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Central venous catheter complications

Recognise mechanical, thrombotic and infectious central venous catheter complications, stabilise the patient, protect the vessel and device, and choose investigation and source control without unsafe line manipulation.

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Unstable patient after central access

Respiratory collapse, shock, neurological deficit, rapidly expanding neck swelling, major bleeding or suspected venous air embolism after catheter insertion or use is a time-critical procedural emergency.

Action: Stop catheter use, call for resuscitation and senior vascular-access help, provide ABC support and identify the likely mechanism. Clamp an open system for suspected air entry; do not blindly remove a large-bore arterial catheter, and obtain immediate targeted imaging or decompression when the physiology demands it.

Open the sections you need. The overview is shown first.
01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Central venous access devices fail in several distinct ways. Immediate complications arise from needle, guidewire, dilator or catheter injury: arterial puncture or cannulation, bleeding, pneumothorax, haemothorax, arrhythmia, cardiac perforation, malposition and air embolism. Delayed complications include infection, intraluminal thrombosis, fibrin sheath, catheter-related venous thrombosis, fracture, migration and central venous stenosis. The first task is therefore not to label “line failure” but to decide whether the patient is physiologically unstable, whether the line is safe to use and which structure may have been injured.

Timing and catheter function guide the differential. A newly inserted catheter that neither aspirates nor flushes may be kinked, outside the vessel or incorrectly positioned; forceful flushing can cause extravasation or embolisation. A previously reliable dialysis catheter with low flow more often has thrombus or fibrin-related dysfunction. Fever or rigors during access can be bloodstream infection despite an unremarkable exit site. Arm or neck swelling after a PICC or ipsilateral dialysis access suggests thrombosis or central venous outflow obstruction. Each pattern needs its own diagnostic and source-control route.

Key points

  • After suspected large-bore arterial cannulation, stop infusions and leave a catheter or dilator of at least 6 Fr in place; obtain urgent vascular or interventional-radiology advice for imaging and controlled removal or repair.
  • For acute respiratory or circulatory deterioration, stop catheter use and assess immediately for pneumothorax, haemothorax, air embolism, tamponade, malposition and bleeding; treat the life-threatening physiology before routine line troubleshooting.
  • For fever, rigors or shock, obtain appropriate cultures without delaying sepsis treatment, examine the exit site and tunnel, and plan source control; severe, recurrent or S. aureus dialysis-catheter bacteraemia usually favours catheter replacement or removal.
  • Poor flow from the moment of insertion suggests kink, malposition or tip problem; late poor flow more often reflects intraluminal thrombus or a fibrin sheath. Never force a resistant flush.
  • A symptomatic catheter-related venous thrombosis can often be anticoagulated while a necessary, correctly positioned, functioning and uninfected catheter remains, but limb threat, infection or malposition changes that decision.
  • Prevent complications with real-time ultrasound, the smallest suitable catheter and lumen count, a documented guidewire check, aseptic handling, correct tip position and daily review of ongoing need.
  • Preserve future dialysis access in chronic kidney disease: avoid unnecessary PICCs and central venous instrumentation, especially where they may damage veins needed for an arteriovenous fistula.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
01

Insertion injury

Needle, guidewire, dilator or catheter can injure artery, vein, pleura, thoracic duct or myocardium; risk rises with difficult anatomy, repeated attempts and inappropriate device depth.

02

Device-associated failure

Foreign material permits microbial biofilm, activates coagulation and disturbs venous flow; malposition, excessive catheter-to-vein ratio and prolonged dwell amplify thrombosis, dysfunction and stenosis.

03

Handling and maintenance

Breaks in asepsis, wet or loose dressings, contaminated hubs, unsecured connections and failure to remove an unnecessary device increase infection, dislodgement and air-entry risk.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
  1. 1
    Pressure and structural injury

    Large-bore arterial cannulation creates a non-compressible defect that can bleed, dissect, embolise or form a pseudoaneurysm; neck haematoma may rapidly compromise the airway.

  2. 2
    Pleural or cardiac breach

    Apical pleural injury causes pneumothorax or haemothorax, while an excessively deep wire or catheter may trigger arrhythmia, perforation, pericardial effusion and tamponade.

  3. 3
    Thrombus and fibrin sheath

    Endothelial injury, stasis and foreign surface promote mural or intraluminal thrombus; organised fibrin can envelop the tip, impair aspiration and perpetuate inadequate flow.

  4. 4
    Biofilm infection

    Organisms introduced from skin or hubs adhere to catheter material and form biofilm, protecting them from host defence and antibiotics and enabling recurrent bloodstream seeding.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Mechanical complication

Symptoms begin during or soon after insertion: pleuritic pain, dyspnoea, hypotension, neck swelling, neurological change, abnormal pressure waveform, failure to aspirate or unexpected catheter course.

Catheter infection

Exit-site erythema or discharge may remain local, tunnel tenderness suggests deeper infection, while rigors, fever or sepsis during use can represent bacteraemia without visible local inflammation.

Thrombotic dysfunction

Difficulty aspirating, inadequate dialysis blood flow or recurrent pressure alarms after initially good function suggests intraluminal thrombus, tip thrombus or fibrin sheath rather than immediate malposition.

Venous outflow obstruction

Unilateral arm, neck or facial oedema, collateral chest-wall veins, access dysfunction or symptoms aggravated by an ipsilateral fistula suggest catheter-related thrombosis or central venous stenosis.

Air entry or embolismRed flag

Abrupt cough, dyspnoea, chest pain, hypoxaemia, hypotension or neurological change during connection, disconnection or removal should prompt immediate clamping and resuscitation.

Red flags requiring action

  • Sudden dyspnoea, hypoxaemia, pleuritic pain or hypotension after neck or chest access suggests pneumothorax, haemothorax, air embolism or pericardial injury.
  • A new focal neurological deficit, pulsatile neck swelling, rapidly expanding haematoma or arterial pressure waveform suggests arterial cannulation, dissection, embolisation or compressive bleeding.
  • Rigors, hypotension, confusion or new organ dysfunction during catheter use may be catheter-related bloodstream infection even when the exit site appears normal.
  • Arm, neck or facial swelling, collateral veins, catheter dysfunction or unexplained pulmonary symptoms raises catheter-related thrombosis or central venous stenosis.
05InvestigationsWhat to request, why it matters and how to interpret it.
Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

  1. 01
    Immediate bedside ABC and catheter assessmentFirst step
    Why
    Determine physiological threat and whether the catheter is safe to use before diagnostic delay.
    Interpretation and limitations
    Inspect connections and insertion site, attempt aspiration only when appropriate, review pressure waveform and procedure events, and use bedside thoracic or cardiac ultrasound when it can identify pneumothorax, haemothorax or tamponade.
  2. 02
    Chest radiography or targeted fluoroscopic imaging
    Why
    Assess catheter course, tip position and thoracic complication when confirmation is required.
    Interpretation and limitations
    An unexpected course or tip prompts cessation of use and specialist review; a normal radiograph does not exclude vascular injury, small pneumothorax or catheter-related thrombosis.
  3. 03
    Vascular ultrasound and cross-sectional imaging
    Why
    Define accessible-vessel thrombosis, haematoma or arterial injury and investigate deeper central obstruction.
    Interpretation and limitations
    Duplex is useful for neck and limb vessels; CT angiography defines arterial injury or active bleeding, while CT venography or contrast venography may be required for central venous stenosis.
  4. 04
    Blood cultures and infection assessment
    Why
    Confirm bloodstream infection, identify the organism and search for complications or another source.
    Interpretation and limitations
    Obtain paired appropriate cultures before antibiotics when this causes no dangerous delay; persistent S. aureus bacteraemia requires evaluation for metastatic infection and endocarditis with specialist input.
  5. 05
    Catheter function and dialysis adequacy review
    Why
    Separate transient positional flow limitation from persistent catheter dysfunction.
    Interpretation and limitations
    Record aspiration, achieved blood flow and pressure alarms; persistent inability to deliver approximately 300 mL/min in an adult dialysis catheter supports dysfunction and an access plan rather than repeated temporary manoeuvres.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
01

Pulmonary embolism

Sudden dyspnoea and hypoxaemia may reflect catheter-related thrombosis with embolisation rather than pneumothorax, especially when thoracic imaging shows no pleural air.

02

Infusion reaction

Rigors or hypotension during catheter use may be drug or transfusion related, but cultures and line assessment remain necessary because timing also strongly suggests bloodstream infection.

03

Volume or cardiac disease

Facial swelling and dyspnoea may arise from heart failure or fluid overload; collateral veins, unilateral swelling and access dysfunction favour central venous obstruction.

04

Catheter pinch or fracture

Intermittent occlusion with shoulder movement or an abnormal catheter contour suggests compression, fracture or migration rather than simple thrombotic lumen occlusion.

07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Emergency pathwayAcute deterioration during or after insertionFirst stepRespiratory, circulatory or neurological compromise, major bleeding, or suspected large-bore arterial cannulation occurs.
  1. 1Stop catheter use, call the resuscitation and procedural teams, support airway, breathing and circulation, and identify whether air entry, thoracic injury, arterial injury or tamponade best explains the timing.
  2. 2For a catheter or dilator of at least 6 Fr in an artery, leave it in place and obtain urgent vascular or interventional-radiology review for imaging and controlled repair; do not perform blind pull-and-pressure removal.
  3. 3Clamp any open catheter system if air entry is possible, administer high-concentration oxygen and obtain critical-care help; decompress a tension pneumothorax immediately when clinically diagnosed.
  4. 4Document the device, site, number of attempts, guidewire removal, imaging, complication, corrective action and monitoring plan.
02Infection pathwayStable catheter infection assessmentLocal catheter inflammation, bacteraemia or systemic features are present without shock or another immediate mechanical threat.
  1. 1Assess sepsis severity, obtain blood cultures and other indicated samples without delaying antibiotics, examine the exit site and tunnel, and search for another infection source.
  2. 2Treat an isolated exit-site infection without bacteraemia with systemic antibiotics while retaining the dialysis catheter when clinically appropriate; tunnel infection often needs replacement according to severity.
  3. 3AlternativeFor uncomplicated coagulase-negative staphylococcal bacteraemia, initial catheter retention may be considered, but recurrent or severe bacteraemia and S. aureus usually favour exchange or removal with alternative access planning.
  4. 4Confirm culture clearance and assess for endocarditis, septic thrombosis or metastatic infection when organism, symptoms or persistence requires it.
03Dysfunction pathwayPoor aspiration or inadequate catheter flowThe catheter cannot be used safely or delivers inadequate flow without systemic instability.
  1. 1Check clamps, connections, patient position and catheter course; do not force flushing, and treat a newly inserted non-functioning line as possible malposition or kink.
  2. 2For dialysis-catheter late dysfunction, use a lumen-volume thrombolytic lock under the renal unit protocol; if ineffective, replace the catheter, usually by guidewire exchange where fibrin-sheath disruption is available.
  3. 3If arm or neck swelling or recurrent dysfunction suggests thrombosis or central stenosis, obtain appropriate venous imaging and involve vascular-access and renal teams.
  4. 4Reassess ongoing catheter need and protect future access sites rather than repeatedly replacing a poorly planned device.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
01

Haemorrhage and stroke

Arterial injury can produce expanding haematoma, airway obstruction, dissection, embolisation, pseudoaneurysm, major blood loss or cerebral ischaemia.

02

Sepsis and metastatic infection

Catheter bacteraemia can progress to shock, endocarditis, septic thrombosis, vertebral infection or other distant foci, particularly with persistent S. aureus.

03

Loss of venous access

Thrombosis and central stenosis may prevent future catheter placement or fistula drainage, creating long-term dialysis-access failure.

04

Device embolisation

Catheter or guidewire fracture and retained components can embolise to the heart or pulmonary circulation, requiring urgent image-guided or surgical retrieval.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.
  • Record oxygen saturation, respiratory pattern, blood pressure, neurological status and neck or chest swelling after a suspected mechanical event; repeat imaging if symptoms evolve.
  • Review every catheter daily for necessity, function, dressing integrity, exit-site inflammation and systemic infection; remove devices that are no longer required.
  • After bloodstream infection, monitor temperature, haemodynamics and microbiological clearance, and actively look for endocarditis, septic thrombosis or distant seeding when indicated.
  • During treatment of catheter-related thrombosis, monitor bleeding, limb swelling, catheter function and signs of pulmonary embolism; reassess whether the line still meets retention criteria.
  • For dialysis catheters, trend delivered blood flow and dialysis adequacy rather than normalising repeated alarms or lumen reversal as a durable solution.
10Special situationsVariants, exceptions and circumstances that change the usual approach.

Large arterial devices provide their own tamponade

Immediate removal sacrifices temporary control of the arterial defect. Size, site, compressibility, anticoagulation and neurological consequences determine whether open, endovascular or percutaneous closure is safest.

A normal exit site does not exclude bacteraemia

Catheter-related bloodstream infection often presents through systemic physiology during use. Local exit-site appearance classifies one component but cannot rule out intraluminal colonisation or haematogenous complications.

Air embolism is preventable

Secure connections, clamp lumens, use appropriate patient positioning and an occlusive removal technique. Sudden symptoms during disconnection or removal should be treated as air entry until another cause is established.

Preserve veins in chronic kidney disease

PICC-associated thrombosis and central instrumentation can eliminate future fistula options. Discuss access planning early with the kidney team rather than treating every available vein as interchangeable.

Do not treat an image alone

Asymptomatic central venous stenosis with functioning dialysis access is managed conservatively under UKKA guidance; symptoms and access dysfunction, not radiological narrowing alone, drive intervention.

11Common pitfallsFrequent interpretation and management errors.
  1. 01

    Blindly removing a large-bore arterial catheter converts a controlled procedural injury into uncontrolled haemorrhage or stroke risk.

  2. 02

    Forcing a flush through a resistant catheter can worsen extravasation, dislodge thrombus or conceal malposition.

  3. 03

    Calling rigors with a normal exit site “not line infection” misses the common presentation of catheter-related bacteraemia.

  4. 04

    Repeated lumen reversal may complete dialysis temporarily but does not correct thrombus, fibrin sheath or malposition.

  5. 05

    Replacing central lines without considering future dialysis access can create avoidable bilateral central venous stenosis.

Practice

Two practice questions

Question 1 of 20 correct
Vascular surgeryOriginal SBA

Large-bore arterial cannulation

During attempted internal-jugular central access, a 7 Fr dilator and catheter are inadvertently advanced into the carotid artery. The patient is currently stable. What is the safest next action?

Sources and review status3 sources · checked 13 Sept 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 13 Sept 2026; clinical approval remains outstanding.

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom