Carcinoma of the Tongue

Anatomy Relevant to Tongue Cancer

• Oral tongue (anterior 2/3): The freely mobile portion, demarcated posteriorly by the circumvallate papillae (ICD-10 C02). Subdivided into tip, dorsum, lateral borders, and ventral surface.
• Base of tongue (posterior 1/3): Part of the oropharynx; generally presents at a later stage.

• Motor: Hypoglossal nerve (CN XII) - all muscles except palatoglossus (vagus, CN X)
• Sensation: Lingual nerve (branch of V3)
• Taste (anterior 2/3): Chorda tympani branch of CN VII

Epidemiology

• Oral tongue is the second most common site of oral cancer (30% of cases); in non-tobacco-chewing populations it accounts for 22-39% of oral cancers.
• Site distribution: Most tumors arise in the middle third, predominantly on the lateral border, followed by the ventral surface. Only 4-5% occur on the dorsum.
• Age: Usually presents in the 6th-8th decade; 90% of patients are over 40.
• Sex: Slightly more common in males; the male-to-female ratio has narrowed with increasing alcohol use in women.
• Risk factors: Tobacco (smoking and chewing), alcohol, immunosuppression, and possibly poor oral hygiene. Up to 70% of patients report significant tobacco and alcohol use.
• Emerging trend: Incidence in young adults (<40 years) has been increasing (from 4% in 1971 to 18% by the 1990s in the USA), often without identifiable risk factors - increased genetic susceptibility is postulated.

Clinical Presentation

Early Disease

• Erythroplakia (red inflammatory lesion) is the most common presentation of early SCC.
• Asymptomatic ulcer, lump, or persistent white patch on the lateral tongue.
• Most oral tongue cancers present at Stage I or II (unlike base of tongue tumors, which typically present at Stage III/IV).

Late/Advanced Disease

• Pain (may radiate to the ear via the lingual/auriculotemporal nerves)
• Ulceration with raised, rolled, indurated margins
• Tongue fixation (invasion of intrinsic/extrinsic muscles)
• Decreased tongue sensation
• Alteration in speech (dysarthria) and swallowing (dysphagia)
• Trismus (masseter/pterygoid involvement)
• Cervical lymphadenopathy

Cervical Metastases

• Clinically positive nodes at presentation: 21-34%
• Occult cervical metastasis: up to 53%
• Contralateral occult disease: up to 4.5%
• Tumors on the midline dorsum or ventral surface carry a greater risk of bilateral cervical node metastases
• Primary nodal drainage: upper jugular nodes (73%), submandibular (18%), middle jugular (18%), submental (9%)

Key prognostic factor: Depth of tumor invasion >2-4 mm significantly increases the risk of regional metastasis, recurrence, and mortality.

Clinical Images

Histopathology

• Vast majority are Squamous Cell Carcinoma (SCC).
• Most tongue tumors are well-to-moderately differentiated.
• Features that worsen prognosis: perineural invasion, lymphovascular invasion, positive/dysplastic margins, and advancing tumor thickness.
• Multifactorial histological malignancy grading of the invasive front helps assess cervical metastasis risk.

Staging (TNM - AJCC 8th Edition)

• Depth of Invasion (DOI) was incorporated into AJCC 8th edition staging (not just tumor size), reflecting its major prognostic importance.

Workup / Investigations

• Biopsy: Most lesions are amenable to office biopsy; should include deep margin and peripheral mucosa. Deep biopsies provide tumor thickness information.
• Intraoral ultrasonography: Accurately assesses tumor thickness and aids in determining neck management.
• CT/MRI neck: To assess lymph node involvement (though sensitivity is moderate). MRI is preferred for soft tissue extent; CT for bone invasion.
• PET-CT: For advanced disease or suspected distant metastases.
• Chest imaging: To rule out pulmonary metastases and synchronous lung primaries.
• Panendoscopy: To assess for synchronous primary tumors.

Treatment

Primary Site Management

• Partial glossectomy with 1 cm margins in three dimensions is the treatment of choice.
• Reconstruction by primary closure, secondary intention, or skin graft.
• For patients unsuitable for surgery: external beam radiation ± brachytherapy.
• Ultrasonography can aid intraoperative margin assessment, particularly for the deep margin.

• Near-total or total glossectomy may be necessary.
• Glossectomy carries significant morbidity: dysphagia, aspiration; may require laryngectomy in select cases.
• For T4 with bone involvement: surgical resection ± composite resection (marginal or segmental mandibulectomy).
• Marginal mandibulectomy: For periosteal involvement.
• Segmental mandibulectomy: For medullary bone invasion (especially in edentulous patients with reduced bone stock).
• For T4: chemoradiation may be considered if surgery is not feasible.

Management of the Neck

• Selective neck dissection (supraomohyoid): levels I-III minimum.
• Elective neck dissection (END) should include levels I-IV because of skip metastases.
• Bilateral neck dissections for midline tongue cancers.
• Sentinel lymph node biopsy (SLNB): Validated as feasible and accurate for T1-T2 N0 oral cavity cancers.

Adjuvant Therapy

• Post-operative radiotherapy (PORT): Indicated for positive margins, perineural invasion, lymphovascular invasion, multiple positive nodes, or extracapsular spread (ECS).
• Concurrent chemoradiotherapy (cisplatin-based): For ECS or positive margins.

Prognosis

• pN- (node negative): 5-year OS ~75%
• pN+/ECS- (node positive, no extracapsular spread): 5-year OS ~50%
• pN+/ECS+ (extracapsular spread): 5-year OS ~30%

• Tumor thickness >9 mm (5-year survival 66% vs. 100% for <3 mm)
• Perineural invasion
• Positive or dysplastic resection margins
• Cervical metastasis
• Young patients (<40 years) with tongue cancer paradoxically have a poorer long-term prognosis

Base of Tongue Carcinoma

• More commonly associated with HPV (especially p16-positive oropharyngeal SCC)
• Typically presents at Stage III/IV (later presentation)
• Often silent until advanced - first sign may be neck mass
• Management: primary chemoradiation or surgery (transoral robotic surgery, TORS)
• Better prognosis in HPV-positive cases

Key Points Summary

• Most common site: lateral border of the middle third of the oral tongue
• Erythroplakia is the earliest visible sign
• Depth of invasion is the single most important factor for neck management and prognosis
• Most oral tongue cancers present at Stage I/II - early detection is achievable
• Elective neck dissection (levels I-IV) is preferred even for clinically N0 necks when DOI >4 mm
• ECS (extracapsular spread) is a major adverse prognostic factor that mandates adjuvant chemoradiation
• Reconstruction after glossectomy must maximize residual tongue function

Umbilical Hernia

Definition

Embryology and Anatomy

• The fascial margins of the umbilical defect form by the 3rd week of gestation.
• In the 6th week, the intestinal tract migrates outside the coelom through the umbilicus (physiological herniation); it returns at the 10th week as the midgut undergoes rotation.
• After this, the four folds of the somatopleure fuse inward, forming the tight umbilical ring that allows passage of only the umbilical vessels.
• At birth, ligation of the cord causes thrombosis of the umbilical arteries and vein, and the umbilical aperture closes.
• Any defect in this closure process results in an umbilical hernia.

Classification

1. Exomphalos (Omphalocele)

2. Congenital Umbilical Hernia (in infants)

• Comes out through the centre of a congenital weak umbilical scar.
• Appears within the first few months of birth.
• Higher incidence in premature babies and Black infants (up to 8x higher than White infants).
• Incidence: up to 10-30% of newborns in general; higher in premature infants.
• The neck is generally wide - strangulation is extremely uncommon below age 3.
• Swelling is easily reducible; increases in size on crying (classic conical shape); impulse on coughing.
• About 90-95% resolve spontaneously within the first 5 years as the umbilical scar thickens and contracts.

3. Acquired Umbilical Hernia (true umbilical hernia in adults)

• Protrudes directly through the umbilical scar in adult life.
• Relatively rare compared to paraumbilical hernia.
• Due to raised intra-abdominal pressure forcing through the umbilical scar.
• Causes: pregnancy, ascites, bowel distension, large ovarian cysts, fibroids.

4. Paraumbilical Hernia (most common acquired type)

• Occurs through a defect adjacent to (usually just above) the umbilicus, in the linea alba between the two recti.
• The lower half of the sac fundus is covered by the umbilicus.
• Affects middle-aged to older, obese women predominantly; female:male ratio ~3:1.
• Common symptoms: pain, swelling, discomfort.
• Many are irreducible when contents (omentum or bowel) become adherent to the sac.
• Due to the firm, fibrous, narrow neck - prone to incarceration and obstruction (though strangulation is less common than incarceration).

Clinical Features

• Soft bulge at or adjacent to the umbilicus, often to one side, creating a crescent-shaped appearance.
• Usually reducible; the fascial defect can be palpated on reduction.
• Pain due to tissue tension or intermittent bowel obstruction.
• In large hernias, overlying skin becomes very thin; rarely, skin ulceration may occur; spontaneous rupture is extremely rare.
• Small hernias may contain only extraperitoneal fat or omentum (firm to palpation).
• Larger hernias may contain small or large bowel (soft, resonant on percussion).

• Abdominal wall varices (in portal hypertension/cirrhosis)
• Umbilical granuloma
• Sister Mary Joseph's nodule - metastatic tumor implant at the umbilicus (must be excluded in any atypical presentation)
• Urachal cyst or patent urachus (usually presents below the umbilicus)

Predisposing Conditions

Complications

• Incarceration (contents cannot be reduced) - common due to narrow fibrous neck
• Obstruction - intermittent or acute
• Strangulation - vascular compromise; may occur in one loculus of a multiloculated sac while other areas appear soft and non-tender
• Skin necrosis and ulceration - in very large hernias with thin overlying skin
• Rupture - extremely rare

The narrow neck relative to sac size makes adult umbilical hernias more prone to incarceration and strangulation than congenital ones in children.

Treatment

Children

• Small curvilinear "smile" incision just inferior to the umbilicus.
• Sac dissected free, contents reduced or inverted.
• Fascial defect closed transversely with interrupted slowly absorbable or permanent sutures.
• Skin closed subcuticularly; umbilical skin tacked to fascia.
• Day-surgery procedure under general anaesthesia; recurrence is rare.

Adults

• Hernia containing bowel (high strangulation risk - surgery advised)
• Symptomatic hernias (pain, obstruction)
• Enlarging hernias
• Small asymptomatic hernias may be observed, but tend to enlarge with time

• Repair is associated with significantly increased morbidity and mortality (haemodynamic instability, infection, electrolyte disturbance, high recurrence).
• Reserved for progressive symptoms or incarceration.
• Ascites should be controlled (medically or with transjugular intrahepatic portosystemic shunt) before elective repair.

Surgical Repair Techniques (Adults)

Open Repair

• Simple suture repair (0 polypropylene or nylon, interrupted) - as long as fascia is not closed under tension.
• "Darn" technique: non-absorbable monofilament suture criss-crossed across the defect.

• Transverse incision below the umbilicus.
• Sac dissected, opened, contents reduced, peritoneum closed.
• Defect extended transversely; fascial edges approximated with interrupted non-absorbable sutures.

• Mesh placement reduces recurrence (recommended by current guidelines for defects >1-2 cm).
• Onlay mesh: placed on the anterior surface of the closed defect.
• Sublay/retromuscular mesh (Rives-Stoppa principle): placed posterior to the rectus, superior to the posterior sheath - preferred for lower recurrence.
• Intraperitoneal onlay mesh (IPOM): used in laparoscopic repair.

• The classic overlapping fascial repair described in 1901.
• Transverse elliptical incision; upper flap sutured over lower flap in overlapping fashion.
• Now less commonly used as overlapping closures have been shown to weaken overall wound strength compared to mesh repair.

Laparoscopic Repair

• Indicated for larger defects and recurrent hernias.
• IPOM (intraperitoneal onlay mesh) is most common laparoscopic approach.
• The bulky falciform ligament must be taken down to create a smooth surface for mesh placement.
• Comparable or better outcomes vs. open for larger defects.

Emergency Repair

• Most performed by open surgery.
• In the presence of established strangulation: mesh should be avoided (high infection risk).
• Priority is to deal with the strangulated tissue (resect if necessary) and perform a suture repair.
• A more definitive mesh repair can be performed electively at a later date if needed.

Mesh vs. Suture - Current Evidence

Summary / Key Points

Gangrene, Necrosis, Dead Tissue, Near-Dead Tissue, and Ischemia: Proper Relations and Definitions

ISCHEMIA (reduced blood flow)
    ↓
HYPOXIA (reduced oxygen delivery to cells)
    ↓
REVERSIBLE CELL INJURY ("near-dead tissue")
    ↓  [point of no return]
IRREVERSIBLE CELL INJURY → NECROSIS (dead tissue at cell level)
    ↓  [when necrosis involves macroscopic tissue portions]
GANGRENE (a clinical/macroscopic form of necrosis, usually with specific context)

1. Ischemia

• It is the upstream cause - the initial insult - in the chain leading to necrosis and gangrene.
• Ischemia is distinct from simple hypoxia: in hypoxia, only oxygen is reduced (e.g., high altitude, anaemia), while metabolites are still washed away. In ischemia, both oxygen delivery and waste removal are impaired, making ischemia more damaging.
• Caused by: arterial thrombosis, embolism, atherosclerotic occlusion, external compression, vasospasm, prolonged hypotension.
• Consequences depend on duration and severity:
  • Brief ischemia → reversible injury (stunning)
  • Prolonged ischemia → irreversible injury → necrosis
  • Restoration of blood flow after ischemia can paradoxically worsen injury: ischemia-reperfusion injury (mediated by reactive oxygen species, calcium overload, and inflammation).

1. Oxygen falls → mitochondrial oxidative phosphorylation fails → ATP depletion
2. Loss of ATP → failure of Na⁺/K⁺-ATPase pump → cell swelling (reversible stage)
3. Anaerobic glycolysis → lactic acidosis, pH falls
4. Ca²⁺ influx → activates destructive enzymes (phospholipases, proteases, endonucleases)
5. Membrane phospholipid degradation → plasma membrane rupture → irreversible

2. Reversible Cell Injury ("Near-Dead Tissue")

• The cell is alive but impaired - this is "near-dead tissue."
• Morphology: cell swelling (oncosis), organelle swelling (mitochondria, ER), membrane blebbing, fatty change (in hepatocytes), reduced ATP, reduced pH.
• The cell membrane remains intact - this is the key difference from irreversible injury.
• Clinically this corresponds to a tissue that is viable but at risk: pale, cold, painful, not yet infarcted.

1. Inability to reverse mitochondrial dysfunction - failure of oxidative phosphorylation and ATP generation persists even if the original injury is corrected.
2. Profound disturbances in membrane function - irreversible damage to lysosomal membranes leads to enzymatic dissolution of the cell.

3. Necrosis (Dead Tissue at the Cellular Level)

• Necrosis is a passive, chaotic, unregulated process - "messy and destructive."
• It is the microscopic/cellular-level term for dead tissue.
• The inflammatory response it triggers is the key clinical feature - swelling, redness, pain around necrotic tissue.

Morphological Patterns of Necrosis

Nuclear Changes in Necrosis (histological hallmarks)

• Karyolysis - basophilia of chromatin fades (loss of DNA by enzymatic degradation)
• Pyknosis - nuclear shrinkage with increased basophilia (condensed, shrunken nucleus)
• Karyorrhexis - fragmentation of the pyknotic nucleus
• After 1-2 days, nucleus disappears completely.

Necrosis vs. Apoptosis

4. Gangrene (Dead Tissue at the Macroscopic/Clinical Level)

• Gangrene is not a distinct pattern of cell death (Robbins) - it is a clinical/macroscopic term that describes what happens when coagulative necrosis (or coagulative + liquefactive in wet gangrene) involves a large volume of tissue, typically a limb.
• It represents the same process as necrosis but at a gross, visible scale.
• Usually affects the most distal part of a limb (poor collateral circulation): toes, feet, fingers.
• The black discoloration is not simply a colour of dead tissue - it is specifically from haemoglobin breakdown → iron sulphide formation.

Types of Gangrene

Dry Gangrene

• Mechanism: Gradual, slow reduction in arterial blood flow (e.g., atherosclerotic occlusion) without infection.
• Tissue state: Desiccated, mummified, shrunken, dry, leathery, black-brown.
• Infection: Absent or minimal.
• Line of demarcation: Clear, well-defined - separates dead tissue from living tissue; granulation tissue forms between the two zones; if proximal blood supply is good, demarcation appears within days and separation occurs neatly.
• Spread: Does not spread proximal; the process is self-limiting.
• Management: Can often be managed conservatively (wait for auto-amputation at demarcation); elective amputation when line is established.

Wet (Moist) Gangrene

• Mechanism: Arterial obstruction plus superimposed bacterial infection and putrefaction.
• Tissue state: Soft, moist, swollen, foul-smelling; partially perfused; retains some turgor.
• Infection: Present - bacteria (often mixed) cause liquefactive digestion superimposed on coagulative necrosis.
• Line of demarcation: Poorly defined or absent - infection spreads into adjacent living tissue, pushing the demarcation more proximally than in dry gangrene.
• Spread: Spreads rapidly proximally if untreated.
• Management: Surgical emergency - urgent debridement or amputation.
• Commonly seen in: diabetic foot, venous gangrene, intestinal ischemia.

Gas Gangrene

• Mechanism: Invasion of anaerobic bacteria (classically Clostridium species, e.g., C. perfringens) into devitalized muscle, releasing exotoxins (histotoxins, lecithinase) and gas (CO₂, H₂) locally and systemically.
• Clinical features: Crepitus on palpation (gas in tissues), rapidly spreading necrosis, systemic toxaemia, extreme toxicity.
• Management: Surgical emergency - immediate wide debridement, amputation, high-dose penicillin, hyperbaric oxygen.

Other Named Gangrenes

• Diabetic gangrene: Wet gangrene in diabetics - due to small vessel disease (microangiopathy), neuropathy (painless trauma), and impaired immunity combined.
• Fournier's gangrene: Rapidly spreading necrotizing fasciitis and gangrene of the perineum and genitalia; polymicrobial synergistic infection.
• Synergistic (Meleney's) gangrene: Progressive bacterial synergistic gangrene of the abdominal wall.
• Intestinal gangrene: Ischemic necrosis of bowel following mesenteric arterial occlusion or strangulated hernia.

Line of Demarcation

• A zone develops between truly viable and dead or dying tissue.
• Granulation tissue forms between the dead and living parts.
• In dry gangrene with adequate proximal blood supply: clear, neat, rapid demarcation.
• In moist gangrene: demarcation is proximal, irregular, and delayed due to infection extending into living tissue.
• If proximal blood supply is poor: line of demarcation is slow to form or absent; gangrene may spread or "skip" areas - skip lesions can appear higher up the limb.
• Bone demarcates more slowly than soft tissue (better blood supply); the stump tends to be conical.

5. Putting It All Together: The Hierarchy

ISCHEMIA
(reduced blood flow - cells alive but stressed)
        ↓ short duration / mild
REVERSIBLE CELL INJURY = "NEAR-DEAD TISSUE"
(cell swollen, ATP depleted, membrane blebbing - but membrane intact, can recover)
        ↓ prolonged / severe - point of no return crossed
IRREVERSIBLE CELL INJURY → NECROSIS
(membrane ruptures, lysosomal enzymes released, inflammation - cell is DEAD)
        ↓ when macroscopic - many cells / tissues involved
INFARCTION
(area of necrosis in an organ caused by ischemia; typically coagulative)
        ↓ when limb involved + blackening + macroscopic putrefaction
GANGRENE
(clinical/macroscopic term; coagulative necrosis ± infection in a limb or part)

Key Conceptual Distinctions

Important Additional Points

• Ischemia does not equal necrosis - ischemia is the cause; necrosis is the outcome if ischemia is not corrected. Reversible ischemia resolves without necrosis.
• Necrosis does not equal gangrene - necrosis is the microscopic event. Gangrene is the gross/clinical manifestation when necrosis involves a large tissue volume in a specific pattern (limb, blackening, putrefaction).
• Gangrenous necrosis is not a separate cellular mechanism - it is coagulative necrosis ± liquefactive (when infected), just in a limb context at macroscopic scale.
• All gangrene involves necrosis, but not all necrosis is gangrene.
• All necrosis involves dead tissue, but dead tissue can arise from causes other than ischemia (infection, toxins, physical injury).
• Ischemia is the most common cause of gangrene and infarction, but gangrene can also follow trauma, cold injury, sepsis, or vasoconstriction.