Pharyngeal carcinoma

Source: OHCS pg 570

• Often advanced at presentation.
• M:F = 5:1.
• Histologically, 85% are squamous.
• Typical pt: Elderly smoker with sore throat, sensation of a lump, referred otalgia, and local irritation by hot and cold foods.
• Risk factors:
  - Chewing or smoking tobacco.
  - Alcohol alone is not a risk factor but is synergistic with smoking.
  - Oral HPV (especially HPV-16) infection.
• 30% of pharyngeal SCCs will have a second primary within 10y.
• 20% are LN positive at presentation.
• Hypopharyngeal tumours may give dysphagia, voice alteration, otalgia, stridor, throat pain; trismus is a late sign.
• Note any sign of premalignant conditions:
  - Leukoplakia.
  - Paterson-Kelly-Brown syndrome (Plummer-Vinson): Pharyngeal web associated with iron deficiency, glossitis, koilonychia: 2% risk post-cricoid ca.
• Imaging: MRI with STIR (short tau inversion recovery), contrast-enhanced CT.
• Rx: Surgery, sometimes with:
  - Jejunal flaps.
  - Tubed skin flaps (e.g. radial forearm or anterolateral thigh flaps).
  - Gastric pull-ups.
• Rx: Radiotherapy (e.g. intensity-modulated) may be used first line if the tumour is small. i.e. T1 (less than 2cm) or T2 (less than 4cm).
• T3 = >4cm, T4 = beyond oropharynx.

Inhalational agents

These are volatile liquids which readily vaporise, permitting administration by inhalation in oxygen-enriched air or an O2/N2O mix.They help maintain anaesthesia and decrease awareness (by an unclear mechanism).

Halothane

A colourless, pleasant-smelling gas (which, unlike the other agents, is not an ether). First used as an anaesthetic in the 1950s. It has little analgesic effect, but decreases cardiac output (vagal tone increased, leading to bradycardia, vasodilation, hypotension. It sensitises the myocardium to catecholamines (beware in patients with arrhythmias and in surgical infiltration with local anaesthetic and adrenaline). Halothane has now been replaced by safer inhalational agents due to the rare but serious complication of post-op hepatitis (uo to 1 in 4,000 for multiple exposures).

Isoflurane

A halogenated ether. Theoretically induction should be quick, but isoflurane is irritant, so coughing, laryngospasm, or breath-holding may complicate the onset of anaesthesia.

Sevoflurane

Well-tolerated halogenated ether. Agent of choice for inhalation induction of general anaesthesia with low blood:gas solubility.

Desflurane

Another halogenated ether with a pungent smell, rapid onset of anaesthesia and quick recovery.

All can cause malignant hyperthermia.

Post-operative N&V

Anaesthesia SE experienced by at least 25% of patients.

Vomiting is initiated in the vomiting centre of the medulla, which itself receives input from higher centres, the chemoreceptor trigger zone (CTZ), afferent somatic and visceral fibres, and the vestibular apparatus of the middle and inner ear. Of these, the CTZ in the area postrema (floor of 4th ventricle) is probably the most important.

Complications:

Dehydration

Electrolyte imbalance

Metabolic imbalance (metabolic alkalosis)

Pulmonary aspiration

Hernia formation

Damage to site of surgery (direct e.g. ENT or indirect e.g. neurosurgery).

Inability to take oral medication.

Delayed discharge.

Risk factors:

• Patient: Female, younger than 16y, Hx, obesity, motion sickness, pre-op anxiety.
• Anaesthetic agents: Opioids, N2O nitrous oxide, etomidate, ketamine.
• Surgery: GI, GU, neurosurgery, middle ear, ophthalmic.
• Post-op: Dehydration, hypotension, hypoxia, early oral intake.

Entiemetics:

• H1: Cyclizine (GI causes), cinnarizine (Vestibular causes).
• D2: Metoclopramide (GI causes, prokinetic), domperidone (prokinetic), prochlorperazine (vestibular/GI causes), haloperidol (chemical causes e.g. opioids).
• 5HT3: Ondansetron - doses can be high e.g. for emetogenic chemotherapy.
• Others:
  • Hyoscine hydrobromide (antimuscarinic therefore also antispasmodic and antisecretory - don't prescribe with a prokinetic).
  • Dexamethasone (unknown mode of action).
  • Midazolam (unknown mode of action; anti-emetic effect outlasts sedative effect).

  
  
  
  

Premedication

• Analgesia: Pre-emptive analgesia aims to dampen the pain pathways before the signals starts to arrive. It is not often used, and effects are hard to determine as few studies are in agreement and there are many variables.
• Antacid: For reflux either ranitidine 150mg PO or omeprazole 40mg PO/IV the night before and then 2h pre-op. Ranitidine reduces both gastric pH and volume. High risk of aspiration in: Emergency surgery, pregnancy, DM, hiatus hernia.
• Anti-emesis
• Antibiotics: Depends on surgery e.g. cefuroxime + metronidazole for colorectal or biliary surgery.
• Anti-autonomic: B-blockers can be used to reduce risk of perioperative ischaemia.
• Steroids: Minor operations 25-50mg hydrocortisone IV at induction, major operations 50mg at induction then repeat 3 times 8 hourly before restarting oral. Ditto if adrenal insufficieny or adrenal surgery, or >10mg prednisolone/day over last 3m.
• Bronchodilators: E.g. salbutamol nebuliser.
• Anxiolytics and Amnesia: Amnesia may add to the unpleasantness of the experience, though it can be useful in those not wanting to know, and children.
  • The most common agents used are benzodiazepines. E.g. lorazepam 2mp PO, temazepam 10-30mg PO, diazepam 5mg PO. Some anaesthetists still use morphine 10mg IM (SE dysphoria) or atropine 0.6mg IM.
  • Children: Midazolam 0.5mg/kg (tastes bitter so often put in Calpol).
    Local anaesthetic creams for children: Tetracaine 4% applied 45min before inserting IVI.
    The presence of a parent at induction is more powerful than any premedication in reducing anxiety.

The patient should be aware of what will happen, where she will wake and how she will feel. Premedication aims to to allay anxiety and contribute to a smooth induction of anaesthesia by decreasing secretions (much less important than when ether was used), promoting amnesia and analgesia, and decreasing vagal reflexes.

Timing: 2h pre-op for oral drugs, 1h pre-op if IM.

Where does the oculomotor nerve like to get squashed?

Berry aneurysm at the junction between the posterior communicating artery and the internal carotid artery is an important cause of oculomotor nerve palsy.

The oculomotor nerve runs through the lateral wall of the cavernous sinus superiorly. It enters the cavernous sinus just above the petroclinoid ligament and inferior to the interclinoid ligament. Masses invading the cavernous sinus from within the sella are most likely to cause third cranial nerve dysfunction prior to involvement of the other cranial nerves in the cavernous sinus. This is probably because of the oculomotor nerve's close proximity to the unyielding interclinoid ligament above and the petroclinoid ligament below.

The axons for most of the muscles are uncrossed from the nucleus to the eye, but there are 2 exceptions: (1) Axons for the levator palpebrae come from both sides of the central caudal subnucleus via crossed and uncrossed pathways. (2) Those for the superior rectus muscle come from the superior rectus subnucleus on the contralateral side.

The pupillomotor and ciliary muscle neurons derive from the Edinger-Westphal subnucleus, which is in the midline in the most rostral and anterior part of the oculomotor nerve nucleus. These autonomic pathways are all ipsilateral or uncrossed.

From emedicine.

Kernig's sign

Positive when the leg is bent at the hip and knee at 90 degree angles, and subsequent further extension in the knee is painful (leading to resistance).

SAH

Rx: Renounce raw conceit; find notes, morphine and pennies.

Refer neurosurgery

Reexamine CNS often

Chart BP, pupils, GCS

Fluids: SBP >160 (HHT = hypertensive hypervolaemic therapy... because hypotension causes vasospasm).

Nimodipine. Start by day 4 (asap on diagnosis!) till day 21 - three weeks.

Morphine + laxatives (opiates cause constipation).

Angiography: Sensitivity: 4 vessel angiography > CTA > MRA

Procedures: Clipping (craniotomy) or coiling (endovascular).

Tests

• Angiogram: Sensitivity - 4 vessel angiography > CTA > MRA. CT detects >90% of SAHs.
• LP: If CT negative and no c/i >12h after headache onset.
  Early CSF uniformly bloody; later CSF shows xanthochromia.

S&S

• Thunderclap headache, vomiting, collapse, seizures, coma, neck stiffness, Kernig's sign, retinal or subhyaloid haemorrhage.
• Focal signs at presentation may suggest site of aneurysm (e.g. pupil change suggests CNIII palsy suggests PCA aneurysm).
• Sentinal headache due to small warning leak from the offending aneurysm.

DD of thunderclap headache = D SUMMIT V

Dissection of carotid/vertebral artery

SAH

Unknwon cause

Meningitis

Migraine

Intracerebral bleed

Thrombosis cortical vein

Valsalva maneuvre

Complications

1. Rebleed.
2. Vasospasm à stroke.
3. Hydrocephalus.
4. Hyponatraemia.

Prognosis

⅓ die immediately.

⅓ die within 1m from vasospasm or rebleed.

⅓ survive with or without neurological problems.

Grade I = No signs = 0% mortality.

Grade II = Necks stiffness, CN palsies = 11%.

Grade III = Drowsiness = 37%.

Grade IV = Drowsiness + hemiplegia = 71%.

Grade V = Prolonged coma = 100%.

Causes

Aneurysm rupture 80%.

AVM.

Unknown.

Risk factors

Smoking, hypertension, mycotic aneurysm, alcohol, bleeding disorder, low oestrogen (post-menopause).

Berry aneurysms are associated with:

1. Polycystic kidneys.
2. Coarctation of aorta.
3. Ehlers-Danlos syndrome.