Dysphagia For Medical Finals (based On Newcastle University Learning Outcomes)

Hospital Based Practice – Dysphagia. • • •

Always requires investigation to exclude malignancy. If symptoms are progressive or prolonged then urgent investigation is required. Causes. ○ Mechanical blockage  Malignant stricture. • Oesophageal cancer • Gastric cancer • Pharyngeal cancer  Benign strictures. • Oesophageal web or ring • Peptic stricture.  Extrinsic pressure. • Lung cancer

○

○

•

• •

Mediastinal lymph nodes

•

Aortic aneurysm

Retrosternal goitre

• Left atrail enlargement.  Pharyngeal pouch.  Oral Motility disorders  Achalasia  Diffuse oesophageal spasm  Systemic sclerosis  Myasthenia gravis  Bulbar palsy  Pseudobulbar palsy  Syringobulbia  Bulbar poliomyelitis  Chagas’ disease Others.  Oesophagitis • Infection ○ Candida ○ Herpes simplex • Reflux  Globus hystericus

Clinical features. ○ There are a number of key questions to ask.

1. Was it difficult to swallow liquids and solids from the start. • Yes:Motility disorder. • No: Stricture if solids became difficult first. 2.

3.

Is it difficult to initiate swallowing movement? • If yes, suspect bulbar palsy. • Especially if coughing on swallowing. Is swallowing painful? • If yes, suspect.

○

Cancer

○ Severe oesophagitis ○ ○

Achalasia Oesophageal spasm

4. Is dysphagia intermittent or constant, and is it getting worse? • Intermittent: Oesophageal spasm • Constant & worsening Suspect malignant stricture 5.

•

Signs. ○

○

○

Does the neck bulge or gurgle on drinking. • If yes, suspect pharyngeal pouch.

Look for  Cachecsia  Anaemia  Signs of systemic disease. • Systemic sclerosis • CNS disease Examine mouth. Feel for supraclavicular nodes.

 Virchow’s node (left supraclavicular) suggests intra – abdominal malignancy. •

Investigations. ○ FBC.  ○ U&E  ○ CXR.

Anaemia Dehydration

 Mediastinal fluid level. ○ ○ ○

 Absent gastric bubble  Aspiration Barium swallow ± video fluoroscopy. GI endoscopy + biopsy. Further investigations  Oesophageal manometry • If barium swallow is normal  ENT opinion • If suspected pharyngeal cause.

Diffuse oesophageal spasm.

•

Intermittent dysphagia.

•

Chest pain

•

Barium swallow. ○ Abnormal contraction. ○ Eg. Corkscrew oesophagus.

Achalasia.

• •

Failure of relaxion of lower oesophagus sphincter.

•

Clinical picture. ○ Dysphagia ○ Regurgitation ○ Substernal cramps

Due to degeneration of myenteric plexus.

○ Weihgt loss • •

Barium swallow. ○ Dilated tapering oesophagus. Treatment. ○ Endoscopic balloon dilatation. ○ Heller’s cardiomyotomy. + PPIs ○ Botulism toxin.

Benign oesophageal stricture. •

•

Caused by. ○ GORD ○ Corrosives ○ Surgery ○ Radiotherapy. Management. ○ Endoscopic balloon dilatation.

Paterson – Brown – Kelly/ Plummer – Vinson syndrome •

Post – cricoids web + iron – deficiency.

Anti – emetics. Receptor H1 D2

Antagonist Cyclizine Cinnarizine Metoclopramide

Notes GI causes Vestibular disorders GI causes

5HT3

Domperidones Prochlorperazine Haloperidol Ondansetron

Prokinetic Prokinetic Vestibular & GI causes Chemical causes, eg. Opioids Can use high doses.

Others

Hyoscine butylbromide

Eg. For emetogenic chemotherapy. Antimuscarinic. Hence, antispasmodic and antisecretory.

Dexamethasone

Don’t give with a prokinetic. Unknown mode of action

Midazolam

Used as adjuvant therapy. Unknown action. Anti – emetic effect outlasts sedative effect.

Gastro – oesophageal Reflux Disease. • •

•

•

Dysfunction of the lower oesophageal sphincter predisposes to acid reflux. If reflux is prolonged or excessive, it may cause: ○ Oesophaitis ○ Benign oesophageal stricture ○ Barrett’s oesophagus. Associations. ○ Smoking ○ Alcohol ○ Hiatus hernia ○ Pregnancy ○ Obesity ○ Large meals ○ Achalasia surgery. ○ Drugs.  Tricyclics  Anticholinergics  Nitrates ○ Systemic sclerosis ○ H. pylori

Symptoms.

○

○ ○

○ ○ ○

Heartburn.  Burning  Retrosternal discomfort.  Related to meals  Exacerbated by. • Lying down • Stooping • STraining  Relieved by antacids. Belching Acid brush.  Acid or bile regurgitation. Waterbrush.  Excessive salivation. Odynophagia.  Painful swallowing Nocturnal asthma.  Cough  Wheeze  Minimal aspiration of gastric contents.

•

Differential diagnoses. ○ Oesophagitis  Corrosives  NSAIDs ○ Infection.  CMV  Herpes  Candida ○ Peptic ulcer ○ Gastric cancer ○ Non – ulcer dyspepsia.

•

Complications ○ Oesophagitis ○ Ulcers ○ Benign stricture ○ Barrett’s oesophagus ○ Oesophageal adenocarcinoma ○ Iron deficiency anaemia.  Rarely.

•

Investigations. ○ Isolated symptoms don’t require investigation. ○ Indication for upper GI endoscopy.  Age > 55  Symptoms > 4 weeks  Dysphagia  Persistent symptomsin spite of treatment

○

○

○

•

 Relapsing symptoms  Weight loss Barium swallow may show hiatus hernia. 24 hour oesophageal pH monitoring ± oesophageal manometry help diagnose GORD.  Use if endoscopy is normal

Endoscopic classification.  According to Los Angeles classification.  The term mucosal break describes a well demarcated area of slough or erythema • Covers old classification of erosion and ulceration. 1. One or more mucosal breaks < 5 mm long. Doesn’t extend beyond 2 mucosal folds. 2. Mucosal breaks > 5 mm long. Limited to the space between 2 mucosal fold tops. 3. Mucosal break continuous between the tops of 2 or more mucosal folds. Involves less than 75% of the oesophageal circumference. 4. Mucosal break involving > 75% of oesophageal circumference.  Grading can be useful, but it is important to also document the qualitative findings of endoscopy.  Also record any complications of GORD.

Treatment. ○ Lifestyle.  Encourage. • Weight loss • Smoking cessation • Small, regular meals  Avoid. • Hot drinks • Alcohol • Eating within 3 hours of bed. • Drugs reducing oesophageal motility. ○ Nitrates ○ Anticholinergics ○ Tricyclics ○ Caclium channel blockers •

Drugs that damage oesophageal mucosa. ○ NSAIDs. ○ Potassium salts ○ Bisphosphonates. Raise head of bed.

○

 Drugs.  Antacids.



○

○ ○

•

Magnesium trisilicate mixture (Gaviscon).

• •

If oesophagitis confirmed on endoscopy.

PPI

Eg. Lanzoprazole. Refer for endoscopy if.  Symptoms persist for > 4 weeks.  Weight loss  Dysphagia  Excessive vomiting  GI bleeding Prokinetic drugs.  Encourage gastric emptying  Eg. Metoclopramide. Surgery  Eg. Nissen fundoscopy.  Not indicated unless • Symptoms are severe • Resistant to medical therapy. • Severe reflux on pH monitoring.  Laparoscopic repairs are gaining favour.

Motor Neurone Disease. •

• •

Caused by degeneration of neurones ○ Motor cortex ○ Cranial nerve nuclei ○ Anterior horn cells. Upper and lower motor neurones are affected. No sensory loss or sphincter disturbances. ○ Distinguishes from MS and polyneuropathies.

•

No affect on external eye movements. ○ Distinguishes from myasthenia gravis.

•

Fronto – temporal dementia is seen in 10 – 35%.

•

Prevelence of 7:10000 ○ Male: Female ratio of 3:2 ○ Up to 10% of cases are familial.

•

Cause is unknown. ○ As affects anterior horn cells in the same way as polio, is thought that viruses may be implicated. ○ Higher levels of oxidative damage from free radicals are found in MND brains than normal brains.  Also, MND more sensitive to free radicals causing damage than normal brian.  Affect motor neurons preferentially due to • Long length free to be attacked • Lower levels of protective calcium – buffering proteins

○ ○

Oxidative damage has not yet been fully shown to be the cause of MND. No diagnostic tests, but 3 clinical patterns.

○

Bulbar palsy.  Palsy of. • Tongue • Chewing muscles • Swallowing muscles • Facial muscles  Due to loss of motor nuclei function in the medulla.  Signs include. • LMN lesions. ○ Flaccidity ○ Fasiculating tongue.  Like “sack of worms”



•

Jaw jerk may be normal or absent.

•

Speech is. ○ Quiet ○ Hoarse ○ Nasal

Causes. • MND

•

Gullian – Barre

• • •

Polio Syringobulbia Brainstem tumours

•

○

Central pontine myelinolysis ○ Malnourished alcoholics ○ Rapid correction of hyponatraemia ○ Causes  Progressive and fatal quadriparesi  Mutism  Dysarthria  Bulbar palsy ○ Recovery can occur Amyotrophic lateral sclerosis.  50% of cases.  Combined LMN wasting and UMN signs. • Loss of fine finger movement. • Spasticity ○ Arm flexors ○ Leg extensors • Hyperreflexia

•  

Upgoing plantars

• Clonus Risk doubled in Gulf war veterans Possibly due to copper/ zinc superoxide dismutase (SOD1) mutations.

○

• • •

•

• •

•

Progressive muscular atrophy.  25% of cases.  Anterior horn cell lesions  Affect distal muscles before proximal ones.  Better prognosis than ALS.

Think of MND in those > 40 with stumbling. ○ May be due to spastic gait or foot drop. Also consider in unexplained aspiration pneumonia. Look for UMN signs. ○ Weakness ○ Spasticity ○ Brisk reflexes ○ Upgoing plantars Look for LMN signs. ○ Weakness ○ Muscle wasting ○ Fasiculation.  Tongue  Abdomen  Back  Thighs Consider if speech or swallow is affected. MND strongly suggested in patients with a mixture of progressive UMN and LMN signs. ○ If affecting 2 limbs ○ If affecting 1 limb and bulbar muscles. ○ Fasiculation alone is not enough to diagnose LMN lesion, also requires weakness. Investigations. ○ Tend to rule out other differentials. ○ MRI of brain and cord helps eliminate structural causes. ○ Lumbar puncture helps eliminate inflammatory causes. ○ Neurophysiology helps exclude motor neuropathies. Can detect subclinical denervation.

•

Treatment. ○ MDT approach is best due to MND rapid course and relative rarity. ○ Antiglutamate drugs.

 Riluzole. • • • •

•

○ ○

○ ○ ○

Inhibits glutamate release. Prolongs life by about 3 months. Expensive. Be cautious in liver disease. ○ Check LFTs monthly for 3 months, then 3 monthly for 9 months, then annually. Side effects. ○ Vomiting ○ Weakness ○ Tachycardia ○ Somnolence ○ HEadahce ○ Dizziness ○ Vertigo ○ Pain ○ Raised LFTs.

Vitamin E  As antioxidant, may reducerisk of developing MND by 50% Anti – drooling.  Propantheline  Amitriptyline Anti – dysphagia.  Pureed foods  Consider NG tube or PEG. Anti – spasticity.  As for MS. Respiratory failure & sleep apnoea.  NIV at home may give valuable palliation.

Why do anti – glutamate drugs work in MND. • •

Glutamate is chief excitatory neurotransmitter. MND brains tend to have higher than normal levels of glutamate. ○ Reduced activity of excitatory amino acid transporter, EAAT2, which ‘mops up’ glutamate. ○ High levels may be neurotoxic.

•

Prognosis ○ Incurable ○ Often fatal within 5 years. ○ Median age at death in UK is 60 years. ○ With bulbar disease, prognosis is to survive only about 1.5 years. ○ Death from choking is rare/



Reassure patients that a dignified death is the norm.