Author: Rodrigo Arrangoiz MS, MD, FACS, FSSO

• Background and Rationale:
  • Human papillomavirus (HPV)-associated (p16-positive) oropharyngeal squamous cell carcinoma (OPSCC):
    • Is a biologically distinct, prognostically favorable disease compared with HPV-negative disease
  • Historically, patients received definitive chemoradiation or surgery followed by uniform adjuvant chemoradiation:
    • Producing excellent cancer control but substantial long-term toxicity:
      • Dysphagia, xerostomia, fibrosis, osteoradionecrosis
  • The central question of E3311 was:
    • Whether upfront transoral surgery (TOS), by providing accurate surgical pathology:
      • Could be used to stratify patients by recurrence risk and thereby safely de-intensify adjuvant therapy:
        • Reducing radiation dose (or omitting radiation entirely) in lower-risk patients while reserving full-intensity chemoradiation for high-risk pathology
    • A secondary but pivotal aim was:
      • To demonstrate that a multi-institutional cooperative-group transoral surgical trial, with formal surgeon credentialing, was feasible (Ferris et al., Journal of Clinical Oncology, 2022)
  • Study Design:
    • Phase:
      • II, prospective, multi-institutional (ECOG-ACRIN Cancer Research Group):
        • With randomization embedded in the intermediate-risk group
    • Population:
      • Resectable, p16+ OPSCC
      • AJCC 7th edition T1 to T2
      • Clinical stage III / IVa
      • No matted nodes
      • Candidates for transoral resection
    • Surgical quality control:
      • Participating surgeons underwent formal credentialing:
        • To ensure consistent transoral oncologic technique
    • Intervention:
      • All patients underwent primary transoral surgery (robotic or laser) plus neck dissection:
        • Followed by assignment to one of four pathology-based arms (Ferris et al., Journal of Clinical Oncology, 2022)
• Risk Stratification and Treatment Arms

• Key operational definitions used in E3311 (important when comparing with other trials):
  • Positive margin = tumor-on-ink
  • Close margin = < 3 mm (contrast with ORATOR / MC1675, which used > 5 mm as clear)
• Patients in the intermediate-risk group were randomized between 50 Gy (Arm B) and 60 Gy (Arm C)
  • The trial was not powered for a direct head-to-head comparison of B vs. C:
    • Instead each arm was independently compared against a historical efficacy benchmark (Ferris et al., Journal of Clinical Oncology, 2022)
• Primary Results (Ferris et al., Journal of Clinical Oncology, 2022) – see Table 1
  • Interpretation:
    • Among 359 evaluable patients (median follow-up 35.2 months):
      • Approximately 70% of patients were de-intensified relative to standard adjuvant chemoradiation
      • Two-year progression-free survival (PFS) was excellent across all arms, and both intermediate-risk arms cleared the prespecified efficacy boundary (lower limit of the 90% CI > 85%)
        • Both intermediate-dose arms exceeded the historical benchmark:
          • Supporting 50 Gy as an adequate adjuvant dose for intermediate-risk disease
        • Functional and quality-of-life measures (FACT-H&N, MD Anderson Dysphagia Inventory):
          • Favored the reduced-dose approach, reinforcing the clinical value of de-escalation (Ferris et al., Journal of Clinical Oncology, 2022)
• Long-Term Follow-Up (Burtness et al., Journal of Clinical Oncology, 2025): Table 2
  • Mature data at 54 months confirmed durable efficacy across the cohort:
    • Overall 54-month PFS 90.6% and OS 95.3%
  • Key long-term observations (Burtness et al., Journal of Clinical Oncology, 2025):
    • Outcomes did not differ by primary subsite or smoking history
    • Among observed (Arm A) patients:
      • All 4 recurrences occurred in N1 patients:
        • Signaling that patients with N1 disease remain at some risk for late recurrence when radiation is omitted, and warrant careful surveillance or individualized decision-making
• Guideline Integration:
  • NCCN Head and Neck Cancers Guidelines:
    • E3311 is cited to support de-escalation of adjuvant radiotherapy to 50 Gy (category 2B) in p16+ OPSCC with ≤ 4 positive ipsilateral nodes (largest ≤ 6 cm), T1 to T2 resected to negative or close (< 3 mm) margins, and ≤ 1 mm ENE — mirroring the E3311 intermediate-risk criteria (National Comprehensive Cancer Network, Head and Neck Cancers, 2026)
  • ASCO Transoral Robotic Surgery (TORS) Guideline (2025):
    • E3311 is the largest prospective trial underpinning pathology-driven, risk-adapted adjuvant therapy after TORS
    • It supports adding concurrent cisplatin for positive margins (tumor-on-ink) or ENE, and informs the risk-based selection of radiation dose (Holsinger et al., Journal of Clinical Oncology, 2025)
• Contextual Comparisons and Caveats:
  • Definitional heterogeneity:
    • E3311’s 3 mm close-margin and tumor-on-ink positive-margin thresholds differ from other de-escalation trials (e.g., ORATOR, MC1675), which affects cross-trial comparison of toxicity and control
  • Postoperative vs. definitive setting:
    • E3311’s favorable de-escalation outcomes contrast with NRG-HN005, where dose reduction to 60 Gy in the definitive chemoradiation setting did not meet non-inferiority:
      • This suggests the smaller tumor volume of the postoperative setting may better tolerate dose reduction (Ma et al., Lancet Oncology, 2025)
  • Trial scope:
    • Phase II design and lack of power for direct B-vs-C comparison mean 50 Gy and 60 Gy were each validated against a benchmark rather than against each other
• Distinguishing E3311 from E1308:
  • If the trial of interest was E1308 (a separate ECOG-ACRIN study):
    • The trial tested induction chemotherapy (cisplatin / paclitaxel / cetuximab) followed by reduced-dose IMRT (54 Gy) with cetuximab in HPV-associated resectable OPSCC:
      • Among primary-site complete responders, 2-year PFS and OS were 80% and 94%, with improved swallowing at the lower dose (Marur et al., Journal of Clinical Oncology, 2017)
      • E1308 uses an induction / organ-preservation strategy, distinct from E3311’s surgery-first, pathology-guided strategy
• Key Takeaways:
  • E3311 established that upfront transoral surgery can guide risk-based de-intensification of adjuvant therapy in HPV+ OPSCC within a credentialed, multi-institutional framework
  • ~ 70% of patients were safely de-intensified, with excellent 2-year and durable 54-month PFS / OS across all arms
  • 50 Gy is adequate for intermediate-risk pathology:
    • Clear margins, 2 to 4 nodes or ENE ≤ 1 mm)
  • Observation alone yielded outstanding control in low-risk disease:
    • But N1 patients accounted for the Arm A recurrences and merit vigilance
  • E3311 now anchors NCCN (50 Gy, category 2B) and ASCO TORS guidance on adjuvant management after transoral surgery

• Cisplatin is the cornerstone systemic agent in locally advanced head and neck squamous cell carcinoma (HNSCC)
• Concurrent Chemoradiation (Definitive Setting):
  • Standard of care for locally advanced, unresectable HNSCC (or when organ preservation is desired, e.g., larynx, oropharynx).
• High-dose cisplatin: 100 mg/m² IV every 3 weeks × 3 cycles concurrent with radiation therapy.
• Alternative (for toxicity or frailty): weekly low-dose cisplatin (30–40 mg/m²).
• Evidence: Landmark trials (EORTC, RTOG) showed improved overall survival and locoregional control when cisplatin was added to radiation versus radiation alone.

2. Adjuvant (Postoperative) Chemoradiation

• Indicated for high-risk features after surgery:
  • Positive margins
  • Extracapsular nodal extension
• High-dose cisplatin concurrent with adjuvant radiation reduces recurrence and improves survival (EORTC 22931, RTOG 9501).

3. Palliative / Metastatic Disease

• Cisplatin combined with 5-FU or taxanes, historically standard in recurrent/metastatic disease.
• More recently, cisplatin used in combination with immune checkpoint inhibitors (e.g., pembrolizumab, nivolumab) in first-line regimens (KEYNOTE-048).

Key Points for Clinical Use

• Highly emetogenic → requires aggressive antiemetic prophylaxis (NK1 antagonist + 5HT3 antagonist + dexamethasone).
• Toxicities: nephrotoxicity, ototoxicity, neurotoxicity, myelosuppression.
• Alternative for cisplatin-ineligible patients: carboplatin ± 5-FU, or immunotherapy-based regimens.

✅ Summary: Cisplatin exerts its anti-cancer effects by forming DNA crosslinks that trigger apoptosis. In head and neck cancer, it is the backbone of definitive chemoradiation, adjuvant chemoradiation for high-risk patients, and palliative regimens. High-dose cisplatin remains the gold standard for fit patients, with weekly dosing or alternative agents reserved for those with comorbidities.

Would you like me to also prepare a slide-ready summary table comparing cisplatin 100 mg/m² q3w vs 40 mg/m² weekly in head and neck chemoradiation (efficacy, toxicity, compliance)? That’s a common journal club/board question.

You said:

mechanism of acton

ChatGPT said:

Here’s a clear explanation of the mechanism of action of cisplatin (the essence, without the broader oncology indications):

Mechanism of Action of Cisplatin

1. Cell Entry
   • Cisplatin enters tumor cells by passive diffusion and through membrane transporters (notably copper transporters such as CTR1).
2. Activation (Aquation)
   • In the bloodstream, cisplatin is relatively stable because of high chloride concentrations.
   • Once inside the cell (where chloride concentration is lower), cisplatin undergoes aquation: its chloride ligands are replaced by water molecules, creating a highly reactive, positively charged complex.
3. DNA Interaction
   • The activated cisplatin binds strongly to guanine and adenine bases in DNA.
   • It forms:
     • Intrastrand crosslinks (most common: between adjacent guanines or guanine–adenine)
     • Interstrand crosslinks
     • DNA–protein crosslinks
4. Cellular Consequences
   • These DNA adducts distort the double helix, blocking replication and transcription.
   • DNA damage response pathways are activated (p53-dependent and independent).
   • When repair is unsuccessful, this leads to cell-cycle arrest and apoptosis (programmed cell death).
5. Other Effects
   • Cisplatin can also interact with RNA and proteins, contributing to its cytotoxicity.
   • Oxidative stress and mitochondrial dysfunction also play a role in cell death.

✅ In short: Cisplatin kills cancer cells by forming DNA crosslinks that prevent proper replication and transcription, ultimately triggering apoptosis.

Cisplatin is the cornerstone systemic agent in locally advanced head and neck squamous cell carcinoma (HNSCC).

1. Concurrent Chemoradiation (Definitive Setting)

• Standard of care for locally advanced, unresectable HNSCC (or when organ preservation is desired, e.g., larynx, oropharynx).
• High-dose cisplatin: 100 mg/m² IV every 3 weeks × 3 cycles concurrent with radiation therapy.
• Alternative (for toxicity or frailty): weekly low-dose cisplatin (30–40 mg/m²).
• Evidence: Landmark trials (EORTC, RTOG) showed improved overall survival and locoregional control when cisplatin was added to radiation versus radiation alone.

2. Adjuvant (Postoperative) Chemoradiation

• Indicated for high-risk features after surgery:
  • Positive margins
  • Extracapsular nodal extension
• High-dose cisplatin concurrent with adjuvant radiation reduces recurrence and improves survival (EORTC 22931, RTOG 9501).

3. Palliative / Metastatic Disease

• Cisplatin combined with 5-FU or taxanes, historically standard in recurrent/metastatic disease.
• More recently, cisplatin used in combination with immune checkpoint inhibitors (e.g., pembrolizumab, nivolumab) in first-line regimens (KEYNOTE-048).

Key Points for Clinical Use

• Highly emetogenic → requires aggressive antiemetic prophylaxis (NK1 antagonist + 5HT3 antagonist + dexamethasone).
• Toxicities: nephrotoxicity, ototoxicity, neurotoxicity, myelosuppression.
• Alternative for cisplatin-ineligible patients: carboplatin ± 5-FU, or immunotherapy-based regimens.

✅ Summary: Cisplatin exerts its anti-cancer effects by forming DNA crosslinks that trigger apoptosis. In head and neck cancer, it is the backbone of definitive chemoradiation, adjuvant chemoradiation for high-risk patients, and palliative regimens. High-dose cisplatin remains the gold standard for fit patients, with weekly dosing or alternative agents reserved for those with comorbidities.

Would you like me to also prepare a slide-ready summary table comparing cisplatin 100 mg/m² q3w vs 40 mg/m² weekly in head and neck chemoradiation (efficacy, toxicity, compliance)? That’s a common journal club/board question.

You said:

mechanism of acton

ChatGPT said:

Here’s a clear explanation of the mechanism of action of cisplatin (the essence, without the broader oncology indications):

Mechanism of Action of Cisplatin

1. Cell Entry
   • Cisplatin enters tumor cells by passive diffusion and through membrane transporters (notably copper transporters such as CTR1).
2. Activation (Aquation)
   • In the bloodstream, cisplatin is relatively stable because of high chloride concentrations.
   • Once inside the cell (where chloride concentration is lower), cisplatin undergoes aquation: its chloride ligands are replaced by water molecules, creating a highly reactive, positively charged complex.
3. DNA Interaction
   • The activated cisplatin binds strongly to guanine and adenine bases in DNA.
   • It forms:
     • Intrastrand crosslinks (most common: between adjacent guanines or guanine–adenine)
     • Interstrand crosslinks
     • DNA–protein crosslinks
4. Cellular Consequences
   • These DNA adducts distort the double helix, blocking replication and transcription.
   • DNA damage response pathways are activated (p53-dependent and independent).
   • When repair is unsuccessful, this leads to cell-cycle arrest and apoptosis (programmed cell death).
5. Other Effects
   • Cisplatin can also interact with RNA and proteins, contributing to its cytotoxicity.
   • Oxidative stress and mitochondrial dysfunction also play a role in cell death.

✅ In short: Cisplatin kills cancer cells by forming DNA crosslinks that prevent proper replication and transcription, ultimately triggering apoptosis.

• The adverse prognostic significance of tumor extension beyond the thyroid has been recognized for decades:
  • Remarkably, local tumor extent or invasion appears repeatedly in nearly every major historical prognostic system developed for DTC:
    • Despite these systems originating independently at different institutions and during different eras
• These observations established the principle that ETE is not simply an anatomic descriptor:
  • But a marker of more aggressive thyroid cancer biology

• Locally advanced differentiated thyroid cancer (DTC) refers primarily to:
  • Gross macroscopic extension beyond the thyroid gland into adjacent cervical structures, including the:
    • Strap muscles, recurrent laryngeal nerve (RLN), larynx, trachea, pharynx or esophagus, subcutaneous soft tissues, prevertebral fascia, or major cervical and mediastinal vessels
  • Among these structures, the strap muscles and RLN are most frequently involved, followed by the trachea, laryngotracheal junction, pharyngoesophageal tract, and major vessels
• The clinical significance of ETE, however, is heterogeneous and is strongly influenced by the:
  • Extent of invasion
  • The specific structure involved
  • The presence of regional or distant metastatic disease
  • Tumor biology
  • The ability to achieve complete gross resection (Figure)
     

https://www.instagram.com/p/Ddl5vk-F8LI/?img_index=7&stkn=bDRhbjdsOWJvcnk1

Why Not All Thyroid Cancers Need Aggressive Treatment

Not all thyroid cancers behave the same. Modern care is personalized—the goal is to treat what matters while avoiding unnecessary treatment.

🧠 The key concept: Risk-adapted management

Many thyroid cancers—especially low-risk papillary thyroid cancers—are:

Slow-growing Unlikely to spread Associated with excellent long-term survival

Because of this, more treatment is not always better.

⚖️ Treatment options today

Depending on risk, options may include:

Active surveillance (careful ultrasound follow-up, no immediate surgery) Thyroid lobectomy instead of total thyroidectomy Selective use of radioactive iodine (not routine for everyone)

➡️ These approaches are evidence-based and safe for appropriately selected patients.

📉 Why avoid overtreatment?

Unnecessary aggressive treatment can:

Increase risk of hypocalcemia and voice changes Require lifelong thyroid hormone replacement Affect quality of life without improving outcomes

🦋 What matters most

Treatment decisions should be guided by:

✔️ Tumor size and ultrasound features

✔️ Pathology and risk of recurrence

✔️ Patient age, preferences, and values

✔️ Expertise of a multidisciplinary thyroid team

👨‍⚕️ Dr. Rodrigo Arrangoiz, MD

Surgical Oncologist – Thyroid, Head & Neck, Breast

Mount Sinai Medical Center

📌 Take-home message:

The best thyroid cancer treatment is the right treatment for the right patient—not the most aggressive one.

📚 References

Haugen BR et al. ATA Guidelines for Differentiated Thyroid Cancer. Thyroid Tuttle RM et al. Active surveillance for low-risk papillary thyroid cancer. JAMA Brito JP et al. Overdiagnosis and overtreatment of thyroid cancer. BMJ

Summary

Lobectomy may be considered in select patients with sporadic medullary thyroid cancer (MTC), though total thyroidectomy with central neck dissection remains the standard of care. The evidence base is evolving, with growing data supporting comparable oncologic outcomes for carefully selected patients.

Guideline Recommendations

The NCCN Thyroid Carcinoma Guidelines (v2.2026) recommend total thyroidectomy with central neck dissection (level VI) as the standard primary treatment for MTC. However, the guidelines now explicitly state that “lobectomy can be considered in select cases without RET pathogenic variant if no concerns for contralateral nodules.” This represents a notable shift toward acknowledging lobectomy as an option.

For MTC diagnosed after initial thyroid surgery (e.g., lobectomy), the NCCN notes that completion thyroidectomy may not be necessary unless there is a positive germline RET pathogenic variant or radiographic evidence of disease (biopsy-proven residual neck disease).

The ATA Guidelines similarly state that completion thyroidectomy following hemithyroidectomy is not indicated unless the patient has a RET germline mutation, significant postoperative calcitonin elevation, or imaging showing residual MTC. In a prospective study of 15 patients with sporadic MTC treated by hemithyroidectomy, 80% achieved biochemical cure.

Hereditary MTC (MEN2A/MEN2B) remains a strict indication for total thyroidectomy, as the likelihood of bilateral disease approaches 100%.

Key Evidence Supporting Lobectomy in Sporadic MTC

A 2026 systematic review and meta-analysis in JAMA Otolaryngology (9 studies, 1,371 patients) found that lobectomy was associated with comparable oncologic outcomes to total thyroidectomy in selected patients with sporadic MTC:

– Mortality: No difference at 5 years (RR 0.30; 95% CI 0.07–1.35) or beyond (RR 1.00; 95% CI 0.40–2.47)

– Overall survival at 5 years: Similar (RR 1.02; 95% CI 0.94–1.11)

– Biochemical cure: No difference at 5 or beyond 5 years

– Structural recurrence at 5 years: No difference (OR 0.45; 95% CI 0.14–1.49), though total thyroidectomy was associated with lower recurrence beyond 5 years (OR 7.26; 95% CI 1.07–49.21) — a finding with very wide confidence intervals

– Postoperative complications: More common with total thyroidectomy

Multiple SEER-based analyses corroborate these findings:

– A propensity-matched study (122 pairs, median follow-up 99 months) showed no significant difference in 10-year overall survival (85.2% vs. 83.1%) or disease-specific survival between total thyroidectomy and lobectomy for localized MTC.

– Another SEER analysis of T1N0/1M0 MTC (398 patients, median follow-up 8.75 years) found no survival difference between approaches (cancer-specific mortality HR 0.44, p = 0.23).

– A 2025 SEER analysis with Chinese cohort validation confirmed no survival difference and demonstrated significantly more adverse events with total thyroidectomy, including transient hypocalcemia (p < 0.001) and vocal cord paralysis (p < 0.025).

Occult Contralateral Disease

A key concern with lobectomy is missing contralateral foci. A multi-institutional JAMA Otolaryngology study found that the prevalence of sonographically occult contralateral disease in sporadic MTC was only 5.0%, with a 95.7% reduction in odds compared to germline disease (adjusted OR 0.034). Among patients who underwent lobectomy alone, 41.7% achieved undetectable calcitonin levels. A 2026 European study found zero cases of occult contralateral disease in 48 patients with sporadic MTC when high-quality preoperative ultrasound was available.

Patient Selection Criteria for Lobectomy

Based on the available evidence, lobectomy with ipsilateral central neck dissection may be appropriate when all of the following are met:

– Sporadic disease (no germline RET pathogenic variant)

– Unifocal tumor confined to one lobe with no contralateral nodules on ultrasound

– Clinically node-negative (cN0) with preoperative calcitonin ≤250 pg/mL

– No extrathyroidal extension

– Tumor size <2 cm (most studied population)

– Absence of desmoplastic stroma reaction on intraoperative frozen section (if available)

—Important Caveats

Important Caveats

All existing data are retrospective, with inherent selection bias — patients who underwent lobectomy likely had lower-risk disease. The meta-analysis signal of potentially higher structural recurrence beyond 5 years with lobectomy warrants attention, though confidence intervals were very wide. Calcitonin surveillance is more complex after lobectomy, as residual normal C cells may produce low-level calcitonin, complicating interpretation. Prospective randomized trials are needed to definitively establish the safety of lobectomy in this setting.

Key References

– Lincango EP et al. Total Thyroidectomy vs Lobectomy for Sporadic Medullary Thyroid Cancer: A Systematic Review and Meta-Analysis. JAMA Otolaryngol Head Neck Surg. 2026.

– Mao YV et al. Extent of Surgery for Medullary Thyroid Cancer and Prevalence of Occult Contralateral Foci. JAMA Otolaryngol Head Neck Surg. 2024.

– Wells SA et al. Revised American Thyroid Association Guidelines for the Management of Medullary Thyroid Carcinoma. Thyroid. 2015.

– Liang W et al. Total Thyroidectomy vs Thyroid Lobectomy for Localized Medullary Thyroid Cancer in Adults: A Propensity-Matched Survival Analysis. Surgery. 2022.

– Yang J et al. Comparison of Lobectomy vs Total Thyroidectomy for Medullary Thyroid Carcinoma: A SEER Analysis With Chinese Cohort Validation. Oncologist. 2025.

– Spörlein A et al. Is Hemithyroidectomy Enough? Low Risk of Occult Contralateral Disease in Sporadic Medullary Thyroid Cancer. Eur Arch Otorhinolaryngol. 2026.

– Park H et al. Preoperative Identification of Low-Risk Medullary Thyroid Carcinoma: Potential Application to Reduce Total Thyroidectomy. Sci Rep. 2023.

– NCCN Thyroid Carcinoma Guidelines, v2.2026.

Overview

A totally implantable venous access port (TIVAP / port-a-cath) provides reliable long-term central venous access for chemotherapy, parenteral nutrition, blood products, and antibiotics. Overall reported complication rates range from about 2% to 14.4%, and are broadly lower with ultrasound-guided internal jugular vein (IJV) access and standardized protocols (Tabatabaie et al., American Journal of Clinical Oncology, 2017; Camargo et al., Scientific Reports, 2026). Complications are grouped by timing (intraoperative/immediate, early ≤30 days, late >30 days) and by anatomic origin (incision/pocket, catheter, reservoir/port).

Complication Categories and Reported Incidence

Complication Timing Reported incidence Key management Pneumothorax Intraoperative ~0.5–6% (higher with subclavian/landmark technique; ~0 with US + IJV) Observation vs. chest tube depending on size; US guidance largely eliminates risk Hemothorax Intraoperative Rare Drainage/chest tube; vascular repair if arterial laceration Arterial puncture (carotid ~3%, subclavian rarer) Intraoperative ~3% carotid Manual compression; vascular surgery if large-vessel injury Air embolism Intraoperative Rare Trendelenburg/left lateral position, 100% O2, aspiration Cardiac arrhythmia (guidewire/tip) Intraoperative Up to ~9% with tip migration Withdraw guidewire/reposition tip to cavoatrial junction Catheter malposition Early ~0.3% Fluoroscopic/endovascular repositioning (pigtail, gooseneck snare) Hematoma / pocket bleeding Early Low (minor) Compression; evacuation if expanding Wound dehiscence / skin erosion / port extrusion Early–late ~0.6% extrusion Wound care; often requires revision/explantation Infection (pocket, tunnel, exit site, CRBSI) Early–late (most common) ~1.5–5% pocket/site; CRBSI ~0.05–0.9/1000 catheter-days Systemic antibiotics ± antibiotic lock; removal for complicated infection Catheter-related thrombosis / venous stenosis Late Thrombosis ~0.3–28% (series-dependent); venous stenosis ~7% Anticoagulation; thrombolysis or removal in severe cases Catheter occlusion / fibrin sheath Late Variable Thrombolytic instillation (e.g., alteplase); fibrin sheath stripping Catheter fracture / disconnection / embolization Late Rare Endovascular retrieval; surgical revision Port flip / rotation Late Rare (single cases) Manual or surgical repositioning Extravasation Late Rare Stop infusion, aspirate, antidote per agent, surgical consult

Timing Patterns from Recent Cohorts

• Standardized US-guided IJV series (n=175): 100% procedural success, no early complications, 8.0% late complications (all skin ulceration around port/catheter). Concurrent diabetes + hypertension was the only independent risk factor (HR 12.2) (Ma et al., The American Surgeon, 2026).
• >1000 TIVAP series: No intraoperative/perioperative complications; 12% total complications (26.7% early, 73.3% late). Most common were infection (4.7%) and thrombosis (3.6%). Infectious complications carried the highest explantation rates; thrombotic complications were usually managed conservatively (Thiel et al., Langenbeck’s Archives of Surgery, 2022).
• Large oncology cohort (n=1180): 100% technical success; early events mostly minor (pain 24.7%, bruising 9.2%). Late: site cellulitis 3.8%, CRBSI 0.25%, thrombosis 0.25%, port extrusion 0.6% (Tashi et al., Annals of the Academy of Medicine, Singapore, 2024).
• Vascular surgeon image-guided series (n=443): No intraoperative/early complications; 2.0% late (infection, thrombosis, erosion, malfunction) (Kim, Journal of Surgical Research, 2025).
• Infection is both the most frequent and earliest category, with a steep early rise; catheter- and port-related events accrue more gradually (Tsuruta et al., Supportive Care in Cancer, 2020).

Management Principles

Infection

• Systemic antimicrobial therapy is the treatment of choice; device removal is required for complicated infection (tunnel/pocket infection, severe sepsis/septic shock, endocarditis, septic thrombophlebitis, osteomyelitis, hematogenous seeding).
• Infections due to S. aureus or Candida spp. generally warrant removal. Uncomplicated CRBSI not caused by these organisms may be treated conservatively with systemic antibiotics + antibiotic lock therapy.
• Remove if blood cultures remain positive 72 h after starting antibiotics (Lebeaux et al., The Lancet Infectious Diseases, 2014).
• Most guidelines cite ~0.3 infections/1000 catheter-days as an acceptable upper threshold (Walser, Cardiovascular and Interventional Radiology, 2012).

Thrombosis / occlusion

• Mechanical occlusions need cause-specific treatment; thrombotic occlusions usually resolve with thrombolytic instillation (e.g., alteplase).
• Catheter-related thrombosis: anticoagulation for ~6 weeks to a year depending on extent and persistence of risk factors; balance against bleeding/coagulopathy risk. Anticoagulation prophylaxis is not routinely recommended (Baskin et al., Lancet, 2009).
• Preventive measures: correct tip positioning at the cavoatrial junction and infection prevention.

Mechanical (fracture, migration, port flip)

• Endovascular retrieval/repositioning (pigtail catheter, gooseneck snare) under fluoroscopy; surgical revision or replacement for breakage or port separation (Wang et al., Current Medical Research and Opinion, 2025).

Local skin/pocket problems

• Port repositioning to a new pocket may salvage the device in selected local infections, avoiding full re-implantation (Sun et al., European Journal of Medical Research, 2025).

Prevention

• Ultrasound-guided venous puncture and fluoroscopic tip confirmation reduce pneumothorax, arterial injury, and malposition.
• Right IJV access is associated with lower rates of malposition, thrombosis, and pneumothorax than subclavian access.
• Operator experience matters: complication likelihood is roughly halved for operators with ≥50 insertions.
• Strict sterile access technique and standardized maintenance/locking protocols reduce CLABSI and occlusion.

https://www.jscimedcentral.com/journal-article-info/JSM-Head-and-Neck-Cancer-Cases-and-Reviews/oral-cavity-squamous-cell-carcinoma-contemporary-evidence-based-management-and-multidisciplinary-care-12782

I am pleased to share our recent publication:

“Oral Cavity Squamous Cell Carcinoma: Contemporary Evidence-Based Management and Multidisciplinary Care”

In this comprehensive review, Fernando Cordera and I examine the evolving management of oral cavity squamous cell carcinoma (OCSCC), a disease in which surgery remains the cornerstone of treatment, but where optimal outcomes increasingly depend on precise risk stratification and coordinated multidisciplinary care.

Several important concepts emerge from the contemporary evidence:

🔹 Depth of invasion (DOI) matters. DOI has become a critical prognostic variable in oral cavity SCC, influencing T classification, the risk of occult cervical nodal metastasis, and decisions regarding management of the clinically N0 neck.

🔹 The neck must be addressed appropriately. Elective neck treatment remains a fundamental component of management for patients at meaningful risk of occult nodal disease. Sentinel lymph node biopsy is also emerging as an effective alternative to elective neck dissection in appropriately selected early-stage patients and experienced centers.

🔹 Pathology drives postoperative treatment. Margin status, nodal burden, extranodal extension, perineural invasion, lymphovascular invasion, and DOI are central to postoperative risk stratification and decisions regarding adjuvant radiation or chemoradiation.

🔹 Surgery is evolving toward oncologic control with functional preservation. Achieving adequate oncologic resection remains paramount, but contemporary treatment must simultaneously consider speech, swallowing, reconstruction, appearance, and long-term quality of life.

🔹 Immunotherapy is changing the treatment landscape. The KEYNOTE-689 trial represents an important shift in the management of selected patients with locally advanced, resectable head and neck squamous cell carcinoma, demonstrating improved event-free survival with the integration of perioperative pembrolizumab into standard treatment.

Perhaps the most important message is that oral cavity cancer can no longer be approached as surgery alone. Optimal care requires integration of head and neck surgical oncology, reconstructive surgery, radiation oncology, medical oncology, pathology, radiology, dentistry, speech and swallowing rehabilitation, nutrition, psychosocial support, and survivorship care.

Our goal with this review was to bring together the contemporary evidence—from epidemiology, anatomy and staging to surgical management, neck dissection, reconstruction, adjuvant therapy, immunotherapy, surveillance, recurrence, and survivorship—into a practical framework for clinicians treating patients with oral cavity cancer.

Reference:
Arrangoiz R, Cordera F. Oral Cavity Squamous Cell Carcinoma: Contemporary Evidence-Based Management and Multidisciplinary Care. JSM Head Neck Cancer Cases Rev. 2026;6(1):1013.

#OralCancer #HeadAndNeckCancer #HeadAndNeckSurgery #SurgicalOncology #CancerSurgery #OralCavityCancer #SquamousCellCarcinoma #NeckDissection #Immunotherapy #MultidisciplinaryCare #CancerResearch