mcg/kg IV, titrated every 5–10 minutes to effect, because opioid analgesia can control renal colic while definitive evaluation proceeds.
If a distended bladder or acute retention is suspected: place a urethral catheter; if passage meets resistance or there is known urethral injury, stop and seek urologic guidance rather than force it.
If infected obstruction is suspected: obtain cultures without delaying treatment and give ceftriaxone 1–2 g IV, then arrange urgent drainage; it treats common urinary pathogens but does not relieve the obstruction.
If hyperkalemia causes ECG changes or is severe: give calcium gluconate 1 g IV (10 mL of 10% solution), repeat if ECG changes persist; give regular insulin 10 units IV with dextrose 25 g IV, because insulin shifts potassium intracellularly. Add nebulized albuterol 10–20 mg if appropriate; it provides an additional intracellular shift.
Do not let symptom improvement, antibiotics, or a Foley catheter falsely reassure you when the upper tract remains obstructed.
Definitive Care & Disposition
Infected obstruction requires urgent source control—usually ureteral stent or percutaneous nephrostomy—plus IV antibiotics and admission. Anuria, AKI, bilateral obstruction, a solitary kidney, uncontrolled pain/vomiting, or significant electrolyte disturbance generally warrants admission and urgent urology consultation. Stable patients with uncomplicated unilateral obstruction may be discharged only if pain is controlled, renal function is acceptable, there is no infection or high-risk anatomy, and follow-up is reliable. A Foley treats bladder-outlet obstruction, not an obstructed ureter.
How This One Kills
Treating an infected obstructed kidney with antibiotics alone. Bacteria remain trapped behind the blockage; deterioration to septic shock can occur despite apparently appropriate antimicrobial therapy.
The Differential — What Else Looks Like This
Pyelonephritis without obstruction — no obstructed collecting system; missing obstruction delays source control.
Renal colic without high-risk obstruction — unilateral stone with preserved renal function and no infection; overcalling risk can lead to unnecessary intervention.
Acute tubular injury — AKI without hydronephrosis or retention; attributing it to obstruction delays the actual renal work-up.
Abdominal aortic aneurysm — vascular risk, pulsatile mass, or unexplained shock; mislabeling it as renal colic can be fatal.
The Second-Day Story
Older adults may have delirium, falls, nausea, or vague abdominal discomfort rather than flank pain; neuropathy, immunosuppression, or analgesics can blunt pain and fever. A patient with obstruction of a solitary kidney—or bilateral obstruction—may present mainly with low urine output and rising creatinine. When the story is quiet but renal function or urine output is changing, check bladder volume and image the kidneys rather than relying on symptoms.
Back to Our Patient
Back to our 68-year-old man with right flank pain, low urine output, and new fogginess. Recognize possible obstruction with AKI; risk-stratify him as high risk until infection, bilateral disease, and solitary-kidney obstruction are excluded. Check a bladder scan and renal imaging, obtain urine and blood studies, and give fentanyl for severe pain while monitoring his renal function and electrolytes. If imaging shows an infected obstructed system, give IV antibiotics and arrange urgent urologic decompression; if the bladder is distended, catheterize, but confirm that this resolves the obstruction. He is admitted for AKI and urgent urology evaluation rather than discharged based on pain relief.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“This is a 68-year-old man presenting with acute right flank pain, oliguria, and confusion. His daughter reports markedly reduced urine output since yesterday and new fogginess this morning; he has no known trauma or dysuria. He is uncomfortable but currently hemodynamically stable, with right flank tenderness and no peritoneal signs. His creatinine is more than twice baseline, and we are checking potassium, urinalysis, bladder volume, and renal imaging now. I’m concerned about obstructive uropathy with AKI and will assess for infection and high-risk anatomy. I’ll treat his pain, catheterize if retention is demonstrated, and involve urology urgently if imaging confirms upper-tract obstruction or infection. He needs admission if AKI or a high-risk obstruction is confirmed.”
Study Directive
Draw a two-branch pathway from memory: bladder-outlet obstruction versus upper-tract obstruction, including the first test and definitive intervention for each.
Work through three cases: infected stone, retention with AKI, and obstruction of a solitary kidney; state the disposition and source-control plan for each.
Review your local hyperkalemia treatment protocol and recite the calcium, insulin/dextrose, and albuterol doses without looking.
A blocked or displaced nephrostomy can recreate the obstruction it was placed to relieve. Forceful manipulation risks injury, while delay in infected...
Also known asnephrostomy tube malfunction · nephrostomy catheter obstruction · percutaneous nephrostomy complications
A 61-year-old woman arrives clutching the side of her coat, where a damp patch is spreading beneath a taped dressing. Her nephrostomy bag is nearly empty, and she says the tubing stopped draining sometime overnight. She has a dull ache under her ribs but is not sure whether she has had a fever. The tube and its connections are in view; the next move has not yet been made.
Before You Read
What can you safely check at the bedside before imaging?
When is flushing reasonable, and when should you stop?
Which tube problems need urgent interventional radiology or urology involvement?
Why It Matters
A blocked or displaced nephrostomy can recreate the obstruction it was placed to relieve. Forceful manipulation risks injury, while delay in infected obstruction can lead to sepsis.
When to Think of It
Suspect a tube problem with reduced or absent drainage, leakage around the skin, new flank pain, fever, hematuria, or visible change in external tube length. First inspect the bag, tubing, connections, and dressing; establish whether the patient is still draining urine through the bladder or another kidney.
Sick or Not Sick
The key call is whether the patient has infection or loss of drainage from an obstructed/solitary kidney. Sepsis, worsening AKI, anuria, severe pain, or a solitary functioning kidney with a non-draining tube demands urgent urology/interventional radiology (IR) involvement.
The First Fifteen Minutes
If unstable or septic: monitor, establish IV access, obtain cultures and renal function/electrolytes, and give ceftriaxone 1–2 g IV for a suspected community urinary source while arranging urgent tube assessment; broaden coverage and adjust for renal function and local risk.
If pain is severe: give fentanyl 0.5–1 mcg/kg IV, titrated every 5–10 minutes, because it provides rapid analgesia while the tube is evaluated.
Check for a closed clamp, kink, dependent loop, full bag, or loose connection; correct an obvious external issue without pulling on the tube.
If the tube appears intact but is not draining, follow the patient’s tube-specific instructions and local protocol. Gentle sterile-saline flushing may be appropriate only if authorized and trained; use the prescribed volume, often 5–10 mL, and stop if there is resistance, pain, or leakage. Do not force a flush or blindly advance, remove, or replace the catheter.
If the tube is partly or fully out, newly longer, or leaking with pain/fever: treat it as possible displacement and contact IR/urology urgently; do not wait for a bedside flush to prove patency.
Definitive Care & Disposition
Confirm position and drainage with appropriate imaging—often ultrasound or fluoroscopic evaluation, with CT when the cause or anatomy is unclear. IR commonly performs an exchange or repositioning; urology may be needed for the underlying obstruction. Admit patients with sepsis, AKI, significant electrolyte disturbance, inadequate drainage of a solitary kidney, or need for urgent intervention. Discharge is reasonable only when the patient is stable, drainage is restored or a safe plan is made, and specialist follow-up is reliable.
How This One Kills
Forcing saline or manipulating a displaced tube can cause bleeding, false passage, or collecting-system injury—and can delay definitive drainage of an infected kidney.
The Atypical Presentation
Frail or immunosuppressed patients may have little pain or fever despite a blocked tube and evolving infection. A patient with two kidneys may continue to make urine from the unobstructed side, masking failure of the affected nephrostomy. Compare current output and external tube position with baseline, review renal function, and image when patency or position is uncertain.
Back to Our Patient
Back to our 61-year-old woman with a nearly empty nephrostomy bag, damp dressing, and flank ache. Recognize possible obstruction or displacement, then risk-stratify by checking her vital signs, urine output, renal function, and signs of infection; a non-draining tube with sepsis or compromised renal drainage is urgent. Inspect the external system for a kink or closed clamp, but do not pull or force a flush. Because her drainage has stopped and leakage has begun, contact IR/urology for prompt assessment and imaging; if she is febrile or septic, obtain cultures and give IV antibiotics without delaying tube intervention. Admit if drainage is not promptly restored or infection/AKI is present.
Patient Presentation to Attending
“This is a 61-year-old woman with a left nephrostomy tube presenting with overnight loss of drainage, leakage at the dressing, and new flank discomfort. Her bag is nearly empty, and the dressing is damp; she is uncertain about fever. I’ve checked the external tubing and bag for a clamp, kink, or full reservoir and have not manipulated the catheter. I’m assessing her vital signs, urine output, renal function, and urinalysis, and will image to evaluate tube position and hydronephrosis. I’m concerned about tube obstruction or displacement with recurrent urinary obstruction. I’ll contact IR or urology now, give analgesia, and add IV antibiotics promptly if infection is suspected. She will be admitted if drainage is not restored or she has infection or AKI.”
Study Directive
Practice a 60-second nephrostomy check: bag, clamp, kink, dependent loop, connection, external length, output, and patient stability.
Review your institution’s nephrostomy flush and escalation protocol; write down who to call after hours and what flush volume is authorized.
Verbalize a “stop” rule for resistance, pain, leakage, suspected displacement, and sepsis.
Key Medications
Fentanyl: 0.5–1 mcg/kg IV, titrate every 5–10 minutes for severe pain.
Ceftriaxone: 1–2 g IV every 24 hours for suspected community urinary infection; broaden for sepsis, resistant-organism risk, or healthcare-associated infection, with renal adjustment as appropriate.
Sterile saline for flushing: use only when permitted by the tube-specific plan and local protocol; the prescribed volume varies (often 5–10 mL). Do not force against resistance.
Pediatric dosing is weight-based; nephrostomy-specific flush instructions require specialist/local guidance.
High-Yield Pearls
Compare the tube’s external length with its documented baseline; a new length change raises concern for migration.
A patent-looking tube can still be obstructed internally—persistent symptoms or absent output warrant assessment rather than repeated flushing.
The urine output from the other kidney can conceal failure of the nephrostomy side.
The Mimics
Full or kinked drainage bag/tubing — corrects with simple external inspection; unnecessary tube manipulation creates avoidable risk.
Urine leakage from a patent tube — may reflect a loose connection or pressure, but persistent leakage with pain can signal obstruction or displacement; dismissing it can miss loss of drainage.
Hematuria after recent placement/exchange — small, improving blood staining may be expected; heavy bleeding or clots can indicate significant injury.
Pyelonephritis with a functioning tube — fever and flank pain may occur despite drainage; assuming a mechanical failure can delay recognition of infection.
Board Question
A patient with a nephrostomy tube has new flank pain, no drainage, and resistance when a clinician attempts a saline flush. What is the best next step?
AApply firm pressure to force the flush through
BRemove the tube and place a larger catheter at bedside
CStop manipulation and urgently contact IR/urology for assessment
DClamp the tube and reassess in several hours
Reveal answer
Correct: C
Resistance and pain during flushing are reasons to stop; forcing fluid or blindly replacing the tube can cause injury and delay needed drainage. Urgent specialist assessment is especially important when obstruction or displacement is possible.
Recognizing nephrostomy tube malfunction and complications helps guide immediate assessment and when to involve interventional radiology.
3 of 5
Bleeding Dialysis Fistula
Hemorrhage from a dialysis access can become fatal within minutes. Secure hemostasis without sacrificing a potentially usable access—and identify aneurysm,...
Also known asAV fistula bleeding · AVF hemorrhage · dialysis access hemorrhage
A 59-year-old man arrives with his left sleeve soaked through and a red towel pressed tightly against his forearm. Blood wells between his fingers each time he loosens his grip. He says the access began bleeding after dialysis, and his face has gone pale while he waits. The bleeding has not yet been brought under control.
Before You Read
What is the first maneuver for active fistula hemorrhage?
When should a tourniquet enter the plan?
Which access findings make this more than a simple puncture-site bleed?
Why It Matters
Hemorrhage from a dialysis access can become fatal within minutes. Secure hemostasis without sacrificing a potentially usable access—and identify aneurysm, infection, or outflow problems that need urgent repair.
When to Think of It
Treat ongoing bleeding from an arteriovenous fistula or graft as a time-critical hemorrhage. Look for a focal puncture-site bleed versus spontaneous bleeding, a thin/shiny skin defect, enlarging aneurysm or pseudoaneurysm, infection, or repeated prolonged bleeding after dialysis.
Sick or Not Sick
The essential call is whether bleeding is controlled with direct pressure. Persistent brisk bleeding, shock, recurrent hemorrhage, skin breakdown over an aneurysm, or suspected infected access requires immediate escalation to vascular surgery and/or the dialysis access team.
The First Fifteen Minutes
For active bleeding: apply firm, continuous focal pressure directly over the bleeding point with gauze; do not repeatedly lift it to check. Add a hemostatic dressing if available and appropriate.
If hemorrhage persists or the patient is unstable: activate the major hemorrhage pathway, obtain IV access away from the access arm, send CBC/coagulation studies/type and crossmatch, and involve vascular surgery immediately. A tourniquet proximal to the bleeding site may be used as a lifesaving rescue if direct pressure fails; document the time and reassess distal perfusion when feasible.
If shock is present: give blood products according to the local major hemorrhage protocol rather than large volumes of crystalloid.
If life-threatening bleeding occurs in a patient taking warfarin: give 4-factor PCC 25–50 units/kg IV, based on INR/product protocol, plus vitamin K 10 mg IV; PCC dosing varies, so check the product and institutional protocol. For life-threatening bleeding on a direct oral anticoagulant, use agent-specific reversal guidance and consult the local protocol.
Avoid blind clamping, suturing, or circumferential dressings that conceal ongoing bleeding or compromise the access.
Definitive Care & Disposition
Once controlled, keep the patient for reassessment and urgent vascular/access-team review if there was brisk or recurrent bleeding, aneurysm or skin compromise, infection, or need for reversal/transfusion. Definitive management may include repair or revision of aneurysm/pseudoaneurysm, treatment of infection, or evaluation for stenosis/outflow obstruction. A small, controlled needle-site bleed may be discharged only after sustained hemostasis, stable vital signs, and a clear dialysis/access follow-up plan.
How This One Kills
Assuming a puncture-site bleed is harmless and loosening pressure repeatedly. A fragile aneurysm or eroded skin can rupture catastrophically, with rapid exsanguination before routine laboratory results return.
The Atypical Presentation
Patients may minimize repeated small bleeds, especially if bleeding stops with pressure before arrival. A quiet puncture site does not exclude high-risk skin erosion, aneurysm, infection, or central/outflow stenosis; ask about prolonged bleeding after prior dialysis sessions and inspect the entire access, not just the current puncture point.
Back to Our Patient
Back to our 59-year-old man with the blood-soaked sleeve and bleeding left-arm access. Recognize an access hemorrhage and immediately apply firm, uninterrupted pressure; risk-stratify by whether it stops and whether he is developing shock. If bleeding persists, escalate to the major hemorrhage pathway, consider a proximal tourniquet as a rescue maneuver, and call vascular surgery urgently. Review anticoagulant exposure and reverse life-threatening warfarin-associated bleeding if present. Because his bleeding is ongoing and he appears pale, he needs emergency hemostasis and hospital evaluation, not discharge after a brief dressing change.
Patient Presentation to Attending
“This is a 59-year-old man with active bleeding from his left-arm dialysis access after today’s treatment. He reports no trauma beyond the dialysis needle removal, and blood continues to well through the towel when pressure is released. He is pale, and I’m reassessing his hemodynamics while maintaining direct pressure over the bleeding point. I’m examining for aneurysm, skin erosion, infection, and other bleeding sites, and have obtained access away from the fistula arm for labs and type and crossmatch. This is a potentially life-threatening access hemorrhage, with concern for aneurysmal or puncture-site bleeding. I’m activating the hemorrhage pathway if he is unstable, involving vascular surgery now, and will use a tourniquet only if pressure fails. He requires admission or observation until durable hemostasis and an access-team plan are established.”
Study Directive
Rehearse a verbal hemorrhage sequence: direct pressure, escalation, rescue tourniquet, vascular call, and anticoagulant reversal decision.
Review your local major hemorrhage and warfarin reversal protocols, including where PCC is stocked.
Practice identifying access aneurysm, skin erosion, and infection on three clinical images or exam cases.
Key Medications
4-factor PCC: for life-threatening warfarin-associated bleeding, 25–50 units/kg IV according to INR and product protocol.
Vitamin K: 10 mg IV with PCC for life-threatening warfarin-associated bleeding.
Blood products: use the local major hemorrhage protocol when shock or ongoing major blood loss is present.
PCC dosing varies by INR, product, and indication; check an institutional protocol or dosing reference if uncertain. Pediatric use is specialist- and weight-based.
High-Yield Pearls
A thrill or bruit does not make an access safe: inspect for thin, shiny, ulcerated, or scabbed skin over an aneurysm.
Prolonged bleeding after dialysis can be the clue to outflow stenosis, even when the access still has a thrill.
Never place routine IVs or blood-pressure cuffs on the access arm when another option is available.
The Mimics
Prolonged post-dialysis needle-site bleeding — recurrent or unusually prolonged bleeding can signal outflow stenosis; overlooking it risks future access failure or hemorrhage.
Access infection — erythema, warmth, purulence, or fever; treating it as simple mechanical bleeding misses a potentially life-threatening infection.
Pseudoaneurysm or aneurysm rupture — focal bulging, skin thinning, or spontaneous bleeding; missing it risks recurrent catastrophic hemorrhage.
Generalized coagulopathy — bleeding at multiple sites or abnormal coagulation studies; focusing only on the access misses a systemic cause.
Board Question
A hemodialysis patient arrives with brisk, persistent bleeding from an AV fistula despite firm focal pressure. He is becoming hypotensive. What is the most appropriate next step?
ARelease pressure every minute to locate the exact vessel
BPlace a proximal tourniquet as a rescue maneuver and activate emergency hemorrhage/vascular response
CWrap the entire arm tightly with an elastic bandage and discharge
DDelay intervention until coagulation studies return
Reveal answer
Correct: B
Persistent life-threatening access bleeding requires immediate escalation; a proximal tourniquet can be a lifesaving rescue when direct pressure fails. Do not delay hemostasis for laboratory results.
A practical reference for recognizing bleeding dialysis access and determining when hemorrhage or other access complications require urgent vascular evaluation.
4 of 5
Calciphylaxis
Calciphylaxis causes severe ischemic skin injury and carries high mortality, especially when wounds become infected. Early recognition can prevent the pain...
A 56-year-old woman with kidney failure winces as a bedsheet brushes a dark, netlike patch on her thigh. She says the pain began days before the skin changed, and now even light touch makes her pull away. There is no obvious drainage, but the center of the patch has started to look dusky. The question of how urgently to escalate is still open.
Before You Read
What skin finding and pain pattern should raise concern before ulceration appears?
Which mimics require urgent exclusion?
What can the ED do now, given that definitive treatment is multidisciplinary?
Why It Matters
Calciphylaxis causes severe ischemic skin injury and carries high mortality, especially when wounds become infected. Early recognition can prevent the pain and skin change from being dismissed as routine bruising or cellulitis.
When to Think of It
Consider calciphylaxis in a patient with advanced kidney disease—especially on dialysis—with severe, often disproportionate pain and indurated plaques that progress to retiform purpura, necrosis, and ulceration. Common sites include thighs, abdomen, and buttocks; lesions may be proximal or distal.
Sick or Not Sick
The key call is whether there is superimposed infection, sepsis, or rapidly progressive tissue necrosis. Fever, purulence, crepitus, hemodynamic instability, or rapidly spreading erythema requires urgent evaluation for infection and surgical involvement; the skin diagnosis does not exclude a concurrent emergency.
The First Fifteen Minutes
If pain is severe: give fentanyl 0.5–1 mcg/kg IV, titrated every 5–10 minutes, because severe ischemic pain often needs prompt parenteral analgesia.
If the patient is septic or the wound appears infected: obtain cultures when feasible and give vancomycin 20–25 mg/kg IV as a loading dose plus cefepime 2 g IV, adjusted for renal function and local protocol; these provide empiric coverage while source and organisms are assessed.
If stable without signs of infection: avoid reflexive antibiotics; document lesion distribution and progression, assess pain and wound status, and involve nephrology and wound care early.
Check calcium, phosphate, renal function, CBC, and coagulation studies as indicated; results may inform the work-up but a normal value does not exclude the disease.
Definitive Care & Disposition
Admit patients with suspected infection, uncontrolled pain, rapidly progressive lesions, or diagnostic uncertainty requiring urgent specialist assessment. Coordinate nephrology, dermatology, wound care, pain specialists, and surgery as appropriate. Care may include wound management, optimization of mineral-bone disease and dialysis, review of contributing medicines, and specialist-directed sodium thiosulfate; evidence and dosing vary, so this is not a stand-alone ED fix. Debridement decisions are individualized—particularly when infection or necrosis is present.
How This One Kills
Calling a profoundly painful, evolving retiform lesion “cellulitis” or “bruising” and delaying recognition until necrosis or infection is advanced. Conversely, assuming calciphylaxis explains fever or shock can miss a treatable superinfection.
The Atypical Presentation
Early lesions can be subtle—deep tenderness, induration, or bruiselike discoloration before the retiform pattern or ulcer appears. Older or immunocompromised patients may lack fever despite infection, and patients with diabetes or neuropathy may not describe pain reliably. In a patient with advanced kidney disease, escalating focal skin pain or a changing plaque deserves direct inspection and early specialist discussion even when the initial appearance is nonspecific.
Back to Our Patient
Back to our 56-year-old woman with kidney failure, severe pain, and a dusky netlike thigh lesion. Recognize possible calciphylaxis from the disproportionate pain and evolving retiform appearance; risk-stratify immediately for infection, systemic illness, and tissue progression. Treat her pain with titrated IV fentanyl, examine and document the lesion, and obtain targeted labs without using them to rule the disease out. If she has signs of infection, obtain cultures and begin renal-adjusted empiric antibiotics while involving the appropriate teams. Given severe pain and evolving skin injury, she needs urgent nephrology and wound/dermatology assessment and likely admission for coordinated care.
Patient Presentation to Attending
“This is a 56-year-old woman with kidney failure on dialysis presenting with several days of severe thigh pain and a progressive dark, netlike skin lesion. The pain began before the discoloration and is triggered by light contact; she has not noticed drainage. The lesion is dusky centrally, and I’m assessing for spreading erythema, fluctuance, crepitus, and systemic toxicity. I’m checking her vital signs and relevant labs, but I recognize these tests do not exclude calciphylaxis. I’m concerned for calciphylaxis with evolving tissue injury, while actively evaluating for superinfection and necrotizing infection. I’ll provide titrated IV analgesia, involve nephrology and wound/dermatology teams urgently, and start renal-adjusted broad-spectrum antibiotics if infection is suspected. Given her severe pain and progression, I recommend admission for multidisciplinary management.”
Study Directive
Sketch the progression from early painful plaque to retiform purpura, necrosis, and ulceration; label the key bedside clues at each stage.
Compare calciphylaxis with necrotizing infection, warfarin skin necrosis, and cellulitis using one discriminating feature for each.
Review your local dialysis-specific vancomycin/cefepime dosing guidance and identify who coordinates suspected calciphylaxis after hours.
Key Medications
Fentanyl: 0.5–1 mcg/kg IV, titrate every 5–10 minutes for severe pain.
Vancomycin: 20–25 mg/kg IV loading dose when severe infection is suspected; subsequent dosing and monitoring must be individualized for dialysis and renal function.
Cefepime: 2 g IV for empiric severe infection, with renal adjustment and repeat-dose timing based on dialysis status and local protocol.
Sodium thiosulfate: commonly 25 g IV during or after hemodialysis three times weekly in specialist-directed regimens; evidence and dosing vary, and adverse effects include metabolic acidosis and hypotension. Check a current reference and local protocol.
Pediatric experience and dosing are limited; involve specialists.
High-Yield Pearls
Severe pain can precede visible necrosis; do not wait for an ulcer before involving specialists.
A normal calcium or phosphate level does not rule out calciphylaxis.
Biopsy may help when the diagnosis is uncertain but can worsen tissue injury; specialist discussion should guide the decision.
The Mimics
Cellulitis — diffuse warmth and erythema without the characteristic retiform ischemic pattern; confusing it may delay recognition, while missing superinfection remains dangerous.
Necrotizing soft-tissue infection — rapid progression, systemic toxicity, or pain beyond visible findings; mislabeling it as calciphylaxis delays emergency surgery.
Warfarin-induced skin necrosis — typically follows warfarin initiation and often involves fatty areas; confusing them can lead to the wrong medication plan.
Cholesterol emboli/vasculitis — livedo or purpura with clues such as recent vascular instrumentation, renal findings, or systemic involvement; misattribution can delay the relevant work-up.
Board Question
A patient receiving hemodialysis has severe thigh pain followed by indurated, retiform purpura. Which additional finding most strongly supports calciphylaxis?
APainful skin lesions in a patient with advanced kidney disease
BPruritic wheals that disappear within hours
CPainless unilateral edema that improves with elevation
DA sharply demarcated dermatomal vesicular eruption
Reveal answer
Correct: A
Severe pain with evolving indurated retiform lesions in advanced kidney disease is a classic pattern for calciphylaxis. Early lesions may precede ulceration, so absence of an open wound does not exclude it.
Recognizing painful, necrotic skin lesions early can prompt urgent wound care, risk-factor modification, and specialist treatment for this high-mortality disease.
Multicenter outcome data help frame prognosis and reinforce the need for prompt escalation when calciphylaxis is suspected.
5 of 5 · Procedure Corner
Suturing a Bleeding Dialysis Fistula
Persistent, focal bleeding from a dialysis access needle puncture or small skin opening despite sustained, correctly placed direct pressure.Use as a...
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Indications
Persistent, focal bleeding from a dialysis access needle puncture or small skin opening despite sustained, correctly placed direct pressure.
Use as a temporizing hemostatic maneuver while arranging vascular-access or nephrology follow-up when needed. Uncontrolled hemorrhage requires simultaneous resuscitation and urgent specialty consultation.
Contraindications
Do not suture blindly when the source is unclear, bleeding appears to arise from a ruptured aneurysm or pseudoaneurysm, or there is extensive tissue loss, infection, or suspected access disruption. Obtain urgent vascular surgery input.
Avoid deep or circumferential bites, which can narrow or occlude the access. A suture must not delay escalation for ongoing major bleeding.
Equipment & Prep
Gloves, eye protection, sterile prep and drapes, gauze, and a nonabsorbable monofilament suture with a small curved needle (commonly 3-0 or 4-0; select to fit the wound and local practice).
Have pressure dressings and resuscitation supplies available. Assess hemodynamic status; expose and inspect the access, identify the precise bleeding point, and document the pre-procedure thrill/bruit and distal perfusion.
Apply firm, focused direct pressure first. If bleeding persists, use aseptic technique and involve vascular-access expertise early. Avoid injecting local anesthetic into the access or bleeding point.
Steps
Position the patient so the access is visible and accessible. Maintain focused pressure until ready to place the stitch; do not use blind clamping.
Prepare the skin and identify the puncture or small opening. Plan a superficial stitch that compresses the bleeding point without encircling or deeply traversing the access.
Place a small figure-of-eight or purse-string-style hemostatic stitch across/around the skin opening, taking shallow bites in healthy skin adjacent to the puncture. Keep the needle path controlled and away from the access lumen.
Tie gradually while observing the wound. Stop tightening once bleeding is controlled; avoid strangulating skin or compressing the fistula.
Reassess bleeding, access thrill/bruit, and distal hand perfusion. If bleeding continues or the access signal is diminished, do not add blind or tighter stitches—maintain pressure and escalate urgently.
Confirmation & Success Criteria
No active bleeding after releasing focused pressure and during a period of observation.
Access thrill/bruit remains present and distal perfusion is unchanged. A palpable thrill alone does not exclude access injury; arrange specialist assessment when injury is suspected.
Complications & Rescue
Persistent or recurrent hemorrhage: Resume firm direct pressure, reassess hemodynamics, obtain urgent vascular surgery/nephrology support, and escalate resuscitation as indicated. Do not delay definitive control with repeated blind sutures.
Loss of thrill/bruit or impaired distal perfusion: Loosen or remove the stitch if safe, apply pressure to the bleeding site, and obtain immediate vascular consultation for possible thrombosis, stenosis, or arterial compromise.
Access damage, infection, skin injury, or stenosis: Avoid further manipulation and arrange urgent specialist evaluation. Do not place a circumferential ligature or clamp across the access.
Aftercare & Documentation
Apply a light protective dressing that permits access monitoring; avoid a tight circumferential wrap. Recheck for bleeding, thrill/bruit, and distal perfusion before disposition and after any dressing change.
Arrange prompt vascular-access follow-up and communicate any concern for access injury. Provide return precautions for recurrent bleeding, increasing pain or swelling, hand coolness/numbness, or loss of the thrill.
Document the bleeding source and duration, pressure and suture technique/material, hemostasis, post-procedure access and distal neurovascular findings, consultations, and follow-up plan.
Yesterday’s Differential
The daily puzzle — from editions past
A quick test of recall from prior editions. Commit to an answer before you check.
From yesterday's edition
A 79-year-old man is referred to the ICU with coma, hypothermia, and hypotension that is not responding to inotropes. He is profoundly bradycardic. What’s the diagnosis, and the first move?
Check your answer
Hypothyroidism (Myxedema). Let the triad trigger thyroid testing (TSH, T4) in the coma/hypothermia/bradycardia patient and start thyroid hormone replacement for myxedema coma; expect the rate and T-wave changes to correct with treatment rather than chasing them cardiac-first.
From the September 20 edition
Today, three days ago: Esmolol. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
Aortic dissection/rate control: optional 500 mcg/kg IV load over 1 min, then 50 mcg/kg/min; titrate every 5 min, commonly up to 200 mcg/kg/min or protocol max. Severe bradycardia, heart block without pacer, cardiogenic shock, decompensated heart failure, severe reactive airway disease caution.
From the September 13 edition
A patient has plantar ecchymosis and midfoot pain after axial loading. Non-weight-bearing radiographs are equivocal. What is the best next diagnostic step?
ADischarge with an ankle brace
BCT of the foot
CImmediate MRI of the ankle
DRepeat radiographs in 6 weeks
Reveal answer
Correct · B
CT of the foot. CT identifies subtle fractures and tarsometatarsal malalignment when plain films are nondiagnostic. Lisfranc injury should not be dismissed as a sprain based on equivocal non-weight-bearing films.
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Podcast Picks
Two for the shift
Critical Care Perspectives in Emergency Medicine2026-09-01
Brain damage and death from ischemic encephalopathy is common after cardiac arrest. Animal studies and limited observational studies suggest that high oxygen exposure after ROSC may result in neuronal death. As such, it is hypothesized that limiting oxygen exposure (conservative oxygen) many attenuate reperfusion injury and improve outcomes. At present,...
Source
Critical Care Perspectives in Emergency Medicine
Published
2026-09-01
Host
Critical Care Perspectives in Emergency Medicine, Critical Care Perspectives in Emergency Medicine
Pulse-dose methylprednisolone is common across many medical fields (defined here as giving ≧500 mg methylprednisolone daily for ≧3 days). However, providing such a high dose of steroids may increase the risk of...
Pharmacology Corner
Two drugs for the shift
One antimicrobial and one other ED workhorse — selected daily, with sources and last-reviewed dates so every dose is cross-checkable.
Antimicrobial of the Day
Azithromycin
Macrolide
Indication
Atypical coverage in CAP (combined with a beta-lactam), pertussis, chlamydia, and select traveler's diarrhea.
What’s your dose? — reveal dosing & cautions
ED Dose
500 mg IV/PO once, then 250 mg PO daily x 4 days (CAP). 1 g PO single dose for chlamydia. 500 mg IV q24h for hospitalized pneumonia.
Renal Adjustment
No adjustment for renal impairment; use caution in severe hepatic disease.
Contraindications
History of cholestatic jaundice with prior macrolide use; congenital long QT.
Baseline ECG if other QT-prolonging drugs or risk factors present. LFTs with prolonged use.
ED Pearl
In a septic patient already getting ondansetron, haloperidol, and a quinolone — stack QT risks; check the QTc and consider doxycycline as the atypical agent instead.
Cardiac arrest, anaphylaxis, severe asthma adjunct, peri-intubation hypotension/pressor support, and selected bradycardic shock states.
What’s your dose? — reveal dosing & cautions
ED Dose
Cardiac arrest: 1 mg IV/IO q3–5 min of 0.1 mg/mL solution. Anaphylaxis: 0.3–0.5 mg IM of 1 mg/mL into lateral thigh q5–15 min. Infusion: commonly 0.01–0.5 mcg/kg/min titrated to effect.
Renal Adjustment
No renal adjustment; titrate to clinical effect.
Contraindications
No absolute contraindication in cardiac arrest or anaphylaxis. Relative caution in severe tachyarrhythmia/ischemia when used for non-life-threatening indications.
Interactions
MAOIs/TCAs/cocaine potentiate effects; beta-blockers may blunt bronchodilation and leave unopposed alpha effects; halogenated anesthetics increase arrhythmia risk.
Monitoring
Continuous ECG, BP, perfusion, extravasation, lactate interpretation after high doses.
ED Pearl
For anaphylaxis, the route/concentration error kills: IM thigh uses 1 mg/mL; IV push arrest dosing uses 0.1 mg/mL and belongs in cardiac arrest or expert titration contexts.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Pacing
Pacemaker Malfunction
A paced patient with syncope, a runaway tachycardia, or unexpected bradycardia may be showing failure to capture, oversensing, or a pacemaker-mediated tachycardia hiding in plain sight.
The Tracing
A 78-year-old with a dual-chamber pacemaker arrives feeling faint and short of breath. Heart rate is 38 and blood pressure is soft. The monitor shows a P wave before each QRS, and tiny pacing spikes march out ahead of the ventricular complexes, most visible in V3 through V6 and again in I, aVR and V1. But the spikes are not followed by a QRS — the ventricle does not respond. The native P waves themselves fail to reach the ventricles, and between the dropped paced beats there is a long, silent pause before an escape complex crawls through. The spike is there; the depolarization is not.
Failure to capture: a pacing spike is present but is NOT followed by myocardial depolarization (no QRS after the spike)
Undersensing: pacing spikes appear within or on top of native QRS complexes because the device fails to sense intrinsic activity and paces asynchronously
Output failure: an expected pacing spike is entirely absent, from oversensing, wire fracture, lead displacement, or interference
Pacemaker-mediated tachycardia: a paced ventricular tachycardia driven by retrograde P waves sensed as native atrial activity, rate capped by the programmed upper limit (usually 160-180 bpm)
Runaway pacemaker: paroxysms of low-amplitude, high-rate pacing spikes that may fail to capture, seen with a depleted battery
Pearls
If the patient's native rate is above the pacemaker's set rate, no pacing is expected — so failure to capture and output failure simply cannot be diagnosed on that ECG. Absence of spikes is not proof of malfunction.
A change in paced QRS morphology from LBBB (RV lead) to RBBB (LV lead) suggests the lead has eroded through the interventricular septum; a chest x-ray helps confirm lead position.
Oversensing of pectoral or rectus muscle activity can inhibit output — ask the patient to isometrically contract those muscles while you watch the monitor to unmask it.
Pitfalls
Failure to capture has causes you can fix at the bedside — electrolyte disturbance (especially hyperkalemia), acute MI, and exit block — not just hardware failure. Check a potassium and a 12-lead before assuming a dead lead.
A rapid paced rhythm with no preceding atrial activity is not automatically malfunction: it may be pacemaker-mediated tachycardia, sensor-induced tachycardia, or an entirely appropriate response to exercise. Don't reflexively call it a device failure.
Diagnosing malfunction on the surface ECG is genuinely difficult and often impossible; the definitive answer is device interrogation, not your read of the strip.
At the Bedside
Place a magnet to force asynchronous pacing (VOO) — this can terminate a pacemaker-mediated or sensor-induced tachycardia and can be life-saving in runaway pacemaker while definitive replacement is arranged. For a symptomatic PMT you can also slow AV nodal conduction with adenosine. Correct reversible causes of failure to capture (potassium, ischemia), and get urgent cardiology for interrogation and reprogramming; have transcutaneous pacing ready if the patient is bradycardic and unstable.
For educational use only. Verify ECG interpretation against the LITFL entry and your institution’s practice before clinical decision-making.
Case of the Day
From the lead · Obstructive Uropathy
Self-Examination
Test Your Understanding
A 72-year-old with fever, hypotension, and flank pain has a ureteral stone with hydronephrosis on CT. After cultures and IV antibiotics, what is the next essential intervention?
ADischarge with oral antibiotics and medical expulsive therapy
BUrgent urinary decompression
CRepeat CT after 24 hours of antibiotics
DImmediate extracorporeal shock-wave lithotripsy
Reveal answer
Correct answer · B
An infected obstructed collecting system requires urgent drainage by ureteral stent or nephrostomy in addition to antibiotics. Antibiotics alone do not provide source control.
Study Pace4 topics today; Issue 71 of 94 — Renal and Urogenital (Weeks 39-40)Deadline · June 1, 2026